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COMPARATIVE CLINICAL STUDY TO EVALUATE THE EFFICACY OF NASYA AND VIRECHANA IN THE MANAGEMENT OF HBV INDUCED JAUNDICE BY DR. JEEVAN K. JOSE B.A.M.S Dissertation submitted to the Rajiv Gandhi University of Health Sciences, Bangalore, In Partial fulfillment of the requirements for the degree of DOCTOR OF MEDICINE (AYURVEDA) IN PANCHAKARMA Under the Guidance of DR.PRASHANTH.A.S M.D (Ay), Ph.D., MHA, PGMH PROFESSOR DEPARTMENT OF POST GRADUATE STUDIES IN PANCHAKARMA, AYURVEDA MAHAVIDYALAYA, HUBLI. Co-Guide DR.PADMAVATHI VENKATESH M.D (Ay) ASST. PROFESSOR DEPARTMENT OF POST GRADUATE STUDIES IN PANCHAKARMA AYURVEDA MAHAVIDYALAYA, HUBLI - 580024 DEPARTMENT OF POST GRADUATE STUDIES IN PANCHAKARMA AYURVEDA MAHAVIDYALAYA, HUBLI 2014

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COMPARATIVE CLINICAL STUDY TO EVALUATE THE

EFFICACY OF NASYA AND VIRECHANA IN THE

MANAGEMENT OF HBV INDUCED JAUNDICE

BY

DR. JEEVAN K. JOSE B.A.M.S

Dissertation submitted to the

Rajiv Gandhi University of Health Sciences, Bangalore,

In Partial fulfillment of the requirements for the degree of

DOCTOR OF MEDICINE (AYURVEDA)

IN

PANCHAKARMA

Under the Guidance of

DR.PRASHANTH.A.S

M.D (Ay), Ph.D., MHA, PGMH

PROFESSOR

DEPARTMENT OF POST GRADUATE STUDIES IN PANCHAKARMA,

AYURVEDA MAHAVIDYALAYA, HUBLI.

Co-Guide

DR.PADMAVATHI VENKATESH

M.D (Ay)

ASST. PROFESSOR

DEPARTMENT OF POST GRADUATE STUDIES IN PANCHAKARMA

AYURVEDA MAHAVIDYALAYA, HUBLI - 580024

DEPARTMENT OF POST GRADUATE STUDIES IN PANCHAKARMA

AYURVEDA MAHAVIDYALAYA, HUBLI

2014

DEPARTMENT OF POST GRADUATE

STUDIES IN PANCHAKARMA AYURVEDA MAHAVIDYALAYA, HUBLI

DECLARATION BY THE CANDIDATE

I hereby declare that this dissertation entitled

COMPARATIVE CLINICAL STUDY TO EVALUATE THE

EFFICACY OF NASYA AND VIRECHANA IN THE

MANAGEMENT OF HBV INDUCED JAUNDICE is a bonafide and

genuine research work carried out by me under the guidance of DR. A. S.

PRASHANTH, M.D. (Ayu) Ph.D., Professor, Department of Post-Graduate

studies in Panchakarma, AYURVEDA MAHAVIDYALAYA, HUBLI.

Date:

Place: Hubli

DR. JEEVAN K. JOSE.

P.G. SCHOLAR

DEPARTMENT OF POST-GRADUATE

STUDIES IN PANCHAKARMA

AYURVEDA MAHAVIDYALAYA,

HUBLI, KARNATAKA

DEPARTMENT OF POST GRADUATE

STUDIES IN PANCHAKARMA,

AYURVEDA MAHAVIDYALAYA, HUBLI

Certificate

This is to certify that the dissertation entitled COMPARATIVE

CLINICAL STUDY TO EVALUATE THE EFFICACY OF NASYA

AND VIRECHANA IN THE MANAGEMENT OF HBV INDUCED

JAUNDICE is a bonafide research work done by DR. JEEVAN K.

JOSE , under the guidance of DR. A. S. PRASANTH, M.D. (AYU) PH.D.,

PROFESSOR, Department of Post-Graduate studies in Panchakarma,

Ayurveda Mahavidyalaya, Hubli.

Date:

Place: Hubli

H.O.D. DR. A. I. SANAKAL M.D. (Ayu)

Professor and Head

Department of Post-Graduate studies in Panchakarma,

Ayurveda Mahavidyalaya, Hubli, Karnataka

DEPARTMENT OF POST GRADUATE

STUDIES IN PANCHAKARMA

AYURVEDA MAHAVIDYALAYA, HUBLI

Certificate

This is to certify that the dissertation entitled COMPARATIVE

CLINICAL STUDY TO EVALUATE THE EFFICACY OF NASYA

AND VIRECHANA IN THE MANAGEMENT OF HBV INDUCED

JAUNDICE is a bonafide research work done by DR.JEEVAN K.

JOSE., in partial fulfillment of the requirement for the degree of

DOCTOR OF MEDICINE (AYURVEDA) in PANCHAKARMA.

Date:

Place: Hubli

Guide

DR. A. S. PRASANTH M.D. (Ayu) Ph.D. MHA, PGMH

Professor

Department of Post-Graduate studies in Panchakarma,

Ayurveda Mahavidyalaya, Hubli, Karnataka

DEPARTMENT OF POST GRADUATE

STUDIES IN PANCHAKARMA

AYURVEDA MAHAVIDYALAYA, HUBLI

Certificate

This is to certify that the dissertation entitled COMPARATIVE

CLINICAL STUDY TO EVALUATE THE EFFICACY OF NASYA

AND VIRECHANA IN THE MANAGEMENT OF HBV INDUCED

JAUNDICE is a bonafide research work done by DR.JEEVAN K.

JOSE, in partial fulfillment of the requirement for the degree of

DOCTOR OF MEDICINE (AYURVEDA) in PANCHAKARMA.

Date:

Place: Hubli

Co-Guide

Dr.PADMAVATHI VENKATESH M.D. (Ayu)

Lecturer,

Department of Post-Graduate studies in Panchakarma,

Ayurveda Mahavidyalaya, Hubli, Karnataka

DEPARTMENT OF POST GRADUATE

STUDIES IN PANCHAKARMA

AYURVEDA MAHAVIDYALAYA, HUBLI

Certificate

This is to certify that the dissertation entitled COMPARATIVE

CLINICAL STUDY TO EVALUATE THE EFFICACY OF NASYA

AND VIRECHANA IN THE MANAGEMENT OF HBV INDUCED

JAUNDICE is a bonafied research work done by DR. JEEVAN K. JOSE.

under the guidance of DR. A. S. PRASANTH, M.D. (AYU) PH.D. ,

PROFESSOR, Department of Post-Graduate studies in Panchakarma,

Ayurveda Mahavidyalaya, Hubli.

Date:

Place: Hubli

PRINCIPAL

DR. P. G. SUBBANAGOWDA

MD (Ayu) P.G.C.R

AYURVEDA MAHAVIDYALAYA,

HUBLI, KARNATAKA

COPYRIGHT

DECLARATION BY THE CANDIDATE

I, DR. JEEVAN K. JOSE., hereby declare that the Rajiv Gandhi

University of Health Sciences, Karnataka shall have the rights to preserve,

use and disseminate this dissertation / thesis in print or electronic format

for academic / research purpose.

Date:

Place: Hubli

DR. JEEVAN K. JOSE

P.G. SCHOLAR

DEPARTMENT OF POST-GRADUATE

STUDIES IN PANCHAKARMA

AYURVEDA MAHAVIDYALAYA,

HUBLI, KARNATAKA

© Rajiv Gandhi University of health sciences, Karnataka

A C K N O W L E D G E M E N T P a g e | I

Comparative clinical study to evaluate the efficacy of Nasya and Virechana in the

management of HBV induced Jaundice

ACKNOWLEDGEMENT

On the occasion of successful accomplishment of this work, I bow down to

Lord Dhanvantari, whose blessings made me to learn and work in the field of

Ayurveda.

I would like to Express My Profound Respect and Deepest Gratitude,

Courtesy, To The Most Dynamic Paragon, Exceedingly Precious Dr. Prashanth A.S.

M.D. (Ayu) PHD, Professor, Department of PG Studies in Panchakarma. His

Collaboration, Out Rightness, Keen Observation, Valuable Suggestions, Inspiring

Spirits, Paternal Affection and Close Involvement with this work gave me

considerable confidence to accelerate and complete my work.

I Express My Profound Gratitude From The Core of My Heart To Dr.

A.I.Sanakal MD. (Ayu) Sir, Professor and Head, Department of PG studies in

Panchakarma, , for His Eminent Guidance, Constant Encouragement Throughout My

Course of Study.

I am really grateful to my Co-Guide Dr. Padmavthi Venkatesh M.D (Ayu) for

her untiresome guidance throughout the study.

It is very difficult to find a vocabulary to appraise My Sincere and Hearty

Gratitude to my beloved and respected teachers Dr. B.B.Hungund, Dr. Shrivatsa

Navalur for their valuable suggestions and timely guidance benefited me in

completing this thesis work.

I extend my gratefulness and heartfelt thanks to Ex-Principal Dr. S.J.

Deshpande for their encouragement and help. I extend my gratefulness and heartfelt

thanks to Principal Dr. P.G. Subbanna Gowda, and Dean of P.G. Studies, Dr. S.K.

Bannigol for their timely support.

I would also feel a great pleasure to thank Dr. B.B. Joshi, Professor& Head.

Dept. of Rasa Shastra & Bhaishajya Kalpana, Dr. J.R. Joshi Professor & Head,

Dept. of Moulika Siddhanta and Dr. M.A. Hullur, Professor and Head, Dept. of

Kayachikitsa for their inspirational support & guidance throughout my study.

I take this opportunity to thank, Dr. Mahesh Desai, Dr. S.A. Patil, Dr.

Prabhu Tashin, Dr. Gourish for his continuous helping hand and for their support in

making Statistical Data and Dr. K.M Jaggal, Dr. Agnihotri, Dr. Anita for guidance

A C K N O W L E D G E M E N T P a g e | II

Comparative clinical study to evaluate the efficacy of Nasya and Virechana in the

management of HBV induced Jaundice

during the preparation of my clinical trial drugs.

I am also thankful to Physicians of Ayurveda Mahavidyalaya & Hospital,

Hubli, who supported me throughout my study.

It was not possible to complete this work without Patients therefore I am very

much great full to each and every patient who co-operated me for this work.

I acknowledge my revered seniors Dr. Hari, Dr. Krishnakumar, Dr .Ashok,

Dr. Kiranath, Dr. Sandeep, and Dr. Pratibha, for assisted me to entire my work.

I am thankful to my batch mates Dr. Ganesh Namboothiri, Dr. Ranjith R

Warrier, Dr.Suraj D., Dr. Arun Mohan, Dr. Sridhar Badgal, Dr. Abhinav Rathore,

Dr. Abhishek Kaushal, Dr. Swapnil Dhoran, Dr.Ritesh, Dr. Hemanth, Dr.

Devendra, Dr. Divya D., Dr. Divya K., Dr. Mumtaz, Dr. Shashikant, Dr. Raygonda,

Dr. Sourabh, Dr.Chaitra, Dr. Dinesh, Dr. Nikita. Their timely support helped me a

lot to overcome the device of hindrances in my research work, let it be physical or

intellectual.

I extend my gratefulness and heartfelt thanks to All Lovely Juniors especially

Dr. Sanjay, Dr. Gautam , Dr. Aswathy, Dr. Vishnu, Dr. Sneha, Dr. Priyadarshini, ,

Dr. Ashwini, Dr. Shrihari, Dr. Rachangouda, Dr. Lokendra, Dr. Rashmi, Dr.

Shaila, Dr. Deepika, Dr. Sandeep, Dr.Sameer for their timely support.

It is my pleasure to thank Mr. Rajashekar, Librarian, PG Library and Mr.

Prashant, Librarian of UG Library, Mr. Prabhakar, Mr.Venkatesh and all staffs of

College and Hospital, Ayurveda Mahavidyalaya, Hubli.

I am thankful to All the Students of BAMS, College and Hospital staff,

Ayurveda Mahavidyalaya, Hubli.

Thanks to family might seem strange but without their support and love I

would not complete my studies successfully.

Shri. Jose T. Kuttikattu and Mrs. Valsamma Jose Kuttikattu – My Father

and Mother deserve special mention for the inspirational support and guidance it is

only because of their that I have reached this stage in my life, I also dedicate this

work to them.

I would also feel a great pleasure to thank My Grandfather, My

Grandmother (Maternal and Paternal) and all other Family members for their

advices, love and affection.

A C K N O W L E D G E M E N T P a g e | III

Comparative clinical study to evaluate the efficacy of Nasya and Virechana in the

management of HBV induced Jaundice

I fail in my duty if I don’t recall My Idol & Brother Mr. Joval K. Jose, My

Sister-in-law Mrs. Sawmya, Baby Joanna and all other Brothers and Sisters for

their inspirational support.

I feel proud in expressing my sincere gratitude to my best friends who not

only helped me each and every step of my study but stood by me during hours of stress

and dejection.

At this moment I cannot forget my B.A.M.S teachers especially Dr.Rethnakar

MD (Ayu), Dr.Shukkoor MD (Ayu), Dr.Roshini MD (Ayu), Dr.Sreeja MD (Ayu),

Dr.Sethu MD (Ayu), Dr.Remani Bai MD (Ayu), Dr.Prasanna MD (Ayu),

Dr.Sarasa MD (Ayu), Dr.Remani K. K. MD (Ayu), Dr.Ravishankar MD (Ayu),

Jayaprakash M.A (Sanskrit), and my UG Batchmates Dr. Laljish, Dr. Kishor R, Dr.

Jery Joji, Dr. Akhil C., Dr. Jinoop P., Dr. Mohd. Anwar, Dr. Hariprasad P., Dr.

Hemesh, Dr. Nahasudeen, Dr.Sonia., Dr.Bardisha and Dr. Neema for their

inspiration and moral support.

Last but not least I express my thanks to each and every person, who has

given their “Pound of flesh” in accomplishing this task without any blemishes.

I apologize for errors and short comings of the work.

PLACE: HUBLI

DATE: DR. JEEVAN K. JOSE

L I S T O F A B B R E V I A T I O N P a g e | IV

Comparative clinical study to evaluate the efficacy of Nasya and Virechana in the

management of HBV induced Jaundice

LIST OF ABBREVIATIONS

1. Ath.Ve. - Atharva veda

2. Rig.ve. - Rigveda

3. Sh.K. - Shabdha Koustabha

4. Ch. - Charaka Samhita

5. S.S. - Sushruta Samhita

6. Su. - Sutrasthana

7. Ch.Kr. - Chakrapani Datta

8. M.M.W. - Monier Williams

9. Sh.M. - Shabdha sthana Mahanidhi

10. Sh.Ki. - Shabdha Kalpadruma

11. Va. - Vachaspatya

12. U. - Uttar tantra

13. Ah.Hr. - Asthang Hridaya

14. Ni. - Nidana sthana

15. Chi. - Chikitsa sthana

16. M.K. - Madhukosh Vyakhya

17. Ma.Ni. - Madhava Nidana

18. Y.R. - Yoga Ratnakara

19. Ch.D. - Chakradatta

20. Br.Ni.Ra. - Brihat Nighantu Ratnakar

21. Br.Yo.Ta. - Brihat Yoga Tarangini

22. Dh.Ni. - Dhanwantari Nighantu

23. Ra.Ni. - Raja Nighantu

24. Bh.Pr. - Bhavaprakash

25. Ma.Vi.Ni. - Madana Vinoda Nighantu

26. Ky.Ni. - Kaiydev Nighantu

27. B.R. - Bhaishajya Ratnavalli

28. R.R.S. - Rasa Ratna Samuchaya

29. V.K. - Vaidya Kalpadruma

A B S T R A C T P a g e | VI

Comparative clinical study to evaluate the efficacy of Nasya and Virechana in the

management of HBV induced Jaundice

ABSTRACT

The present clinical study, entitled as, “Comaparitive Clinical Study To

Evaluate The Efficacy Of Nasya And Virechana In The Management Of HBV

Induced Jaundice”, was completed and the details of the study are presented in this

dissertation.

Hepatitis B is one of the major problems Worldwide in medicine, which can

produce Jaundice severely. Hepatitis B is claimed to be 100-200 times more

infectious than AIDS and results in approximately one million deaths each year,

making it the World’s Tenth leading cause of death.

It is also observed that the drug belongs to Cucurbitaciae family (Luffa

species), and some of the Upavisha dravyas are getting absorbed from a particular site

in the body and getting resecreted from the same site. Jimutaka is a magic drug if

instilled through the nostrils getting absorbed through the mucosa of nasopharynx and

getting resecreted from the same site along with mucopolypeptides, bile and other

accumulated enzymes.

Virechaka dravya are mainly irritants. They induce mild inflammatory

changes on the digestive mucosa and localized tissues.Owing to the increased

permeability of the membranes the transportation and excretion of the waste materials

takes place easily. Most of the Drugs in Patolamooladi Kashaya have Madhura, Katu

Thikta Rasa, Ushna Veerya, Laghu, Snigdha, Sara, Vikashi, Tikshna Guna, and

Madhura Vipaka. Most of the Drugs are Raktashodaka, Pithasaraka,and Deepana.

Patola, Brahmi Katuki, Visala, and Hareetaki which are present in Kashaya have

Bhedana property which are the main drugs acting in Virechana Karma. All the other

drugs are supporting drugs in Amapachana or Pithasamana.

In the present study, subjects suffering from HBV induced Jaundiced were

selected and investigated. However inclusion thoroughly examined and randomly

divided into two groups namely Group A and Group B.

In Group – A, Amapachana with Hareetakyadi Yoga (5-10 gms) for 3-

5 days was given. Mukhabhyanga with Taila and Baashpa sweda was performed

initially as Poorva Karma followed by Pradhana karma Nasya with Jeemoothaka

phala swarasa for 7 days initially followed by 14 days of Parihara Kala. Then one

more course of Nasya with the same swarasa for 7 days after which 14 days of

A B S T R A C T P a g e | VII

Comparative clinical study to evaluate the efficacy of Nasya and Virechana in the

management of HBV induced Jaundice

Parihara Kala was followed again. During course of Parihara Kala internally

Nimbatwakadi Kashaya(45-60ml), was given as Shamanoushadhi.

In Group – B, Amapachana with Hareetakyadi Yoga (5-10 gms) for

3-5 days was given followed by Snigdha bhojana (Eshad pramana of Goghrita along

with Ahara), only for 3 days was advised as a part of Poorva Karma. Bahya Prayoga

of Murchita Tila Taila in the form of Mrudu Abhyanga was suggested to the patients.

Sukhoshna Jala Snana was followed later as a part of Parisheka Sweda. Virechana

with Patolamooladi Kashaya(60-90 ml) and 3 days of samsarjana krama initially

followed by 14 days of Parihara Kala. Then one more course of virechana with the

same medicine and samsarjana karma for 3 days after which 14 days of Parihara Kala

was followed again. During course of Parihara Kala internally Nimbatwakadi

Kashaya(45-60ml), was given as Shamanoushadhi.

Comparing the total response of Therapy and Parameters of both groups in this

study, Group A and Group B showed similar results. The mean difference and

corresponding percentage reduction shows Nasya and Virechana are highly effective

in the treatment of Hepatitis B Virus induced Jaundice.

Thus it can be stated that Jeemootaka Nasya and Virechana with

Patolamooladi kashaya along with Nimbatwakadi Kashaya as Shamana Aushadi are

excellent methods of managing Hepatitis Virus induced Jaundice.

Keywords: Kamala, Hepatitis B Virus induced Jaundice, Nimbatwakadi kashaya,

Patolamooladi kashaya, Jeemootakaphala Nasya, .

T A B L E O F C O N T E N T S P a g e | VIII

Comparative clinical study to evaluate the efficacy of Nasya and Virechana in the

management of HBV induced Jaundice

TABLE OF CONTENTS

Acknowledgement

Abbreviations

Abstract

List of Tables, Graphs and Figures

1. Introduction………………………………………………… 1 – 3

2. Objectives of the Study …………………………………….. 4

3. Previous works done ....…………………………………….. 5

4. Review of Literature………………………………………… 6-158

5. Drug review…………………………………………………. 159-162

6. Methodology………………………………………………… 163-176

7. Observations and Results……………………………………. 177-220

8. Discussion…………………………………………………… 221-251

9. Conclusion…………………………………………………… 252-254

10. Summary…………………………………………………….. 255-256

11. References & Bibliography ……………………………….... 257-263

Annexure

a. Case Proforma with consent form

b. Master chart

T A B L E O F C O N T E N T P a g e | IX

LIST OF TABLES

Sl.No Contents Page

No.

1. Various Parts Of Drugs Used For Nasya 17

2. Classification Of Nasya According To Various Acharyas 20

3. Dose Of Sneha Nasya 21

4. Dose Of Shodhana Nasya 22

5. Time Of Administration Of Nasya According To Season 22

6. Time Of Administration Of Navana Nasya According To

Season

22

7. Dose Of Shirovirechana And Avapida Nasya 23

8. Indications Ofavapida Nasya 23

9. Length Of Nadi According To The Types Of Dhuma Nasya 25

10. Drugs For Of Dhuma Nasya 25

11. Indications Of Pratimarsha Nasya 26

12. Contraindications Of Pratimarsha Nasya 26

13. Various Timings For Pratimarsha Nasya According To

Acharyas

26

14. General Indications Of Nasya 30

15. General Contraindications Of Nasya 31

16. Time Schedule Based On Doshic Involvement (Kala Of Nasya) 32

17. Time Schedule Based On Different Seasons 32

18. Course Of Nasya Karma 33

19. Showing Dosage Of Nasya Karma 33

20. Difference In Opinions In Nasya Procedure 35

21. Samyakyoga Lakshana Of Shirovirechana 36

22. Samyak Yoga Lakshana Of Nasya 36

23. Heena Yoga Of Shirovirechana 36

24. Heena Yoga Of Nasya 37

25. Atiyoga Of Shirovirechana 38

26. Atiyoga Of Nasya 38

27. Vyapat Of Nasya 39

T A B L E O F C O N T E N T P a g e | X

28. Nasya Vyapat And Complication 41

29. Treatment For Vyapat Of Nasya 41

30. Parts Used For Virechana- Plant Orgin 45

31. Virechana Drugs According To Seasons 48

32. Some Of The Agrya Drugs Mentioned In Classics 48

33. According To Sushruta 48

34. Virechna Drug According To Prakriti 49

35. Virechana Drug According To Dosha 49

36. Indications Of Virechana Karma 52

37. Contraindications Of Virechana Karma 53

38. Samyak Yoga Lakshanas Of Virechana Karma 63

39. Ayoga Lakshanas Of Virechana Karma 64

40. Atiyoga Lakshanas Of Virechana Karma 65

41. Samsarjana Karma 70

42. Showing Paittika (Pitta Vardhaka) Ahara Which Acts As

Nidana For Kostasrita Kāmalā

94

43. Showing Paittika (Pitta Vardhaka) Viharas Which Acts As

Nidana For Kostasrita Kāmalā

94

44. Showing The Comparision Of Lakshanas Of Shahkashrita

Kamala And Prodromal Symptoms Of Hepatitis-B

95

45. Lakshana Of Kamala Roga According To Different Acharyas 108

46. The Arishta Lakshanas Of Kumbha Kamala 118

47. Risks Of Occupational Groups 140

48. Showing The Comparison Of Histopathological Changes In

Different Types Of Viral Hepatitis

142

49. Jeemootaka Phala For Nasya 160

50. Patolamooladi Kashaya For Virechana 160

51. Nimbatwakadi Kashaya As Shamana Aushadi 161

52. Hareetakyadi Choorna For Amapachana 170

53. Showing The Incidence Of Sex In The Subjects Of Hbv Induced

Jaundice

177

54. Group A - Showing The Incidence Of Age In The Subjects Of

Hbv Induced Jaundice

177

T A B L E O F C O N T E N T P a g e | XI

55. Group B - Showing The Incidence Of Age In The Subjects Of

Hbv Induced Jaundice

178

56. Showing The Incidence Of AGE In The Subjects Of Hbv

Induced Jaundice

178

57. Showing The Incidence Of Religion In The Subjects Of Hbv

Induced Jaundice:

179

58. Showing The Incidence Of Marital Status In The Subjects Of

Hbv Induced Jaundice:

179

59. Showing The Incidence Of Habitat In The Subjects Of Hbv

Induced Jaundice:

180

60. Showing The Incidence Of Food Habits In The Subjects Of

Hbv Induced Jaundice:

180

61. Showing The Incidence Of Duration Of Illness The Subjects Of

Hbv Induced Jaundice

181

62. Showing The Incidence Of Socio-Economic Status In The

Subjects Of Hbv Induced Jaundice

182

63. Showing The Incidence Of History Of Previous Treatment

Received In The Subjects Of Hbv Induced Jaundice

182

64. Showing The History Of Hepatitis B Vaccine Received In The

Subjects Of Hbv Induced Jaundice

183

65. Showing The Incidence Of Education In The Subjects Of Hbv

Induced Jaundice:

183

66. Showing The Incidence Of Habits In The Subjects Of Hbv

Induced Jaundice:

184

67. Showing The Incidence Of State Of Agni In The Subjects Of

Hbv Induced Jaundice

184

68. Showing The Incidence Of Nature Of Koshta In The Subjects

Of Hbv Induced Jaundice

184

69. Showing Dominent Rasa Wise Diet Of 30 Subjects Of Kamala 185

70. Showing Dominent Guna Wise Diet Of 30 Subjects Of Kamla 185

71. Showing The Incidence Of Deha Prakruti In The Subjects Of

Hbv Induced Jaundice

186

T A B L E O F C O N T E N T P a g e | XII

72. Showing The Incidence Of Aetiological Factors In The Subjects

Of Hbv Induced Jaundice

186

73. Showing The Incidence Of Occupation In The Subjects Of Hbv

Induced Jaundice

187

74. Showing The Incidence Of Poorva Roopa In The Subjects Of

Hbv Induced Jaundice

188

75. - Showing The Incidence Of Symptomatology (Roopa) In The

Subjects Of Hbv Induced Jaundice

189

76. Showing The Incidence Of Objective Parameters / Invetigations

In The Subjects Of Hbv Induced Jaundice

190

77. Nasya Karma Observation Chart In 15 Subjects Of Kamala 191

78. Parameters Of Nasya Observed In 15 Subjects Of Kamala 191

79. Complication Observed In Nasya Karma In 15 Subjects Of

Kamala

191

80. Average Time Taken To Relieve Complication Observed In

Nasya Karma In 15 Subjects Of Kamala

192

81. Showing B.P And Pulse Reported Before And After Nasya

Karma

192

82. Virechana Karma Observation Chart In 15 Subjects Of

Kamala

192

83. Assessment Of Virechana In 15 Subjects Of Kamala 193

84. Virechana Sudhi Lakshanas Wise Distribution Of 15 Subjects

Of Kamala

193

85. Complication Observed In Virechana Karma In 15 Subjects Of

Kamala

194

86. Samyak Virechana Lakshan Observed In 15 Subjects Of

Kamala

194

87. B.P And Pulse Reported Before And After Virechana Karma 194

88. Results Of Symptom Relief In Group A (Nasya): 204

89. Results Of Symptom Relief In Group B (Virechana) 207

90. Results Of Biochemical And Other Objective Parameters In

Group A (Nasya):

210

91. Results Of Bio-Chemical And Other Objective Parameters In 211

T A B L E O F C O N T E N T P a g e | XIII

Group B (Virechana)

92. Results Of Test For Hbsag (Hbv) By Hepacard Method In

Group A (Nasya) And Group B (Virechana)

213

93. Group A Showing Sr.Bilirubin (Total) Before And After Nasya 213

94. Group B Showing Sr.Bilirubin (Total) Before And After

Virechana

214

95. Total Response Of Therapy (Objective Parameters) In Group

A And Group B

214

96. Comparative Efficacy Of Therapies On Assessment Parameters

In Group A And Group B Using Unpaired Student ‘T’ Test:

215

97. Total Response Of Therapy (Subjective Parameters) In Group

A And B

220

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HBV induced Jaundice

LIST OF FIGURES

SL.NO FIGURES

1. NIMBATWAKADI KASHAYA

2. PATOLAMOOLADI KASHAYA

3. JEEMOOTHAKAPHALA FOR NASYA

4. ANATOMY AND HISTOLOGY OF LIVER

5. STUCTURE OF HBV

P a g e | XV

LIST OF GRAPHS

Sl.No Contents Page

No.

1. Showing The Incidence Of Sex In The Subjects Of Hbv Induced

Jaundice

194

2. Group A - Showing The Incidence Of Age In The Subjects Of

Hbv Induced Jaundice

194

3. Group B - Showing The Incidence Of Age In The Subjects Of

Hbv Induced Jaundice

194

4. Showing The Incidence Of AGE In The Subjects Of Hbv

Induced Jaundice

195

5. Showing The Incidence Of Religion In The Subjects Of Hbv

Induced Jaundice:

195

6. Showing The Incidence Of Marital Status In The Subjects Of

Hbv Induced Jaundice:

195

7. Showing The Incidence Of Habitat In The Subjects Of Hbv

Induced Jaundice:

196

8. Showing The Incidence Of Food Habits In The Subjects Of

Hbv Induced Jaundice:

196

9. Showing The Incidence Of Duration Of Illness The Subjects Of

Hbv Induced Jaundice

196

10. Showing The Incidence Of Socio-Economic Status In The

Subjects Of Hbv Induced Jaundice

197

11. Showing The Incidence Of History Of Previous Treatment

Received In The Subjects Of Hbv Induced Jaundice

197

12. Showing The History Of Hepatitis B Vaccine Received In The

Subjects Of Hbv Induced Jaundice

197

13. Showing The Incidence Of Education In The Subjects Of Hbv

Induced Jaundice:

198

14. Showing The Incidence Of Habits In The Subjects Of Hbv

Induced Jaundice:

198

15. Showing The Incidence Of State Of Agni In The Subjects Of

Hbv Induced Jaundice

198

16. Showing The Incidence Of Nature Of Koshta In The Subjects

Of Hbv Induced Jaundice

199

17. Showing Dominent Rasa Wise Diet Of 30 Subjects Of Kamala 199

18. Showing Dominent Guna Wise Diet Of 30 Subjects Of Kamla 199

19. Showing The Incidence Of Deha Prakruti In The Subjects Of

Hbv Induced Jaundice

200

20. Showing The Incidence Of Aetiological Factors In The Subjects

Of Hbv Induced Jaundice

200

21. Showing The Incidence Of Occupation In The Subjects Of Hbv

Induced Jaundice

200

22. Showing The Incidence Of Poorva Roopa In The Subjects Of

Hbv Induced Jaundice

201

23. Showing The Incidence Of Symptomatology (Roopa) In The

Subjects Of Hbv Induced Jaundice

201

P a g e | XVI

24. Parameters Of Nasya Observed In 15 Subjects Of Kamala 202

25. Complication Observed In Nasya Karma In 15 Subjects Of

Kamala

202

26. Virechana Sudhi Lakshanas Wise Distribution Of 15 Subjects

Of Kamala

203

27. Complication Observed In Virechana Karma In 15 Subjects Of

Kamala

203

28. Samyak Virechana Lakshan Observed In 15 Subjects Of

Kamala

203

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INTRODUCTION

Nature has its own initiate ways of expressing itself and colour has been its

unique expression of awry or peace, as is red-hot sun and soothing blue moon. Man is

nothing but an epitomized version of nature, so does his body express the status of

homeostasis through colour. This has an unparalleled description in the texts of

Ayurveda. Vaivarnya or discoloration is so an alarming situation in a human body

indicating a disease. Pandu, Kamala, Kusta etc are examples of these phenomena.

The colour yellow has always been associated as a sign for education, hence

we find yellow atmosphere in renowned temples of education. But this Yellow colour

unearths a dubious significance in the human body.

Yellow discolored skin, conjunctiva, urine signals the onset of a deadly

disease called Kamala, which in modern parlance is correlated with disease of biliary

system in general and Hepatitis with jaundice in particular.

Hepatitis B is an infectious inflammatory illness of the liver caused by

the hepatitis B virus (HBV) that affects hominoidea, including humans. Originally

known as "serum hepatitis", The disease has caused epidemics in parts

of Asia and Africa, including India and it is endemic in China. About a third of the

world population has been infected at one point in their lives, including 350 million

who are chronic carriers. Professional blood donors constitute the major high risk

group for HBV infection in India, with a hepatitis B surface antigen positivity rate of

14%. Blood transfusions represent the most important route of HBV transmission

among adults. However, most of India's carrier pool is established in early childhood,

predominantly by horizontal spread due to crowded living conditions and poor

hygiene. Acute and subacute liver failure are common complications of viral hepatitis

in India and HBV is reckoned to be the aetiological agent in 45% of adult cases. HBV

is reported to be responsible for 70% of cases of chronic hepatitis and 80% of cases of

cirrhosis of the liver. About 60% of patients with hepatocellular carcinoma are HBV

marker positive.

The virus may be present in the oropharyngeal secretions, in seminal fluid, in

menstrual blood, in stool, in urine and in remaining all physiological and pathological

secretions. Hepatitis B is claimed to be 100-200 times more infectious than AIDS and

results in approximately one million deaths each year, making it the World’s Tenth

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leading cause of death1.

In spite of vaccination present today, the chronic Asymptomatic carriers HBV

and its complications still do not have drugs, which can be employed satisfactorily in

the management of Hepatitis B in modern science. Specific therapies are not available

either to counteract the viral infection or to promote the Hepatocellular regeneration.

The cure of disease is left to the mercy of nature and time. Ayurveda do possess

effective antiviral and Hepatoprotective herbs in pharmacopoeia.

Charaka and Vagbhata have opined that the nomenclature of the diseases need

not be over emphasized. Instead, management is more stressed on the basis of Dosha

and Dushya. It is also concluded that some of the old diseases will disappear while

new diseases emerge2. Ayurveda documented that infectious disease in the form of

Agantuka rogas or Sankramaka rogas. Therefore we need not worry that Hepatitis is

not directly mentioned in ancient texts. The management of Hepatitis B is neither

impossible nor new for Ayurvedic physicians.

In classics the term Kamala has been explained by different names. In Atharva

veda, Kamala was known as Haridraka, Harima, Harit, Vilohitatwa. Dalhana, while

commenting Sushrutacharya’s view, opined that Kamala, Panaki, Kumbha kamala,

Lagharaka, Alasa, Alasakhya,…etc., are different stages of panduroga and all these

terms are considered as the synonyms of Kamala.

The present study comprises of 2 parts. The first part mainly concerned with

the review of literature regarding Kamala, Virechana, Nasya, Jaundice and Hepatitis

B. Various aspects of the disease such as History, Nirukti, Paribhasha, Nidana

panchaka etc. are reviewed and discussed.

The second part consists of details of clinical trial of the effect of Nasya with

Jimutakaphala and Virechana with Patolamooladi Kashaya along with

Nimbatwakadi kashaya as Shamana Oushadi. It comprises of the materials and the

methods used for the study, the results and observations of the study and discussion

on them. A summary of the study is provided in the last part of the dissertation.

In the present study, subjects suffering from HBV induced Jaundiced were

selected and investigated. However inclusion thoroughly examined and randomly

divided into two groups namely Group A and Group B.

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In Group – A, Amapachana with Hareetakyadi Yoga (5-10 gms) for 3-

5 days was given. Mukhabhyanga with Taila and Baashpa sweda was performed

initially as Poorva Karma followed by Pradhana karma Nasya with Jeemoothaka

phala swarasa for 7 days initially followed by 14 days of Parihara Kala. Then one

more course of Nasya with the same swarasa for 7 days after which 14 days of

Parihara Kala was followed again. During course of Parihara Kala internally

Nimbatwakadi Kashaya(45-60ml), was given as Shamanoushadhi.

In Group – B, Amapachana with Hareetakyadi Yoga (5-10 gms) for

3-5 days was given followed by Snigdha bhojana (Eshad pramana of Goghrita along

with Ahara), only for 3 days was advised as a part of Poorva Karma. Bahya Prayoga

of Murchita Tila Taila in the form of Mrudu Abhyanga was suggested to the patients.

Sukhoshna Jala Snana was followed later as a part of Parisheka Sweda. Virechana

with Patolamooladi Kashaya(60-90 ml) and 3 days of samsarjana krama initially

followed by 14 days of Parihara Kala. Then one more course of virechana with the

same medicine and samsarjana karma for 3 days after which 14 days of Parihara Kala

was followed again. During course of Parihara Kala internally Nimbatwakadi

Kashaya(45-60ml), was given as Shamanoushadhi.

The vital informations regarding the patients along with demographical data

were discussed, subjective and objective parameters belonging to both of the groups

before and after treatment were systematically analyzed. The subjective findings and

objective parameters (Bio-chemical and other objective findings) were found highly

significant in both of the groups (Group A and B), test for HBsAg by Hepacard

method found negative for maximum subjects after treatment in both of the groups.

Hence the treatment principles adopted in either groups shown highly significant

response, during the follow-up period it was observed that all the bio-chemical and

other objective parameters were not exceeding their physiological range in most

subjects. It can be said that the treatment of Group A and Group B found effective in

inactivating the virus and allowing the virus and other toxic materials to be driven

away from the body.

At the end, dissertation comprises the Bibliography and Annexure. Master

charts were prepared containing all the details of clinical study in compact versions,

which yield the bird’s eye view on the practical work done.

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OBJECTIVES OF THE STUDY

1. To study Virechana Karma and Nasya Karma in detail.

2. To study Hepatitis B Virus induced Jaundice in detail and Kamala according to

Ayurvedic texts.

3. To study the efficacy of Virechana Karma with Patolamooladi Kashaya in the

management of Hepatitis B Virus induced Jaundice (Kamala).

4. To study the efficacy of Nasya Karma with Jeemoothaka Phala Swarasa in the

management of Hepatitis B virus induced Jaundice (Kamala).

5. To compare the efficacy of Patolamooladi Kashaya Virechana and Jeemoothaka

Nasya in the management of Hepatitis B Virus induced Jaundice.

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PREVIOUS WORKS DONE

1. Singh N. R. – Role of Phyllanthus niruri In Koshta-Sakhasritha Kamala,

(Hepatocellular Jaundice), State Ayurvedic College, University of

Lucknow,1991.

2. Jaiswal A.K. – Role of Phalatrikadi Kwada in cases of Koshtasritha Kamala

w.s.r.to Hepatic Jaundice, State Ayurvedic College, University of

Lucknow,1992.

3. Rao Subramanyeswar – The study of effect of Pathyadi Lehyam in Kamala

(Sakasritha Kamala), with Virechana or without Virechana Karma, Dr

B.K.R.R. Govt. Ayurveda College, A. P University, Vijayawada, 1994.

4. Gupta.S.K. – Clinical evaluation of some indigenous drugs in the treatment of

Kamala Roga. Faculty of Ayurveda Institute of Medical Sciences, Banaras

Hindu University, Varanasi,1998.

5. Sreevatsa.A.K. – A study on the effect of indigenous drugs in the

management of Hepatitis (Kamala Roga) w.s.r.to membrane- stabilizing effect

of these drugs. Faculty of Ayurveda Institute of Medical Sciences, Banaras

Hindu University, Varanasi,1999.

6. Lavanya.V.K.M – Clinical and experimental study on Viral Hepatitis

(Kamala), and its management with an indigenous compound, Faculty of

Ayurveda Institute of Medical Sciences, Banaras Hindu University,

Varanasi,2001.

7. Naik Sameer N. – Management of Sakasritha Kamala w.s.r.to Viral Hepatitis

B – An observational study. Mysore Govt Ayuvedic Medical College, Rajiv

Gandhi University of Health Sciences, Banglore, 2001.

8. Yadav.P.S. – Clinical evaluation of Markandyadi Hima in the management of

Kamala Roga w.s.r.to Viral hepatitis, National Institute of Ayurveda,Rajastan

University,Jaipur,2003.

9. Hadimani Gangadhar – An evaluation of the efficacy of Phalatrikadi Yoga

in Kamala (Jaundice), D.G.M. Ayurveda Medical College, Gadag, Rajiv

Gandhi University of Health Sciences, Banglore,2003.

10. Pankaj Doshi – Management of Hepatocellular B virus induced Jaundice

w.s.r. to virechana and nasya, Ayurveda Mahavidyalaya Hubli, RGUHS 2006

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HISTORICAL REVIEW

HISTORICAL REVIEW OF KAMALA

To understand the subject in better manner one must know Historical Review,

which has been, studied under three headings.

1. Aadi Kala (Purana Kala) – 230BC – 1300 AD.

2. Madhyama Kala – 1300 AD – 1800 AD

3. Adhunika Kala – 1800 AD onwards

Aadi Kala (Purana Kala – 230BC – 1300AD):

Vedas are the oldest sources of information regarding the diseases and

medicinal uses of plants.

In Rig Veda we get references stating that by chanting mantras the disease

Kamala (Harima or Harita)3 can be transferred from the patient to the yellow coloured

birds and yellow coloured plants like Turmeric etc4.

In Atharva Veda, some references regarding the disease Kamala is available.

“Harima” is one of the twelve diseases mentioned in Atharva Veda.

The word “Harima” means yellowish discoloration: which is one of the main

symptoms of Kamala. Apart from medical treatment for the diseases, Atharva Veda

prescribes “Emperico religious” approach also for the management of the disease.

In Atharva Veda we find the term “Harima” and Harita, which are said to be

synonyms of Kamala, and was advised to be treated with „suryasnana‟, consumption

of milk obtained from the red cow5 and Anjana therapy

6, are also available.

In Garuda purana and Agni purana there are references of Kamala. Garuda

purana opines Kamala as paratantra to Pandu roga. It says that neglecting Pandu roga

and indulging in unwholesome food and other habits, which provokes Pitta dosha,

endangers Kamala.

Samhita Kala:

Charaka and Sushruta Samhita are the two great works of this era. Description

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of the disease Kamala is available in Nidana sthana and Chikitsa sthana of Charaka

Samhita and Uttara tantra of Sushruta Samhita.

Kashyapa, the author of Kashyapa Samhita mainly deals with Kaumarbrutya

explained the disease Kamala in sutra sthana of Vedana adhyaya and Pleeha Halimaka

adhyaya of Chikitsa sthana.

Harita has not explained the Nidana aspect of the disease Kamala, but

however he has considered Kamala as a variety of Pandu roga.

Sangraha Kala:

Sangraha Kala is considered as the golden period of Indian Medicine.

Important works in the period are Astanga Sangraha and Astanga Hridaya. Vagbhata

wrote these scripture, which borrowed many things from Charaka Samhita and

Sushruta Samhita.

In Chakradatta, the author Chakrapani has described only Chikitsa aspects of

Kamala and has even commented on the description of Kamala in Charaka Samhita.

Dalhana and Indu the commentators at Sushruta Samhita and Astanga Hridaya

respectively have commented on Kamala.

Madhyama Kala (1300 AD – 1800 AD):

In Sharangadhara Samhita reference regarding treatment of Kamala is

available. But while classifying Kamala. He has not mentioned regarding

Shakhashrita Kamala. Bhavaprakasha also followed the same.

In Yoga Ratnakar explanation regarding Nidana, Chikitsa and laxana of

Kamala are available. In Bhaishajya ratnavali only Chikitsa aspects of Kamala are

explained. Even in Brihat Nigantu Ratnakar, Kalyanakaraka, Yoga Tarangini, Brihat

Yoga Tarangini, Basavarajeeyam, Chikitsa kramakalpavaleeyam and Rasaratna

samucchya plenty of references are available and they have explained its treatment

with different formulations.

Adhunika Kala (18th

Century onwards):

The period after 18th

century is called as Adhunika kala. Many authors such as

Dr.Ranjit Roy Desai, Dr.Ramraksha Pathak, Dr.Shivacharan Dhyani, Dr.Vidhyadhar

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Shukla, Dr.Ramharsh Singh etc, and others have compiled the disease by going

through various classical texts in their respective textbooks by stating their views.

Hepatitis is a clinical disease state, which has been recognized from antiquity.

The delineation of its viral cause is relatively a recent event.

The first reference to epidemic Jaundice has been ascribed to Hippocrates,

which is found in Western Europe, in a letter written in 751 A.D. by Pope Zacharious

to St.Boniface, Arch Bishop of Mainz. Since then there have been numerous accounts

of epidemics particularly during wars. Hepatitis was a problem in Franco-Persian war,

American civil war and 1st world war. In 2

nd World War huge epidemics were

reported particularly in the Middle East and Italy7.

In 1947, Mac Callum suggested that the virus that gives rise to Serum

Hepatitis should be called as Virus-B.

(Ref.Mac Callum FO: Early Studies of Viral Hepatitis, Br.Med.Bull.28: 105, 1972).

Throughout the 1950‟s and early 1960‟s the Epidemology of parentally

transmitted Hepatitis was extensively studied and a number of important human

transmission studies were performed.

A new era in the history of Viral Hepatitis began with the discovery of

Australia antigen by Blumberg and Colleagues in 1963.

(Blumberg BS et al; 'A New Antigen in leukemia sera-JAMA‟ 191, 101, 1965).

Blumberg and Colleagues in Philadelphia found an antibody in two multiple

transfuse haemophilic patients, which reacted with an antigen in a single serum in

their panel, which came from an Australian aborigine. Later the antigen was found

in patients with Viral Hepatitis.

Because of its discovery in an Australian aborigine serum, the antigen was called

„Australian Antigen. In 1977 Blumberg was awarded Nobel prize for his discovery. The

Australian Antigen is now known to be the surface antigen of Hepatitis B Virus and is

termed as Hepatitis B surface antigen (HBsAg).

HBV of humans and Hepatitis B like viruses found in wood chucks (Marmota

monex) Beechy ground squirrels (Spermophilus Beecheyi) and Pekin ducks (Anas

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domesticus) share many features and belong to a family of Hepatotrophic. „DNA

viruses called Hepadna viruses‟ type 1.

(Melnick JL; classification of Hepatitis Virus as entero virus type 72 and of

Hepatitis B virus as Hepadna virus type 1 Interovirology 18: 105, 1982).

HISTORICAL REVIEW OF NASYA KARMA

It is natural that accumulation of knowledge of any topic occurs gradually and

same is the case with Nasya Karma, which has developed since Vedic era to Modern

era.

Description Of Nasya In Veda Kala

There is a mantra in Rigveda in which eradication of Roga is mentioned by

routes of Nasa, Chibuka, Shira, Karna, and Rasna. This can be considered as a

primitive picture of Nasya Karma.

In Krishna Yajurveda, Shatpatha Brahmana, Upanishada, the term Nasya

Karma has been used frequently.

In Valmiki Ramayana, when Lakshmana became unconscious by the blow of

Meghanada, Vaidya Sushena administered the juice of Sanjivani through nasal route

bringing him to consciousness instantaneously.

In Bauddha Kala“Jeevaka” the famous Vaidya of Bauddha kala had utilized

Nasya Karma in many cases such as

In Shirahshoola, he prescribed Nasya of medicated Ghrita to the wife of

Shreshthi of Saketa Nagar.

Once when Jeevaka wanted to give Virechana to Lord Buddha, he gave

him Aushadhi by Nasya for Virechana.

In Vinaya Pitika, it is mentioned that one Utpala Hasta of Nasya has potency to

induce 10 Vegas of Virechana.

Samhita Kala

Literature written during this period is the heart of Ayurvedic literature. In all

the Samhita, Nasya Karma has been elaborately described especially in Charaka

Samhita, Sushruta Samhita and Ashtanga Samgraha. All the Brihathrayi‟s gave

detailed explanation regarding the Nasya Karma in separate chapters. The research

conducted on this therapy was at such a height that it was used to achieve expected

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sex of foetus. Nasya Karma is utilized in treatment of many diseases in Brihatrayis.

HISTORICAL REVIEW OF VIRECHANA

Description Of Nasya In Veda Kala

No clear cut description of Virechana is available in Vedas. At various places

several Mantras are described in Rigveda, which indirectly refer towards the Karma

which are included under Panchakarma procedures, which includes Virechan Karma.

It is interesting to note from the historical point of view that the Virechana was

popular and was in practice in other pathies also. In Mesopotamia Virecana was in

practice for pain in abdomen along with Vamana. Svarnapatri and Indrayana drugs

were used for Virecana (Jacquetta Hawks and Leonard wooley)

In Buddha Kala 1425-353 B.C. In the text "Vinayapitaka" it is mentioned that

by inhaling some powder spread over Utpalapatra, Virecana was given to Bhagavan

Buddha.

Samhita Kala

In Bhrihatrayee, Laghutrayee and other Ayurvedic texts we get elaborative

description of Virechana Karma.In Charaka Samhita Sutrasthana Virechana dravya

Sangraha, Virechana yoga‟s,procedure of Virechana is mentioned, in Kalpasthana

complete explanation of Virechana Kalpas is mentioned, in Siddhi sthana Virechana

samyak yoga, ayoga,atiyoga, Virechana yogya, ayogya, Virechana Vyapad and

chikitsa is mentioned.

In Sushruta Samhita Sutrasthana Virechana dravyas, explanation of Trivrit

differentpreparations are mentioned, in chikitsa sthana Virechana karma vidhana,

samyakayoga, atiyoga, Vyapad and their treatment is mentioned.

In Ashtanga Hridaya Sutrasthana Virechana Vidhi is explained, in

Kalpasthana

Virechana dravyas, Virechana Vyapad and Siddhi is explained. In Ashtanga Sangraha

Sutrasthana complete Virechana Vidhi is explained.

We find well contribution of Virechana in Sharangadhara samhita,Kasyapa

samhita Siddhi sthana, Bhavaprakasha poorva khanda,

YogaratnakaraVirechanadhikara and Chakradatta Virechanadhikara

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VYUTPATTI - NIRUKTI - PARIBHASHA

KAMALA

„Kalaha‟ substitutes the term Kamala is formed by the root „Kamu‟ which

means „Kanthi‟ by suffixing „Nhin‟ pratyaya. Thus the term Kamala is Kamu + Nhin

(Kalaha)8.

Nirukti

Kaman Itchan lunathi iti Kamala‟

„Kamam na lati iti Kamala‟

Here „Kamam‟ means „Aasham‟ or desires and „Lati‟ means „Runaddhi‟ or

„Badhnati‟ or to diminish. Hence Kamala means one which checks or struck the desires or

in other words Kamala is a disease in which an individual looses interest in all aspects.

Paribhasha

There are several types of Paribhasha described in classics for the term

Kamala. All of them describe the different phases and laxanas of Kamala.

“Atha Kamalethi Kama Shabdha Ayama Sadharana Shabdha Visheshata

Swalpe Bhaktadhihi abhilasha Prawartate Tam Lunathi iti Kamala” 9

This implies that Kamala is a disease in which hunger and appetite for food is

diminished in a particular sense.

“Kanthim Lunathi Lunatho Hinasthi Ve Iti Kamala Roga Bhedah” 10

This indicates the pratyatma laxanas of disease Kamala. The term „Lunathi‟

means nasha and „Kanthim Lunathi‟ means a pathological condition in which normal

colour of the skin is affected. Thus Kamala would indicate the diseased state in which

the colour change sets in. Even discolouration of urine, faecal matter, conjunctiva,

dorsum of tongue, nails etc, also can be considered on the basis of above definition.

Thus Kamala can be defined as a diseased state in which hunger and appetite

for food is diminished and normal colour of the skin, urine, and conjunctiva is lost.

(Peeta or Haridra / Harita).

The term Kamala means dry and sterile soil, desert, libidinous and lustful11

. In

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Jaundice, excessive secretion of bile (Bahupitta Kamala) is seen On the contrary, in

the clinical type of Kamala (Rudhapatha Kamala- Alpapitta Kamala) obstructs the

bile in the biliary pathway12

.

The term Viral Hepatitis is formed by two words Viral and Hepatitis. Hepatitis

is a condition in which inflammation of Liver is observed. Thus the inflammation of

Liver caused due to Hepatitis B Virus is called as Viral Hepatitis-B.

Hepatocellular means concerned to Hepatocytes.

Viral Hepatitis may be defined as a systemic viral infection in which hepatic

cell necrosis and hepatic inflammation are responsible for a characteristic

constellation of clinical, biochemical immunoserological and morphological features.

All though several viruses may cause Hepatitis, the term viral hepatitis is

reserved for inflammation of Liver caused by HAV, HBV, HCV, HDV, and HEV13

.

Thus the term viral hepatitis can be defined as the inflammation of Liver

caused by specific group of viruses having affinity towards Liver. Hepatitis B is an

infection of Liver caused by Hepatitis B virus.

NASYA KARMA

The word Nasya Karma is composed of two words Nasya and Karma.

Nasya: „ Nas‟ is substituted for Nasa when it is followed by the suffix „Yath‟.

Nasika + Yath = Nasadeshancha

Nirukthi

Nasikaayai hitam – Nasya

In Sanskrit language each word is derived from a specific Dhatu and each

Dhatu bears an inherent meaning which is the crux of the word. The derivation of the

word Nasya is from “Nasa” Dhatu. It conveys the sense of Gati – motion. Vyapti

bears the meaning pervasion. Here, the Nasa Dhatu is inferred in sense of nose. The

word “Nasata” means beneficial for nose, or belonging to or being in nose, as breath.

Acharya Chakrapani explains that “Nastha Prachardanam iti

Shirovirechanam.”, Nasya can be defined as that which is administered through nose

by using the medicines to alleviate Jatrurdhva Vikaras in particular.

The medicine or any oil processed with medicine administrated through nose

is known as Nasya.The medicine administrated through nose is Nasya.The drug

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administrated to Shiras through nose is Nasya.The drug which is administrated slowly

through nose or absorbed through nose is Nasya.

Paribhasha

In context of Ayurveda, the word Nasya suggests the nasal route for

administration of various drugs. As per Acharya Sushruta, administration of medicine

or medicated oils through the nose is known as Nasya. Arunadatta and

Bhavaprakasha opine that all drugs that are administered through the nasal passage

are called Nasya. Sharangadhara and Vagbhata also hold the same view.

VIRECHANA KARMA

Virehana shabda is formed by the root “Rich” dhatu and “Vi” upasasga. “Nich

and “Lout” pratyaya are also take part in the derivation of the word virechana.

“Visheshena rechateeti” “Vi + rich + Nich + Lyu.”

Nirukthi

The word Rechana is commonly used for evacuation. As both Vamana and

Virechana do the evacuation of Doshas, therefore some times the word Virechana

broadly applies for both. But in general, the word Virechana denotes evacuation of the

Doshas through „Guda‟.

Paribhasha

The act of expelling Doshas through Adhobhaga is known as Virechana. Here

the meaning of Adhobhaga is „Guda‟ commented by Chakrapani.

Indu commenting on Astanga sangraha opines that,Virechana is the procedure

in which the orally administered drug acts on internally vitiated Doshas, specifically

on Pitta and expels them out through anal route.

Virechana Karma is considered as the best treatment for evacuation of morbid

Pitta Dosha. It also performs the function of elimination of doshas in condition like

kapha samsrishta pitta dosha, vata sthana gata kapha. It can also be employed for the

purpose of anulomana of vata.

KARMA:

The action by Kartru is known as Karma. The treatment of diseases done with

Nasya is called Nasya Karma and with Virechana , Virechana Karma, where Karma is

used in the meaning of Chikitsa.

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PARYAYA

Paryaya of Kamala

In classics the term Kamala has different synonyms.

In Atharva Veda, Kamala was known as Haridraka, Harima, Harita,

Vilohitatwa. Dalhana, while commenting Sushruta Acharyas view, opined that

Kamala, Panaki, kumbha Kamala, Langharaka, Alasa, Alasakhya etc. are different

stages of Pandu roga and all these terms are considered as the synonyms of Kamala.

Astanga Hridaya has noted Lodhara as the synonym of Kamala.

Chakrapani has used the term Alpapitta Kamala as the synonym of

Shakhashrita Kamala and Bahupitta Kamala as the synonym of Koshtashakhashrita

Kamala. Thus Haridraka, Harita, Vilohitatwa, Harima, Panaki, Kumbha Kamala,

Langharaka, Alasa, Alasakhya, Lodhara and Bahupitta Kamala are the synonyms of

Kamala14

and Alpapitta Kamala is the synonym of Shakhashrita Kamala.

Paryaya of Nasya:

Shirovirechana, Shirovireka, Murdhavireka, Navana, Nasta Karma, Nasta

Prachardana.Sirovirechana, Murdha Virechana, Sirovireka indicates its main function,

elimination of morbid Dosha from the parts above the clavicle. Acharya Charaka used

the term Nasta Prachardana, for Nasya which denotes Shodhana done by Nasya.

Navana and Nasta Karma denotes the site of administration and the measures which

are beneficial to nose or regions near to nose

Paryaya of Virechana :

Kayavirechanam according to Ashtanga Hridaya, Rechanam

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according to Bhavaprakasha and Vangasena, Praskandana told in Charaka Samhita,

and Prakledanam told in Gudarthadeepika are the major synonyms told in Classics for

Virechana.

According to the Sanskrit – English dictionary-purgative, cathertic, aperient

and evacuant are the different meanings of Virechana (M.Monier Williams).

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REVIEW OF NASYA KARMA

The administration of either medicine (drug) or medicated oil through the nose

is known as Nasya Karma. Nasya is especially desired for diseases of parts above the

base of the neck, nasal passage being the gateway of the head, permeating through

this aperture, it cures such diseases. The drug administrated to Shiras through nose is

Nasya.

Nasa is the Adhishtana for Ghrahanendriya which is one of the

jnyanendriya,perception of smell is its function,it is supported by prana vata.Its

activities are mentioned by prana vata which assists it in smell

perception.Ghranendriya is nourished by tarpaka kapha.

CLASSIFICATION OF NASYA KARMA

Nasya is classified in various ways by different Acharyas. Each classification

has its own salient features and each is done with different angles.

Acharya charaka’s classification of nasya:

According to Acharya Charaka the Nasya is of five types viz. Navana,

Avapidana, Dhmapana, Dhuma and Pratimarsha. Navana is further divided in to

Snehana and Shodhana, Avapidana into Shodhana and Stambhana, Dhuma into

Prayogika, Vairechanika and Snaihika while Pratimarsha is divided into Snehana and

Virechana.

Nasya

Navana

Snehana

Shodana

Avapida

Shodhana

Sthambana

Dhmapana Dhuma

Prayogika

Snaihika

Vairechanika

Pratimarsha

Snehana

Virechana

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According to the mode of action of Nasya therapy

The above mentioned five types of Nasya are regrouped according to their

pharmacological action into three groups viz. – Rechana, Tarpana and Shamana.

According to various parts of the drugs utilized in Nasya therapy

Acharya Charaka has also mentioned 7 types of Nasya according to parts of

the drugs to be used in Nasya Karma – Phala, Patra, Mula, Kanda, Pushpa, Niryasa,

Tvaka.

Table 1. Various Parts of Drugs used for Nasya

PARTS DRUGS

Phala/Fruit Pippali, Vidanga, Apamarga, Shigru, Sarshapa, Shirisha,

Mareecha, Bilwa, Vatharka

Moola/Root Karaveera, Bimbi, Aparajitha, Vacha, Karanja, Arka,

Jyothishmati, Kushta, Barngi, Shwetha, Nagadanthi,

Kanda/Tuber Lashuna, Athivisha, Nagara, Haridra

Pathra/Leaf Thaleesapathra, Thamala Pathra, Surasa, Tharkari, Sarshapa,

Haridra, Nagara, Lashuna, Moolaka

Twak/Bark Ingudi, Meshasrungi, Shigru, Tejaswini, Meshasrungi, Ela,

Bruhathi, Kantakari

Pushpa/Flower Mathulunga, Shigru, Peelu, Jati, Jyothishmathi, Gavakshi,

Harithaki, Vrushchikali, Lavanga

Sara/Heart wood Shala, Thala, Madhooka, Thamala, Darvi

Niryasa/ Exudate Hingu, Laksha, Agaru, Suradaru, Shallaki, Jingani, Asana,

Rasanjana

Beeja/seed Lodhra, Madana, Peelu, Sapthaparna, Nimba

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Classification of nasya according to acharya sushruta

According to Acharya Sushruta, Nasya is of 5 types viz. Nasya, Avapida,

Pradhamana, Shirovirechana and Pratimarsha. These 5 types of Nasya are further

classified according to their functions into two groups; Shirovirechana and Snehana.

Shirovirechana, Avapida and Pradhamana are used for Shirovirechana purpose. i.e.

for the elemination of morbid Dosha from Shira while Pratimarsha and Nasya may be

used for Snehana.

Vagbhata’s classification of nasya

Ashtanga Samgraha has mainly classified Nasya according to its effect viz.

Virechana, Brumhana and Shamana. Snehana and Brumhana Nasya have been further

subdivided according to the doses into two groups i.e. Marsha and

Pratimarsha.Avapida Nasya may be given for both Virechana and Shamana while

Pradhamana Nasya is given only for Shirovirechana.Ashtanga Hridaya has mainly

classified Nasya in 3 types viz. Rechana, Brumhana and Shamana.

Nasya

Shirovirechana

Shirovirechana Pradhamana Avapida

Snehana

Nasya Pratimarsa

Nasya

Virechana

Pradhaman

Murdha Virechana

Bhrumhana

Sneha Nasya according to

Dose

Pratimarsha

Marsha

Shamana

Avapida

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KASHYAPA’S CLASSIFICATION OF NASYA

According to Kashyapa Samhita, Nasya has been classified into two groups

i.e. Brumhana and Karshana. These are also known as Shodhana and Purana Nasya.

SHARANGADHARA’S CLASSIFICATION OF NASYA

Sharangdhara has also classified Nasya according to their functions into two

groups viz. Rechana and Snehana. Rechana Nasya is further subdivied into Avapida

and Pradhamana while Snehana Nasya is subdivided into Marsha and Pratimarsha.

BHOJA’S CLASSIFICATION OF NASYA

Bhoja has classified two types of Nasya, viz - Prayogika and Snaihika.

VIDEHA’SCLASSIFICATION OF NASYA

Videha has stated two types i.e. Sangyaprabodhaka and Stamabhana.

CLASSIFICATION OF NASYA KARMA

Classification according to various Acharyas is described in a tabular form as below.

Table 2.Classification of Nasya According to Various Acharyas

NAME C.S Su. S A.S A.H Sha.S

Navanam + +

Avapeeda + + +

Dhmapanam +

Dhooma +

Prathimarsha + + + +

Shirovirechanam + +

Nasyam +

Nasya

Rechana

Avapida Pradhamana

Snehana

Marsha Pratimarsha

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Pradhamanam + +

Tharpanam +

Shamanam + + +

Marsha + +

Virechanam + +

Bruhmanam + +

Rechanam +

Snehanam +

Apart from classification on above basis other criteria are also there,

Classification according to preparation e.g. Avapida Nasya which indicates the

use of expressed juice.

Classification according to the dose to be dropped into the nostrils e.g. Marsha

and Pratimarsha described by Acharya Vagbhata.

Considering by par the classification of Acharya Charaka as gold standard we will

have detailed description of each type.

I. NAVANA NASYA

Navana is one of the important and well applicable type of Nasya Karma.

Method: In Navana, the Bindu of medicated oil or ghee are administered.

Instrument: For administration of Sneha in nostrils, use of Pranadi (Pipette or

dropper) is described by Acharya Charaka.

Classification: It is classified in to two types.

a. Snehana Nasya

b. Shodhana Nasya

SNEHANA NASYA: It enhances the strength of all Dhatus and is used as Dhatu

Poshaka i.e. nutritive for Dhatu.

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Table 3 Dose of Sneha Nasya

Hina matra 8 Bindus in each nostril

Madhyama matra 16 Bindus in each nostril (Shukti Pramana)

Uttama matra 32 Bindus in each nostril (Panishukti Pramana)

Benefits of Sneha Nasya:

It is used for the Snehana in the complaints of shiro laghutva . It gives strength

to neck, shoulder and chest and improves eyesight.

Indications of Sneha Nasya

Sneha Nasya can be given in Vatika Shirahshula, Keshapata, Dantapata,

Shmashrupata, Tivrakarnashula, Timira, Nasaroga, Mukhashosha, Avabahuka

Akalaja Valita, Akalaja Palita, Darunaprabodha and Vatapittaja Mukharoga.

SHODHANA NASYA:

Acharya Sushruta’s Shirovirechana type is included in Shodhana type of Navana

Nasya. It eliminates the vitiated Doshas.

Drugs: In this type of Nasya, oil prepared by Shirovirechana Dravyaa are used.

Table 4 Dose of Shodhana Nasya

Uttama 8 Bindus

Madhyama 6 Bindus

Hina 4 Bindus

Indications:

It can be used in the following conditions; Kaphapurna Talu & Shira, Aruchi,

Shirogaurava, Shula, Pinasa, Ardhavabhedaka, Krimi, Pratishyaya, Apasmara,

Gandhagyananasha and Urdhvajatrugata Kapha Rogas and Urdhvajatrugata Shopha, Praseka,

Arbuda and Kotha.In healthy, Navana should be given according to the following

seasonal schedule.

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Table 5 Time of Administration of Nasya According to Season

SEASON TIME OF NASYA KARMA

Shita Kala Noon

Sharada & Vasanta Morning

Grishma Rutu Evening

Varsha Rutu Only when sun is visible.

Time Schedule:

Navana Nasya should be administered according to the following time schedule.

Table 6 Time of Administration of Nasya According to Season

In Kaphaja Roga Fore noon

In Pittaja Roga Noon

In Vataja Roga After Noon

AVAPIDA NASYA

This can be utilized for Shodhana and Shamana depending on the drug utilized.

Definition: In Avapida Nasya, juice is expressed from paste or Kalka of a drug.

Method: The paste of required medicine is placed in a white and clean cloth and

thereafter it is squeezed to obtain the required quantity of juice, directly in the nostrils

of the patients. The administration of the drug in this way is known as Avapida

Nasya. This type of Nasya may also be given with Kalka etc.

It may also be given by dipping the swab into the Kwatha or Sheeta or

Swarasa of the required drug. Though Acharya Sushruta has categorized this under

Shirovirechana, Avapida has also been used for Stambhana purpose in treatment of

Raktapitta where Sharkara and Ikshu rasa are utilized for the same.

1. Stambhana Nasya: For this type ikshu rasa, milk etc. are used.

2. Shodhana Nasya: For this type Saindhava, Pippali etc. are used.

Videha has mentioned two types of Avapida Nasya.

1) Sangya prabodhana : It is one type of Shodhana Nasya.

2) Stambhana : It is one type of Shamana Nasya.

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Table 7 Dose of Shirovirechana and Avapida Nasya

Uttama 8 Bindus

Madhyama 6 Bindus

Hina 4 Bindus

Indications:

Avapida Nasya is indicated in the following conditions.

Table 8 Indications ofAvapida Nasya

Manasaroga

Apatantraka

Murchha

Krodha

Krisharogi

Vishabhighata

Apasmara

Moha

Sanyasa

Bhiru

Stri

Shirovedana

Mada

Bhaya

Sukumara

Raktapitta

Chittavyakulavastha

Sharangdhara recommends the Avapida Nasya for the patients suffering from

Galaroga, Vishamajwara Manovikara and Krimi.

III. DHMAPANA NASYA

It is a specific Shodhana Nasya.

Synonym: Pradhmana Nasya

Definition: This type of Nasya is instilled with Churna specifically for

Shirovirechana. This Nasya is mentioned as Dhmapana in Charaka Samhita and as

Pradhamana in Sushruta Samhita.

Instrument: In this type, fine powder of drug is administered through nasal passage.

For this purpose specific Nadi yantra - A tube like instrument with length of 6 angulas

and with open ends is utilized.

Method: Fine powder of required drug is kept at one end and air is blown from the

other end so that the medicine gets puffed into the nostrils. Videha has advocated a

different procedure in this context according to him, fine powder is kept in a Pottali of

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thin cloth and then patient is asked to inhale deeply, so that the subtle particles of

medicine enter into nostrils.

Dose: According to Videha,

Three Muchuti (3 pinches) for method with Shadangula nadi.

Two Tolas i.e. 20 gms for Pottali method.

Drugs specifically mentioned for Pradhmana Nasya are generally Teekshna

Dravyas, like Rock salt, Guggulu, Maricha, Vidanga etc. Here we observe that the

drugs used in Pradhmana Nasya are Tikshna (irritative) and it would be safe to remain

cautious while executing this Nasya.

Indications: According to Acharya Charaka, its indications are as under

a) Shiroroga

b) Nasaroga

c) Akshiroga

According to Acharya Susrutha, Mano Vikara, Krimi, Visha, Atyutklishta Dosha,

Sajna Nasha are the indications

DHUMA NASYA:-Inhalation of medicated Dhuma by nasal route and elimination of

Dosha by oral route is called Dhuma Nasya. Acharya Sushruta has remained aloof

from description of this Nasya.

Types and Instrument:Acharya Charaka has mentioned special Dhuma Nadi for

Dhuma Nasya. The length of the Nadi depends upon the type of the Dhuma Nasya,

details of which are as under:

Table 9 Length of Nadi According to the types of Dhuma Nasya

Type of Dhuma Nasya Length of Nadi

Prayogika 36 angula

Vairechanika 24 angula

Snaihika 32 angula

Breadth of the Nadi should be as per the measurement of one’s own angula.

Dose:

Two puffs are to be taken for Prayogika Dhuma.

3 to 4 puffs are to be taken for Vairechanika Dhuma.

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A single puff is advised for Snaihika Dhuma.

Drugs: [Cha Su 5/20-26]

Table 10 Drugs for of Dhuma Nasya

Prayogika Dhuma Priyangu, Ushira

Vairechanika Dhuma Aparajita, Apamarga

Snaihika Dhuma Vasa, Ghrita

Indication of Dhuma Nasya :

It is indicated for treatment of Shiroroga, Nasaroga and Akshiroga.

IV. MARSHA – PRATIMARSHA NASYA

The methods shared by both these types are common but the variation occurs in

context of dose. In Pratimarsha Nasya 1 – 2 Bindu is administered while in Marsha

the dose is of 6 to 10 Bindu.

Pratimarsha Nasya :Following method is employed for Pratimarsha Nasya. A finger

is dipped in the Sneha up to 2 phalanges and then oil is allowed to drop from it in both

nostrils. Patient is advised to expel out the Sneha, which comes in oral cavity.

Dose – 2 Bindu

The sneha should be in such an amount that it reaches from nose to gullet but should

not be enough to produce secretions in gullet

Indications:

Pratimarsha can be given in any age, even in not suitable time & season

Table 11 Indications of Pratimarsha Nasya

Bala Vriddha

Bhiru Sukumara

Weak patients Kshtakshama

Trishna Pidita Mukhashosha

Khalitya Palitya

Durdina Varsha Ritu

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Table 12 Contraindications of Pratimarsha Nasya

Dushta Pratishyaya Krimija Shiroroga

Badhirya Bahudosha

Madhyapi Utklishta Doshas

It is contraindicated, because the Sneha Matra is quite insufficient to eliminate

Doshas or Kriminasha and already aggravated Doshas may get vitiated further.

Table 13 Various Timings for Pratimarsha Nasya according to Acharyas

No Time for Pratimarsha Nasya Su. As. H. Sha.

1 After leaving the bed in morning + + +

2 After Dantadhavana + + +

3 Before going outside + - +

4 After exercise + + +

5 After sexual intercourse + + +

6 After walking + + +

7 After urination + + +

8 After passing Apanavayu + - -

9 After Kavala + + +

10 After Anjana + + +

11 After meal + + +

12 After sneezing + - -

13 After sleeping in the noon + + +

14 In the evening + + +

15 After vomiting - + +

16 After Shirobhyanga - + -

17 After defaecation - + +

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18 After laughing - + -

Pratimarsha in Nasya is a very innocent procedure, it never produces any

complication and by its virtue checks any disease process.

Marsha Nasya

The method of administration of Marsha Nasya resembles that of Pratimarsha but as

said earlier, the dose varies.

Dose – In Marsha Nasya, 6 to 10 Bindu of Sneha are administered.

Drugs – Though all Sneha dravya like oil, ghee, etc. can be utilized but use of oil is

advisable because Shira is the place of Kapha and oil is inherently opposite to Kapha

in properties.

Marsha Nasya is quickly effective and more beneficial than its counterpart i.e.

Pratimarsha.

CLASSIFICATION OF NASYA ACCORDING TO KARMA

This type of classification is given in Charaka Samhita as well as Ashtanga Hridaya

Classification according to Karma (Pharmacological Action)

The types Rechana, Tarpana and Shamana are described by Acharya Charaka

and Acharya Vagbhata. Acharya Sushruta has not described the Shamana Nasya. He

has given only two types viz. Shirovirechana and Snehana.

Kashyapa has mentioned Brumhana and Karshana types of Nasya Karma i.e. Sangya

Prabodhana and Stambhana, according to their pharmacological action. All these

Rechana

Sangyaprabodana

(Shodana) Krimigna

Brimhana Shamana

Sthambana

Rakthasthambana

Dosha sthambana

Karshana

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types can be included into the classification of Acharya Charaka, as in previous pages.

Details of each type of Nasya according to the Karma are as under:

a. RECHANA NASYA

The Rechana Nasya denotes eliminations of vitiated Doshasfrom Urdhvajatrugata

part of the body. It is also termed as Karshana Nasya. Churna (powder) of the

required drug or the Sneha prepared with the Shirovirechana drugs can be used.

Drugs:Drugs like Apamarga, Pippali, Maricha etc. could be used. It could also be

given with Tikshna Sneha, Kwatha or Swarasa of Shirovirechana drugs or by

dissolving these drugs in Madya, Madhu, Saindhava, Asava, Pitta and Mutra or mixed

with the drugs specific for that diseases.

Indications:It is indicated specifically in Kaphaja type of Shiroroga like Stambha,

Supti and Guruta of Shira. According to Acharya Sushruta and Acharya Vagbhata, it

is used in Shleshma abhivypta like Talukantaka, Shirokrimi, Arochaka, Pinasa,

Pratishyaya, Urdhvajatrugata Shopha, Praseka, Vairasya, Arbuda, Dadru and Kotha.

The patients of Galaroga, Sannipataja Jwara, Atinidra, Manovikara, Abhishyanda

Sarpadansha and Murchha may be given Shirovirechana Nasya with Kalka, Churna

and Svarasa also, but if the immediate effect is required, then Churna (powder) should

be used.

If Rechana Nasya is to be given in patients of weak will power then Sneha preparation

of Rechana dravya is applied.

b. TARPANA NASYA

Tarpana is that type of Nasya, which is specially indicated in a Dhatukshaya

(degeneration). Tarpana Nasya resembles Snehana Nasya described by Acharya

Sushruta and Sharangadhara and Brumhana Nasya mentioned by Acharya Vagbhata

in its properties and actions.

Drugs:The Sneha prepared with Vatapittahara drugs should be used and the drugs of

Madhura Skandha may also be employed. According to Vagbhata, Sneha prepared

with Snigdha and Madhura drugs or with the drugs described useful for that particular

disease should be used. Exudations of certain trees, meat soup and blood also may be

administered.

Indications :Vatika Shiroroga, Dantapata, Keshapata, Darunaka and other Vata-

Pittaja Roga. Acharya Sushruta advises Sneha Nasya for increasing general strength

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and to improve the vision power and its acuity. It is also used for curing the Shirah

Kampa and Ardita.

c. SHAMANA NASYA

As the name indicates, Shamana Nasya is used for the alleviation of Dosha

situated in Shirah (head). Shamana Nasya has been described by Charaka and

Vagbhata only. It may be correlated with Snehana and Pratimarsha. The Sneha

prepared with the beneficial drugs may be used for Shamana Nasya.

Definition :The type of Nasya which is used for alleviation of Dosha of Shira is

called Shamana Nasya.

Drugs :Usually drugs beneficial for particular diseases are chosen for this type and

the carrier is a Sneha Dravya.

Indication :It is indicated to check the bleeding occurring in the course of Raktapitta.

It is also indicated in Vali, Palita, Khalitya, Darunaka, Raktaraji, Vyanga and Nilika.It

can also be used to improve the power of eyes, ears and nose.

Anutaila Nasya as a measure of Svasthavritta should be administered in Pravrita,

Sharada and Vasant Ritu to promote the functions of eyes, ears and nose to prevent

Khalitya and Palitya and diseases like Manyastambha, Shirahshula, Ardita,

Hanustambha, Pinasa, Ardhavabhedaka, Shirokampa.

INDICATIONS OF NASYA

Nasya therapy may be given in all diseases except in the conditions mentioned

earlier. The specific indications of Tarpana Nasya, Shodhana Nasya, Shamana Nasya,

Shirovirechana, Navana, Avapida, Dhmapana and Dhuma Nasya etc. have already

been discussed in the classification of Nasya, but Charaka has described the following

general indications, where Nasya therapy should be used.

Table 14 General Indications of Nasya

Shirostambha

Ardhavabhedaka

Shira shula

Akshishula

Gadgadatva

Vaggraha

Grivaroga

Kamala

Galashundika

Galashaluka

Galaganda

Upajihvika

Hanugraha

Mukharoga

Apatantraka

Apatanaka

Danta Stambha

Danta Shula

Danta Harsha

Danta Chala

CONTRAINDICATION OF NASYA

In classics some special conditions have been mentioned where Nasya should

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not be administered, otherwise various complications may occur. In general, in all

patients Nasya should not be administered on Durdina or in Anrutu. Contra

Indications of Nasya mentioned in Brihattrayi have been tabulated below:

Table 15 General Contraindications of Nasya

Sr. Nasya Anarha Charaka Sushruta Vagbhata

1 Bhuktabhakta + + +

2 Ajirni + + -

3 Pitta Sneha + + +

4 Pitta Mad + + +

5 Pitta Toya + + +

6 Snehadi Patukamah + - +

7 Snatah Shirah + - +

8 Snatukamah + + +

9 Kshudharta + - +

10 Shramarta + + -

11 Matta + - -

12 Murcchita + - -

13 Shastradandahrita + - -

14 Vyavayaklanta + - -

15 Vyayamaklanta + +(Shranta) -

16 Panaklanta + - -

17 Navajwara Pidita + - -

18 Shokabhitapta + - -

19 Virikta + - +(Shuddha)

20 Anuvasita + +(Datta

Basti)

+(Datta Basti)

21 Garbhini + + +

22 Navapratishyayarta + - -

23 Apatarpita - + +(Shuddha)

24 Pittadravah - + +

25 Trishnarta + + -

26 Gararta - + +

27 Kruddha - + -

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28 Bala - + -

29 Vriddha - + -

30 Vegavarodhita - + +(Vegarta)

31 Raktasravita - - +

32 Sutika - - +

33 Shvasapidita - - +

34 Kasapidita - - +

SUITABLE TIME FOR GIVING NASYA

According to Acharya Charaka generally Nasya should be given in Pravrita,

Sharada and Vasant Rutu. However in emergency it can be given in any season by

providing artificial conditions of the above mentioned seasons, for example in

summer, Nasya can be given in cold places and in cold season, it can be given in hot

places.

BASED ON DOSHA :

Table 16 Time schedule based on Doshic Involvement (Kala of Nasya)

In Kaphaja Vikara Morning/Prathah

In Pitta Vikara Afternoon / Madhyahna

In Vata Vikara Evening/ Syam or Night /Rathri

Table 17 Time schedule based on Different Seasons

In Swastha, Sharath and Vasntha Poorvahna

Sheeta kala Madhyahna

In Greshma Syam/ Piranha

In Varshakala When Sunlight is there

In Vathabhibhootha Shira, Ayama,

Apathanaka, Manyasthambha and

Swarabhramsha

Daily Sayan and Prathah

Lalasrava, Pralapa, Danta Katakatayana,

Kruchronmeelana, Poothimukha, Karna

Nada, Thrushna, Ardida, Shiroroga, Shwasa

and Kasa

Sputa, Rathri/ Night

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According to Acharya Sushruta in normal condition Nasya should be

given on empty stomach. Nasya should be given daily in morning and evening in

Vataja Shiroroga, Hikka, Apatanaka, Manyastambha and Swarabhramsha.

Sharangadhara has described same time schedule for different seasons as Acharya

Sushruta has mentioned. He further states that – Nasya can be given in night, if the

patient is suffering from Lalasrava, Supti, Pralapa, Putimukha, Ardita, Karnanadi,

Trishna, Shiroroga and such conditions like excessive vitiated Doshas.

Table 18 Course of Nasya Karma

No. Name of Acharaya Days

1 Acharya Sushruta 1,2,7,21

2 Bhoja 9

3 Vagbhata 3,5,7,8

Vagbhata

Nasya Karma may be given for seven consecutive days. In conditions like

Vata Dosha in head, hiccough, loss of voice etc. it may be done twice a day (in

morning and evening).Nasya should be given for 3 days, 5 days, 7 days & 8 days or

till the patient shows the symptoms of Samyak Nasya as stated in Ashtanga

Samgraha.

Acharya Sushruta

According to Acharya Sushruta, Nasya may be given repeatedly at the interval

of 1, 2, 7 or 21 days depending upon the condition of the patient and the disease he

suffer

Acharya Charaka

Acharya Charaka has not mentioned specific duration of the Nasya therapy,

but instead suggested to give it according to the severity of disease.

DOSE OF NASYA

The dose of Nasya drug depends upon the drug utilized for it and the variety

of the therapy. Charaka has not prescribed the dose of the Nasya. Acharya Sushruta

and Vagbhata have mentioned the dose in form of Bindu, here one Bindu means, the

amount of liquid that falls, after dipping the two phalanges of Pradeshini Anguli that

is index finger in Drava Dravya.

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Table 19 Showing Dosage of Nasya Karma

No.

TYPE OF NASYA

Mathra in Bindu Pramana

Hrasva Madhyama Uttama

1 Shamana Nasya 8 16 32

2 Shodhana Nasya 4 6 8

3 Marsha Nasya 6 8 10

4 Avapida Nasya (Kalka Nasya) 4 6 8

5. Pratimarsha Nasya 2 2 2

Acharya Sharangadharahas described the following dosage schedule for Nasya

Karma depending upon the variety of material used.

Tikshnaushadhi Churna - 1 Shana (4 Masha)/(24 Ratti)

Hingu – 1 Yava (½ Ratti)

Saindhava – 1 Masha (6 Ratti)

Dugdha – 8 Shana (64 Drops)

Jala (Aushadha Siddha) – 3 Karsha (3 Tola)

Madhura Dravya – 1 Karsha (1 Tola)

If the Nasya is given in less quantity than the prescribed dose then it does

not eliminate the Doshas completely and cause heaviness, loss of appetite, cough,

salivation, coryza, vomiting and disorders of the throat etc. If the Snehana Nasya is

administered in the excessive dose it may produce the symptoms of Atiyoga

SUITABLE AGE FOR NASYA KARMA

According to Acharya Vagbhata Nasya should not be given before the age of

seven years and after the age of 80 years. But Pratimarsha Nasya may be administered

from birth to death. Acharya Sarangadhara has also given the same opinion as

Acharya Vagbhata. Acharya Charaka has not mentioned the exact age.

ADMINISTRATION OF NASYA

The procedure of Nasya Karma may be classified under following headings :

1) Purva Karma (Pre-measures)

2) Pradhana Karma (Chief measure)

3) Pashchat Karma (Post-measures)

PURVA KARMA

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It is advisable that all materials, drugs and equipments like napkin, utensils

necessary for Nasya Karma are collected in sufficient quantity prior to Nasya Karma.

Patient should be prepared for Nasya Karma. It can be described in detail as under.

Special room for Nasya should be prepared which should be free from atmospheric

effects like direct blow of air or dust and it should be lighted properly

Nasya Asana :It should be placed in Nasya room. It consists of -

a) A chair for sitting purpose

b) Droni for lying purpose

Nasya Aushadhi : Drug required for Nasya Karma in the form of Kalka, Churna,

Kwatha, Kshira, Udaka, Sneha, Asava etc. should be collected in sufficient quantity.

Drug for counter acting any complications during or after the Nasya should also be

kept ready.

Nasya Yantra :It should be collected according to the types of Nasya such as :

A Gokarna or Pichu : For Snehana, Avapida, Marsha and Pratimarsha

Shadangula Nadi : For Pradhmana Nasya

Dhuma Yantra : For Dhuma Nasya

Besides, it is also necessary that a stove, bowl, napkins, spitting pits and an efficient

assistant are kept handy.

Selection of The Patient :The patient should be selected according to the indications

and contra-indications of Nasya described in classics.

Preparation of The Patient :To prepare the patient for the Nasya Karma following

matter should be considered according to Acharya Sushruta.

Patient should have passed his natural urges like urine and stool.

He should have completed his routine activities.

Light breakfast prior (1 hour) to Nasya Karma is advised.

After preparation of patient by above said regimens, Snehana and Svedana

should be done. Here, Snehana means Mridu Abhyanga. It should be done on

scalp, forehead and neck for 3 to 5 minutes by medicated oil.

After Abhyanga, Mridu Svedana should be done on Shira, Mukha, Nasa,

Manya, Griva and Kantha. Though according to Ayurvedic classics, Svedana should

not be done on the head, but for the purpose of elimination and liquification of dosha,

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Mridu Svedana can be done as Purva Karma of Nasya.

PRADHANA KARMA

Patient should lie down in supine position on Nasya table, head of the patient

should be lowered. The position of head should not be excessively extended.After

covering of the eyes with a clean cloth, the tip of patient’s nose should be drawn

upward by the left thumb of the Vaidya. At the same time with the right hand Vaidya

should instil lukewarm medicine in both the nostrils, alternately, with the help of

proper instrument like Pichu, dropper, Gokarna, Shadangula Nadi etc. according the

type of Nasya. The drug should be proper in dose and temperature.Patient should

remain relaxed at the time of administration of Nasya and he should avoid speech,

anger, sneezing, laughing and shaking his head

PASHCHAT KARMA

According to Acharya Charaka, Acharya Sushruta and Acharya Vagbhata,

following regimen should be followed after administration of Nasya. Patient in lying

position is asked to count up to 100 Matra i.e. approximately 2 minutes.

After administration of Nasya feet, shoulders, palms and ears should be

massaged. Again mild fomentation should be done on forehead, cheeks and neck. For

pacifying Vata dosha, Rasna churna is rubbed on head.The patient is asked to expel

out the drug which comes in oropharynx.

Medicated Dhumpana and Gandusha are advocated to expel out the residue

mucous lodged in Kanda.

Patient should be advised to stay in a windless place. A light meal and

lukewarm water are advised. One should avoid dust, smoke, sunshine, hot bath, anger,

riding, excessive intake fat and liquid diet.

Acharya Charaka further says that the patient should avoid day sleep and

should not use cold water for any purpose like pana, snana, etc. Patient should stay at

windless place. Laghu Aahara and Sukhoshna Jala is allowed.

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Tabel 20 DIFFERENCE IN OPINIONS IN NASYA PROCEDURE

A.H. A.S. C.H Su.Sa

Snehana-Svedana of

Uttamanga

Snehana-

Svedana of

Shiras

PrakSurya,

MadhyaSurya

Kala

Snehana-Svedana

of Uttamanga

Void Mala Mutra Mukha

Prakshalana Head tilted down Bhuktavatte

Lye in Nivatastana Void Mala

Mutra Spread Pani Pada Vyabhra Kale

Spread Pani Pada 3 parts Aushada Void Mala Mutra Void Mala Mutra

Leg- raised and head

tilted down wards

Svedana of

Urdvajatru by

Pani

Svedana before

and After Nasya

Not to shake his

head

Mardana of Pada,

Skanda,Hasta,Karna

Eyes covered

with 4 folded

cloth

Dhumapana as

Paschat Karma

Not to talk, laugh

nor sneeze

Spit Aushada on both

the sides

Raise tip of Nose

by middle Finger

Complication-

excessive head

tilting

Apathya leads to

rogas like Kasa

etc.

Repeat twice or thrice. Prayogika

Dhumapana Lye in Nivatastana

Svedana,

Dhumapana-

Pascat Karma

SAMYAK YOGA, AYOGA AND ATIYOGA OF NASYA KARMA

After Nasya Karma, Samyakyoga, Ayoga and Atiyoga should be observed, which

are being described here as under.

Samyak Yoga:The symptoms of adequate, Nasya according to Acharya Charaka are

Urah-shiro-laghava. Indriyavishuddhi and Srotovishuddhi. Acharya Sushruta has

described Sukhaswapna-prabodhana, Chitta-Indriya-prasannata and Vikaropashama.

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Table 21 Samyakyoga Lakshana of Shirovirechana

Criteria Ch Su A.S A.H Sh

Shiro Lakhavam + +

Urah Lakhavam +

Indriya Aachyam + + +

Srotho Vishudhi + +

Sukha swapna probodhanam + + +

Vikara upaShamanam + + +

Manassukham +

Sukhauchwasa + +

Sukhanishwasa +

Kshavadhu +

Vadana Shudhi +

Shiro Shudhi +

Akshapatavam +

Shareera Lakhavam +

Table 22 Samyak Yoga Lakshana of Nasya

CRITERIA Ch Su A.S A.H Sh

Shiraso Lakhavam + + +

Sukha Svapna + + +

SukhaPrabodhana + + +

Vikaropashama + +

IndriYanam Shudhi + + +

Manassukham + +

Akshaavapatanam +

Ayoga

If Nasya is not given in proper way or the dose is less, features of inadequate

Nasya arise which are Shirogaurava (heaviness in head), Galopalepa and Nishthivana.

According to Acharya Sushruta, Kandu, Upadeha, Guruta, Srotasam Kapha Srava are

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the symptoms of Hina Shuddhi. Vitiation of Vata, dryness in Indriya, no relief in the

symptoms of the disease, dryness in mouth and noseare other symptoms of Ayoga of

Nasya Karma.

Table 23 Heena Yoga of Shirovirechana

Criteria Ch Su A.S A.H Sh

Galopalepa +

Shiraso Guruthwam +

Shteewanam +

Vata Vaigunyam +

IndriYanam

Rogashanthi

Vatavikara +

Kantu +

Upadeha +

Gurutha +

Srothasam Kapha Samsravam +

Rogaadhikya +

Table 24 Heena Yoga of Nasya

CRITERIA Su A.H Sh

Akshi Sthabdatha +

Shosha +

MoordhaShoonyata +

Kandu +

Upadeha + +

Gurutha + +

Atiyoga

According to Charaka, the general features of excessive Nasya are, feeling of

Arati and Toda. Kapha Srava, Shirahshula and Indriya Vibhrama are the symptoms of

Atiyoga of Nasya. Mastulungagama, Vatavriddhi, Indriyavibhrama and Shiroshunyata are

also the symptoms of Atiyoga of Shirovirechana.

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Table 25 Atiyoga of Shirovirechana

CRITERIA Ch Su A.S A.H Sh

Shira Toda +

Akshi Toda +

Sravana Toda +

Shiro Arthi +

Akshi Arthi +

Sravana Arthi +

Thimiram Pashyeth +

Vata Vaigunyam + +

IndriYanam Rookshatha +

Kshaamatha or Krushatha +

Masthulungagama + +

Indriya Vibhrama + +

ShiraShoonyata + +

Table 26 Atiyoga of Nasya

Criteria Su A.H Sh

Kapha Praseka + + +

ShiroGuruta + +

Indriya Vibhrama + +

Kandu +

Aruchi +

Peenasa +

Nasya phala:

Thebenefits of Nasya Karma are

Khanata and Prasannata of Tvak, Skanda, Greeva, Asya, Vaksha

Drudatha of Indriyas

Shamana of Urdhajathrugatha Vyadhi

Indriya Vimalatha

Asya sugandham

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Bala in Hanu, Greeva, Shira, Trika, Bahu, Uras

Prevents Vali, Palithya, Khalithya, Vyanga

Ghanonnatha Prasanna Twak, Greeva, Aasya, Vaksha

Snigdha Niswana

Vyapath and its management:

The patients after taking the Nasya Karma if does not follow the regimen

given above then the Prakopa of Dosha may again occur leading to many

complications which are known as Vyapath.

Many complications of Nasya Karma may occur due to:-

(i) Administration of Nasya when it is contraindicated

(ii) Due to technical failure.

These complications occur through following two modes.

(a) Doshotklesha

(b) Dosha Kshaya

Nasya Vyapath is due to Dosha utklesha and where as that of Shirovirechana

is due to Dosha Kshaya. Dosha utklesha is treated with Shodhana and Shamana

Chikitsa and Dosha Kshaya with Bruhmana Chikitsa.

Table 27 Vyapat of Nasya

NASYA KARMA VYAPAT CHIKITHSA

Nasya Doshothklesha Shamana aushadha

Shirovirechana Kshaya Bruhmana

If Nasya is given in contraindicated conditions than many Vyapaths can occur.

When Nasya is administered to the patient just after lunch or who is suffering from

indigestion than diseases like Kasa, Shvasa, Chhardi, Pratishyaya etc. may occur due

to obstruction of channels situated in upper part of body.

Treatment :

In above-mentioned conditions treatment should be done with Kapha Nashaka

Upchara like use of Ushna, Tikshna Aushadha and Kapha Nashaka Karma

If Nasya is given in Krisha, Kshina, Virikta, Aatura, Garbhini, Vyayama

Klanta and a thirsty person then vitiation of Vata takes place which may produce Vata

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Vikara.In this condition, Vatanashaka treatment like Snehana, Svedana, Brumhana

should be specially done, pregnant lady should be treated with Ghrita and Ksheera.

If Nasya is administered in a Madya peeta, person having fever and in

Shokabhitapta then Timira Roga may occur.

Treatment :

Ruksha, Sheeta, Lepa and Putapaka should be applied.

VYAPATHS DUE TO TECHNICAL FAILURE

This can occur in following conditions -

If the drug used for Nasya is very hot or cold.

The dose is not proper i.e. very less or in excess quantity.

If the posture is not proper i.e. patient has lowered his head more during

Nasya.

In such conditions complications like Trishna and Udgara occur. Treatment should be

done according to the disease.

If Moorcha, happens to the patient then, Sheeta Jala should be sprinkled all over the

body avoiding head.

Table 28 Nasya Vyapat and Complication

CONDITION COMPLICATION

Ajeerna, Bukthabaktha Kasa, Shvasa, Chardi, Prathishyaya,

Krusha, Garbhini, Klantha, Thrushnartha. Vata Roga

Peeta or Pathukama of Sneha, Madya, Toya Mukha Nasa Srava, Upadeha, Timira

Snatha shira Prathishyaya

Kshudartha Vataprakopa

Thrushnartha Thrushna, Mukha Shosha

Moorchitha, Asthapitha Dosham Janayeth

Vyavaya, Vyayama, Pana, Klantha, Siranetraskantha peedanam

Navajwara, Shoka Abhithaptha Timira,Jwara Vrudhi

Virikta Indriyopagatham

Anuvasitha Shiroguruthwa, Kandu, Kimi Dosha

Nava Pratishyaya Srothamsi Vyapathayeth

Anrutha Sheetha Dosha, Shirorogam,

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Table 29 Treatment for Vyapat of Nasya

CRITERIA CH SU A.H

Tharpanam which is Mrudu and drava +

Snigdha +

Shamana for Doshotkleshana +

Shodhana for Doshothkleshana +

Bruhmana for Kshaya +

Sheeta Thoya Shirasinchana for Moorcha +

MODE OF ACTION OF NASYA KARMA:

AYURVEDIC VIEW:

In Aayurvedic classics, the mode of action of Nasya karma is explained.

According to Caraka Samhitaa, the drug administered through the nose enters in the

Uttamaanga and liminates the morbid doshas residing there (C. Si. 2/22).

According to ashtangasamgraha:

Drug administered through nose – i.e. the doorway to Sira Reaches the

S’r`ngaat’aka marma of Head (Shira), which is a Siraa marma and formed by the

Siraas of Naasaa, cakshu, kant’ha and shrotra. The drug spreads by the same

routeEliminates the morbid Doshas of Oordhwajatru and extracts them from the

Uttamaanga (As. Sam. Su.29/2).

Indu, the commentator of Ashtaangasamgraha, opined that Sringaataka is

theinner side of middle part of head i.e. “Shiraso antar madhyama”. In this context

Sushruta has clarified that Srngaataka marma is a Siraamarma formed by the union of

Siraa’s supplying to nose, ear, eye and tongue. Thus it can be stated that drug

administered through Nasya may enter the above Siraa and purifies them(S. S’aa.

6/27).

Under the complications of Nasya karma, Sushruta has mentioned that

excessive eliminative errhine may cause Mastulunga Sraava (flow of cerebrospinal

fluidout to the nose) (S. Ci. 40/40), which suggest the direct relation of Nasal pathway

tobrain.All ancient Aacaryas have considered Naasaa as the gate way of S’iras.

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REVIEW OF VIRECHANA KARMA

The word Virechana is derived from the „Rica‟ dhatu after applying „Lyut‟

Pratyaya and „Vi‟ Upasarga. Thus, Virechana means Maladeh Nirharanam i.e.

expelling out of Malas.

Definition

The process applied for the elimination of morbid humors through the

Adhobhaga is known as Virechana. Acharya Chakrapani while commenting on

Adhobhaga clarifies it as the Guda (anal route). In certain circumstance the expulsion

of Dosha through both their route i.e. „Urdhva‟ and „Adho‟ are collectively known by

the term Virechana. According to opinion of Gangadhara, Dosha Nirharana from any

route of the body is termed as Virechana. Thus since Niruha Basti and Sirovirechana

has capacity of expelling the Malas from the Pakvashaya, so these should also be

considered as Virechana. But Acharya Chakrapani is not ready to accept Niruha Basti

and Sirovirechana under term Virechana since Niruha Basti has only capacity of

expelling the Mala from Pakvashaya but not from the total body as in Virechana.

Placement of Virechana:

This can be explained on the basis of its effect on Dosha, Dushya, Srotas, Agni &

Ama.

Dosha

Virechana is said to be beneficial for Pitta Dosha, since it eliminates vitiated

Pitta from its root. According to Vagbhata, Virechana is helpful even in Pitta

combined with Kapha or Kapha in Pitta sthana (A.S.Su.27). But Bhela mentions

Virechana in Sannipata conditions also.

Dushya

Virechana is mentioned as Shodhana procedure in Dusthi of Rasa, Rakta,

Mamsa, Asthi, Majja & Shukra Dhatus. Hence in majority of the Dhatupradoshaja

Vikaras Virechana is the better option (Ch.Su.28/25-28).

Srotas

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Since on the above mentioned Dushyas Virechana is helpful, we can say that it

is beneficial in Rasavaha, Raktavaha, Mamsavaha, Asthivaha, Majjavaha &

Shukravaha Srotodushti also.

Agni

In the Samyak Virikta Lakshana, Deeptagni is mentioned. Hence Virechana

improves the Mandagni state also.

Ama

It is indicated in the state of Ama but before that Langhana-Pachana should be

done (Ch.Su.22).

Classfication of Virechana dravya

Classification of Virechana dravya can be done as follows.

Depending upon the origin and part used.

Depending upon intensity of action.

Classification on base of Kalpna.

According to safety of their use.

According to seasons.

Depending upon the origin and part used :

1. Animal Origin :

Urine (A. S. Su. 14/4; Ch. Su. 1/94-97)

Milk (Ch. Su. 1/107-114)

Takra (A. S. Su. 14/4)

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2. Plant Origin

Table 30 Parts used for Virechana- Plant orgin

Part Used Charaka (Ch.Su.1/77-

85)

Sushruta Su. Su. 39/4) Vagbhata (A. S. Su.

14)

Mula

(Mulini)

Hastidanti

Shyama trivritta

Shweta

Saptala

Danti

Gavakshi

Visanika

Avartaki

Dravanti

Snuka

Shyama trivritta

Raktamula

Saptala

Danti

Gavakshi

Swarnakshiri

Dravanti

Chitraka

Kusa, Kasa

Kinihi

Salaparni

Prasnaparni

Kantakari

Vartaki

Gokshura

Punarnava

Vastuka

Salavriksha

Phala

(Phalini)

Sankhini

Vidanga

Anupklitaka

(Madhuyasti)

Prakirya

(Latakaranja)

Abhaya

Antahakotarpushpi

Kampillaka and

Aragawadha

Udkirya

Puga

Eranda

Haritaki

Amalaki

Bibhitaka

Nilini

Chaturangula

Kampillaka

Triphala, Pilu,

Eranda, Priyala

Badara

Kuvala

Karkandhu

Kashmari

Puga

Parusaka

Vidanga

Draksha

Nil, Yashtimadhu

Putikaranja

Kshira Snuhikshira

Arkakshira

Saptacchada

Jyotishmati

Saptaparna

Jyotishmati

Tvacha Putika

Tilvaka

Kampillaka

Ramyaka

Patala

Tilvaka

Kampillaka

Lodhra

Mahanimba

Classification depending upon intensity of action:

Mrudu Virechaka Drugs

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As the term indicates. The drugs which are mild in action causing lesser

degree of purgation, to be given in low dosage and which are combined with drugs

having antagonistic action.

Indications

Alpa Dosha, unknown Kostha, Purva Shodhita weak patients with ample

Dosha, Mrudu Kostha patients

e.g. Draksha, Dugdha, Ushna Jala (Su. Ut. 4/13-14).

Madhyama Virechaka Drugs

The drugs which are moderate in qualities and action, is known as Madhyama

Virechaka.

Indications

Madhyama Roga, Madhyama Bala (Ch.Ka.12/55-58),

e.g. Trivrita, Katuki, Aragvadha (Su. Ut. 4/13-14).

Tikshna Virechaka Dravya

The drugs which induces several motions and eliminates the Dosha in large

quantity. In quick and gentle way without causing Glani (uneasiness), pain in

precordial region or anus or any other internal organ are termed as Tikshna Virechaka.

(Ch. Ka. 12/51-52)

Indication

Balavana, Krura Kostha

e.g. Hemakshiri, Danti, Jayapala.

Classification on base of Kalpana

Various pharmaceutical preparations of drugs are prepared for enhancing the

potency, shelf life and convenience; Acharya Sushruta has given eight preparations as

follows in context of Virechana –

Kshira Yoga Madhya yoga

Ghrita Yoga Taila Yoga

Mutra Yoga Mamsa Rasa Yoga

Bhakshanna Yoga Avaleha Yoga

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Besides these few other Kalpana like Kashaya, Panaka, Tarpana, Shadava,

Raga, Yavagu, Modaka, Dadhi etc.

Virechana Drugs according to the safety of their use (Ch. Su. 25/40)

Mrudu Virechana

They are mild in nature and may be used in Mrudu Kostha.

Indication : Mrudu Kostha

e.g. Aragwadha

Sukha Virechana

The drug which cause Samyaka Virechana without any complications may be

referred as Sukha Virechana.

Indication: Madhyama Kostha

e.g. Trivrita.

Tikshna Virechana

The drugs of this group are drastic in their action.

Indication: Krura Kostha

e.g. Snuhi Kshira

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Table 31 Virechana Drugs according to Seasons (Sh. U. 4/21-27)

Varsha Sharada Hemanta Shishira

and

Vasanta

Grishma All seasons

Preparations Trivrita

Kutaja

Bija

Pippali

Shunthi

Trivrita

Duralabha

Musta

Sharkara

Bala

Chandana

Trivrita

Chitraka

Patha

Jivaka

Sarala

Vacha,

Hemakshiri

Trivrita

Pippali

Nagara

Saindhav

Shyama

Trivrita Trivrita

Danti

Hapusha

Saptala

Katuki

Svarnakshiri

Anupana Draksha

Swarasa

&

Honey

Yashti in

Draksha

Decoction

Warm

water

Honey Sugar Bhavana

with cow‟s

urine

Table 32 Some of the Agrya drugs mentioned in classics are: (Ch.Su.25/40)

Mridu virechana Aragwadha

Sukha virechana Trivrit

Teekshna virechana Snuhi

Purisha janana Yava

Table 33 According to Sushruta: (Su.Su.44/3,4)

Mula virechana Arunabha trivrit mula

Twak virechana Tilwaka

Phala virechana Haritaki

Taila virechana Eranda taila

Swarasa virechana Karavellaka

Paya virechaba Sudha paya

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Table 34 Virechna drug according to Prakriti

Prakriti Virechana Drug

Pitta Kashaya and Madhura Rasa Aushadhi

Kapha Katu Rasa Aushadhi

Vata Snigdha, Ushna & Lavanayukta Aushadhi

Table 35 Virechana drug according to Dosha

Dosha Virechana Drug

Pitta Trivrita with Draksha Kwatha

Kapha Triphala or Gomutra + Trivrita + Triphala

Vata Trivrita + Saindhava + Sunthi with Amla

Mansa Rasa

Kaphaja Vyadhi Pippali, Shunthi, Yavakshara, Trivrita

with honey

CLASSIFICATION OF VIRECHANA :

Acharya Sharangadhara was the first person who has mentioned the

classification of Virechana as per the action, potency of drug, onset consistency of

excretory products (Sha. Pu. 4)

Anulomana

The drug which make the digestion of Mala and breaks its compactness and

after that bring toward Adhobhaga is known as Anulomana e.g. Haritaki.

Sramshana

The drugs which expels the half digested and sticky Mala without its prior

digestion is known as Sramshana e.g. Aragwadha.

Bhedana

The drug which breaks all types of Mala like Abaddha, Baddha, Pindita and

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throws them through anal route are called Bhedana e.g. Katuki.

Rechana

The drugs which eliminates digested as well as undigested Mala by making

them watery, though Anal route are known as Rechana e.g. Trivrita.

Classification of Virechana on drugs Properties :

Sneha Virechana

The preparation containing (oil) Sneha is known as Sneha Virechana. Sneha

Virechana should be used in all patients except Snigdha patients (A. H. Su. 18/57). It

is contraindicated in patients who have been given higher dose of Sneha (Su. Chi.

33/41; Ch. Si. 6/9).

Ruksha Virechana

The preparation which is devoid of Sneha is known as Ruksha Virechana. It is

prescribed in the patients who have taken more Sneha because in such bodies due to

increased. Sneha (unctuousness), the Dosha may adhere instead of being detached.

Procedure for Virechana Karma

The main procedure can be classified as, Purvakarma karma, Pradhana karma,

Paschat karma.

Purva Karma

This includes -

1. Sambhara Samgraha

2. Aatura Pariksha

3. Aatura Siddhata

4. Matra Vinishchaya

1) Sambhara Sangraha: Acharya Charaka advocated that Virechana Karma

should be performed by collecting the necessary equipment at first. He advised

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to do same in order to carry out the Virechana safely and to avoid the

complication and if complication arises that can be handled safely. The storage

of these things will be helpful in the condition of emergency (Ch. Su. 15/3).

Different types of drugs to be collected before going to Virechana.

a) Deepana Pachana Drugs : Trikatu, Panchakola, Chitrakadi Vati etc.

b) Sneha Dravya: Pancha tikta ghrta, Dadimaadi ghrta etc. according to the

requirement of patients.

c) Virechana Drugs: Like Aragvadha, Katuki, Eranda Taila, Icchabhedi Rasa,

Abhyadi Modak etc. according to Kostha and Prakriti of the patients.

d) Virechanopaga Drugs: Acharya Charaka has mentioned a group of 10 drugs

which are helpful in inducing the Virechana. These drugs are – Draksha, Kashmarya,

parushaka, Abhaya,

Amalaka, Bibhitaka, Kuvala, Badara, karkandu and Pilu (Ch. Su. 4/13).

e) Emergency Drugs : Certain drugs for counter acting various emergencies like

Kutaja Ghanavati, Karpura Rasa etc. Along with this Pichchha Basti drugs, Mocha

Rasa etc. must also be collected prior to Virechana.

Collection of Instruments:

Along with these drugs sphegmomanometer, stethoscope, thermometer should

also be arranged. Dietic food required for the previous night and for Sansarjana

Karma should also be kept ready.

2) Aatura Pariksha:

There are certain diseases and certain physiological as well as pathological

conditions in which Virechana may prove hazardous. Patients should be thoroughly

examined in this context. After choosing the right patient appropriate sneha for

snehana and appropriate drug for Virechana should be chosen. During Snehapana,

patient should be monitored daily for any unexpected conditions.

In persons who are Sneha Satmya, first Rukshana is done after which

Virechana is executed.

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Patients who have Ruksha Sharira, dominancy of Vata dosha, possessing

Krura Koshtha, habituated of doing exercise daily, having fulminating appetite

should be given Sneha basti prior to Virechana. If this is not done then

Virechana aushadhi is digested itself.

Indications and Contraindications

Table 36 Indications of Virechana karma

Diseases Cha

Su.

A. H.

Diseases Cha

Su.

A. H.

Jwara + + + Udavarta + - -

Kustha + + + Ashyadaha + + -

Prameha + + + Hrudroga + + -

Urdvaga

raktapitta

+ + + Vyanga + - +

Bhagandara + + + Neelika + - -

Arsha + + - Aruchi + + -

Pliha + + + Netrasrava + - -

Gulma + + - Nasasrava + - -

Arbuda + - - Halimika + - +

Galaganda + - - Shwasa + - +

Granthi + + + Kasa + - +

Gara - + + Kamala + - +

Vishuchika + + - Apachi + - +

Alasaka + + - Apasmara + + -

Mutraghata + + + Unmada + - -

Krimikoshta + + + Vatarakta + + +

Visarpa + + + Yonidosha + + +

Pandu + + + Raktadosha + - +

Shirashula + + + Timira + + +

Parswashula + - - Udara + + +

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Table 37 Contraindications of Virechana Karma

Diseases Cha.

Su.

A. H.

Diseases Cha.

Su.

A.

H.

Shubhaga + - - Atisthoola + + +

Kshataguda + - + Atikrisha + - +

Muktanala + - - Bala-vrudha + + +

Adhoga raktapitta + + + Durbala + + +

Langita + - - Shranta + + -

Durbalendriya + - - Pipashita + + -

Alpagni + + + Karmabhara

advahata

+ - -

Niruda + - + Upavasita + + -

Kamadivyagra + - - Maituna Prashakta + - -

Ajeerna + + + Adhyana Prashakta + - -

Navajwara + + + Vyayama

Prashakta

+ - -

Madatyaya + + + Chinta Prashakta + - -

Admana + - + Kshama + - -

Shalyardita + - + Garbini + + +

Abhihata + - + Navaprasuta - + +

Atisnigda + + + Navapratishaya - + -

Ativruksha + + + Rajayakhmi - - -

Dharunakoshta + + - Atisara - - +

Kshataksheena + + + Hrudrogi - - +

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Reason for indication:

Pitta Pradhana Vyadhi‟s are indicated since Virechana is best in those diseases

(Ch.Su.25/40) e.g. Pandu, Kamala.

Rakta Pradoshaja Vyadhi: Since there is a indication of Virechana in those

diseases. e.g.: Kustha, Visarpa, Raktapitta, Gudapaka (Ch.Su.24/18).

Diseases wherein there is extreme need to eliminate Doshas like in Gara

Visha, Krimi Kostha & Udavarta.

Diseases having Viparita Gati like Urdhwaga Raktapitta & Chardi etc,

Virechana is indicated to reverse the Gati of the disease.

Diseases in which there will be excessive vitiation of Doshas & also having

Tridosha Prakopa & also those diseases requiring Ubhaya bhaga Shodhana

like Kustha, Virechana is indicated.

Those diseases wherein Pitta has its location:

Eg: Hridroga- Sadhaka pitta

Jwara- Pachaka pitta

Kamala- Ranjaka pitta.

Reason for contra-indication

Patient who is incapable of tolerating the stress produced during Virechana

like Langhita, Durbalendriya.

Ashukari roga: Hridroga, Kshata Ksheena which may collapse the patient.

Sama avasthas, wherein Snehapana itself is contra indicated.

Local problem: To guda pradesha like in kshata guda.

Altered or disturbed mental conditions of the patients like in bhaya bheeta,

kamadi vyaghra wherein there may be the risk of mithya yoga.

Certain altered physiques like Atisthula, Atikrisha & in weak physical

conditions like Bala, Vriddha conditions.

Pathology involving the elimination of Doshas through Adhomarga like in

Atisara, Adhoga Raktapitta.

3) Aatura Siddhata

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Vamana Karma should be done before Virechana because if it is not done then

Kapha doshas may cause Avarana of Grahani. (Sha. Ut. 4/1-2, Vangasena,

Hemadri)

It is also advisable the Asthapana Basti to be administered before Virechana.

If patient is [Vata dominated] Krura Kosthi, then there is no need to give

Vamana before carrying the Virechana. (A.S. Su. 27/27)

Deepana And Pachana :

The condition of patient must be examined before giving Virechana. The

condition of patient must be Nirama. If Samshodhana medicine is taken in the

condition of Ajirna, it will lead to Vibandha and Glani (Ch. Si. 6/14). If the condition

of patient is associated with Ama then Shodhana can only be done after the Pachana

of Ama by Deepana, Pachana, Snehana and

Swedana measures (A. H. Su. 13/28-30; Ch. Chi. 3/53).

If the Doshas are in Ama conditions and anybody tries to remove these Dosha

forcefully then it will destroy the Dhatu. That is why prior giving the Snehana,

Deepana and Pachana should be carried out to enhance Agni. So that Snehana can be

easily digested and patients will be properly oleated, for the purpose of Deepana and

Pachana Agnitundi Vati, Trikatu Churna, Chitrakadi Vati etc. can be used.

Diet before Virechana:

After preparing the patient properly with Snehana and Swedana, he may be

subjected to Virechana. A day before Virechana patient should be advised to take

Laghu, Snigdha, Drava, Ushna diet, Mamsa rasa should be provided (Ch. Si. 1/9,

6/13). Diet should be as such that it should not increase Kapha as that may cause

Vamana and for carrying Virechana there should be state of Manda Kapha (Ch. Si. 1).

Manasopachara:

Patient should be counseled in sound manner and prepared mentally also,

because disturbance in mental state can cause Mithya Yoga. Patient should also

perform Swastika Vachana, Homa Bali etc. on auspicious day for peace of mind (Ch.

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Su. 15/17).

4) Matra Vinishchaya:

Matra plays a profound role in a samyaka Virechana. It should be elaborately

counted by taking various factors like Roga bala, Rogi bala, Agni bala, Aushadha

virya, etc. in account. While deciding the matra of Virechana aushadhi prime

importance is to be given to the koshtha of the patient as well as the form of

Virechana aushadhi i.e. whether it is in form of Churna, Kwatha, Swarasa or Modaka.

Various doses depending the koshtha and kalpana are described below in tabulated

form:-

Kalpana Hina for Mrudu

Kostha

Madhyama for

Madhyama

Kostha

Uttam for Krura

Kostha kwatha

Kwatha 2 tolas 4 tolas 8 tolas

Kalka, Churna,

Modaka

1 tolas 2 tolas 4 tolas

Swarasa (Half of

Kwatha)

1 tolas 2 tolas 4 tolas

Ushnodaka(As

Anupana)

4 tolas 8 tolas 12 tolas

If the Kostha of patient is unknown then he should be administered mridu

aushadhi.

If the patient is weak, having alpa dosha, devoid of strength, whose shodhana

has been done and whose Kostha is unknown then in such patients mridu

aushadhi is advisable and that also in alpa matra.

B) Pradhana Karma

This includes:

1) Administration of Virechana Yoga.

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2) Observation: a) Aushadi Jeerna-Ajeerna Lakshana.

b) Hritadosha Lakshana.

3) Suddhi Lakshana.

4) Management of Vyapada.

1) Administration of Virechana Yoga.

Purva karma:

Acharya Charaka elaborately described the method of administration of

Virechana drug which is as follows.

After successfully administration of Snehana and Swedana, finding the patient

to be cheerful, to have slept well, to have full digested his/her meal and empty

stomach. It is essential that patient should remain in calm mood, because intestinal

motility, secretion of various enzymes and that of mucous are very sensitive towards

emotional disturbance. Any emotional stress may alter the intestinal motility as well

as secretions causing hurdle in Samyaka Virechana.

Patient has performed Dharmik karma like Homa, Bali, Swasti Vachana, etc.

These things help in boosting up the will power of patient. When Tithi, Muhurat are

ideal.

Virechana drugs are administered in „Shleshma kale gate‟ i.e. after Shleshma

kala has passed i.e. not in early morning like Vamana. The suitable time is 8 to 10 am.

It should preferably be administered empty stomach.

Aushadha pane kartavya

Virechana Aushadha should take in Kwatha form with Luke warm water in a

single bout, without feeling its smell and taste.

Aushadha pite kartavya

After intake of Virechana yoga, it is possible that patient may feel nauseatic

due to odour and irritative nature of Virechana drugs, to prevent that cold water is

sprinkled on face. Patient is asked to gargle hot water and have fragrance of flowers,

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lemon, etc. Exposure to cold wind is prohibited. Patient is asked to relax and take rest

in bed. He is advised that neither the Vegas should be induced nor should be retained.

Vega pravartanopaya

For Vatanulomana and Yogavahi action lukewarm water is taken. If medicine

composed of Jayapala is given then hot water is contraindicated. If Vegas are not

induced then Swedana is done over abdomen by Pani tala.

2) Observation :-

a) Aushadi Jeerna-Ajeerna Lakshana

Virechaka Dravya plays a role after „Aushada Jeerne‟ digestion through

stomach. Symptoms of Aushadhi Jeerna and Ajeerna are

Aushadhi Jeerna Lakshana Aushadhi Ajeerna Lakshana

Vatanulomana Klama, Daha

Swasthya Angasada

Kshudha Bhrama

Trusha Murccha

Urjamanasvita Shiroruja

Indriya laghuta Arati

Udgara shuddhi Balahani

If Ajeerna of Aushadhi is observed then medicine should not be administered

again, as it may cause Atiyoga.

If Aushadhi Jeerna symptoms are present and Virechana is not induced then

Virechaka dravyas are given on next day.

If still Virechana is not induced then after 10 days again the whole procedure

should be initiated. If the medicine itself obstructs the Doshas and there is no

induction of Vamana or Virechana along with body ache then fomentation

should be executed over abdomen.

If Pittaja symptoms like Trushadhikyata, Bhrama occur then they should be

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treated by Madhura, Sheeta Virya aushadhi.

If Aushadhi Jirna Lakshana are available, but Hritdosha Lakshana are not

found then Virechana Yoga should be given on next day.

Even then if Virechana does not occur then Snehana and Swedana should be

done again and thereafter Virechana drug should be administered after 10

days. (A. H. Su. 18/36-38)

b) Hritadosha Lakshana:

There should be sequential elimination of Vita, Pitta and Kapha along with

Gatra, Daurbalya and Laghuta. If Hrita-dosha Lakshana are present, Kaphanta

condition is observed and still Virechana is not terminated then Vamana should be

induced (Ch. Si. 6/21).

3) Shuddhi Lakshana:

Chaturvidha Shuddhi Lakshana

Chakrapani has categorized this assessment by naming as Antiki, Vaigiki,

Manikia and Laingiki criteria (Ch.Si. 1/14-16).

Shuddhi

Prakara

Pravara

Shodhana

Madhyama

Shodhana

Avara

Shodhana

Vaigiki 30 Vegas 20 Vegas 10 Vegas

Maniki 4 Prastha 3 Prastha 2 Prastha

Antiki Kaphanta Kaphanta Kaphanta

1 Prastha = 648 gm

There is a lot of controversy regarding these criteria as which is the best one.

Several explanations are given by different scholars. After detailed explanation

regarding these four criteria, Chakrapani counts Antiki Shuddhi under Laingiki one

(Chakrapani on Ch. Si. 1/14-16). Chakrapani at last accepted Laingiki Shuddhi is

most acceptable one and important in assessing the Shodhana procedure.

Vaigiki Criteria

After the administration of the medicine while counting the Vegas, the first 2 –

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3 Vegas mixed with Mala should not be counted (Ch. Ka. 14). The purification may

occur in varying number of Vega which are influenced by the factors like body

consistency, age, strength of an individual drug and vitiation of Doshas (amount of

vitiated doshas).

Maniki Criteria

Maniki Shuddhi is defined as the Shuddhi, in which the proportion of Avara,

Madhyama and Pravara Shuddhi are 4, 3 and 2 Prastha respectively. This criteria

seems impractical as nowadays it is verydifficult to assess in different condition.

Vaigiki and Maniki criteria are important for decide the Samsarjana Karma. Actually

“Jaghyanyadi Shuddhi” must be decided for Samsarjana Krama and this is to be

decided on the basis of Vega and Mana. Because the number of Vega and expelled

humor (Dosha) is going to disturb our body physiology right from Agni (digestive

juices) to homeostasis of all the physiological process, nourishment of body,

electrolyte balances etc. To fulfill these requirements and to act according to state of

Agni, Samsarjana Krama should be followed (Ch. Si. 1)

Antiki Criteria

Antiki Shuddhi is just like indicator of any titration reaction, it means this is

the stage where we have to stop as our ultimate aim is achieved, we must not go

beyond this stage otherwise condition will be worsened.

Laingiki Criteria

The sign and symptoms described under the head of Samyaka – Lakshana can

be considered under Laingiki criteria.

This criteria is observed to see whether our Karma has reached to our ultimate

goal of Shodhana or not, as we have to act further for treatment regimen. This has

given due importance by all Acharyas.

Explanation

Chakrapani had described Jaghanya, Madhyama and Avara Shuddhi to

understand the proportion of Dosha vitiated inside the body which is eliminated out.

What is Kaphanta Virechana?

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This is a sign of Samyaka Virechana. We can consider it as indicator as

present in any titration reaction. Because this is the endpoint where we must stop as

this is our ultimate aim, if we go beyond this level there may be chances of

complications. In Virechana, there is sequential elimination of Vita, Pitta, Kapha and

Vata. Our aim is to eliminate the Pitta and up to some extent small quantity of Kapha.

The great preponderance of secretion in the large intestine is mucus. This

mucus contains moderate amount of bicarbonate ions secreted by a few non-mucus

secreting epithelial cells that lie between the mucus secreting epithelial cells.

After the elimination of Mala and Pitta, this mucus is secreted by gut and can

be taken as Kapha in Virechana process.

The rate of secretion of mucus is regulated principally by direct, tactile

stimulation of the mucus cells on the internal surface of the large intestine and by

local nervous reflexes to the mucus cell in crypts of Lieberkuhn. Stimulation of the

pelvic nerves from the spinal cord, which carry parasympathetic innervations to the

distal one – half to two third of the large intestine, also can cause marked increase in

peristaltic motility of the colon. Therefore, during extreme parasympathetic

stimulation, so much mucus can occasionally be secreted into the large intestine.

Mucus in the large intestine protects the wall against excoriation. Furthermore,

it protects the intestinal wall from the great amount of bacterial activity and provides a

barrier to keep acids formed in the feces from attacking the intestinal wall.

Main function of this mucus is to protect intestinal wall from excoriation, as if

we continue the process of Virechana after Kaphanta condition is reached then there

are chances of rupture of intestinal wall and capillaries vessels etc. and it may lead to

blood loss (Jivadana). So to avoid this condition, as primary stage mucus is secreted

by intestine to protect the wall and if the process of Virechana is stopped then there is

no harm.

Hence, we can say this is an indicator (alarm) for Samyaka Virechana and also

for avoidance of Vyapada.

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Table 38 Samyak Yoga Lakshanas of Virechana Karma

Lakshana Charaka Sushruta Vagbhata

Sroto Vishuddhi + - -

Indriya Prasada + + -

Laghuta + + -

Agnivrddhi + - -

Anamayatva + + -

Kramat Vit Pitta Kaphagamana + + -

Vatanulomana - + -

Absence of Ayoga Lakshanas - - +

Table 39 Ayoga Lakshanas of Virechana Karma

Lakshana Charaka Sushruta Vagbhata

Kapha Prakopa + + +

Pitta Prakopa + + +

Vata Prakopa + - -

Agnimandya + + -

Gaurava + + -

Pratishyaya + - +

Tandra + - -

Chardi + - -

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Aruci + + +

Vata Pratilomana + - Vatagraha

Daha - + +

Hrdaya Ashuddhi - + +

Kukshi Ashuddhi - + +

Kandu - + +

Vit Sanga + + +

Mutrasanga - + -

Pidika - - +

(Ca. Si. 1/18, Su.Ci. 33/24, A.H.Su. 18/38-39)

Table 40 Atiyoga Lakshanas of Virechana Karma

Lakshana Charaka Sushruta Vagbhata

Kapha Kshaya Vikara + + -

Pitta Kshaya Vikara + - -

Vata Kshaya Vikara + - -

Supti + - -

Angamarda + - -

Klama + - -

Vepathu + - -

Nidra + - -

Balabhava + - -

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Tamah Pravesha + - -

Unmada + - -

Hikka + - -

Murcha - + -

Guda Bhramsa - - -

Kapha Pitta Rahita Shveta

Udaka Nihssarana

- - +

Kapha Pitta Rahita Lohita

Udaka Nihssarana

- - +

Mamsa Dhavana vat udaka

srava

- - +

Medokhandavat Srava - - +

Trishna - - +

Bhrama - - +

Netrapraveshanam - - +

Raktaksayaja Vikara + - -

Management of Atiyoga

Due care should be taken in case of Atiyoga and it should be managed by

following measures –

1) Water should be sprinkled on the patient‟s body.

2) Tandulodaka should be given with honey.

3) Juice of Kapittha should be given with honey.

4) Padmakastha, Nagakesar, Raktachandana should be administered with honey.

5) If Mala kshaya occurs then soup of Udana should be given with Kulmasha.

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4) Management of Vyapada

Vyapda means complication occurred due to improper handling of Shodhana

Karma. These are symptoms observed other than Shamaka Yoga symptoms. Charaka

has explained 10 Vyapada as-

1. Adhmana (Distension of abdomen)

2. Parikartika (Gripping pain)

3. Parisrava (Excessive discharge)

4. Hritgraha (Cardiac spasm)

5. Gatragraha (Spasms of limbs)

6. Jivadhanam (Discharge of blood)

7. Savibhramasha

8. Stambha (Rigidity)

9. Upadrva (Serious afflicatios)

10. Klama (Exhuastion)

Vyapada Lakshana Chikitsa

Adhamana Adhamana, Udvarta,

Nabhi, Prustha, Parshva,

Shiroruja, Shvasa, Vit

Mutra, Vata Sanga

Abhyanga, Sweda,

Phalavarti,

Niruha, Anuvasana,

Udavartahara, Chikitsa

Parikartika Gud Parikartana,

Tivrashula,

Pichcha, Rakta, Mala

Pravritti

Langhana, Pachana,

Ruksha,

Ushna Bhojana

Yashtimadhu

Sneha Basti

Parisrava Alpa Mala Pravritti,

Kandu, Shopha, Kustha,

Gaurava, Agnimandya,

Staimitya, Aruchi, Panduta

Vamana, Virechana,

Grahani roga Chikitsa,

Asava, Arishta

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Hridgraha Hikka, Swasa, Kasa,

Parshvashula, Lalasrava,

Akshivibhrama, Shula,

Dantatikitkitayana, Jihva,

Snigdha Lavana, Sweda,

Yashti Taila,

Anuvasana, Tikshna

Nasya, Vamana, Basti

Angagraha Stambha, Vepathu, Toda

Pindikodveshtana,

Manthanavat Pida

Vatahara

Snehana

Swedana

Jivadana Rakta Chandrika,

Udakasrava,

Guda Bhransha, Trishna,

Murchha,

Mada

Pittahara, Raktapana,

Rakta

Basti, Pichcha Basti,

Ghrita

Manda, Anuvasana

Vibhransh Only Mala Excreted not

Doshas, Shodhana Occurs

Gudabhransha, Sanjna

Bhransha, Kandu, Pidika,

Kustha.

Kashaya Lepa, Snehana

Mrudu Sweda,

Manonukal Chikitsa,

Tikshna Shodhana After

Snehapana

Stambha Vatavarodha,

Gudastambha,

Gudshula, Alpalpa Mala

Pravritti

Langhana, Pachana,

Tikshna Basti,

Virechana

Upadrava Stambha, Shula,

Gatragraha, Sarvanga

Vedana

Snehana, Swedana

Vataghna Chikitsa

Klama Tandra, Gaurava, Klama,

Daurbalya, Angasada

Langhana, Pachana,

Sneha,

Tikshna, Shodhana

Sushruta has mentioned 15 complications, out of which Adhmana, Jivadana,

Parikartika, Parisrava, Angagraha, Vibandha, Hridayo pasaranam are common

Savasesaudhatvam, Jirna Aushadhatvam, Hina dosha pritatvam, Vamansyadhogati

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and Virechanasya Urdhva (movement of humors in opposite direction) are different in

Sushruta which are included in the causes of complication by Charaka (Su. Chi. 34/3).

Acharya Sushruta has mentioned some other complications which are

explained as follows.

Savisesha Aushadhi Vyapada

Dosha Vigrathita drug when given in small dose is unable to eliminate dosha

and may lead to Savisesha Vyapada.

Signs & Symptoms: Thirst, pain in sides, vomiting, unconsciousness, pain in joints

and nausea.

Management: Such condition should be managed by Vamana (emesis).

Jirna Aushadhi Vyapada

When the Virechana drug of low potency is given in small doses to the patient

having Krura Kostha and Tikshnagni, then it may be digested like food without

causing purgation. This leads to Vyadhi and Bala Vibhramsha and the condition is

known as Jirna Aushadhi Vyapada.

Management: This should be managed with Tikshna drug in sufficient quantity after

Snehana.

Vibandha

If patient gets exposed to cold water or air during Virechana then the dosha

gets retained in their respective Srotasa and causes retention of Vayu, urine and

faeces. This condition is known as Vibandha Vyapada.

Sign and symptoms: Atopa, burning sensation, fever and acute pain.

Management: Vamana, Virechana, Asthapana Basti and Anuvasana Basti should be

advised.

Pratiloma Gati Vyapada

If the Virechana drug is given before digestion of previous meal or the Kapha

is aggravated or the drug is of offensive smell, then it causes vomiting, means

Pratiloma Gati.

Management : In this condition, Snehana and Swedana should be done and again

Virechana should be given.

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C) Paschat Karma

This includes

1) Samsarjana Karma.

2) Tarpanadi Karma.

3) Astha Mahadoshkar Bhava

4) Subsequnt Shodhana procedure.

5) Internal Medicine.

1) Samsarjana Krama :

This is special dietary protocol that is to be followed after Virechana. Jejjata

says “The liquefied vitiated doshas come in Amashaya, which causes irritation in

Amashaya weakening its Agni”. To boost this weakened Agni of Amashaya

Samsarjana is followed. There is description of Samsarjana krama at two places in

Charaka Samhita, one in Sutrasthana and other at Siddhisthana.

In this Krama, Peya, Vilepi, Akruta yusha, Kruta yusha, Akruta mamsa rasa

and Kruta mamsa rasa are given for 3, 2 and 1 Anna kala for Pradhana, Madhyama

and Avarashuddhi respectively (Ch. Si. 1/11).

It can be tabulated in summarized form as follows –

Table 41 Samsarjana krama

Days Annakala Pravara Suddhi Madhyama

Suddhi

Avara Suddhi

I day 1 morning - - -

2 evening Peya Peya Peya

II day 1 morning Peya Peya Vilepi

2 evening Peya Vilepi Krtakrt Yusa

III day 1 morning Vilepi Vilepi Krtakrt

Mamsarasa

2 evening Vilepi Akrta Yusa Normal diet

IV day 1 morning Vilepi Krta Yusa -

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2 evening Akrta Yusa Akrta

Mamsarasa

-

V day 1 morning Krta Yusa Krta Mamsarasa -

2 evening Krta Yusa Normal diet

VI day 1 morning Akrta

Mamsarasa

- -

2 evening Krta Mamsarasa - -

VII day 1 morning Krta Mansarasa - -

2 evening Normal diet - -

Acharya Sushruta is of opinion that Yusha of Kulatha, Adhaki or Mamsa rasa

can also be given. Here, Dalhana explains that Peyadi krama is also admitted by

Sushruta, but if there is dominancy of Vata then Mamsa rasa, if there is diminished

Kapha then Peya and if there is Kapha vriddhi then Yusha of Kulatha and Adhaki

should be given.

Sushruta has also opined the Samsarjana Krama in respect to Bala of patient.

But this Bala can be assessed by Upachaya of patient. It is more appropriate to

consider the Bala of patient after Shodhana Karma as existent Bala of patient for

following the Samsarjana Krama (Su. Chi. 39/17-18). For the individuals having good

strength, three Anna Kala are advocated, two Anna Kala for the individual of medium

strength and the individuals with lesser strength only one Anna Kala is advised (Su.

Chi. 39/17-18).

2) Tarpanadi Karma :-

Usually Peyadi krama is observed after Virechana, but under certain

circumstances Santarpana is preferred. Acharya Charaka says that if Shodhana is

improper, patient is addicted to alcohol, patient is of Vatapitta prakriti then

Santarpana is advisable.

In this procedure in place of Peya, Swachchha Tarpana and in place of Vilepi

Ghana Tarpana are given. Jejjata has considered Mudaga Yusha and Mamsa rasa as

Tarpana. Arundatta prescribes Sattu, Purana Shalyodana and Mamsa rasa in 1st, 2nd

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and 3rd Anna kala respectively.

3) Ashta Mahadoshakara Bhava :

The following Ashta Mahadoshakara Bhava and some other activities are to be

strictly avoided after Virechana till Prakriti sthapana is achieved.

They are as under,

1) Loud speeches

2) Excessive ingestion of food

3) Sedentary habit

4) Excessive roaming – traveling

5) Anger – misery

6) Sleeping at noon

7) Remaining awake at night

8) Either inducing natural urges or retaining them (Ch. Si. 12).

After Virechana when patient acquires adequate strength, complexion, serene

mood, sufficient sleep, normal digestion then he should take a bath and apply lepa of

Chandana, wear garland, new clothes and ornaments. Then after he is advised to

communicate with his friends and relatives and do appropriate Ahara - Vihara.

4) Subsequent Shodhana Procedure

If Basti is to be given after Virechana then it should be administered from 8th

or 9th day onwards. It is more plausible that Basti given on 9th day is Anuvasana and

3 days after it Niruha should be given.

5) Internal Medicine

If internal medicine is thought to be ideal after Virechana, then it should be

sought for after 7 days.

Probable Mode of action

Ayurvedic View

Deepana

Due to its inherent properties it enhances the Agni which is helpful in the

digestion of Sneha taken during Snehapana.

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Snehapana

Main purpose of Purvakarma is to eliminate doshas from Shakha to Kostha. It

is done by Snehana and Swedana. Acharya Charaka has given a verse, which

describes how Doshas from Shakha enter the Kostha.

The elevated doshas on Vriddhi, Vishyandana, Paka, and Srotomukha

Vishodhana and Vatanirodha re-enters the Kostha from Shakha. Detail description of

this is given below.

Vriddhi

Sneha is able to elevate the quantity of Dosha with help of its Snigdha and

Drava properties.

(1) Snigdha : Due to its Kledana action Sneha increases the Dosha. When any Sneha

is metabolized than maximum quantity of water is produced as a byproduct in the

compatison of metabolism of proteins and carbohydrates. This liberated water may

dissolve the local

Doshas in itself and help them in coming to Kostha.

(2) Drava : Due to its Vilodana action Sneha liquefies morbid humours and causes an

increase in its quantity. Drava is opposite of the Sandra guna. Here we can consider

that Sneha decreases the

concentrated Doshas of the body by its Drava guna. It helps in elimination of Kapha

and Pitta which are having Drava Guna and Dosha‟s present in liquid Dhatu like

Rasa, Rakta and Mala like Mutra, Purisha are also get increase. So their easy

elimination takes place during Virechana Karma.

Vishyandana :- Vishyandana means liquification. Sneha converts the Dosha in a

liquid form so that may be facilitated for transport. This is done by its Snigdha,

Mridu, Drava, and Sara properties.

(1) Snigdha : On account of its Kledana action Sneha increases and liquefies the

doshas as explained earlier.

(2) Mridu : Due to this property Sneha loosens and softens the Dosha so that they may

be mobilized.

(3) Drava : Sneha increases the liquidity of Dosha on behalf of its panchabhautika

configuration, thus mobilizing them.

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(4) Sara : With help of Sara guna Sneha directs the doshas in its proper direction e.g.

Shakha to Kostha.

Paka :- Sneha increases Agni at all levels i.e. Jatharagni, Bhutagni, and Dhatvagni

thus digest the Doshas and Ama.

Srotomukha Vishodhana :- On account of its Sukshama and sara gunas Sneha does

this function.

(1) Sukshama : Due to its vivarana() action Sneha penetrates subtle channels and

opens the blocked one, allowing proper motion of Dosha.

(2) Sara : Sara guna of Sneha also helps this process. Sara has the property of Prerana

i.e. it puts the things into motion as a result of this quality Sneha helps in redirecting

the Dosha, Dhatu, and Mala in proper direction.

Vayoshcha Nigrahat : Sneha has specific action over Vata Dosha. Vata is the chief

culprit for mobilizing Doshas from the Kostha to Shakha. On pacifying this Vata

Dosha by it inherent antagonist Sneha guna, this process can be terminated.

In the process of bringing Doshas from Shakha to Kostha, Mridu and Guru

guna are also helpful. By Mrudu Guna Sneha loosens and softens the Dosha. Sneha

softens the Ruksha organ or Srotasa. Mrudu Guna causes Shaithilya of various organs.

Sneha also increases the permanent type of Bala which remains helpful after the

process of Virechana and during the Samsarjana Krama. This all properties of Sneha

helps to prevent the lodging of transported Dosha from Shakha to Kostha in the way

in Srotasa (micro-channels). This shows the importance of Sneha.

If Snehapana is not done and if we tries to remove the Dosha from Ruksha

Sharira, there may be possibility of lodging the Dosha in the way due to Rukshata

(roughness) in Srotasa and this creates another pathogenesis in that particular Srotasa.

To avoid this, patients should be oleated properly. Dosha smear easily in Snigdha

body without any hurdle just as water smears smoothly on oil applied utensil and

easily come out to kostha.

(3) Swedana :- The qualities of Swedana drugs are Ushna, Tikshna, Sara, Snigdha,

Ruksha, Sukshma, Drava, Sthira and Guru (Ch.Su.22/16).

Klinna doshas which are present either in kostha, dhatu, srotas & shakhas &

asthi (includes madhyama roga marga) are liquified by swedana & brought to kostha,

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thereby eliminated through shodhana karma.

By Swedana there is dilatation of various srotasa and the flow is resumed

which helps in eliminating vitiated Doshas.Vagbhata and Dalahana say that with the

help of Snehana and Swedana Doshas are being liquefied and they dissolve in Sneha

and make the path for excretion by bringing them to Kostha.

Swedana pacifies the Vata, which causes rigidity, contracture due to its

Ruksha and Sheeta guna. On the contrary, Swedana removes it by its Ushana guna. Its

also increases Agni, thus digesting Ama and clearing the path for excretion of Dosha.

Swedana drugs also possesses Drava and Sara properties which adds itself in

mobility of sluggish Dosha.

Acharyas have explained the dual nature of Snehana and Swedana as Purvakarma by

giving following examples.

In the case of cleansing the dirty cloth, we first use the detergent and water in

the same way for removing the Dosha of body we can use Snehana and

Swedana.

The wood which is not properly oleated and fomented destroys if we try to

bend it, in the same way our body (dhatu - tissue) destroys by Shodhana

procedure if not properly oleated and formented.

Modern View :-

(1) Snehapana :- Our cell membrane is made up of Phospholipids. Watersoluble

substance cannot cross the cell membrane while lipid and lipid soluble substance are

permeable to the cell membrane. Cell membrane acts as a barrier to the passage of

water soluble molecules, but provides free passage to lipids and lipid soluble

substances.

From above description it can be said that Sneha, by its Sukshma Guna

reaches at the cellular level and it can be correlate with the “Anutva of Sneha”.

Phospholipids which are a part of class of fat could be increased by snehapana.

Phospholipids function as a carrier of various cellular elements. Increase in their level

may enhance this transport which may helpful in some way in various diseases. This

could also be compared with gati of Dosha from Shakha to Kostha.

Snehapana produce Kledana in body because 1 gm of fat on combustion gives

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1.07 gms of water as a side product while combustion of protein produces 0.41 gms of

water and carbohydrate produces 0.55 gms of water. This water may help in

dissolution of various Doshas and this can be compared with the Kledana property

described to Sneha dravya.

Lipid consuming is helpful in excretion of lipid soluble substance. It suggests

that Sneha liquefies the compact Dosha and destroy morbid mala.

The Membrane permeability is crucial important for it‟s functioning and it

depends on its lipid components. Phospholipds composed of chains of poly

unsaturated fatty acids increased the membrane permeability by banding some chains

and double bonds prevent them from compacting themselves.

“This can be correlated with “Pravanatava of Sneha” because by increasing

cellular permeability Sneha directs the Dosha from Sakha to Kostha.”

(2) Swedana :- During Swedana, heating the tissues results in rise in temperature, the

main reaction to which are as follows.

(a) Increase Metabolic rate :

By Swedana process, our body temperature is increased and due to increased

body temperature, sympathetic activities are also increased. Because of increased

sympathetic activities hormones like Epinephrine, Norepinephrine, Cortisol, Thyroid

hormones are released which accelerate the metabolic rate and stimulate the process

of lipolysis. As a result of increased metabolism there is increased demand for oxygen

and increased output of west products. It can be correlated with digestion of Ama.

(b) Increase blood supply :

If the body temperature rises a negative feedback action is become active to

reach at normal temperature. Higher temperature of the blood stimulates thermo

receptors that send nerve impulses to the preoptic area of the brain. Which in turn

stimulate the heat losing center and inhibit the heat promoting center. Nerve impulses

from the heat losing center cause dilation of blood vessels in the skin so the excess

heat is lost to the environment via radiation and conduction. As a result of

Vasodilation there is an increased blood flow through the area so that the necessary

oxygen and nutritive materials are supplied and west products are removed. It can be

correlated with Srotomukhavishodhanat.

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(C) Stimulation of Sweat Glands:

A high temperature of blood stimulates sweat glands of the skin – via

hypothermic activation of sympathetic nerves and by this procedure excessive sweat

production take place. With the increase Sweat production more west products is

expel out of the body through the media of sweat. Hence, it can be said that Swedana

corrects Swedavahasrotodushti.

Probable mode of action of Virechana :

Ayurvedic View :-

The properties of Virechana dravyas are Ushna, Tikshna, Sukshma, Vyavayi,

Vikasi etc. are mentioned in Ayurvedic classics which play a vital role in the mode of

action of Virechana Karma.

(1) Ushna

Ushna guna has Agneya property & hence “Vishyandana” occurs i.e.

„Vilininam Kurvanti‟ (Chakrapani). Hence it facilitates movement of morbid Doshas

towards Kostha. It also assists to Tikshana property to perform its action.

(2) Tikshana

Tikshna property performs the function of “Sanghatabhedana”, „Chakrapani‟

quoted the word „Vicchindayanti‟ (Ch. Ka. 1/5 - Chakrapani). It means to break the

complex morbid matter into smaller molecules. According to Dalhana, it is

responsible for quick excretion. Thus, Tikshna property breaks the Mala and morbid

Dosha in micro form.

(3) Sukshma

Sukshma guna due to its Anupravanabhava, i.e. “Anutvat

Pravanabhavach……(Ch. Ka. 1/5 – Chakrapani) its helps to dilate the channel and to

pass the drug into micro-channel. This property helps to remove the morbid matter

from micro-channels and brings them to Kostha for expulsion.

(4) Vyavayi

Due to this, drugs spreads quickly throughout the body & starts their action

before its digestion. Due to Vyavayi Guna, Virechaka drugs spreads all over the body

without changing their form. Some scholars included this property under „Drava‟

property.

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(5) Vikasi

Due to this property drugs loosens the dhatu bandhana (Sh.Sam.Pu.Kh.4). It

creats the dhatu shaithilyata (Dalhana). Hence drugs initiates their action without

being digested. From all these properties doshas are driven to kostha.

Now from above description of Virechana dravya‟s properties it can be

conclude that due to their Vyavayi, Vikasi, Sukshma, guna Virechana Drugs reaches

to the micro channels and by virtue of its Ushna, Tikshna Guna it scrapes out and

liquefies morbid Mala and compact Doshas. In this way, Virechana Drugs brings

Shakhagat Mala to Koshtha and consequently expels out form the body.

Virechaka drugs carry out the Virechana due to the Prabhava (potency) of

drug rather than its above properties. No doubt these properties help to do so but drug

should have that Prabhava. The drugs which are having Jala and Prithvi Mahabhutas

dominancy have a natural tendency to go downwards and thus they can assist in

induction of Virechana. If drugs are having all above said properties but if it is not

having Virechaka Prabhava then it will not induce the Virechana. Hence we can say,

drugs act by its active principle can be said as Virya or Prabhava not by property, but

properties assist in carrying the function of drug.

It can be summarized that the above mentioned properties of drug reaches

hridaya by swaveerya & then with the help of the large & small dhamanis it pervades

the whole body. Due to agneya property, it causes vishyandana i.e.oozing of doshas &

by tikshna property causes vicchandana (disintegration) of doshas.

The drugs due to their Virya reach to the „Hridaya‟ from where they spread to

all over the body. To reach the micro level throughout the body in a very short time,

there are two chief systems in the body i.e. circulatory and nervous. By traveling

through CVS or by activating the action of CNS, Virechana drug performs their

function.

In case of Ghreya Yoga, Virechana is induced only by smelling the few drug,

it shows the action of drugs by nervous system. Here Hridaya can be taken as brain

and heart too.

Mode of Action of Virechana Karma :

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Modern View :-

Mode of action of Virechana Karma can be divided in the following two ways.

Systemic action: Doshas are brought to Kostha from Snehana & Swedana, from there

they are eliminated by Virechana, which suggests action throughout the body.

Local action: Locally mild inflammation occurs which is transient due to Ushna and

Tikshna properties of drugs which irritate the intestinal mucosa. Hence hyperemia

results due to arteriolar & capillary dilatation & also exudation of protein substances

which helps in dilution of toxins.

From the modern point of view we can say that the Ayurvedic Shodhana

karma are “physician induced mild inflammation” mainly Vamana and Virechana

drugs are quite irritant to the stomach and the intestinal mucosa respectively, to cause

inflammation. Due to this the permeability of the membrane changes and those

substances come out due to the changed permeability which can not come out in

normal condition.

To further understand the action of Virechana Karma we should go through

the mode of action certain modern purgatives.

LAXATIVES:

These are the drugs that promote the evacuation of bowels.

Depending on the intensity of action, they are classified into:

1. Laxative or aperient: This has milder action, & eliminates soft but formed stools.

2. Purgative or cathartic: It has stronger action resulting in more fluid evacuation.

Many of the drugs in low doses act as laxatives & in larger doses as purgatives.

Classification:

1. Bulk forming :

Dietary fibre – bran. Dietary fibre consists of unabsorbable cell wall & other

constituents of vegetable food- cellulose, pectins, glycoproteins & other

polysaccharides. Bran consists of 40% dietary fibre. It absorbs water in the intestines,

swells, increases water content of the faeces, softens it & facilitates colonic transit.

Dietary fibre supports bacterial growth in colon which contribute to the faecal mass.

Certain dietary fibres like gums, lignins, pectins bind bile acids & promote their

excretion in faeces, leads to degradation of cholesterol in liver & then lowering of

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plasma LDL cholesterol.

Psyllium (plantago) & Isabgole : They contain natural colloidal mucilage

which forms a gelatinous mass by absorbing water.

Methyl cellulose & carboxymethyl cellulose: These are semi-synthetic,

colloidal, hydrophilic derivaties of cellulose.

Generous amounts of water must be taken with all bulk forming agents.

So, we can say that Bulk Purgatives work by one or more of the following actions.

Non-metabolizing

Retaining water

Promoting peristalsis

2. Stool softener :

Dicotyl sodium sulfosuccinate: Is an anionic detergent softens the stools by

net water accumulation in the intestinal lumen by action on the intestinal mucosa. It

emulsifies the colonic contents. By a detergent action, it can disrupt the mucosal

barrier & enhance the absorption of many non absorbable drugs. Eg: liquid paraffin

should not be combined with it.

Lubricant: Liquid paraffin – is a viscous liquid, a mixture of petroleum hydrocarbons.

Taken for 2-3 days, it softens stools & is said to lubricate hard scybali by coating

them.

3. Stimulant purgatives :

They are powerful purgatives & often produce griping. They may irritate the

intestinal mucosa & thus stimulate motor activity. The more important mechanism of

action is accumulation of water & electrolytes in the lumen by altering absorptive &

secretory activity of the mucosal cell. They inhibit Na + K+ ATpase at the basolateral

membrane of villous cells transport of Na+ & accompanying water into the

interstitium is reduced. Secretion is enhanced by activation of CAMP in crypt cells &

by increased PG synthesis. Larger doses of stimulant purgatives can cause excess

purgation, leads to fluid & electrolyte imbalance.

Anthraquinones: Senna obtained from leaves & pod of certain cassia species. They

contain an anthraquinone glycoside called emodins. Glycosides not active as such.

Unabsorbed in the small intestine, they are passed to the colon where bacteria liberate

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the active anthrol form, which either acts locally or is absorbed into circulation.

Excreted in bile to act on small intestine. They take 6-7 hours to produce action.

The active principle is believed to act on the myenteric plexus to increase

peristalsis & decrease segmentation. They also inhibit salt & water absorption in the

colon. Senna anthraquinone has been found to stimulate PGE2 production in rat

intestine.

Castor oil: Is one of the oldest purgatives. It is a bland vegetable oil obtained from the

seeds of Ricinum communis, has been used on skin as emollient. It mainly contains

triglyceride of ricinoleic acid, which was believed to irritate the mucosa & stimulate

intestinal contracations. The primary action has shown to be decreased intestinal

absorption of water & electrolytes & enhanced secretion by a detergent like action on

the mucosa.

4. Osmotic purgatives :

Solutes that are not absorbed in the intestine retain water osmotically &

distend the bowel increasing peristalsis indirectly. Magnesium ions release

cholecystokinin which may aid purgative action of magnesium salts. All inorganic

salts are used as osmotic (saline) purgatives have similar action.

On the other hand, they may also be classified according to the pattern of

laxative effect following the therapeutic doses into :

1) Slow Onset : Those which produce softening of the stool after one to three days of

daily use - bulk laxatives, mineral oil, Dioctyl Sodium Sulphosuccinate, lactulose.

2) Intermediate Onset : Those which lead to soft or semisolid stool in 6 – 12 hours

of a single dose – Saline laxative (low dose), phenolphthalein, bisacodyl (oral)

anthraquinone group.

3) Rapid Onset : Those which leads to watery evacuation in 2 – 6 hours of a single

dose – saline laxative (high dose), castor oil, bisacodyl. Our Virechaka drugs belong

to this category.

Out of these, certain drugs increase the motility of intestine certain modify the

fluid dynamics of the mucosal wall and may cause fluid accumulation in lumen.

Mechanism of Virechana :

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Michanism of Virechana occurs due to following three actions

1. Increase propulsive movement.

2. Reduced absorption.

3. Fluid Accumulation in Gut.

1. Increase Propulsive Moment:

Due to its irritant property Virechana Dravya stimulate motor activity of GI

track. Some of them increase motility by acting on mesenteric plexuses and because

of increase, propulsive activity there is a less time for absorption of colonic contain.

2. Reduced Absorption:

By virtue of its irritative nature Virechan Dravya produced structural injury to

the absorbing mucosal cell and thus absorbing capacity of mucosal cell is decreased.

3. Fluid Accumulation in Gut:

Virechana Dravya cause structural injury in GIT and leads to inflammation in

mucosal cell. Due to inflammatory changes vasoactive amines and polypeptides

increases membrane permeability in GIT and cause Vasodilation. Some chemical

factors are also responsible which increase the permeability in response to acute

inflammation.

In this way all these factors together initiate the Virechana process.

Action on nerves: Here the defecation centre is irritated in Medulla oblongata. The

vagus nerve stimulates pancreas, liver to produce secretions. Bile is secreted due to

contraction of G.B., & also due to irritant & vagal stimulation, Brunner‟s glands are

stimulated which secretes mucus. Due to increased peristalisis, sacral & lumbar

plexus are irritated, ileo caecal & anal sphincters are relaxed & these secretions are

excreted out & is said to be purgation.

Hormonal action: It causes irritation of liver & pancreas, secretions are increased

which adds to further irritation of mucosa. Some other hormones also increase small

intestinal secretions like secretin & cholecystokinin. Whenever a segment of large

intestine becomes irritated, then mucosa secretes large quantities of water &

electrolytes in addition to alkaline mucus. This acts to dilute irritating factors & to

cause rapid movement of the faeces towards anus.

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The mechanism by which marked secretion of watery fluid by crypts of

Lieberkuhn is unknown. However, 2 active secretory processes occurs. Active

secretion of chloride ions into the crypts & bicarbonate ions. The secretion of chloride

ions causes electrical drag of sodium ions through the membrane. Finally all these

cause osmotic movement of water & hence fluidity in the purgation occurs. In

diarrhoea, both sodium & potassium are excreted out of the body. The crypts of

lieberkuhn are located at jejuna region of small intestine, causes extreme rate of fluid

secretion.

Regulation of Virechana process:

The process of Virechana is regulated & controlled by a special centre situated

near Medulla oblongata in the brain. This centre is close to respiratory & vomiting

centre. When the Virechana drugs stimulate the purgation centre, indirectly vomiting

centre is relaxed. Sacral plexus of the spinal cord also helps in controlling &

regulating the act of purgation, & it is also controlled & regulated by local reflex

actions. Hence during the act of defaecation, the respiration is arrested momentarily;

diaphragm is activated & presses transverse colon. Simultaneously, the accessory

muscles of the abdomen are also activated & helps in propelling the faecal matter

towards anus along with the diaphragm.

Faecal matter, when it reaches the intestine, stimulates local nerve plexuses &

then enforced peristalisis further helps in expelling contents of intestines towards

rectum & finally to anal canal. When these voluntary or involuntary act of defaecation

starts, finally results in evacuation of bowels.

Elimination of Pitta :

Bile can be considered as Pitta Vargiya Dravya. Bile production is increased due to

increase uptake of Lipids (Sneha) in following manners.

Polyunsaturated fatty acids stimulate oxidation of cholesterol to bile acids.

It also stimulates the cholesterol excretion through bile in intestine.

Fatty food itself when enter the duodenum hormone cholycystokinin is

released which stimulate the gall bladder contraction and thus bile come out in

intestine.

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In this way, Snehapana stimulate bile production.

Beside this the gall bladder is also stimulated by acetrylcholine – secreting

nerve from both the vagi and the intestinal enteric nervous system. They are

the same nerves that promote motility and secretion in other part of upper

Gastro intestinal Tract.

In the Virechana process during the relaxation phase of peristaltic wave the

sphincter of oddi is also relaxed then bile comes out in GIT.

Bile serves as a means for excretion of several important waste products from

the blood. These include especially bilirubin, end product of haemoglobin

destruction and excesses of cholesterol synthesized by the liver cells.

It can be staited that Virechana become helpful in elimination of vitiated Pitta as

well as Rasa – Rakta Gata Meda (Cholesterol)

Elimination of Kapha :

The large intestine chiefly secret mucous. This mucus contains moderate amount of

bicarbonate ions secreted by a few non-mucus secreting epithelial cells that lie

between the mucus secreting epithelial cells.

After the elimination of Mala and Pitta, this mucus is secreted by gut and can

be taken as Kapha vargiya Dravya in Virechana process.

The rate of secretion of mucus is regulated principally by direct, tactile

stimulation of the mucus cells on the internal surface of the large intestine and by

local nervous reflexes to the mucus cell in crypts of Lieberkuhn. Stimulation of the

pelvic nerves from the spinal cord, which carry parasympathetic innervations to the

distal one – half to two third of the large intestine, also can cause marked increase in

peristaltic motility of the colon. Therefore, during extreme parasympathetic

stimulation, so much mucus can occasionally be secreted into the large intestine.

In this way, Virechana helps in elimination of Kapha.

Elimination of Waste Products:

Waste product present in the body either in extra-cellular, intracellular or in

plasma can be brought into intestine by means of Dhamani i.e. through circulatory

system from where it can be eliminated out of body by the action of intestine, which

is induced by Virechaka drug.

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The active chemical medium of the liver is well known for its ability to

detoxify or excrete into the bile. Several of the hormones secreted by the endocrine

glands are either chemically altered or excreted by the liver, including thyroxine and

essentially all the steroid hormone such as estrogen, cortisol and aldosterone. Finally,

one of the major routes for excreting calcium from the body is secretion by the liver

into the bile, which then passes into the gut and is lost in the feces.

Thus chemically altered substances or toxic substances are excreted by liver

and Virechana process can enhance these functions by various routes, by initiation of

bile excretion, by increasing blood circulation etc.

During the Swedana process also west products are expelled out of the body

through the increase Sweda it suggests that Virechana become helpful in elimination

of west products (Mala) through the different media.

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CONCEPT OF RANJAKA PITTA

Sushruta has designated this Pitta as Ranjakagni. He has indicated its

location in the Yakrit or Liver and Pliha or Spleen. In function, he has stated that,

it confers colour to rasa i.e. rasaragakrit. Vagbhata has identified location of

Ranjaka Pitta in the amashaya or stomach and ascribed to it the same function as

Sushruta has done. According to the ancient Ayurvedic view, rasadhatu is stated to

contribute to the formation of Rakta or blood with the help of Ranjaka Pitta, which

is claimed to impart to rasa, its colour. It would, therefore, appear that Ranjaka

Pitta plays an essential part in the formation of Rakta.

Chronologically speaking, Sushruta appears to have been the first authority, in

this world, who had associated some principle present in the Liver and Spleen to the

formation of blood. He has recommended the administration of raw-Liver of goats,

together with the Pitta contained in it, for the treatment of loss of blood in Rakta-Pitta

(idiopathic haemorrhagic states). He has also indicated its use in night-blindness.

Latter, Vagbhata indicated the existence of a haemopoietic principle in the

stomach. He does not appear to have taken note of the earlier observations of

Sushruta, who associated this principle with the Liver and Spleen. Nonetheless, it is

significant to note that the functions ascribed by him to this stomach-principle was the

same as those attributed by Sushruta to the Liver-principle.

The fact that, between them, the stomach and Liver contribute an identical

factor – the Ranjaka Pitta – essential for the formation of Rakta which makes blood

appear red, was visualized by Sushruta and Vagbhata has now experimentally

confirmed by modern workers in the late twenties of the present century. Minot and

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Murphy showed (1926) that the Liver was the most effective ingredient in the diet for

the treatment of anaemia in dogs. He tried to asses the effect of adding Liver to the

diet of patients with pernicious anaemia, which was followed by dramatic results.

Today, lightly cooked-Liver, half to one pound or preferably, an extract of Liver, has

been recognised as a specific in anaemia. The factor in the Liver, which is essential

for the maturation of erythrocytes has, since been, demonstrated to be associated with

the non-protein fraction of the Liver-substance, which is known as the anti-anaemic or

haematenic principle.

It is of interest to note, in this connection, that both Sushruta and Vagbhata

have stated that, the main venue of Rakta is Yakrit or Liver and Pliha or Spleen. The

former has stated that the blood, having its seat in these organs, lends support to and

augments the functions of other seats of Rakta. These authorities have noted that the

two main seats of Rakta viz., Yakrit and Pliha are the seats or Ranjaka Pitta. By

implication, it would follow that, these sthanas or sites have to do either with the

formation of Rakta or serve as its reservoir or both. The term sthana may mean a

storage depot or the place of production or both. Hence the Yakrit and Pliha are the

sthanas of Rakta which can very well appreciated from both the points of view. This

observation is fully supported by the developments in modern physiology.

There is however, no direct reference, in the samhita granthas, about other

sthanas of Rakta. The concept of the formation of Rakta, according to Ayurveda, will

remain incomplete today if the contributions made by modern physiology about the

role played by the red-bone-marrow in the formation of blood is not taken into

account. There are again, no direct references in the samhita granthas regarding the

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part of majja or bone marrow, in the formation of Rakta. Sushruta samhita however,

mentions saraktam meda, corresponding to the red-bone marrow. The context in

which this reference occurs is of significance. Sushruta said that Majja is present

inside the sthulasthi. The substance present within other asthi, is spoken of as

saraktam meda. By implication, the majja present in sthulasthi is saraktam meda.

Metabolic Aspects:

Those authors who are considering two types of dosha i.e. Prasadabhuta and

Malabhuta doshas, consider Yakrit Pitta as malabhuta Pitta.

Yakrit Pitta originates in Yakrita.Yakrita is the largest gland in human body. It

is present on the upper aspect of Udarguha on right and below the shawapatala.

Pratiharini sira which carries vitiated blood from Amashaya both antras, agnyashaya

and Pleeha enters into Yakrit. Thus the dhatupakadimala which enters into the Rakta,

circulating all over the body finally enters the Yakrit. Yakrit kosha performs mala

nirharana from this Rakta through minute ends present in pratiharini sira, kriya of

sanghatana, vighatana and produce Pitta. This Pitta production takes place

continuously in human body.

Yakrit Pitta Vahana and Storage:

Yakrit Pitta has got two functions these are agnyashaya rasa utpadana and

snehapachana. During pachanakala Pitta enters grahani via Yakrit Pittanalika. Other

times it accumulates in Pitta kosha through Pittakoshanalika. Pittakosha is a pear

shaped ashaya. It is present below Yakrit in a fossa. When required Pitta accumulated

in it enters grahani via Pitta praseka.

Swaroopa of Yakrit Pitta and its Karma:

It is yellowish, reddish, brownish liquid. It smells like Kasturi, Tikta-Madhura

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rasatmak and Alkaline in nature.

It contains pigments of Pitta, urea, uric acid etc. Urea from it is eliminated via

kidneys.

Main function of Pitta is to help agnyashaya rasa especially for sneha paka. To

some extent it also helps to kill microorganisms in antra. It also helps in proper

absorption of digested food and proper evacuation of sthulantra.

Obstructive Symptoms of Pitta:

Due to obstruction caused to Pitta in Pittavaha srotas, total Pitta cannot enter

grahani. It is absorbed again and circulates all over the body. If this obstruction

reaches to a particular stage then pita netra, pita twacha and pita mutra develops. This

disease is then named as Kamala. Due to absence or scarcity of Pitta ingested, sneha

dravyas are not digested and absorbed properly. They are excreted via mala in

indigested form which gives shweta varnata to mala.

If Pitta in the body is more than normal, it imparts pita varnata to netra, danta

and sweda. When excessive Pitta and its lavana or Ranjaka dravyas reach lala granthis

in oral cavity, they lead to dantapitata and also tiktasyata. Pitta Ranjaka dravyas

impart colour to purish and mutra.

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CONCEPT OF COMMUNICABLE DISEASE IN AYURVEDA

Prasangat Gatrasamsparshat Nishwasat Sahabhojanat |

Sahashayyasanachyapi Vastramalyanulepanat ||

Kushtam Jwarascha Shoshascha Netrabhishandya Eva cha |

Aoupsargika Rogascha Sankramanthi Naran naram || 15

Kandu Kustoupadanshacha Bhutonmada Vrana Jwarah |

Aoupsargika Rogascha Sankramanthi Naran naram ||16

Darshanath Sparshanath Danath Sankramanti Naran naram ||17

Asmakam Sharirani Vranamukhena, Annapanadi Dwarena Pravishtah ||18

Tatra Nasarandranugatena Vayuna Shwasakasapratishayah…. |

Twakindriyagatena Jwaramsurikadayah ||19

Ayurveda believes communicable diseases. Acharya Sushruta and other

authors like Bhavaprakasha, Urabhra, Sainacharya and Dalhana explains the cause of

communicable diseases. The concept of epidemiology and janapada udhawansa vikara

are also dealt by Acharya Charaka.

Prasanga:

Gatra Prasanga, by the sexual activity a disease may be communicated from

one person to another (sex ual partner).

Gatrasamsprashata:

Cutaneus touch, trauma etc can spread infections from unhealthy to healthy

individuals.

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Nishwasa:

Inspiration and expiration may disease may spread disease from person to

another.

Sahabhojana:

Food items, food poisoning, feco-oral route of contamination etc. can be

considered under this heading.

Sahashayya:

Sharing the bed, copulation, hetero-sexual, homo-sexual activity etc. are

considered under this heading of Vyadhi – Samsarga Hetavaha.

Vastra – Gandhamala, Anulepa:

Wearing the clothes, exchanging clothes within infected individual, sharing

the ornaments, using the cosmetic agents and other instruments, which are already

used by infected person may cause into the spread of the disease to healthy person.

Sushruta while explaining the Raktaja Krimi states that some of the Krimis are

visible to naked eye, some other are invisible to the naked eye some of them are

circular larger and many of them are anuswaroopi causing Kushtadi twachagata

vikara. Though according to manifestation it produces the Kushtadi vikaras, the

morphology, size etc. are more important than its manifestation.

The virus are very much microscopic not visible to naked eye or they are ati

sukshma.

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NIDANA

To understand the disease process properly one should possess a thorough

knowledge of its nidana. A particular factor can be called nidana, only when it is

capable of producing a complete disease process in the body either immediately or

after a certain period. Nidana has been classified in different ways in Ayurvedic

literature. Among them, Bahya hetu and Abhyantara hetu are relevant to the present

discussion.

Bahya hetus are the extrinsic factors causing the disease. It includes ahara, vihara,

kaala, pathogenic organisms and toxins etc.

Abyantara hetus are intrinsic factors causing the disease. They mainly consist of

doshas and dushyas.

Kamala has been classified into 2 types namely Kostasrita and Shākhasrita.

Nidana also varies depending upon the types of the Kamala. The entire nidana aspect

of Kamala can be broadly divided into 5 headings.

1) Kamala as a nidanarthakara vyadhi of Pandu and other diseases.

2) Pittala ahara vihara sevana by pittolbana purisha

3) Specific nidana of Shākhasrita Kamala.

4) Specific nidanas of both the types of Kamala.

5) Indirect nidanas of Kamala.

1) Kamala: Nidanarthakara vyadhi of Pandu and other diseases:

In Ayurveda, Kamala has been mentioned as a sequel of Pandu roga. When

Pandurogi indulges in excessive paithika ahara and viharas the pitta gets aggravated

and leads to Kamala. Gangadhara described that Kamala asnidhanarthakara roga of

Pandu20

. Chakrapani described it is as Paratantraja Kamala.

Susruta regarded Kamala as a synonym of Pandu and considered it is as an

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advanced stage of Pandu. He designated it is as Kamala as it is characterized by a

special set of symptoms21

. Dalhana while commenting upon the word “Amayante”

described “Amayante anayarogante ca” means Kamala may occur after Pandu roga

or after other rogas too. By Amla bhojana and apathya (un-wholesome diet) bhojana

at the end of Pandu or any other roga, pitta gets aggravated and produces Kamala22

.

2) Pittala ahara vihara sevana by pittolbana person:

Vagbhata described that in pittolbana persons, excessive indulgence in pittala

ahara viharas develops Kamala independently23

. The term pittala used in the above

context denotes all the pitta provoking agents in the form of ahara and viharas. .

3) Specific nidana of Shākhasrita Kamala:

A separate set of etiological factors specific to Shakhasrita Kamala is available

in Caraka Samhita. The same version is reproduced in Astanga Hridaya with a minor

change. The etiological factors narrated in Caraka Samhita are one as follows24

:

Intake of food having predominantly seethaguna

Intake of food having predominantly guru guna.

Intake of food having predominantly madhura rasa.

Intake of food having predominantly rooksha guna.

Ativyayama.

Vegadharana.

Vagbhata has considered „bala nigraha’ in lieu of Vegadharana25

. If the

above mentioned nidanas are analyzed it is evident that most of the nidanas are either

kapha provoking factor (or) vata provoking factors. The first three nidanas mentioned

above act as Kapha vitiating factors where as the last three operate as vata provoking

causes. Intake of food having predominantly ruksha guna increases the rooksha

quality of vata resulting in vata prakopa.

Intake of food having seetha guna increases the seetha quality resulting in vata

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& kapha prakopa. Intake of food having predominantly guru guna leads to

agnimandya, amotpatti, and kapha prakopa. By the term guru ahara one should

consider both matra guru (excess quantity) and swabhava guru (heavy in quality).

Intake of food having predominantly madhura rasa especially when it is associated

with guru ahara produces agnimandya and ama. This also results in Kaphaprakopa.

Ati vyayama in terms of excessive exhaustion causes vata vriddhi in general and

ruksha and chala guna in particular.

Vegadharana causes an obstruction to the physiological movement of vata

dosha and results in pratiloma gati. This abnormal movement of vata in the form of

tiryak gati is responsible for the shākhabhigamana of pitta from kosta. Since

ativyayama and vegadharana play a major role in Samprapti it gives a scope to

speculate that they act as vyanjaka hetu. All the remaining causes can be considered

as Utpadaka hetus.

Nidana of Kumba Kamala: Separate nidana has not been described for

Kumba Kamala as it occurs only when Kostasrita Kamala becomes chronic due to

negligence26

.

4) Specific nidanas of both the types of Kamala:

Caraka described certain nidanas of Kamala, which are not mentioned as

specific either for Kostasrita Kamala or Shākhasrita Kamala. Hence such nidanas are

considered as nidanas for both the types of Kamala.

Caraka emphasized that a person who ingests dadhi (curd) in violation of rules will be

subjected to severe Kamala27

. It is contraindicated in pittaja and raktaja vyadhis as it

has amlarasa and ushna virya properties28

. On ingestion, it further vitiates pitta and

causes Kamala in 2 fold manner. By vitiating pitta, either directly it may cause

Kamala or Pandu. Pandu, which in turn leads to Kamala due to continuous usage of

dadhi. In the same manner continuous usage of dadhi in Sarat & Grishma ritu may

also causes Kamala29

. Sarangadhara mentioned that Dadhi is having pichila, guru and

abhisyandi properties30

; due to these gunas it can provoke kapha, which causes

srotorodha (obstruction of channels) and may lead to Shākhasrita Kamala.

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Dr.V.N.Pandey has observed that dadhi, may cause Kamala by acting as a

vehicle, which carries hepatotoxic agents in the body when used against personal

hygiene31

.

Viruddha kala snehapana also leads to Kamala32

. Caraka, Madhavakara described that

pitta dusta sthanya also leads to Kamala in children33

. Here Kamala is produced in a

2-fold manner. It may be due to Sthanya (breast milk) which is acted upon by vitiated

pitta (or) the baby who ingests the sthanya may be lacking specific pitta activity for

pachana (metabolism) of milk. Due to paittika dravya sevana by the mother that

causes vitiation of pitta and this vitiated pitta also vitiates the sthanya. By the

ingestion of this pitta dusta sthanya, the baby develops Kamala. Recent research

workers also concur with this view, and have recorded that the production of Kamala,

is closely associated with breast feeding34

.

5) Paroksha nidanas of Kamala:

As Susruta considers Kamala as a synonym of Pandu the etiological factors of

Pandu should also be considered. Chakrapani also described that Kamala is produced

by Pandu roga nidana35

. It can be assumed that the various karanas attributed for the

causation of Pandu, play an indirect role in the causation of Kamala. They directly

cause Pandu roga, which in turn are capable of producing Kamala. For e.g.

Santarpana36

and viruddhaharas37

are capable of producing Pandu and hence are

indirect causes for Kamala like wise all the etiological factors of Pandu are paroksha

nidanas (indirect causes) of Kamala.

Caraka and Vagbhata have stated that Kamala is Rakta pradoshaja38

and is due

to Rakta vaha sroto dusti39

respectively. Etiological factors which causes raktadusti40

like ushna, Vidahi, Dadhi, Taila, Drava, Snigdha, Kshara, Anupa mamsa sevana,

krodha and Sarath kala etc. are almost similar to that of pitta prakopas, which causes

Kamala. The above-mentioned nidanas causes pittprakopa and rakta dusti when rakta

is vitiated the srotases through which it circulates (Raktavaha srotas) also gets

vitiated41

, ultimately leading to vitiation of mulasthanas i.e., Yakrit and pliha and

causing Kamala. Thus the nidanas of Rata dusti also causes Kamala indirectly.

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Caraka has mentioned that the usage of Katu rasa will cause the „Bhinatti‟ of

„Sonithasanghata42

‟ (destruction of R.B.C) i.e., haemolysis which also may result in

Kamala.

Table 42 Showing Paittika (Pitta vardhaka) ahara which acts as nidana for

Kostasrita Kāmalā 43

Sl.No: Paittika aharas C.S. A.S. A.H.

1. Katu rasa sevana + + +

2. Amla rasa

sevana

+ + +

3. Lavana rasa

sevana

+ + +

4. Ushna dravya

sevana

+ + +

5. Teekshna

dravya sevana

+ + +

6. Laghu dravya

sevana

+

7. Vidahi + + +

8. Tila taila +

9. Pinyaka +

10. Kulutha +

11. Sarshapa +

12. Athasi + +

13. Harithaka varga +

14. Godhamamsa +

15. Matsya +

16. Aja +

17. Avika +

18. Dadhi + +

19. Koorchika +

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20. Mastu + +

21. Souveera +

22. Amla phala +

23. Ksharam +

24. Madya +

25. Tilanna +

26. Bhallatakasthi +

27. Amlika +

Table 43 Showing Paittika (Pitta vardhaka) viharas which acts as nidana

for Kostasrita Kāmalā43

S.No. Paittika

viharas

C.S. A.S. A.H.

1. Maidhuna + +

2. Rajosevana +

3. Dhuma sevana +

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SAMPRAPTI

“Vyadhijanaka vyapara visheshayuktam Vyadhijanmeha Sampraptihi44

The disease is manifested by Dosha Dushya sammoorchana, when all evading

Doshas are in their provoked state, comes in contact with an organ or Srotas that is

termed vaigunya. This manifestation of disease is preceded by the other evaluative

stages. Samprapti means the description of pathology of disease.

Yakrit, according to Ayurveda is mentioned as the Moola of Raktavaha Srotas

and Kamala as a disease of Raktavaha Srotas. Moreover, Kamala belongs to the

category of Pittaja Vyadhi and Ranjaka Pitta is the type of Pitta that is involved in its

pathogenesis. The seat of Ranjaka Pitta is Liver (Yakrit).

The outcome of Sanga in Ranjaka Pitta marga, is Vimargagamana of Pitta to

Shakha producing the characteristic symptoms of Kamala.

Koshtashrita Kamala is BahuPitta because in this type of Kamala, there is

Swabhavataha Vruddhi of Pitta due to its own prakopaka hetus. This is a point of

difference between BahuPitta Kamala and Shakhashrita Kamala45

.

Due to margavarodha Pitta does not reach Mahasrotas. Mala Ranjaka Pitta

does not combine with purish and hence it is more or less whitish in colour.

Prakupita Pitta travels all over the body along with purisha and give rise to

sthana samshraya avastha. That’s why purisha is also haridravarni.

As per Sushruta, those persons who immediately after getting cured of Pandu

take amla ahara or other Pitta prakopaka apathya, prakupita Pitta leads to mukha

panduta, tandra, and bala kshaya. In Koshtashrita Kamala Samprapti, prakupita Pitta

does dusti of rakta and mamsa. By definition it means “Dahana”, modern authors

remind us about heamolysis in this type of Kamala.

Ancient authors had described the relation of Yakrit and Pleeha with rakta,

hence the pradhana lakshana of Pandu roga i.e. Raktakshaya.

Along with doshadusti lack of vyadhi kshamatva (Immunity) of an individual

can also be considered as a cause of Khavaigunya. In the above phase of pathogenesis

vague symptoms are produced. This stage can be considered as incubation period,

which varies from 4 to 26 weeks.

If the disease is not prevented in this stage then the pathological changes takes

place due to physiological derangement. The disseminated tridosha become potent

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enough to become lodged in Yakrit where the defense mechanism is weak or in other

terms Khavaigunya is present.

This is the stage where there is intermixing between the circulating doshas and

sthanika dushyas. The circulating vata and kapha produced vitiation of kapha situated

in Koshta, which can be considered as Sthanika dosha46

.

Later the chaturtha kriyakala is manifested. The Poorvaroopa like Atopa,

Vishtambha, Parshwarthi, and Dourbalya etc. are produced.

Along with this other lakshanas like agnimandya, Aruchi, which are carried

from earlier stages, become more prominent. Ranjaka Pitta mentioned here can be

considered as biliary secretion. Bile is synthesized in Liver and excreted into

intestines. From the point of patho physiology, the above said poorvaroopa mainly

agnimandhya and aruchi can be attributed to the absence of bile in Duodenum. The

symptoms such as anorexia, loss of appetite, nausea and vomiting etc, are produced as

a result of the non-availability of bile for the digestion of fat. This stage can be

considered as an icteric stage, where prodromal symptoms of Viral Hepatitis-B are

produced.

There is a striking similarity between the two systems of medicine regarding

the symptoms, which are said to occur at this stage.

Due to sangatmaka srotadusti in raktavaha srotomoola Ranjaka Pitta, which is

synthesized in Yakrit (Liver) is not excreted properly into the ampulla of vater.

Normal functions of Ranjaka Pitta include rasaranjana and malaranjana47

in other

words it can said that Ranjaka Pitta imparts colour to stools and helps in the

emulsification of fats. Ranjak Pitta is nothing but the bile.

But if Ranjaka Pitta is considered to be bile, it is also possible to speculate that

it helps in the process of digestion. Even though Pachaka Pitta is the sub type of Pitta

dosha, which is responsible for digestion, Ranjaka Pitta may play role in pachana

especially in digestion of fat.

The term mala ranjana means giving a natural colour to the stools. In the large

intestine bilirubin is reduced to stercobilin, which is responsible for the golden yellow

colour of stools.

In the Kamala roga, as in other disorders sanchaya, prakopa and other stages

of Kriyakala are present.

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If the disease process is not checked in the sthanasamshraya avastha it goes to

the further stage, which is the actual stage of manifestation of the disease

(Vyaktavastha). The Ranjaka Pitta, which is not excreted normally into the intestine

will deviate its path. This pathology facilitated by the provoked vata dosha. The

deviated Ranjaka Pitta reaches shakha due to vimargagamana. As stated in classics

there are four major causes for the shakhabhigamana of doshas namely.

Ati vyayamat Ushmanat

Teekshanat Ahitasya anavacharanat48

Ati vyayama plays an important role followed by other causes. Shakha gati of

dosha suggests an advancement of pathologic conditions. In the present context the

shakha which first afflicted is rakta Dhatu.

The Ranjaka Pitta deviated from its normal path gets into Rakta Dhatu

(circulation). This condition may be viewed as the hyper Bilirubinaemia present

in Jaundice. The hyperbilirubinaemia, which is present, is usually of conjugated

variety. Ranjaka Pitta, which is circulated along with the blood, gets settled in

Twak, Dhatu and other areas in loose elastic tissues, which also constitute

shakha. This is the actual stage of manifestation of disease, which can also be

called the Icteric phase of the Hepatocellular Jaundice in general and Hepatitis in

particular. The Ranjaka Pitta just deposited results in the symptoms such as

peetata of netra, mootra, twak, rakta and purish etc.

If the disease is not countered even at this stage, it progresses into the next

stage wherein the complications set in. A permanent organic damage may take place

in Yakrit/Liver and produce irreversible damages such as Cirrhosis of Liver,

Carcinoma of the Liver etc.

All the authors have considered Kamala as a synonym of Jaundice caused due

to Hepatic, Pre-Hepatic or extra Hepatic obstruction.

But if the view of different classical authors are considered it may not be

considered as Hepatic or Post Hepatic Jaundice. In hepatocellular Jaundice there may

be even avarodha to the normal flow of Ranjaka Pitta due to inflammatory changes in

the biliary canaliculi. Hence all varieties of Jaundice caused due to the primary

pathology of Yakrit including cholestasis can be considered as Kamala of different

varieties.

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On the other hand if the cause of obstruction is mainly due to the presence of

foreign materials etc, and if the obstruction is extra hepatic it can be called “Paratantra

Shakhashrita Kamala49

”.

SAMPRAPTI GHATAKA:

Dosha - Pitta - Ranjaka Pitta, Pachaka Pitta

Kapha - Koshtastha Kapha

Vata - Vyana Vayu

Dooshya - Rakta, Twak, Mamsa

Agni - Jatharagni and Rakta dhatwagni

Ama - Jatharagni mandyajanya ama and

Raktadhatwagni mandya janya ama.

Srotus - Raktavaha Srotas

Srotadushti Prakara - Sanga and Vimargagamana

Udbhava sthana - Amashaya

Sancharasthana - Rasayani

Vyakta sthana - Netra, Twak, Mootra

Adhishtana - Yakrit

Roga marga - Abhyantara - Bhaya

SAMPRAPTI AVASTHA OF KOSHTA SHAKHASHRITA KAMALA (SHAT KRIYAKALA):

1. Sanchaya:

Chayo vruddhi swadhamneva50

|

Due to different causative factors all the doshas will get vitiated and

accumulate in their own respective site. These vitiated Doshas also vitiate their own

sites and produce related symptoms.

In Kosthashakhashrita Kamala the Pitta prakopaka ahara vihara vitiates the

Pitta dosha. The vitiated Pitta dosha accumulates in its own place, i.e. in Amashaya

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and Raktavaha srotas and produces symptoms i.e. Pitavabhasita, Agnimandya,

Aruchi51

.

2. Prakopa:

Sanchayeapahruta dosha labhante nottara gatihi |

Te tuttarasu gatishu bhavanti balavattaraha52

|

When the dosha become unmaragami attain the nature of unmaragami, that

stage is called Prakopa Avastha. That means the dosha leave their own site and

produce symptoms.

If the Sanchaya avastha is not treated, that will further lead to Prakopa

avastha.

In Koshta Shakhashrita Kamala if a person indulges in Pitta Prakopaka Ahara

Vihara after the Sanchitavastha, these dosha will attain the Prakopavastha and

produce symptoms like Koshtoda, Pipasa, Daha and Aruchi.

3. Prasaravastha:

If the Prakupita dosha is not treated, then it will spread to sarva shareera

through the srotamsi.

In Kosthashakhashrita Kamala, the outcome of Prakupita Ranjaka Pitta which

results in Vimargagamana of Pitta to the Shakha produce symptoms like Daha,

Aruchi, Avipaka, Chardi and Manda Jwara53

.

4. Sthanasamshraya:

The Prasarita dosha after circulating all over the body accumulates in any one

place causing Srotovaigunya. Further it vitiates the Dhatus and Malas producing

Sthananurupi roga that means the dosha dushya sammoorchana take place.

In Koshtashakhashrita Kamala, the disseminated Pitta pradhana tridosha are

potent enough to lodge in Yakrit where the defense mechanism is weak or in other

terms Khavaigunya is present.

This is the stage when there is intermixing between the circulating dosha and

sthanika dushya.

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Later the chaturtha Kriyakala is manifested. The poorvaroopa like Atopa,

Vishtamba, Parshvarthi, and Dourbalya etc are produced54

.

5. Vyaktavastha:

In case of Sanchaya Prakopa and Sthanasamshraya Avastha if the condition is

not treated further it leads to Abhivyakta vyadhi. In this stage the main symptom will

be produced55

.

In case of Kosthashakhashrita Kamala, the Ranjaka Pitta, which is normally

excreated into intestines will deviate its path. This pathology is facilitated by the

Prakupita vata dosha. The deviated ranjaka Pitta reaches Shakha due to

vimargagamana. As stated in classics, there are four main causes for the

shakhabhigaman of dosha namely,

Ativyayamat Ushmanat

Teekshnat Ahitasya avacharanat

Ativyayam plays an important role followed by other causes. Shakha gati of

dosha suggest an advancement of pathological condition. In the present context the

shakha which first afflicted is Rakta Dhatu. The Ranjaka Pitta deviated from its

normal path gets into Rakta dhatu.

Ranjaka Pitta, which is circulates along with the blood, settles in twacha dhatu

and other areas. This deposited Ranjaka Pitta results in symptoms like Peetata of

Netra, Mootra, Twak, Rakta and Purisha.

6. Bheda Avastha:

Ataurdhvameteshamavadirninam vranabhavamapannanam shashtah kriyakalah56

|

If the disease is not encountered even at Vyaktavastha, it progress into the next

stage, i.e. Bheda Avastha, where in the complications set in.

In Koshtashakhashrita Kamala, a Paratantra vyadhi, manifests as a sequel of

Panduroga or due to some other disease. Charaka Samhita has used the term

BahuPitta Kamala as a synonym for Koshta Shakhashrita Kamala. Shakhashrita

Kamala is a Swatantra vyadhi. Chakrapani termed this Kamala as AlpaPitta Kamala.

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POORVA ROOPA

Poorva Roopa is the prodromal symptoms or the premonitory indications,

which occur before the complete manifestation of disease. The provoked dosha at the

stage of sthana samshraya will manifest the signs and symptoms of the forth-coming

disease.

In classics poorva roopa is classified into two varieties. They are,

1. Samanya poorva roopa 2. Vishishta poorva roopa

Samanya poorva roopa are those which indicate the disease to some extent

without giving any indications of the specific sub-type of the disease and generally

disappear before the onset of the disease.

Vishishta poorva roopa are those which give an idea of the dosha along with

the indication of the disease to some extent and these are likely to continue even after

the commencement of the disease.

Specific Poorvarupas for Kamala have not been mentioned either in Brihatrayi

or in Laghutrayi. Vagbhata defined Poorvarupa as Alpavyaktatvam57

and hence the

rupa with less intensity (Alpabala) can be considesed as Poorva Roopa of Kamala

(Swatantraja).

Susruta described Kamala as synonym of Pandu58

. So the Poorvarupa of

Panduroga may also be considered as Pooorvarupa of Kamala. Also that Pāndu

rogi,on consumption of Atipittala ahara will be afflected by Kamala59

. Hence the

same Poorvarupas of Pandu may be considered for the Paratantraja Kamala

Poorvarupa60

. They are

1. Twak sputana

2. Steevana

3. Gatra sada

4. Mrut bhaksana

5. Aksi kuta shotha

6. Peeta mutrata.

7. Peeta varchah

8. Avipaka

But in ‘Chikitsa krama kalpa vallyam’ the work of 18th

century A.D, a

reference pertaining to the poorva roopa of kaamala is available. The author has

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considered following as poorva roopa;

1. Daha

2. Vipaka

3. Aruchi

4. Agni mandya

5. Manda jwara

6. Sada

7. Karshya

But the author has considered these as poorva roopa of kaamala and has not

specified whether they are of Shakhashrita kaamala or koshtashakhahrita kamala.

Table 44 Showing the comparision of lakshanas of Shahkashrita kamala and

prodromal symptoms of Hepatitis-B

Sl.No Prodromal symptoms of viral

Hepatitis-B

Lakshanas considered as vishishta

Poorva roopa of Shakhashrita kaamala

1

2

3

4

5

6

7

8

9

10

11

12

13

Anorexia

Fatigue

Malaise

Myalgia

Arthalgia

Phyaryngitis

Cough

Coryza

Lowgradefever

Loss of appetite

Headache

Photophobia

Nausea & Vomiting

Aruchi

Daurbalya

Daurbalya

Parswarthi

Parswarthi

Kasa

Kasa

Jwara

Agnimandya

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ROOPA

A disease manifests only on the completion of Dosha Dushya Sammoorchana. The

stage of disease at which symptoms appear is called as ‘Roopa’. They manifest at the 5th

stage of the disease. i.e. ‘Vyaktavastha’.

The dosha remain responsible for each and every symptom of a disease, as they are

the causative factors. Hence Roopa indicates the nature of Dosha Dushya Sammoorchana.

The most common consequence of Hepatitis B is acute inflammatory change of the

entire liver. Clinically acute Hepatitis B is categorized into 4 phases61

, they are

Incubation period

Pre - Icteric phase

Icteric phase

Post - Icteric phase

The first three stages of kriya kala can be considered as the period of incubation.

The stage of sthana samshraya corresponds to the pre-icteric phase. Icteric phase is the

actual stage of the manifestation of the disease identified as ‘Vyaktavastha’. The post-icteric

phase is the stage of the self-resolution or of the organic lesions.

This can also be called the ‘Bheda Avastha’. Hence in the present context of roopa,

the symptoms, which manifest during the stage of icteric phase are discussed62

.

Charaka Samhita has considered the following as the Roopa of Kamala:

Haridra netra

Haridra mootra

Haridra twak

Tila Pishta Nibha Varchas

Aatopa

Vishtambha

Guruna hridayena

Dourbalya

Alpagni

Parswarthi

Hikka

Kasa

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Aruchi

Jwara

Haridra netra, mootra, twak.

Among the symptoms of the icteric phase or the Vyaktavastha, Haridra netra,

Haridra mootra, Haridra twak, can be compared to yellowish discoloration of sclera,

urine, skin and can be considered as the cardinal features of the disease

In Shakhashrita kamala peetavarna of twak, nakha, neetra and mootra is

mainly because of impaired pitta dosha. As kamala is one of the pitta nanatmaja

vyadhi yellowish discolouration of skin ..et.c can be considered as the

pratyatmalakshana of the disease Shakhashritakaamala. The pitta which is vitiated

and deviated from its normal path gets accumulated in shakha. Due to the excess of

accumulation of pitta in shakha the peetata which is amongst the common lakshana

attributed to pitta vriddhi is observed.

Tila Pishta Nibha Varchas

This symptom is one of the most important diagnostic criteria of the

Shakhashrita kamala . Physiologically ranjaka pitta is responsible for mala ranjana.

The absence of ranjaka pitta in the koshta due to avarodha hampers mala ranjana

kriya. As a result of this the stool becomes pale. The normal consistancy of the stool

is also hampered and resembles ‘tila pishta’ as a result of the impaired fat digestion,

as fat digestion is one of the important functions of Ranjaka pitta or bile .

Apart from the above two objective lakshanas which appear specifically in the

icteric phase there are many other subjective lakshana which appear in different stages

of the disease. The most important of them include agnimandya, aruchi, aatopa,

vishtambha, jwara, daurbalya. The first three indicate the impairment of a function of

the digestive system or the annavaha srotas. Agnimandya in particular is observed in

the pre- icteric phase. This symptom is also highlighted by Harana chandra,

This symptom is a direct impact of the nidana sevana. As a consequence of

agnimandya, amotpatti takes place. Aama thus formed results in the other symptoms

of the digestive system such as aruchi, aatopa and vishtambha. There are also other

symptoms of the gastro intestinal tract such as hrillasa and chardi which are not

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explained in Ayurveda. They can be considered as an associated symptoms resulting

out of agnimandya and aruchi. The symptom jwara differentiates infective variety of

Shakhashrita kamala from the other varieties of Shakhashrita kaamala, even though

the pathology of all the varieties of Shakhashrita kamala is one and the same. The

presence of jwara as a lakshana helps to make a specific diagnosis of the infective

hepatitis including Hepatitis-B. This lakshana is seen mainly in the pre icteric phase.

Most of the other symptoms which are mentioned can be considered as the

associated symptoms of the disease caused due to the involvement of pranavaha and

other sroatas.

Apart from the above symptoms which are explained in various classical texts,

some more signs and symptoms are commonly observed , in the day to day practice.

They are mainly kandu, yakrit vriddhi and occasionally pleeha vriddhi

Kandu

The symptom kandu appears in Shakhashrita kamala if the disease is

prolonged for one or two weeks. Kandu is said to be the pratyatma lakshana produced

by kapha. In Shakhashrita kamala along with kapha vriddhi the deposition of the

ranjaka pitta in the twak can also be considered as the cause of kandu.

Yakrit vriddhi

As kamala is raktavaha sroatovikara any disturbance in the raktavaha srotas

causes the vitiation of the srotomoola. In Shakhashrita kamala as khavaigunya is in

the yakrith itself, yakrit vriddhi is observed most of the time .

The roopa taken in relation to Bahupitta Kamala are seen in Hepatitis -B

induced Jaundice.

The type of Kamala namely Bahupitta Kamala (Koshtashrita Kamala) –

Ubhayashrita Kamala has got more clinical significance and resemblance with HBV

induced Jaundice.

However it is difficult to find out an exact correlation for HBV induced

Jaundice in Ayurveda. Majority of the lakshanas mentioned in Kosthashakhashrita

Kamala are observed as signs and symptoms in HBV induced Jaundice, but few of the

symptoms and presentations like Shweta varchas (Tila pistha nibha varchas) a

manifestation in Ruddha patha kamala (Shakhashrita Kamala – Alpa Pitta Kamala) is

seen as a symptom in severe cases of HBV induced Jaundice in the form of clay

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coloured stools.

Table 45 Lakshana of Kamala roga according to different Acharyas63

:

Sl.

No Lakshana Cha. Su. A.Hr. M.Ni. B.P. Y.R.

1 Haridra netra + + + + + +

2 Haridra twacha + + + + + +

3 Haridra mukha + + + + + +

4 Haridra nakha + + + + + +

5 Haridra mutra +

6 Rakta peetha shakrut +

7 Rakta peetha mutra + - + + +

8 Daha + + + + +

9 Avipaka + + + + + +

10 Dourbalya + + + + + +

11 Aruchi + + + + + +

12 Krusha - + - - - +

13 Tandra - + - - - -

14 Balakshaya - + - - - -

15 Indriyadourbalya + - + + + +

16 Bhekavarna + - + + + +

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BHEDA

Charaka samhita for the first time has classified the disease kamala in to two types.

They are as follows : 1)Koshta shakhashrita kamala, 2)Shakhashrita kamala64

.

Koshta Shakhashrita kamala is a paratantra vyadhi. It manifests as a sequel to

panduroga65

, or due to some other disease66

. Charaka samhita has used the term ‘Bahupitta

kamala’ as a synonym to the Koshta Shakhashrita kamala. Shakhashrita kamala is ‘Swatantra

vyadhi’. Chakrapani termed this kamala as ‘Alpapitta kamala67

’. Sushrutasamhita has stated

that, kamala is a later stage of Pandu roga or any other disease. Kumbha kamala, Lagharaka,

Alasa and Haleemaka are its different stages68

.

Harita opines that both kamala and Haleemaka are included under the eight types of

Pandu roga69

. Thus kamala can be classified chiefly according to the dispersal of Pitta in the

body as,

1. Koshta Shakhashraya kamala or Bahupitta kamala

2. Shakhashrita kamala or Alpapitta kamala.

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SAPEKSHA NIDANA OF KAMALA

As per Ayurvedic view Sapeksha Nidana of Kamala can be as,

Pittaja Jwara70

Pittaja Pandu71

Koshta Shakhashrita Kamala

Shakhashrita Kamala

Haleemaka72

Kumbha Kamala73

Haridraka Jwara

Peeta Jwara

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Sapeksha Nidana (Vyavachedaka Nidana):

Lakshana Pittaja

Jwara

Shakha

-shrita

kamala

Koshta

Shakhashri

ta kamala

Peeta

Jwara

Pana

ki

Pittaja

Pandu

Hari-

draka

Jwara

Hal-

eema

Haridra netra + + + + + +

Haridra twacha + + + + + + +

Haridra mukha + + +

Haridra nakha + + + + +

Haridra mutra + +

Daha + + + + +

Avipaka +

Dourbalya + + +

Tandra + +

Krushata

Bala kshaya + +

Bhrumsha + + +

Jwara + + + + +

Pitta Chardi + + +

Sarakta chardi +

Shwasa

Aruchi + + +

Haridra purisha - + +

Tilpishtanibha

varchas + -

Bhinna varcha + + +

Dourgandhya +

Sheeteccha + +

Murcha + +

Ati trishna + +

Ati sara + +

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CHIKITSA

A process by which equilibrium of Tridosha, Saptadhatu and Trimala achieved

is termed Chikitsa. Samanya Chikitsa sutra of Kamala explained in different classics

are as follows:

Kamala can be treated by Snehana, Mrudu, Virechana and

Shamanaoushadhi74

. Astanga Hridaya opines to adopt Pittahara chikitsa along with

the above measures. Even he is in favor of Anjana Chikitsa75

.

In Sushruta samhita, Kamala is considered as one of the varieties of

Panduroga and Panduroga Chikitsa sutra is indicated for Kamala76

. In Yoga Ratnakar

clear Chikitsa krama is mentioned for Kamala. They are Snehana, Virechana and he

has also indicated Anjana and Nasya along with the above measures77

.

From the above classical references we can frame the line of treatment of

Kamala in the following manner.

Deepana and Pachana

Snehana

Virechana

Nasya

Anjana

Shamanoushadhi

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Deepana, Pachana:

Restoration of Agni is one of the main aims of treatment .So Deepana and

Pachana karma is required before proceeding to the main line of treatment. This

Karma is essential when the treatment is aimed to cure Koshta Shakhashrita Kamala.

Snehana78

:

Kamala and Pandu Rogi are to be given Sneha in Eshat pramana in these

conditions prayoga of Sneha in Prabhuta matra is contraindicated as stated by

Vagbhata “Tatra Kamala Panduroginam Nati Snigdhan Virechayet” means the

Virechana should be done later after the introduction of Abhyantara Sneha in a

minimal dosage.

Virechana79

:

In classics it has been advised to undertake Mrudu Virechana in Pandu and

Kamala. Virechana therapy is the choice of treatment for Pitta Pradhana Rakta

pradhoshaja disorders.

Nasya and Anjana:

Regarding Nasya karma no detail explanation are available that whether the

Nasya karma is an Avasthika Chikitsa or Nasya karma is complete procedure

relieving the Kamala janya lakshanas (Roga muktasya lakshana). For Nasya in

classics following drugs are mentioned:

Jimutaka Phala Nasya

JaliniPhala swarasa

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Karkotaka Moola Swarasa.

In Bhaishajya Ratnavalli in Kamala prakarana the Karkotaka moola and Jalini

phala are advised for Nasya.

All the above-mentioned drugs Teekshna, Aashukari, Vyavahi and Vikasi in

property. These drugs produce irritation in the nasal mucosa. Because of irritation a

thin serous secretion starts from the nasal cavity, can be practically observed. The

secretion is slightly yellowish in colour. Thus Nasya karma may help in excretion of

bilirubin deposited in nasal mucosa and the bilirubin present in the circulation.

For Anjana in classics following drugs are mentioned.

Hingu

Dronapushpi swarasa

Rasanjana

NishaGairika Dhatri

Arishta Beeja

Bilirubin has got affinity towards elastin tissues.So Bilirubin gets deposited in

sclera. The above-mentioned drugs seem to increase the lacrimal secretion. Through

lacrimal secretion the Bilirubin which is deposited is eliminated (excreted). Here

along with lacrimation even drugs may be helpful in the removing of Bilirubin from

sclera and circulation.

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Commonly used Ghrita:

Pachagavya Ghrita

Mahatikta Ghrita

Kalyanadi Ghrita

Kaleyakadi Ghrita

Haridradi Ghrita

Dadimadi Ghrita

Choorna:

Nishottara

Indrayana

Sunthi churna

Triphala

Katuki

Navayas choorna

Trikatu

Musta

Gutika Vati:

Punanarva mandur

Triyooshnadimandur

vatika

Arogyavardhini

Navayas loha

Saptramruta loha

Other formulations:

Datryavaleha

Bijakarishta

Rohitakarishta

Kalameghasava

Bhunimbadi

kwatha

Vasaguduchyadi

kashaya

Vidangavaleha

Guduchyadi

kwatha

Daruharidra

kwatha

Patolkaturohinyadi

kashaya

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SADHYASADHYATA

The sadhyasadhyata or the probable outcome of an attack of a disease i.e. the

prognosis should be established before the commencement of the treatment.

Sadhyasadhyata suggests the prognosis of a disease. A disease is called as Sadhya when

it is successfully manageable and the prognosis is good. On the other hand if the disease

is not manageable and the prognosis is very poor it is called Asadhya. Even Sadhya

disease can be of two types, easily manageable (Sukhasadhya) ones and the ones, which

are difficult to manage (Kruchra Sadhya). None of the classical textbooks has

mentioned about the Sadhyasadhyata of Kamala in general or Koshta Shakhashrita

Kamala in particular. Hence the general principle described by Ashtanga Hridaya to

decide the Sadhyasadhyata can be made use of. It is said that a disease is sukha Sadhya

if it is not chronic (nava) has minimum symptoms (alpa roopa) and is devoid of

complications (upadrava).

Certain symptoms produced in a disease suggest the bad prognosis of the

disease. Such dangerous and ominous symptoms are called Arishta. In Brihatrayis and

Laghutrayis description regarding Arishta lakshana of Koshta Shakhashrita Kamala or

Shakhashrita Kamala is not available. The Arishtalakshana told by Madavakara has

been mentioned under the heading Arishta Lakshanas.

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PATHYAPATHYA

PATHYA

In Ayurvedic classics description regarding pathya for Kamala disease is widely

available. This can be broadly classified under the following headings80

.

1. Shooka Dhanya

(Monocotyledons)

2. Shami Dhanya (Dicotyledons)

3. Mamsa varga.

Shooka Dhanya:

Charakacharya has particularly mentioned purana shali, purana yava and purana

Godhooma as the pathya for the Kamala patient. Here it is consumed in the form of

yoosha. For this any one of the above-mentioned ahara dravyas are used.

Shami Dhanya:

Under this heading dravya like Mudgha, Masoor etc. are advised as Pathya for

Kamala Rogi.

Mamsa varga:

In this heading Charakacharya opinioned that Jangala prani mamsa rasa is

beneficial for Kamala Rogi.

Along with this other pathya told are,

Patola, Kadali (banana), Jeeraka, Lasuna, Haritaki, Amalaki, Dadima, Draksha,

Amra etc. All these should be adviced according to Prakruti and Dosha, Rogi bala, Roga.

APATHYA:

According to Classics, Raktamokshana, Dumapana, Vamana, Vegavarodh,

Swedana, Sneha in Bahumatra, Dustaja Guru, Vidahi ahara ,Sarshapa, Madhya, Dadhi,

Ghrita, Matsya, Pittaprakopaka Vihara, like Maithuna, Krodha, Aatapsevana,

Ativayayam, Divaswapana, are considered as Apathya for Kamala Rogi.

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UPADRAVA

The occurrence of another disorder on the wake of a primary disease, as a

complication is termed as Upadrava. However upadrava may exhibit pathology of a

more serious or fulminating nature than that of the main disease and in such cases it

cannot be cured merely by the treatment given for the main disease. In such condition

immediate and appropriate treatment should be given to check the Upadrava.

The upadrava of either Koshta Shakhashrita Kamala or Shakhashrita Kamala

is not explained in the classics under separate and independent heading. But based on

the various descriptions explained in classics pertaining to Kumbha Kamala, it seems

to be the disease Kumbha Kamala is an Upadrava of Kamala. Acharya Harita has

considered Kumbha Kamala as a variety of Pandu roga.

Acharya Sushruta has opined Kumbha Kamala as a type of Kamala.

According to Charaka Kumbha Kamala is the avastha vishesha or next stage of the

disease. While explaining Kumbha Kamala Nidana Charaka has mainly used two

terms “Kalantarat” and “Kharibhoota”. Here the term Kalantarat indicates the laps of

time or period where as Kharibhoota indicates the difficult stage of disease for the

treatment.Charaka has explained Kumbha Kamala immediately after explaining the

Samprapti and Lakshana of Koshta – Shakhashrita Kamala. It implies that if Koshta

Shakhashrita Kamala is neglected then Kumbha Kamala is produced. But most of

Kumbha Kamala lakshanas mentioned in classics seems to cirrhotic condition.

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ARISHTA LAKSHANA

Certain symptoms produced in disease suggest the definite death of a patient.

Such dangerous and ominous symptoms are called Arishtas. Description regarding

arishta lakshanas either Shakhashrita kamala or of Koshtashakhashrita kamala is not

explained either Brahatrayis or in Laghutrayis.

Madhavakara for the first time has mentioned Arishta lakshana of Kumbha

kamala. (Ma. Ni. 1. 8/21). Bhavamishra the author of Bhavaprakasha has followed

Madhavakar and in 8th chapter of Bhavaprakasha nighantu has explained arishta

lakshana of Kumbha kamala.

As discussed earlier Kumbha kamakla can be considered as upadrava of

Shakhashrita kamala. Hence arishta lakshana of Kumbha kamala can be considered as

arishta lakshana of Shakhashrita kamala.

Table No. 46 . The Arishta Lakshanas of Kumbha kamala

Aristha lakshanas Bh.Pr Ma.Ni

Chardi

Aruchi

Hrullasa

Jwara

Klama

Shwasa

Kasa

Arati

Vidbheda

+

+

+

+

+

+

+

+

+

+

+

+

+

+

+

+

+

+

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ANATOMY OF LIVER

The Liver

The Liver is a large, solid gland situated in the right upper quadrant of the

abdominal cavity. In the living subjects the Liver is reddish brown in colour, soft in

consistency, and very friable. It weighs about 1600 gms in males and about 1300 gms

in females. The Liver occupies the whole of the right hypochondrium, the greater part

of the epigastrium, and extends into the left hypochondrium reaching up to the left

lateral line. From the above it will be obvious that most of the Liver is covered by ribs

and costal cartilage, except in the upper part of the epigastrium where it is in contact

with the anterior abdominal wall.

The Liver is largest gland in the body. It secretes bile and performs various

other metabolic functions.

The Liver is also called the „hepar‟ from which we have the adjective „hepatic‟

applied to many structures connected with the organ.

External Features:

The Liver is wedge shaped. It resembles a four sided pyramid laid on one side.

It has five surfaces. These are 1.anterior 2.posterior 3.superior 4.inferior

and 5.right.

The Liver is divided into right and left lobes by the attachment of the falciform

ligament anteriorly and superiorly; by the fissure for the ligamentum teres inferiorly;

and by the fissure for the ligamentum venosum posteriorly.

The right lobe is much larger than the left lobe and forms five sixth of the

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Liver. It contributes to all the five surfaces of the Liver, and presents the caudate

and quadrate lobes.

The caudate lobe is situated on the posterior surface. The quadrate lobe is

situated on the inferior surface. The porta hepatis is deep transverse fissure about

2inches long situated on the inferior surface of right lobe of the Liver.

Relations:

1. Peritoneal Relation

Most of the Liver is covered by peritoneum. The areas not covered by

peritoneum are as follows:

a. A triangular bare area on the posterior surface of the right lobe, limited by

the upper and lower layers of the coronary ligament and by the right

triangular ligament:

b. The groove for the inferior vena cava, on the posterior surface of the right

lobe of the Liver, between the caudate lobe and the bare area:

c. The fossa for the Gall Bladder which lies on the inferior surface of the

right lobe to the right of the quadrate lobe:

d. The porta hepatis

e. Along the lines of reflection of peritoneum.

II. Visceral Relations

Anterior Surface:

This surface is triangular and slightly convex. It is related to the xiphoid

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process and to the anterior abdominal wall in the median plane; and to diaphargm on

each side.

Superior Surface:

It is quadrilateral and shows a concavity in the middle. This is the cardiac

impression.

Inferior Surface:

It is quadrilateral and is directed downwards, backwards and to the left.

Right Surface:

It is quadrilateral and convex. It is related to the diaphragm opposite the 7th

to

11th

ribs in the midaxillary line. It is separated by the diaphragm from the pleura (up

to the 10th

rib), and from the lung (up to the 8th

rib).

Blood Supply:

The Liver receives 20% of its blood supply through the hepatic artery, and

80% through the portal vein. Before entering the Liver, both the hepatic artery and the

portal vein divide into right and left branches. Within the Liver, they redivide to form

segmental vessels, which further divide to form interlobular vessels. Further

ramifications of the interlobular branches open into the hepatic sinusoids. Thus the

hepatic arterial blood mixes with the portal venous blood in the sinusoids. There are

no anastomoses between adjoining hepatic arterial territories and hence each branch is

an end artery.

Venous Drainage:

Hepatic sinusoids drain into interlobular veins, which join to form sub lobular

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veins. These in turn unite to form the hepatic veins, which drain directly into the

inferior vena cava.

The hepatic veins are arranged in two groups, upper and lower. The upper

group consists of three large veins (right, left and middle) which emerge through the

upper part of the groove for the inferior vena cava, and open directly into the vena

cava. The lower group consists of a variable number of small veins (from the right

lobe and the caudate lobe), which emerge through the lower part of the caval groove

and open into the vena cava.

Lymphatic Drainage:

The superficial lymphatics of the Liver run on the surface of the organ beneath

the peritoneum, and terminate in caval, hepatic paracardial and coeliac lymph nodes.

Some vessels from the coronary ligament may directly join the thoracic duct.

The deep lymphatic end partly in the nodes around the end of the inferior vena

cava, and partly in the hepatic nodes.

Nerve Supply:

The Liver receives its nerve supply from the hepatic plexus, which contains

both sympathetic and parasympathetic (vagal) fibres. Nerves also reach the Liver

through its various peritoneal ligaments.

Hepatic Segments:

On the basis of the intrahepatic distribution of the hepatic artery, the portal

vein and the biliary ducts, the Liver can be divided into right and left functional lobes.

These do not correspond to the anatomical lobes of the Liver. The physiological lobes

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are separated by a plane passing on the anterosuperior surface, along a line joining the

cystic notch to the groove for the inferior vena cava. On the inferior surface the plane

passes through the fossa for the Gall Bladder, and on the posterior surface it passes

through the middle of the caudate lobe.

Hepatic Ducts:

The right and left hepatic ducts emerge at the porta hepatis from the right and

left lobes of the Liver. The arrangement of structures at the porta hepatis from behind

forwards is i. The branches of the Portal vein ii. Hepatic artery and iii. Hepatic ducts.

Common Hepatic ducts:

It is formed by the union of the right and left hepatic ducts near the end of the

porta hepatis. It runs downwards for about 3cm and is joined on its right side (at an

acute angle) by the cystic duct to from the bile duct.

Accessory hepatic ducts are present in about 15% of subjects. They usually

issue from the right lobe of the Liver, and terminate either in the Gall Bladder, or in

the common hepatic duct anywhere in its course, or even in the upper part of the bile

duct.

Histology of Liver:

The hepatic parenchyma is composed of numerous hexagonal or pyramidal

classical lobules; each with a diameter of 0.5 to 2 mm. Each classical lobule has a

central tributary from the hepatic vein and at the periphery are 4 to 5 portal tracts or

triads containing branches of bile duct, portal vein and hepatic artery. Cords of

hepatocytes and blood containing sinusoids radiate from the central vein to the

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peripheral portal triads. The functioning lobule or Liver acinus‟s as described by

Rapparport has a portal triad in the centre and is surrounded at the periphery by

portions of several classical lobules. However, in most descriptions on pathology of

the Liver, the term lobule is used in its classical form.

The blood supply to the Liver parenchyma flows from the portal triads to the

central veins. Accordingly, the hepatic parenchyma of Liver lobule is divided into 3

zones.

Zone 1 or the periportal (peripheral) area is closest to the arterial and

portal blood supply and hence bears the burnt of all forms of toxic injury.

Zone 2 is the intermediate mid zonal area.

Zone 3 or the centrilobular area surrounds the central vein and is most

remote from the blood supply and thus suffers from the effects of hypoxic

injury.

The hepatocytes are polygonal cells with a round single nucleus and a

prominent nucleolus. The Liver cells have a remarkable capability to undergo mitosis

and regeneration. Thus it is not uncommon to find Liver cells containing more than

one nuclei and having polyploidy up to octoploidy. A hepatocyte has 3 surfaces: One

facing the sinusoid and space of Disse, the second facing the canaliculus, and the third

facing neighboring hepatocytes.

The blood-containing sinusoids between cords of hepatocytes are lined by

discontinuous endothelial cells and scattered flat Kupffer cells belonging to the

reticuloendothelial system.

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The space of Disse is the space between hepatocytes and sinusoidal lining

cells. A few scattered fat storing Ito cells lie within the space of Disse.

The portal triad or tract besides containing portal vein radicle, the hepatic

arteriole and bile duct, has a few mononuclear cells and a little connective tissue

considered to be extension of Glisson‟s capsule. A limiting plate of hepatocytes

surrounds the portal triads.

The intrahepatic biliary system begins with the bile canaliculi interposed

between the adjacent hepatocytes. The bile canaliculi are simply grooves between the

contact surfaces of the Liver cells and are covered by microvilli. These canaliculi join

at the periphery of the lobule to drain eventually into terminal bile ducts or ductules

(canal of Hering), which are lined by cuboidal epithelium.

Gall Bladder:

This is pear-shaped reservoir of bile situated in a fossa on the inferior surface

of the right lobe of the Liver. The fossa for the Gall Bladder extends from the right

end of the porta hepatis to the inferior border of the Liver. The Gall Bladder is 7 to

10 cm (3 to 4 in) long 3cm broad at its widest part, and about 30 to 50ml in capacity.

The Gall Bladder is divided into 1.The fundus 2.The body and 3.the neck. The

Fundus projects beyond the inferior border of the Liver in the angle between the

lateral border of the right rectus abdominis and the 9th

costal cartilage. The body

lies in the fossa for the Gall Bladder on the Liver. The neck is the narrow upper end of

the Gall Bladder. It is situated near the right end of the porta hepatis.

The postero medial wall of the neck is dilated outwards to form a pouch

(Hermann‟s pouch) which is directed downwards and backwards. Some regard this

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pouch as a normal feature of the Gall Bladder, but others consider it to be

pathological. Stones may lodge in this pouch.

Cystic Duct:

This duct is about 3 to 4cm (roughly 1inch) long. It begins at the neck of the

Gall Bladder, runs downwards, backwards and to the left, and ends by joining the

common hepatic duct at an acute angle to form the bile duct. The mucous membrane

of the cystic duct forms a series of 5 to 12 crescentric folds, arranged spirally to form

the so-called „spiral valve‟ (of Heister). This is not a true valve.

Bile Duct:

It is formed by the union of the cystic and common hepatic ducts near the

porta hepatis. It is 8cm long and has a diameter of about 6mm.

Arteries Supplying the Biliary Apparatus:

1. The cystic artery is the chief source of blood supply; and is distributed to the

Gall Bladder, the cystic duct, the hepatic ducts and the upper part of the bile

duct.

2. Several branches from the posterior superior pancreaticoduodenal artery

supply the lower part of the bile duct.

3. The right hepatic artery forms a minor source of supply to the middle part of

bile duct.

4. An accessory cystic artery may arise from the common hepatic artery, or

from one of its branches.

The cystic artery usually arises from the right hepatic artery passes behind the

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common hepatic and cystic ducts, and reaches the upper surface of the neck of the

Gall Bladder, where it divides into superficial and deep branches. Occasionally, the

cystic artery arises from the hepatic artery proper, and rarely from the gastro duodenal

artery.

Venous Drainage:

1. The superior surface of the Gall Bladder is drained by veins, which enter the

Liver through the fossa for the Gall Bladder and join tributaries of hepatic

veins.

2. The rest of the Gall Bladder is drained by one or two cystic veins, which

commonly enter the Liver, either directly or after joining with the veins

draining the hepatic ducts and the upper part of the bile duct. Rarely the

cystic vein opens into the right branch of the portal vein.

3. The lower part of the bile duct drains into the portal vein.

Lymphatic Drainage:

1. Lymphatics from the Gall Bladder, the cystic duct, the hepatic ducts and the

upper part of the bile duct pass to the cystic node and to the node of the

anterior border of the epiploic foramen. These are the most constant

members of the upper hepatic nodes.

2. The lower part of the bile duct drains into the lower hepatic and upper

pancreaticosplenic nodes.

Nerve-Supply:

The cystic plexus of nerves, supplying the territory of the cystic artery, is

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derived from the hepatic plexus, which receives fibers from the coeliac plexus, the left

and right vagi and the right phrenic nerves. The nerve plexus supplies the lower part

of the bile duct over the superior pancreaticoduodenal artery.

Parasympathetic nerves are motor to the musculature of the Gall Bladder and

bile ducts, but inhibitory to the sphincters. Sympathetic nerves (T7 to T9) are

vasomotor and motor to the sphincters.

Pain from the Gall Bladder may travel along the vagus, the sympathetic

nerves, or along the phernic nerves. It may be referred to different sites through these

nerves as follows.

i. Through the Vagus Nerve to the stomach.

ii. Through the sympathetic nerves to the inferior angle of the right

scapula.

iii. Through the phrenic nerve to the right shoulder.

Functions of the Gall Bladder:

1. Storage of bile, and its release into the duodenum when required.

2. Absorption of water, and concentration of bile. Bile may be concentrated as

much as ten times.

3. The normal Gall Bladder also absorbs small amounts of a loose bile salt-

cholesterol compound. When the Gall Bladder is inflamed the concentration

function becomes abnormal and the bile salts alone are absorbed leaving

cholesterol behind. Bile salts have a powerful solvent action on cholesterol, but

when bile salts are absorbed the cholesterol tends to be precipitated. This can

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lead to the formation of Gall stones.

Bilirubin and the Bile formation:81

Bilirubin: It is an orange coloured or yellow pigment. The bile is formed in the

Liver. Bile salts helps in the digestive and absorptive processes of the intestinal tract.

This is the major end product of haemoglobin degradation.

Briefly when the red blood cells are worn out after their average life span of

120 days, they become too fragile to exist longer in the circulatory system, their cell

membranes rupture. Here the hemoglobin is phagocytosed by tissne macrophages

(also called the reticuloendothelial system) throughout the body. Here the hemoglobin

is first split into globin and haem, and the haem ring is opened to give 1. free iron that

is transported in the blood by transferrin and 2. a straight chain of four pyrrole nuclei

that is the substrate from which bilirubin will eventually be formed. The first

substance formed is biliverdin, but this is rapidly reduced to free bilirubin which is

gradually released from the macrophages into the plasma. The free bilirubin

immediately combines strongly with the plasma albumin and is transported in this

combination throughout the blood and interstitial fluids. Even when bound with the

plasma protein this bilirubin is still called “free bilirubin” to distinguish it from

conjugated bilirubin.

Within hours, the free bilirubin is absorbed through the hepatic cell

membrane. In passing to the inside of the hepatic cells, it is released from the plasma

albumin and soon thereafter conjugated, about 80 percent with glucuronic acid to

form bilirubin glucuronide, about 10 percent with sulphate to form bilirubin sulphate,

, and the final 10 percent with a multitude of other substances. In these forms, the

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bilirubin is excreted from the hepatocytes by an active transport process into the

biliary canaliculi and then into the intestines.

Direct Bilirubin:

Bilirubin is conjugated in the Liver cells to form bilirubin diglucuronide,

which is water-soluble.

Indirect Bilirubin:

Unconjugated bilirubin that is present in blood, is fat-soluble.

Bile:

A thick, viscid, bitter tasting fluid secreted by Liver. It passes from the bile

duct of Liver into the common bile duct and then into the duodenum as needed. The

bile from the Liver is straw coloured, while that from the Gall Bladder varies from

yellow to brown to green colour.

Bile is stored in the Gall Bladder, where it is concentrated, drawn upon as

needed and discharged into the duodenum. Contraction of Gall Bladder is brought

about by cholecystokinin-pancreozymin, a hormone produced by the duodenum. The

entrance of fatty foods into the duodenum stimulates its secretion. Added to water,

bile decreases surface tension giving a foamy solution favouring the emulsification of

fats and oils, this action is due to bile salts, mainly sodium glycocholate and

taurochalate.

Formation and Fate of Urobilinogen:

Once in the intestine, about one half of the conjugated bilirubin is converted

by bacterial action into the substance Urobilinogen, which is highly water-soluble.

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Some of the Urobilinogen is reabsorbed through the intestinal mucosa back into the

blood. Most of this is once again re-excreted by the Liver back into the gut. But the

kidneys excrete 5% of Urobilinogen in the urine.

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JAUNDICE

The word “Jaundice” means a yellowish tint to the body tissues, including

yellowishness of the skin as well as the deep tissues. The usual cause of Jaundice is

large quantities of bilirubin in the extra cellular fluid, either free bilirubin or

conjugated bilirubin. The normal plasma concentration of bilirubin, which is almost

entirely in free form, averages 0.5 mg/dl of plasma. In certain abnormal conditions,

this can rise to as high as 40 mg/dl and most of it is conjugated. The skin usually

appears Jaundiced when the concentration of conjugated Bilirubin rises to about three

times its normal concentration that is above 1.5 mg/dl.

The common causes of Jaundice are

1. Increased destruction of red blood cells with rapid release of bilirubin

into the blood and

2. Obstruction of the bile ducts or damage to the Liver cells so that even

the usual amounts of bilirubin cannot be excreted into the

gastrointestinal tract.

These two types of Jaundice are called hemolytic Jaundice and obstructive

Jaundice respectively. They differ from each other in the following ways.

Haemolytic Jaundice:

In hemolytic Jaundice, the excretory function of the Liver is least impaired,

but red blood cells are haemolysed rapidly and the hepatic cells simply cannot excrete

the bilirubin as rapidly as it is formed. Therefore, the plasma concentration of free

bilirubin rises to levels much above the normal. Likewise, the rate of formation of

urobilinogen in the intestine is greatly increased, and much of this is absorbed into the

blood and later excreted in the urine.

Obstructive Jaundice:

Obstructive Jaundice is caused either by obstruction of the bile ducts (which

most often occurs when a Gallstone or cancer blocks the common bile duct) or by

damage to the hepatic cells (which occurs in hepatitis as in hepatitis B). The rate of

bilirubin formation is normal but the bilirubin formed cannot pass from the blood into

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the intestines. The free bilirubin usually enters the Liver cells and becomes

conjugated in the usual way. This conjugated bilirubin is then returned to the blood,

probably by rupture of the congested bile canaliculi and direct emptying of the bile

into the lymph leaving the Liver. Thus, most of the bilirubin in the plasma becomes

the conjugated type rather than the free type.

Here we are elaborately discussing on the jaundice caused by Hepatitis B virus

called HBV induced Jaundice.

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STRUCTURE OF HEPATITIS –B VIRUS (HBV)

Various synonyms have been used for HBV in contemporary science82

.

1. Initially it was known as Australian Antigen, (Because of its

discovery in an in Australian aborigines).

2. Hepatitis B virus (HBV)

3. Hepatitis B surface antigen (HBsAg)

4. Hepatocellular B virus

Dr. David Dane, is the first person who isolated and discribed the structure of

Hepatitis–B virus, for the first time in 1970. Hence Hepatitis–B virus is also called as

‘Dane particle’83

.

Electron microscopic study on the serum of patients infected with Hepatitis–B

virus shows three type of the viral particles

1. Small 20nm sphere

2. Tubule 20nm in diameter and 100 nm long

3. The large 42nm Dane particle

Spherical and filamentous forms are most numerous and represents excess of

viral surface coat protein (HBsAg), while Dane particle believed to represent the

intact Hepatitis –B virus. The mature intact Hepatitis –B virus is spherical with the

diameter of 42nm. It is the double layered sphere . It has an outer surface analogue

of protein, lipid, carbohydrate enclosing a slightly hexagonal core measuring 27nm in

diameter. Inside the core the genome of Hepatitis –B virus is present. The genome is

partially double stranded and partially single stranded , circular, DNA molecule which

is associated with DNA polymerase, an enzyme that catalyses the production of

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DNA. The surface envelope of DNA particle contains Hepatitis –B surface antigen

(HBsAg) and its sub types . Where as the inner core is made up of hepatitis core

antigen HBcAg and another antigen sub unit of core protein called ‘e’ (HBeAg)

The most abundunt protein of the virion surface is the 24 kd hepatitis B

surface antigen (HBsAg) or `S’ protein , which is infact identical to Australian

antigen. Upstream of `S’ gene are the pre `S’ genes which code for pre `S` gene

products, including receptors on the HBV surface of polymerized human serum

albumin and for hepatocyte membrane proteins. The pre `S` region actually consists

of both pre S1and pre S2. Depending on where translation is initiated three potential

HBsAg gene products are synthesised. The protein product of S gene is HBsAg

(major protein) the product of `S` region plus the adjacent pre S2. region is the

middle protein and the product of the pre S1, plus pre S2. plus `S` region is the large

protein. Compared with the smaller spherical and tubular particles of HBV, complete

42 nm virions are enriched in the large proteins. Both pre `S proteins and their

respective antibodies can be detected during HBV infection.

The envelope of the virion can be removed by treatment with non ionic

detergents to liberate the inner nucleo capsid or core. Nucleo capsid proteins are

coded by the `C` gene. The antigen expressed on the surface of the nucleo capsid core

is referred to as hepatitis `B` core antigen (HBcAg) and its corresponding antibody is

anti HBc.

A third HBV antigen is hepatitis B `e` antigen (HBeAg) a soluble non

particulate, nucleo capsid protein84

that is immunologically distinct from intact

HBcAg but is a product of the same `c` gene. The `c` gene has two initiation codons,

a pre core and a core region. If translation is initiated at the pre core region, the

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protein product is HBeAg which has a signal peptide that binds to the smooth

endoplasmic reticulum and leads to its secrition into the circulation . If translation

begins with the core region, HBcAg is the protein product, it has no signal peptide, it

is not secreted, but it assembles in to nucleo capsid particles, which bind to and

incorporate RNA and which, ultimately, contain HBV DNA.

Within the core is the viral genome85

i.e. DNA and DNA polymerase. DNA is

partially single stranded partially double stranded and is circular. It is approximately

3200 nucleotides in length and has single stranded gap of 600- 2100 nucleotides

.DNA polymerase directs replication and repair of HBV DNA. In vitro, the

polymerase can repair the single stranded gap and render it double stranded.

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AETIOLOGY

Among the causal agents concerned with the Hepatitis there may be one major

factor and number of accessory factor without which the major one would be

impotent. Causal agents may accordingly classified as Exogenous and Endogenous.

Exogenous agents include trauma, deficiency of vitamins, bacteria, virus etc .

Endogenous factors include hereditary factors, hormonal disturbances, disturbances in

the intracellular enzymes etc. Now we are beginning to recognize that the endogenous

factors may be of even greater importance than the exogenous ones , which is very

relevant in the context of Shakhashrita kaamala

Aetiology of Hepatitis-B

The exogenous and mandatory cause recognized for Hepatitis – B is the

infection of a virus namely Hepatitis –B virus (HBV). Hepatitis –B virus (HBV) is the

prototype member of the family ‘hepadna viridae’, other member of which are found

in the several wild animal species. The term hepadna virus stands for hepatotrophic

DNA virus. Hepatitis–B virus, is a hardy virus and can with stand the extremes of

temperature and humidity.

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MODE OF TRANSMISSION

Blood is the major source of Hepatitis-B virus. It can also be found in other

tissues and body fluids, but in much lower concentrations. The risk of transmission

varies according to the specific source86

.

Blood:

Direct contact with infected blood can transmit the Hepatitis-B virus through:

Puncture of the skin with blood contaminated needles, lancets, scalpels or

other sharp instruments.

Splashes to skin bring minute scratches, abrasions, burns or even minor

rashes.

Splashes to mucous membrane in the mouth, nose or eyes.

To a lesser extent indirect contact with blood contaminated surface can also

transmit the Hepatitis-B virus. The virus may be stable in dried blood for up to 7 days

at 25OC. Hand contact with blood contaminated surfaces such as laboratory benches;

test tubes or laboratory instruments may transfer the virus through skin or mucous

membrane.

Saliva:

Saliva of people with Hepatitis B can contain the Hepatitis B virus but in very

low concentration compared with blood. Injections of infected saliva can transmit the

virus. So bite injuries can also spread the disease. There are no reports of people

getting Hepatitis B from mouth contact with infected CPR manikins or mouthpieces

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of musical instruments.

Other Body fluids and Tissue:

Sexual transmission:

Hepatitis B is found in semen and vaginal secretions. HBV infection can

spread by having unprotected sex or otherwise contact with body fluids infected with

HBV.

People who have sex with multiple partners and men who have sex with men

are at highest risk of sexually transmitted HBV infection. Although the ability of latex

condoms to prevent HBV is not known for certain, their proper use may reduce the

chance of transmission.

Pregnant mothers infected with HBV:

Hepatitis B virus is found in breast milk. The virus can be transmitted from

mother to infant during birth through breast-feeding.

Synovial fluid (joint lubricant), Amniotic fluid, CSF, and Peritoneal fluid

(found in Abdominal cavity) can contain the HBV, but the risk of transmission to

workers is not known.

Faeces, nasal secretions, sputum, sweat, tears, urine and vomitus have not

been implicated in the spread of Hepatitis B.

Unless they are visibly contaminated with blood, the risk of getting Hepatitis

B from these fluids in the workplace is practically nonexistent.

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Tattooing/Body piercing:

Equipment, tattoo needles, body-piercing tools contaminated with infected

blood can easily transmit Hepatitis B infection.

Hepatitis B is not transmitted by casual contact. For example, hospital

employees who have no contact with blood and blood products or blood-

contaminated fluids are at no greater risk than the general public. However the

virus can spread through intimate contact with carriers in a household setting.

Why this happens is not completely understood. Somehow, the virus can find its

way into the bloodstream of fellow family members possibly because of frequent

physical contact with the small cuts or skin rashes. The virus can also spread

through biting and possibly by the sharing of toothbrushes or razors.

Table 47 Risks of occupational groups:

% Of people having

evidence of Hepatitis B

infection

Occupational Group

High (Over 20%) Pathologist’s, Biochemistry and hematology

laboratory personnel dialysis staff.

Intermediate (7-20%)

Hospital nurses, laboratory personnel other than those

in high-risk group, staff of institutions for the

developmentally handicapped, dentists.

Low (Less than 7%) Administrative hospital staff, medical and dental

students, healthy adults.

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PATHOLOGY

HEPATITIS B VIRUS REPLICATION87

After the virion enters the host cell, it is uncoated and its genome is delivered

to the nucleus. There the viral genome is converted to covalently closed circular

(CCC) DNA, a minichromosome that serves as the viral transcription template. From

this templete, RNA is translated to yield the viral proteins. In addition the 3.5 Kb

RNA serves as a pregenomic template for reverse transcription to negative strand

DNA which in turn becomes the template for transcription of positive stand DNA.

Nuclo capsid and envelope proteins are assembled around the viral genome to form

capsid that bud from the cell membrane.

Adding to the complexity of HBV is the fact that it has serotypes or genotypes

which vary in frequency among different populations.

Immunopathogenesis of Hepatitis-B87

:

The production of antibodies against HBsAg confers protective immunity and

can be detected in patients who have recovered from HBV infection or in those who

have been vaccinated. Antibody to HBsAg is detected in almost every patients with

previous exposure to HBV. The immunoglobulin, immunoglobulin M (IgM) subtype,

is indicative of acute infection or reactivation, while the immunoglobulin G (IGm)

subtype is indicative of chronic infection. With this marker alone, one cannot

understand the activity of the disease. Antibody to HBsAg is suggestive of a non-

replicative state and the antigen has been cleared.

The pathogenesis and clinical manifestations are due to the interaction of the

virus and the host immune system.

HBV is not cytotoxic but destroys liver cells indirectly by provoking an

immunology response. Kupffer cells endocytose viral antigens and present them

bound to MHC class II molecules to T-helper cells. These CD4 cells recognize the

antigens and release cytokines that direct B-cells and cytolytic T-cell (CTL) activity.

Stimulated B cells produce specific antibodies, including neutralizing

antibodies. CTLs recognize viral peptides bound to MHC class I molecules on

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hepatocyte surfaces, leading to destruction of infected hepatocytes. In persons who

fail to mount a sufficiently vigorous immune response to HBV during acute infection,

chronic infection develops, and the persistent, in effective immune response results in

progressive liver damage and fibrosis.

Histo pathology

Histo pathologically two predominant morphologic changes affect hepatocytes

in viral Hepatitis-B namely, ballooning and apoptosis. These are seen throughout the

acinus in various combinations and not all Hepatocytes in a given acinus are affected.

In some cases of Hepatitis-B ballooning tends to be more severe in Zone-3. Apoptosis

is a type of cell death that leads to elimination of dead cells; it results in fragmentation

of injuced hepatocyte. Recent studies have shown that it is induced by transforming

growth factor-1.

In ultrastructural studies of apoptosis the nuclear out line becomes convoluted

and the chromatin aggregates in dense sharply circumscribed masses that about on the

nuclear membrane. At the same time the condensed cytoplasm of the Liver cell

develops protuberances that separate and are released into spaces of Disse and

sinusoids while the nucleus breaks up in to discrete masses. Ballooning degeneration

refers to the swelling of hepatocytes, often to the several times to the normal size.

Affected cells have indistinct cell membrane and sometimes the membranes between

the adjacent hepatocytes disintegrate. The cytoplasm is rarefield, often with

perinuclear condensation of a small quantity of cytoplasmic remnants. There may be

bile retention in some ballooned hepatocytes in lysin, with disappearance or

“drooping-out”.

In addition to hepatocellular degeneration, the acute phase of viral Hepatitis is

characterized by pronounced hypertrophy and hyper plasia of Kupffer cells. These

cells also contain a light brown, finely granular pigment presumed to be phagocytosed

from necrotic hepatocytes, in addition to apoptotic bodies of various sizes. The portal

area in viral Hepatitis are usually heavily infiltered with inflammatory cells;

lymphocytes predominate, but a small number of plasma cells, eosinophillic

leukocytes and neutrophils may be present. Several Viral Hepatitis’s is associated

with sub massive necrosis. When necrosis occurs in Hepatitis-B it involves Zone-3,

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sometimes with extention in to Zone-2 of the hepatic acini, but causes of several viral

Hepatitis-A are characterized by necrosis predominantly involving Zone-1.

TABLE 48 SHOWING THE COMPARISON OF HISTOPATHOLOGICAL

CHANGES IN DIFFERENT TYPES OF VIRAL HEPATITIS

Histopathologic changes A B C D E

Spoty necrosis + + + + +

Zone 3 ballooning - + + + -

Zone 1 ballooning + - - - -

Panacinar ballooning - + - - -

Massive necrosis + + + + ?

Steatosis + + - + +

Pronounced cholestasis with or without pseudogl and

formation

+ - - - +

Kupffercell hypertrophy and Iron or lipofuscin or both + + + + -

Kupffer cell hypertrophy and bile accumulation + - - - +

Portal inflammation + + + + +

Types of inflammatory cells P

L

E

N

L

P

L

P

L

P

N

N

Ductular proliferation + + + + +

Bile duct degeneration - - + - -

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PRODROMAL SYMPTOMS

The prodromal symptoms of acute viral Hepatitis-B are systemic and quite

variable. Constitutional symptoms of anorexia, nausea and vomiting, fatigue,

malaise, arthalgia, myalgia, headache, photo phobia, pharyngitis, cough and coryza

and low grade fever between 100F -102F may precede the onset of jaundice by 1-2

weeks88

.

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PHASES OF ACUTE HEPATITIS B INFECTION

The most common consequence of Hepatitis B is acute inflammatory change

of the entire liver. Clinically acute Hepatitis B is categorized into 4 phases89

, they are

Incubation period

Pre - Icteric phase

Icteric phase

Post - Icteric phase

Incubation period:

The incubation period varies from 4 to 26 weeks. The patient remains

asymptomatic during the incubation period and the peak infectivity occurs during the

last asymptomatic days of the incubation period and the early days of acute

symptoms.

Pre-Icteric period:

This is marked by the non-specific constitutional symptoms. Malaise is

followed in few days by general fatigue, nausea and loss of appetite. Weight loss,

low-grade fever, headache, muscle and joint pain are inconstant symptoms.

Icteric phase:

In this phase following signs and symptoms are manifested.

1. Yellowish discoloration of sclera

2. High coloured urine

3. Pruritis

On examination,

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Liver is palpable with smooth and tender edge.

Spleenomegaly and cervical adenopathy are present in 10-20% of

patients.

Post-icteric phase:

The icteric phase lasting for about 1 to 4 weeks is followed by clinical and

bio-chemical recovery in 2 to 12 weeks. The recovery phase is more prolonged in

HBV compared to the other varieties of Viral Hepatitis. Up to 1% of causes may

develop Fulminant Hepatitis and 5-10% of cases may progress on to Chronic

Hepatitis and 10-20% of adults contracting Hepatitis - B develop carrier state.

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INVESTIGATIONS

Biochemical investigations are always very useful in confirming the disease.

Liver function tests are useful to confirm the clinical diagnosis and type of Jaundice

produced. LFT indicates whether hepatic cells or biliary tree is primarily involved, in

giving an indication of the extent of Liver damage and in assessing the progress of the

disease.

The entire LFT can be studied under following headings:

Tests to determine the synthetic function of Liver.

Tests to assess the bile secretive capacity.

Tests to assess the damage of Liver cells (Hepatocytes).

Serum Bilirubin:

The usual cause of Jaundice is large quantities of bilirubin in the extra cellular

fluid, either free bilirubin or conjugated bilirubin. Normally total serum Bilirubin is

0.2 to 0.8 mg/dl.

The common causes of Jaundice are:

Increased the destruction of red blood cells with rapid release of

bilirubin in to the blood and.

Obstruction of bile ducts or damage to the Liver cells so that even the

usual amount of bilirubin cannot be excreted into gastro intestinal tract.

Here total bilirubin is combination or a sum of conjugated and Unconjugated

bilirubin.

In Hyper Bilirubin condition

If conjugated bilirubin (direct Bilirubin) level is more than

Unconjugated bilirubin (Indirect bilirubin) level, then it suggest the

jaundice has resulted, either due to hepatic cause or due to post hepatic

cause.

If Un-conjugated bilirubin (Indirect bilirubin) level is more than

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conjugated bilirubin (Direct bilirubin level, then it suggest the Jaundice

has resulted due to prehepatic cause.

Serum Transaminases:

SGOT (Serum Glutamic oxaloacetic Transaminase) Or

AST (Aspartate Amino Transferase) and

SGPT (Serum Glutamic pyruvic Transaminase) OR

ALT (Alanine Amino Transferase)

SGOT – is a mitochondrial enzyme released from heart, Liver skeletal muscle

and kidney. Its normal serum level is 0-35 U/L.

SGPT is a cytosolic enzyme primarily present in the Liver. Its normal serum

level is 0-45 U/L.

SGOT and SGPT reflect inflammation and break down of Liver cells, but they

are not specific for the Liver because raised levels being found in other forms of

tissue damage such as myocardial infarction, muscle necrosis, haematemesis and

intravasclar heamolysis.

In these condition SGOT levels tends to be appreciably higher than SGPT

levels, whereas both enzymes tend to show similar rises in Liver diseases. An

exception to this is found in alcoholic Hepatitis where it is not uncommon to find

SGOT levels of several times, the upper limit of normal with SGPT levels, within the

normal range. Transaminase estimations are useful in the early diagnosis of viral

Hepatitis.

Alkaline Phosphatase:

Serum Alkaline Phosphatase is produced by many tissues especially bone

Liver, intestine and placenta and is excreted in the bile. Most of the serum alkaline

phosphatase (25-85 IU/dl) is derived from bone. Elevation of inactivity of the enzyme

can thus be found in diseases of bone, Liver and pregnancy.

In the absence of bone disease and pregnancy, an elevated serum alkaline

phosphatase levels generally reflect Hepato biliary diseases.

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The greatest elevation (3 to 10 times normal) occurs in biliary tract

obstruction. Slight to moderate increase is seen in parenchymal Liver disease such as

hepatitis and cirrhosis and in metastatic Liver disease.

Physiological elevations occur in children adolescence and the trimester of

pregnancy.

HBsAg:

(Hepatitis-B surface Antigen). This should be looked for in every patient with

the Liver disease in whom there is any uncertainty about the etiology.

Finding of HBsAg in the serum may be an important bearing on the aetiology

of the Liver disease since this is a marker of Hepatitis-B.

The Detection of antigen may have important implications with regard to

safety of healthy persons.

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DIFFERENTIAL DIAGNOSIS OF HEPATITIS-B

Positive and complete findings are the tools to arrive at a definite diagnosis, to

estimate the prognosis and to adopt appropriate line of treatment for the disease. A

correct diagnosis should be made to distinguish from one disease to another, which

will have the similar signs and symptoms. The term Sapeksha Nidana means

differential diagnosis of the disease.

In all types of Viral Hepatitis-B the presenting clinical features are almost

same. Clinical diagnosis in such condition is very difficult hence; with the help of

viral markers (Hepacard method) exact diagnosis is made. Following diseases can be

considered for the differential diagnosis of Hepatitis-B90

.

Viral Hepatitis A

Viral Hepatitis B

Viral Hepatitis C

Viral Hepatitis D

Viral Hepatitis E

Viral Hepatitis G

Alcoholic Hepatitis

Cholestatic Hepatitis

Obstructive Jaundice

Hemolytic Jaundice

Drug induced Hepatitis

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COMPLICATIONS OF HEPATITIS –B INFECTION

Many complications can occur but in practice serious complications are

uncommon. The common complications of viral hepatitis – B are as follows91

.

Fulminant hepatic failure,

Relapsing hepatitis,

Biochemical,

Clinical.

Cholestatic hepatitis,

Post hepatitis syndrome,

Connective tissue disease,

Eg. Polyarteritis nodosa.

Glomerulonephritis(Renal

failure)

Henoch–sehonlein purpura,

Papular acrodermatitis,

Chronic hepatitis,

Cirrhosis,

Hepatocellular carcinoma,

Asymptamatic carrierstate.

Fatalities are rare and are attributed to the development of fulminant hepatic

failure. Return of symptoms and signs of acute hepatitis during recovery are

characteristic of relapsing hepatitis and occur in 5 to 15% of patients. A symptomatic

“biochemical” relapses with increase of plasma amino transferase activity are even

more common. Relapsing hepatitis does not imply a worse prognosis, because it

resolves spontaneously.

Cholestatic viral hepatitis can develop from the onset or during the course of

illness, with more severe Jaundice of a clinically and biochemically obstructive type

which may follow a prolonged course. Debility for 2 –3 months is common following

clinical and biochemical recovery. Some times in anxious patients, there may be

prolonged malaise, anorexia, nausea and right hypochondrial discomfort without

clinical or biochemical evidence of Liver disease. This syndrome is known as post

hepatitis syndrome and is not due to Liver disease. Chronic Hepatitis and cirrhosis

developed when chronic Hepatitis-B infection occurs these chronic viral infections

predispose to Hepato cellular carcinoma.

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POORVA ROOPA

Poorva Roopa is the prodromal symptoms or the premonitory indications,

which occur before the complete manifestation of disease. The provoked dosha at the

stage of sthana samshraya will manifest the signs and symptoms of the forth-coming

disease.

In classics poorva roopa is classified into two varieties. They are,

1. Samanya poorva roopa 2. Vishishta poorva roopa

Samanya poorva roopa are those which indicate the disease to some extent

without giving any indications of the specific sub-type of the disease and generally

disappear before the onset of the disease.

Vishishta poorva roopa are those which give an idea of the dosha along with

the indication of the disease to some extent and these are likely to continue even after

the commencement of the disease.

Specific Poorvarupas for Kamala have not been mentioned either in Brihatrayi

or in Laghutrayi. Vagbhata defined Poorvarupa as Alpavyaktatvam57

and hence the

rupa with less intensity (Alpabala) can be considesed as Poorva Roopa of Kamala

(Swatantraja).

Susruta described Kamala as synonym of Pandu58

. So the Poorvarupa of

Panduroga may also be considered as Pooorvarupa of Kamala. Also that Pāndu

rogi,on consumption of Atipittala ahara will be afflected by Kamala59

. Hence the

same Poorvarupas of Pandu may be considered for the Paratantraja Kamala

Poorvarupa60

. They are

1. Twak sputana

2. Steevana

3. Gatra sada

4. Mrut bhaksana

5. Aksi kuta shotha

6. Peeta mutrata.

7. Peeta varchah

8. Avipaka

But in ‘Chikitsa krama kalpa vallyam’ the work of 18th

century A.D, a

reference pertaining to the poorva roopa of kaamala is available. The author has

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considered following as poorva roopa;

1. Daha

2. Vipaka

3. Aruchi

4. Agni mandya

5. Manda jwara

6. Sada

7. Karshya

But the author has considered these as poorva roopa of kaamala and has not

specified whether they are of Shakhashrita kaamala or koshtashakhahrita kamala.

Table 44 Showing the comparision of lakshanas of Shahkashrita kamala and

prodromal symptoms of Hepatitis-B

Sl.No Prodromal symptoms of viral

Hepatitis-B

Lakshanas considered as vishishta

Poorva roopa of Shakhashrita kaamala

1

2

3

4

5

6

7

8

9

10

11

12

13

Anorexia

Fatigue

Malaise

Myalgia

Arthalgia

Phyaryngitis

Cough

Coryza

Lowgradefever

Loss of appetite

Headache

Photophobia

Nausea & Vomiting

Aruchi

Daurbalya

Daurbalya

Parswarthi

Parswarthi

Kasa

Kasa

Jwara

Agnimandya

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ROOPA

A disease manifests only on the completion of Dosha Dushya Sammoorchana. The

stage of disease at which symptoms appear is called as ‘Roopa’. They manifest at the 5th

stage of the disease. i.e. ‘Vyaktavastha’.

The dosha remain responsible for each and every symptom of a disease, as they are

the causative factors. Hence Roopa indicates the nature of Dosha Dushya Sammoorchana.

The most common consequence of Hepatitis B is acute inflammatory change of the

entire liver. Clinically acute Hepatitis B is categorized into 4 phases61

, they are

Incubation period

Pre - Icteric phase

Icteric phase

Post - Icteric phase

The first three stages of kriya kala can be considered as the period of incubation.

The stage of sthana samshraya corresponds to the pre-icteric phase. Icteric phase is the

actual stage of the manifestation of the disease identified as ‘Vyaktavastha’. The post-icteric

phase is the stage of the self-resolution or of the organic lesions.

This can also be called the ‘Bheda Avastha’. Hence in the present context of roopa,

the symptoms, which manifest during the stage of icteric phase are discussed62

.

Charaka Samhita has considered the following as the Roopa of Kamala:

Haridra netra

Haridra mootra

Haridra twak

Tila Pishta Nibha Varchas

Aatopa

Vishtambha

Guruna hridayena

Dourbalya

Alpagni

Parswarthi

Hikka

Kasa

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Aruchi

Jwara

Haridra netra, mootra, twak.

Among the symptoms of the icteric phase or the Vyaktavastha, Haridra netra,

Haridra mootra, Haridra twak, can be compared to yellowish discoloration of sclera,

urine, skin and can be considered as the cardinal features of the disease

In Shakhashrita kamala peetavarna of twak, nakha, neetra and mootra is

mainly because of impaired pitta dosha. As kamala is one of the pitta nanatmaja

vyadhi yellowish discolouration of skin ..et.c can be considered as the

pratyatmalakshana of the disease Shakhashritakaamala. The pitta which is vitiated

and deviated from its normal path gets accumulated in shakha. Due to the excess of

accumulation of pitta in shakha the peetata which is amongst the common lakshana

attributed to pitta vriddhi is observed.

Tila Pishta Nibha Varchas

This symptom is one of the most important diagnostic criteria of the

Shakhashrita kamala . Physiologically ranjaka pitta is responsible for mala ranjana.

The absence of ranjaka pitta in the koshta due to avarodha hampers mala ranjana

kriya. As a result of this the stool becomes pale. The normal consistancy of the stool

is also hampered and resembles ‘tila pishta’ as a result of the impaired fat digestion,

as fat digestion is one of the important functions of Ranjaka pitta or bile .

Apart from the above two objective lakshanas which appear specifically in the

icteric phase there are many other subjective lakshana which appear in different stages

of the disease. The most important of them include agnimandya, aruchi, aatopa,

vishtambha, jwara, daurbalya. The first three indicate the impairment of a function of

the digestive system or the annavaha srotas. Agnimandya in particular is observed in

the pre- icteric phase. This symptom is also highlighted by Harana chandra,

This symptom is a direct impact of the nidana sevana. As a consequence of

agnimandya, amotpatti takes place. Aama thus formed results in the other symptoms

of the digestive system such as aruchi, aatopa and vishtambha. There are also other

symptoms of the gastro intestinal tract such as hrillasa and chardi which are not

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explained in Ayurveda. They can be considered as an associated symptoms resulting

out of agnimandya and aruchi. The symptom jwara differentiates infective variety of

Shakhashrita kamala from the other varieties of Shakhashrita kaamala, even though

the pathology of all the varieties of Shakhashrita kamala is one and the same. The

presence of jwara as a lakshana helps to make a specific diagnosis of the infective

hepatitis including Hepatitis-B. This lakshana is seen mainly in the pre icteric phase.

Most of the other symptoms which are mentioned can be considered as the

associated symptoms of the disease caused due to the involvement of pranavaha and

other sroatas.

Apart from the above symptoms which are explained in various classical texts,

some more signs and symptoms are commonly observed , in the day to day practice.

They are mainly kandu, yakrit vriddhi and occasionally pleeha vriddhi

Kandu

The symptom kandu appears in Shakhashrita kamala if the disease is

prolonged for one or two weeks. Kandu is said to be the pratyatma lakshana produced

by kapha. In Shakhashrita kamala along with kapha vriddhi the deposition of the

ranjaka pitta in the twak can also be considered as the cause of kandu.

Yakrit vriddhi

As kamala is raktavaha sroatovikara any disturbance in the raktavaha srotas

causes the vitiation of the srotomoola. In Shakhashrita kamala as khavaigunya is in

the yakrith itself, yakrit vriddhi is observed most of the time .

The roopa taken in relation to Bahupitta Kamala are seen in Hepatitis -B

induced Jaundice.

The type of Kamala namely Bahupitta Kamala (Koshtashrita Kamala) –

Ubhayashrita Kamala has got more clinical significance and resemblance with HBV

induced Jaundice.

However it is difficult to find out an exact correlation for HBV induced

Jaundice in Ayurveda. Majority of the lakshanas mentioned in Kosthashakhashrita

Kamala are observed as signs and symptoms in HBV induced Jaundice, but few of the

symptoms and presentations like Shweta varchas (Tila pistha nibha varchas) a

manifestation in Ruddha patha kamala (Shakhashrita Kamala – Alpa Pitta Kamala) is

seen as a symptom in severe cases of HBV induced Jaundice in the form of clay

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coloured stools.

Table 45 Lakshana of Kamala roga according to different Acharyas63

:

Sl.

No Lakshana Cha. Su. A.Hr. M.Ni. B.P. Y.R.

1 Haridra netra + + + + + +

2 Haridra twacha + + + + + +

3 Haridra mukha + + + + + +

4 Haridra nakha + + + + + +

5 Haridra mutra +

6 Rakta peetha shakrut +

7 Rakta peetha mutra + - + + +

8 Daha + + + + +

9 Avipaka + + + + + +

10 Dourbalya + + + + + +

11 Aruchi + + + + + +

12 Krusha - + - - - +

13 Tandra - + - - - -

14 Balakshaya - + - - - -

15 Indriyadourbalya + - + + + +

16 Bhekavarna + - + + + +

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BHEDA

Charaka samhita for the first time has classified the disease kamala in to two types.

They are as follows : 1)Koshta shakhashrita kamala, 2)Shakhashrita kamala64

.

Koshta Shakhashrita kamala is a paratantra vyadhi. It manifests as a sequel to

panduroga65

, or due to some other disease66

. Charaka samhita has used the term ‘Bahupitta

kamala’ as a synonym to the Koshta Shakhashrita kamala. Shakhashrita kamala is ‘Swatantra

vyadhi’. Chakrapani termed this kamala as ‘Alpapitta kamala67

’. Sushrutasamhita has stated

that, kamala is a later stage of Pandu roga or any other disease. Kumbha kamala, Lagharaka,

Alasa and Haleemaka are its different stages68

.

Harita opines that both kamala and Haleemaka are included under the eight types of

Pandu roga69

. Thus kamala can be classified chiefly according to the dispersal of Pitta in the

body as,

1. Koshta Shakhashraya kamala or Bahupitta kamala

2. Shakhashrita kamala or Alpapitta kamala.

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SAPEKSHA NIDANA OF KAMALA

As per Ayurvedic view Sapeksha Nidana of Kamala can be as,

Pittaja Jwara70

Pittaja Pandu71

Koshta Shakhashrita Kamala

Shakhashrita Kamala

Haleemaka72

Kumbha Kamala73

Haridraka Jwara

Peeta Jwara

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Sapeksha Nidana (Vyavachedaka Nidana):

Lakshana Pittaja

Jwara

Shakha

-shrita

kamala

Koshta

Shakhashri

ta kamala

Peeta

Jwara

Pana

ki

Pittaja

Pandu

Hari-

draka

Jwara

Hal-

eema

Haridra netra + + + + + +

Haridra twacha + + + + + + +

Haridra mukha + + +

Haridra nakha + + + + +

Haridra mutra + +

Daha + + + + +

Avipaka +

Dourbalya + + +

Tandra + +

Krushata

Bala kshaya + +

Bhrumsha + + +

Jwara + + + + +

Pitta Chardi + + +

Sarakta chardi +

Shwasa

Aruchi + + +

Haridra purisha - + +

Tilpishtanibha

varchas + -

Bhinna varcha + + +

Dourgandhya +

Sheeteccha + +

Murcha + +

Ati trishna + +

Ati sara + +

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CHIKITSA

A process by which equilibrium of Tridosha, Saptadhatu and Trimala achieved

is termed Chikitsa. Samanya Chikitsa sutra of Kamala explained in different classics

are as follows:

Kamala can be treated by Snehana, Mrudu, Virechana and

Shamanaoushadhi74

. Astanga Hridaya opines to adopt Pittahara chikitsa along with

the above measures. Even he is in favor of Anjana Chikitsa75

.

In Sushruta samhita, Kamala is considered as one of the varieties of

Panduroga and Panduroga Chikitsa sutra is indicated for Kamala76

. In Yoga Ratnakar

clear Chikitsa krama is mentioned for Kamala. They are Snehana, Virechana and he

has also indicated Anjana and Nasya along with the above measures77

.

From the above classical references we can frame the line of treatment of

Kamala in the following manner.

Deepana and Pachana

Snehana

Virechana

Nasya

Anjana

Shamanoushadhi

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Deepana, Pachana:

Restoration of Agni is one of the main aims of treatment .So Deepana and

Pachana karma is required before proceeding to the main line of treatment. This

Karma is essential when the treatment is aimed to cure Koshta Shakhashrita Kamala.

Snehana78

:

Kamala and Pandu Rogi are to be given Sneha in Eshat pramana in these

conditions prayoga of Sneha in Prabhuta matra is contraindicated as stated by

Vagbhata “Tatra Kamala Panduroginam Nati Snigdhan Virechayet” means the

Virechana should be done later after the introduction of Abhyantara Sneha in a

minimal dosage.

Virechana79

:

In classics it has been advised to undertake Mrudu Virechana in Pandu and

Kamala. Virechana therapy is the choice of treatment for Pitta Pradhana Rakta

pradhoshaja disorders.

Nasya and Anjana:

Regarding Nasya karma no detail explanation are available that whether the

Nasya karma is an Avasthika Chikitsa or Nasya karma is complete procedure

relieving the Kamala janya lakshanas (Roga muktasya lakshana). For Nasya in

classics following drugs are mentioned:

Jimutaka Phala Nasya

JaliniPhala swarasa

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Karkotaka Moola Swarasa.

In Bhaishajya Ratnavalli in Kamala prakarana the Karkotaka moola and Jalini

phala are advised for Nasya.

All the above-mentioned drugs Teekshna, Aashukari, Vyavahi and Vikasi in

property. These drugs produce irritation in the nasal mucosa. Because of irritation a

thin serous secretion starts from the nasal cavity, can be practically observed. The

secretion is slightly yellowish in colour. Thus Nasya karma may help in excretion of

bilirubin deposited in nasal mucosa and the bilirubin present in the circulation.

For Anjana in classics following drugs are mentioned.

Hingu

Dronapushpi swarasa

Rasanjana

NishaGairika Dhatri

Arishta Beeja

Bilirubin has got affinity towards elastin tissues.So Bilirubin gets deposited in

sclera. The above-mentioned drugs seem to increase the lacrimal secretion. Through

lacrimal secretion the Bilirubin which is deposited is eliminated (excreted). Here

along with lacrimation even drugs may be helpful in the removing of Bilirubin from

sclera and circulation.

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Commonly used Ghrita:

Pachagavya Ghrita

Mahatikta Ghrita

Kalyanadi Ghrita

Kaleyakadi Ghrita

Haridradi Ghrita

Dadimadi Ghrita

Choorna:

Nishottara

Indrayana

Sunthi churna

Triphala

Katuki

Navayas choorna

Trikatu

Musta

Gutika Vati:

Punanarva mandur

Triyooshnadimandur

vatika

Arogyavardhini

Navayas loha

Saptramruta loha

Other formulations:

Datryavaleha

Bijakarishta

Rohitakarishta

Kalameghasava

Bhunimbadi

kwatha

Vasaguduchyadi

kashaya

Vidangavaleha

Guduchyadi

kwatha

Daruharidra

kwatha

Patolkaturohinyadi

kashaya

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SADHYASADHYATA

The sadhyasadhyata or the probable outcome of an attack of a disease i.e. the

prognosis should be established before the commencement of the treatment.

Sadhyasadhyata suggests the prognosis of a disease. A disease is called as Sadhya when

it is successfully manageable and the prognosis is good. On the other hand if the disease

is not manageable and the prognosis is very poor it is called Asadhya. Even Sadhya

disease can be of two types, easily manageable (Sukhasadhya) ones and the ones, which

are difficult to manage (Kruchra Sadhya). None of the classical textbooks has

mentioned about the Sadhyasadhyata of Kamala in general or Koshta Shakhashrita

Kamala in particular. Hence the general principle described by Ashtanga Hridaya to

decide the Sadhyasadhyata can be made use of. It is said that a disease is sukha Sadhya

if it is not chronic (nava) has minimum symptoms (alpa roopa) and is devoid of

complications (upadrava).

Certain symptoms produced in a disease suggest the bad prognosis of the

disease. Such dangerous and ominous symptoms are called Arishta. In Brihatrayis and

Laghutrayis description regarding Arishta lakshana of Koshta Shakhashrita Kamala or

Shakhashrita Kamala is not available. The Arishtalakshana told by Madavakara has

been mentioned under the heading Arishta Lakshanas.

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PATHYAPATHYA

PATHYA

In Ayurvedic classics description regarding pathya for Kamala disease is widely

available. This can be broadly classified under the following headings80

.

1. Shooka Dhanya

(Monocotyledons)

2. Shami Dhanya (Dicotyledons)

3. Mamsa varga.

Shooka Dhanya:

Charakacharya has particularly mentioned purana shali, purana yava and purana

Godhooma as the pathya for the Kamala patient. Here it is consumed in the form of

yoosha. For this any one of the above-mentioned ahara dravyas are used.

Shami Dhanya:

Under this heading dravya like Mudgha, Masoor etc. are advised as Pathya for

Kamala Rogi.

Mamsa varga:

In this heading Charakacharya opinioned that Jangala prani mamsa rasa is

beneficial for Kamala Rogi.

Along with this other pathya told are,

Patola, Kadali (banana), Jeeraka, Lasuna, Haritaki, Amalaki, Dadima, Draksha,

Amra etc. All these should be adviced according to Prakruti and Dosha, Rogi bala, Roga.

APATHYA:

According to Classics, Raktamokshana, Dumapana, Vamana, Vegavarodh,

Swedana, Sneha in Bahumatra, Dustaja Guru, Vidahi ahara ,Sarshapa, Madhya, Dadhi,

Ghrita, Matsya, Pittaprakopaka Vihara, like Maithuna, Krodha, Aatapsevana,

Ativayayam, Divaswapana, are considered as Apathya for Kamala Rogi.

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UPADRAVA

The occurrence of another disorder on the wake of a primary disease, as a

complication is termed as Upadrava. However upadrava may exhibit pathology of a

more serious or fulminating nature than that of the main disease and in such cases it

cannot be cured merely by the treatment given for the main disease. In such condition

immediate and appropriate treatment should be given to check the Upadrava.

The upadrava of either Koshta Shakhashrita Kamala or Shakhashrita Kamala

is not explained in the classics under separate and independent heading. But based on

the various descriptions explained in classics pertaining to Kumbha Kamala, it seems

to be the disease Kumbha Kamala is an Upadrava of Kamala. Acharya Harita has

considered Kumbha Kamala as a variety of Pandu roga.

Acharya Sushruta has opined Kumbha Kamala as a type of Kamala.

According to Charaka Kumbha Kamala is the avastha vishesha or next stage of the

disease. While explaining Kumbha Kamala Nidana Charaka has mainly used two

terms “Kalantarat” and “Kharibhoota”. Here the term Kalantarat indicates the laps of

time or period where as Kharibhoota indicates the difficult stage of disease for the

treatment.Charaka has explained Kumbha Kamala immediately after explaining the

Samprapti and Lakshana of Koshta – Shakhashrita Kamala. It implies that if Koshta

Shakhashrita Kamala is neglected then Kumbha Kamala is produced. But most of

Kumbha Kamala lakshanas mentioned in classics seems to cirrhotic condition.

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ARISHTA LAKSHANA

Certain symptoms produced in disease suggest the definite death of a patient.

Such dangerous and ominous symptoms are called Arishtas. Description regarding

arishta lakshanas either Shakhashrita kamala or of Koshtashakhashrita kamala is not

explained either Brahatrayis or in Laghutrayis.

Madhavakara for the first time has mentioned Arishta lakshana of Kumbha

kamala. (Ma. Ni. 1. 8/21). Bhavamishra the author of Bhavaprakasha has followed

Madhavakar and in 8th chapter of Bhavaprakasha nighantu has explained arishta

lakshana of Kumbha kamala.

As discussed earlier Kumbha kamakla can be considered as upadrava of

Shakhashrita kamala. Hence arishta lakshana of Kumbha kamala can be considered as

arishta lakshana of Shakhashrita kamala.

Table No. 46 . The Arishta Lakshanas of Kumbha kamala

Aristha lakshanas Bh.Pr Ma.Ni

Chardi

Aruchi

Hrullasa

Jwara

Klama

Shwasa

Kasa

Arati

Vidbheda

+

+

+

+

+

+

+

+

+

+

+

+

+

+

+

+

+

+

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ANATOMY OF LIVER

The Liver

The Liver is a large, solid gland situated in the right upper quadrant of the

abdominal cavity. In the living subjects the Liver is reddish brown in colour, soft in

consistency, and very friable. It weighs about 1600 gms in males and about 1300 gms

in females. The Liver occupies the whole of the right hypochondrium, the greater part

of the epigastrium, and extends into the left hypochondrium reaching up to the left

lateral line. From the above it will be obvious that most of the Liver is covered by ribs

and costal cartilage, except in the upper part of the epigastrium where it is in contact

with the anterior abdominal wall.

The Liver is largest gland in the body. It secretes bile and performs various

other metabolic functions.

The Liver is also called the „hepar‟ from which we have the adjective „hepatic‟

applied to many structures connected with the organ.

External Features:

The Liver is wedge shaped. It resembles a four sided pyramid laid on one side.

It has five surfaces. These are 1.anterior 2.posterior 3.superior 4.inferior

and 5.right.

The Liver is divided into right and left lobes by the attachment of the falciform

ligament anteriorly and superiorly; by the fissure for the ligamentum teres inferiorly;

and by the fissure for the ligamentum venosum posteriorly.

The right lobe is much larger than the left lobe and forms five sixth of the

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Liver. It contributes to all the five surfaces of the Liver, and presents the caudate

and quadrate lobes.

The caudate lobe is situated on the posterior surface. The quadrate lobe is

situated on the inferior surface. The porta hepatis is deep transverse fissure about

2inches long situated on the inferior surface of right lobe of the Liver.

Relations:

1. Peritoneal Relation

Most of the Liver is covered by peritoneum. The areas not covered by

peritoneum are as follows:

a. A triangular bare area on the posterior surface of the right lobe, limited by

the upper and lower layers of the coronary ligament and by the right

triangular ligament:

b. The groove for the inferior vena cava, on the posterior surface of the right

lobe of the Liver, between the caudate lobe and the bare area:

c. The fossa for the Gall Bladder which lies on the inferior surface of the

right lobe to the right of the quadrate lobe:

d. The porta hepatis

e. Along the lines of reflection of peritoneum.

II. Visceral Relations

Anterior Surface:

This surface is triangular and slightly convex. It is related to the xiphoid

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process and to the anterior abdominal wall in the median plane; and to diaphargm on

each side.

Superior Surface:

It is quadrilateral and shows a concavity in the middle. This is the cardiac

impression.

Inferior Surface:

It is quadrilateral and is directed downwards, backwards and to the left.

Right Surface:

It is quadrilateral and convex. It is related to the diaphragm opposite the 7th

to

11th

ribs in the midaxillary line. It is separated by the diaphragm from the pleura (up

to the 10th

rib), and from the lung (up to the 8th

rib).

Blood Supply:

The Liver receives 20% of its blood supply through the hepatic artery, and

80% through the portal vein. Before entering the Liver, both the hepatic artery and the

portal vein divide into right and left branches. Within the Liver, they redivide to form

segmental vessels, which further divide to form interlobular vessels. Further

ramifications of the interlobular branches open into the hepatic sinusoids. Thus the

hepatic arterial blood mixes with the portal venous blood in the sinusoids. There are

no anastomoses between adjoining hepatic arterial territories and hence each branch is

an end artery.

Venous Drainage:

Hepatic sinusoids drain into interlobular veins, which join to form sub lobular

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veins. These in turn unite to form the hepatic veins, which drain directly into the

inferior vena cava.

The hepatic veins are arranged in two groups, upper and lower. The upper

group consists of three large veins (right, left and middle) which emerge through the

upper part of the groove for the inferior vena cava, and open directly into the vena

cava. The lower group consists of a variable number of small veins (from the right

lobe and the caudate lobe), which emerge through the lower part of the caval groove

and open into the vena cava.

Lymphatic Drainage:

The superficial lymphatics of the Liver run on the surface of the organ beneath

the peritoneum, and terminate in caval, hepatic paracardial and coeliac lymph nodes.

Some vessels from the coronary ligament may directly join the thoracic duct.

The deep lymphatic end partly in the nodes around the end of the inferior vena

cava, and partly in the hepatic nodes.

Nerve Supply:

The Liver receives its nerve supply from the hepatic plexus, which contains

both sympathetic and parasympathetic (vagal) fibres. Nerves also reach the Liver

through its various peritoneal ligaments.

Hepatic Segments:

On the basis of the intrahepatic distribution of the hepatic artery, the portal

vein and the biliary ducts, the Liver can be divided into right and left functional lobes.

These do not correspond to the anatomical lobes of the Liver. The physiological lobes

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are separated by a plane passing on the anterosuperior surface, along a line joining the

cystic notch to the groove for the inferior vena cava. On the inferior surface the plane

passes through the fossa for the Gall Bladder, and on the posterior surface it passes

through the middle of the caudate lobe.

Hepatic Ducts:

The right and left hepatic ducts emerge at the porta hepatis from the right and

left lobes of the Liver. The arrangement of structures at the porta hepatis from behind

forwards is i. The branches of the Portal vein ii. Hepatic artery and iii. Hepatic ducts.

Common Hepatic ducts:

It is formed by the union of the right and left hepatic ducts near the end of the

porta hepatis. It runs downwards for about 3cm and is joined on its right side (at an

acute angle) by the cystic duct to from the bile duct.

Accessory hepatic ducts are present in about 15% of subjects. They usually

issue from the right lobe of the Liver, and terminate either in the Gall Bladder, or in

the common hepatic duct anywhere in its course, or even in the upper part of the bile

duct.

Histology of Liver:

The hepatic parenchyma is composed of numerous hexagonal or pyramidal

classical lobules; each with a diameter of 0.5 to 2 mm. Each classical lobule has a

central tributary from the hepatic vein and at the periphery are 4 to 5 portal tracts or

triads containing branches of bile duct, portal vein and hepatic artery. Cords of

hepatocytes and blood containing sinusoids radiate from the central vein to the

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peripheral portal triads. The functioning lobule or Liver acinus‟s as described by

Rapparport has a portal triad in the centre and is surrounded at the periphery by

portions of several classical lobules. However, in most descriptions on pathology of

the Liver, the term lobule is used in its classical form.

The blood supply to the Liver parenchyma flows from the portal triads to the

central veins. Accordingly, the hepatic parenchyma of Liver lobule is divided into 3

zones.

Zone 1 or the periportal (peripheral) area is closest to the arterial and

portal blood supply and hence bears the burnt of all forms of toxic injury.

Zone 2 is the intermediate mid zonal area.

Zone 3 or the centrilobular area surrounds the central vein and is most

remote from the blood supply and thus suffers from the effects of hypoxic

injury.

The hepatocytes are polygonal cells with a round single nucleus and a

prominent nucleolus. The Liver cells have a remarkable capability to undergo mitosis

and regeneration. Thus it is not uncommon to find Liver cells containing more than

one nuclei and having polyploidy up to octoploidy. A hepatocyte has 3 surfaces: One

facing the sinusoid and space of Disse, the second facing the canaliculus, and the third

facing neighboring hepatocytes.

The blood-containing sinusoids between cords of hepatocytes are lined by

discontinuous endothelial cells and scattered flat Kupffer cells belonging to the

reticuloendothelial system.

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The space of Disse is the space between hepatocytes and sinusoidal lining

cells. A few scattered fat storing Ito cells lie within the space of Disse.

The portal triad or tract besides containing portal vein radicle, the hepatic

arteriole and bile duct, has a few mononuclear cells and a little connective tissue

considered to be extension of Glisson‟s capsule. A limiting plate of hepatocytes

surrounds the portal triads.

The intrahepatic biliary system begins with the bile canaliculi interposed

between the adjacent hepatocytes. The bile canaliculi are simply grooves between the

contact surfaces of the Liver cells and are covered by microvilli. These canaliculi join

at the periphery of the lobule to drain eventually into terminal bile ducts or ductules

(canal of Hering), which are lined by cuboidal epithelium.

Gall Bladder:

This is pear-shaped reservoir of bile situated in a fossa on the inferior surface

of the right lobe of the Liver. The fossa for the Gall Bladder extends from the right

end of the porta hepatis to the inferior border of the Liver. The Gall Bladder is 7 to

10 cm (3 to 4 in) long 3cm broad at its widest part, and about 30 to 50ml in capacity.

The Gall Bladder is divided into 1.The fundus 2.The body and 3.the neck. The

Fundus projects beyond the inferior border of the Liver in the angle between the

lateral border of the right rectus abdominis and the 9th

costal cartilage. The body

lies in the fossa for the Gall Bladder on the Liver. The neck is the narrow upper end of

the Gall Bladder. It is situated near the right end of the porta hepatis.

The postero medial wall of the neck is dilated outwards to form a pouch

(Hermann‟s pouch) which is directed downwards and backwards. Some regard this

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pouch as a normal feature of the Gall Bladder, but others consider it to be

pathological. Stones may lodge in this pouch.

Cystic Duct:

This duct is about 3 to 4cm (roughly 1inch) long. It begins at the neck of the

Gall Bladder, runs downwards, backwards and to the left, and ends by joining the

common hepatic duct at an acute angle to form the bile duct. The mucous membrane

of the cystic duct forms a series of 5 to 12 crescentric folds, arranged spirally to form

the so-called „spiral valve‟ (of Heister). This is not a true valve.

Bile Duct:

It is formed by the union of the cystic and common hepatic ducts near the

porta hepatis. It is 8cm long and has a diameter of about 6mm.

Arteries Supplying the Biliary Apparatus:

1. The cystic artery is the chief source of blood supply; and is distributed to the

Gall Bladder, the cystic duct, the hepatic ducts and the upper part of the bile

duct.

2. Several branches from the posterior superior pancreaticoduodenal artery

supply the lower part of the bile duct.

3. The right hepatic artery forms a minor source of supply to the middle part of

bile duct.

4. An accessory cystic artery may arise from the common hepatic artery, or

from one of its branches.

The cystic artery usually arises from the right hepatic artery passes behind the

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common hepatic and cystic ducts, and reaches the upper surface of the neck of the

Gall Bladder, where it divides into superficial and deep branches. Occasionally, the

cystic artery arises from the hepatic artery proper, and rarely from the gastro duodenal

artery.

Venous Drainage:

1. The superior surface of the Gall Bladder is drained by veins, which enter the

Liver through the fossa for the Gall Bladder and join tributaries of hepatic

veins.

2. The rest of the Gall Bladder is drained by one or two cystic veins, which

commonly enter the Liver, either directly or after joining with the veins

draining the hepatic ducts and the upper part of the bile duct. Rarely the

cystic vein opens into the right branch of the portal vein.

3. The lower part of the bile duct drains into the portal vein.

Lymphatic Drainage:

1. Lymphatics from the Gall Bladder, the cystic duct, the hepatic ducts and the

upper part of the bile duct pass to the cystic node and to the node of the

anterior border of the epiploic foramen. These are the most constant

members of the upper hepatic nodes.

2. The lower part of the bile duct drains into the lower hepatic and upper

pancreaticosplenic nodes.

Nerve-Supply:

The cystic plexus of nerves, supplying the territory of the cystic artery, is

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derived from the hepatic plexus, which receives fibers from the coeliac plexus, the left

and right vagi and the right phrenic nerves. The nerve plexus supplies the lower part

of the bile duct over the superior pancreaticoduodenal artery.

Parasympathetic nerves are motor to the musculature of the Gall Bladder and

bile ducts, but inhibitory to the sphincters. Sympathetic nerves (T7 to T9) are

vasomotor and motor to the sphincters.

Pain from the Gall Bladder may travel along the vagus, the sympathetic

nerves, or along the phernic nerves. It may be referred to different sites through these

nerves as follows.

i. Through the Vagus Nerve to the stomach.

ii. Through the sympathetic nerves to the inferior angle of the right

scapula.

iii. Through the phrenic nerve to the right shoulder.

Functions of the Gall Bladder:

1. Storage of bile, and its release into the duodenum when required.

2. Absorption of water, and concentration of bile. Bile may be concentrated as

much as ten times.

3. The normal Gall Bladder also absorbs small amounts of a loose bile salt-

cholesterol compound. When the Gall Bladder is inflamed the concentration

function becomes abnormal and the bile salts alone are absorbed leaving

cholesterol behind. Bile salts have a powerful solvent action on cholesterol, but

when bile salts are absorbed the cholesterol tends to be precipitated. This can

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lead to the formation of Gall stones.

Bilirubin and the Bile formation:81

Bilirubin: It is an orange coloured or yellow pigment. The bile is formed in the

Liver. Bile salts helps in the digestive and absorptive processes of the intestinal tract.

This is the major end product of haemoglobin degradation.

Briefly when the red blood cells are worn out after their average life span of

120 days, they become too fragile to exist longer in the circulatory system, their cell

membranes rupture. Here the hemoglobin is phagocytosed by tissne macrophages

(also called the reticuloendothelial system) throughout the body. Here the hemoglobin

is first split into globin and haem, and the haem ring is opened to give 1. free iron that

is transported in the blood by transferrin and 2. a straight chain of four pyrrole nuclei

that is the substrate from which bilirubin will eventually be formed. The first

substance formed is biliverdin, but this is rapidly reduced to free bilirubin which is

gradually released from the macrophages into the plasma. The free bilirubin

immediately combines strongly with the plasma albumin and is transported in this

combination throughout the blood and interstitial fluids. Even when bound with the

plasma protein this bilirubin is still called “free bilirubin” to distinguish it from

conjugated bilirubin.

Within hours, the free bilirubin is absorbed through the hepatic cell

membrane. In passing to the inside of the hepatic cells, it is released from the plasma

albumin and soon thereafter conjugated, about 80 percent with glucuronic acid to

form bilirubin glucuronide, about 10 percent with sulphate to form bilirubin sulphate,

, and the final 10 percent with a multitude of other substances. In these forms, the

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bilirubin is excreted from the hepatocytes by an active transport process into the

biliary canaliculi and then into the intestines.

Direct Bilirubin:

Bilirubin is conjugated in the Liver cells to form bilirubin diglucuronide,

which is water-soluble.

Indirect Bilirubin:

Unconjugated bilirubin that is present in blood, is fat-soluble.

Bile:

A thick, viscid, bitter tasting fluid secreted by Liver. It passes from the bile

duct of Liver into the common bile duct and then into the duodenum as needed. The

bile from the Liver is straw coloured, while that from the Gall Bladder varies from

yellow to brown to green colour.

Bile is stored in the Gall Bladder, where it is concentrated, drawn upon as

needed and discharged into the duodenum. Contraction of Gall Bladder is brought

about by cholecystokinin-pancreozymin, a hormone produced by the duodenum. The

entrance of fatty foods into the duodenum stimulates its secretion. Added to water,

bile decreases surface tension giving a foamy solution favouring the emulsification of

fats and oils, this action is due to bile salts, mainly sodium glycocholate and

taurochalate.

Formation and Fate of Urobilinogen:

Once in the intestine, about one half of the conjugated bilirubin is converted

by bacterial action into the substance Urobilinogen, which is highly water-soluble.

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Some of the Urobilinogen is reabsorbed through the intestinal mucosa back into the

blood. Most of this is once again re-excreted by the Liver back into the gut. But the

kidneys excrete 5% of Urobilinogen in the urine.

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JAUNDICE

The word “Jaundice” means a yellowish tint to the body tissues, including

yellowishness of the skin as well as the deep tissues. The usual cause of Jaundice is

large quantities of bilirubin in the extra cellular fluid, either free bilirubin or

conjugated bilirubin. The normal plasma concentration of bilirubin, which is almost

entirely in free form, averages 0.5 mg/dl of plasma. In certain abnormal conditions,

this can rise to as high as 40 mg/dl and most of it is conjugated. The skin usually

appears Jaundiced when the concentration of conjugated Bilirubin rises to about three

times its normal concentration that is above 1.5 mg/dl.

The common causes of Jaundice are

1. Increased destruction of red blood cells with rapid release of bilirubin

into the blood and

2. Obstruction of the bile ducts or damage to the Liver cells so that even

the usual amounts of bilirubin cannot be excreted into the

gastrointestinal tract.

These two types of Jaundice are called hemolytic Jaundice and obstructive

Jaundice respectively. They differ from each other in the following ways.

Haemolytic Jaundice:

In hemolytic Jaundice, the excretory function of the Liver is least impaired,

but red blood cells are haemolysed rapidly and the hepatic cells simply cannot excrete

the bilirubin as rapidly as it is formed. Therefore, the plasma concentration of free

bilirubin rises to levels much above the normal. Likewise, the rate of formation of

urobilinogen in the intestine is greatly increased, and much of this is absorbed into the

blood and later excreted in the urine.

Obstructive Jaundice:

Obstructive Jaundice is caused either by obstruction of the bile ducts (which

most often occurs when a Gallstone or cancer blocks the common bile duct) or by

damage to the hepatic cells (which occurs in hepatitis as in hepatitis B). The rate of

bilirubin formation is normal but the bilirubin formed cannot pass from the blood into

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the intestines. The free bilirubin usually enters the Liver cells and becomes

conjugated in the usual way. This conjugated bilirubin is then returned to the blood,

probably by rupture of the congested bile canaliculi and direct emptying of the bile

into the lymph leaving the Liver. Thus, most of the bilirubin in the plasma becomes

the conjugated type rather than the free type.

Here we are elaborately discussing on the jaundice caused by Hepatitis B virus

called HBV induced Jaundice.

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STRUCTURE OF HEPATITIS –B VIRUS (HBV)

Various synonyms have been used for HBV in contemporary science82

.

1. Initially it was known as Australian Antigen, (Because of its

discovery in an in Australian aborigines).

2. Hepatitis B virus (HBV)

3. Hepatitis B surface antigen (HBsAg)

4. Hepatocellular B virus

Dr. David Dane, is the first person who isolated and discribed the structure of

Hepatitis–B virus, for the first time in 1970. Hence Hepatitis–B virus is also called as

‘Dane particle’83

.

Electron microscopic study on the serum of patients infected with Hepatitis–B

virus shows three type of the viral particles

1. Small 20nm sphere

2. Tubule 20nm in diameter and 100 nm long

3. The large 42nm Dane particle

Spherical and filamentous forms are most numerous and represents excess of

viral surface coat protein (HBsAg), while Dane particle believed to represent the

intact Hepatitis –B virus. The mature intact Hepatitis –B virus is spherical with the

diameter of 42nm. It is the double layered sphere . It has an outer surface analogue

of protein, lipid, carbohydrate enclosing a slightly hexagonal core measuring 27nm in

diameter. Inside the core the genome of Hepatitis –B virus is present. The genome is

partially double stranded and partially single stranded , circular, DNA molecule which

is associated with DNA polymerase, an enzyme that catalyses the production of

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DNA. The surface envelope of DNA particle contains Hepatitis –B surface antigen

(HBsAg) and its sub types . Where as the inner core is made up of hepatitis core

antigen HBcAg and another antigen sub unit of core protein called ‘e’ (HBeAg)

The most abundunt protein of the virion surface is the 24 kd hepatitis B

surface antigen (HBsAg) or `S’ protein , which is infact identical to Australian

antigen. Upstream of `S’ gene are the pre `S’ genes which code for pre `S` gene

products, including receptors on the HBV surface of polymerized human serum

albumin and for hepatocyte membrane proteins. The pre `S` region actually consists

of both pre S1and pre S2. Depending on where translation is initiated three potential

HBsAg gene products are synthesised. The protein product of S gene is HBsAg

(major protein) the product of `S` region plus the adjacent pre S2. region is the

middle protein and the product of the pre S1, plus pre S2. plus `S` region is the large

protein. Compared with the smaller spherical and tubular particles of HBV, complete

42 nm virions are enriched in the large proteins. Both pre `S proteins and their

respective antibodies can be detected during HBV infection.

The envelope of the virion can be removed by treatment with non ionic

detergents to liberate the inner nucleo capsid or core. Nucleo capsid proteins are

coded by the `C` gene. The antigen expressed on the surface of the nucleo capsid core

is referred to as hepatitis `B` core antigen (HBcAg) and its corresponding antibody is

anti HBc.

A third HBV antigen is hepatitis B `e` antigen (HBeAg) a soluble non

particulate, nucleo capsid protein84

that is immunologically distinct from intact

HBcAg but is a product of the same `c` gene. The `c` gene has two initiation codons,

a pre core and a core region. If translation is initiated at the pre core region, the

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protein product is HBeAg which has a signal peptide that binds to the smooth

endoplasmic reticulum and leads to its secrition into the circulation . If translation

begins with the core region, HBcAg is the protein product, it has no signal peptide, it

is not secreted, but it assembles in to nucleo capsid particles, which bind to and

incorporate RNA and which, ultimately, contain HBV DNA.

Within the core is the viral genome85

i.e. DNA and DNA polymerase. DNA is

partially single stranded partially double stranded and is circular. It is approximately

3200 nucleotides in length and has single stranded gap of 600- 2100 nucleotides

.DNA polymerase directs replication and repair of HBV DNA. In vitro, the

polymerase can repair the single stranded gap and render it double stranded.

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AETIOLOGY

Among the causal agents concerned with the Hepatitis there may be one major

factor and number of accessory factor without which the major one would be

impotent. Causal agents may accordingly classified as Exogenous and Endogenous.

Exogenous agents include trauma, deficiency of vitamins, bacteria, virus etc .

Endogenous factors include hereditary factors, hormonal disturbances, disturbances in

the intracellular enzymes etc. Now we are beginning to recognize that the endogenous

factors may be of even greater importance than the exogenous ones , which is very

relevant in the context of Shakhashrita kaamala

Aetiology of Hepatitis-B

The exogenous and mandatory cause recognized for Hepatitis – B is the

infection of a virus namely Hepatitis –B virus (HBV). Hepatitis –B virus (HBV) is the

prototype member of the family ‘hepadna viridae’, other member of which are found

in the several wild animal species. The term hepadna virus stands for hepatotrophic

DNA virus. Hepatitis–B virus, is a hardy virus and can with stand the extremes of

temperature and humidity.

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MODE OF TRANSMISSION

Blood is the major source of Hepatitis-B virus. It can also be found in other

tissues and body fluids, but in much lower concentrations. The risk of transmission

varies according to the specific source86

.

Blood:

Direct contact with infected blood can transmit the Hepatitis-B virus through:

Puncture of the skin with blood contaminated needles, lancets, scalpels or

other sharp instruments.

Splashes to skin bring minute scratches, abrasions, burns or even minor

rashes.

Splashes to mucous membrane in the mouth, nose or eyes.

To a lesser extent indirect contact with blood contaminated surface can also

transmit the Hepatitis-B virus. The virus may be stable in dried blood for up to 7 days

at 25OC. Hand contact with blood contaminated surfaces such as laboratory benches;

test tubes or laboratory instruments may transfer the virus through skin or mucous

membrane.

Saliva:

Saliva of people with Hepatitis B can contain the Hepatitis B virus but in very

low concentration compared with blood. Injections of infected saliva can transmit the

virus. So bite injuries can also spread the disease. There are no reports of people

getting Hepatitis B from mouth contact with infected CPR manikins or mouthpieces

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of musical instruments.

Other Body fluids and Tissue:

Sexual transmission:

Hepatitis B is found in semen and vaginal secretions. HBV infection can

spread by having unprotected sex or otherwise contact with body fluids infected with

HBV.

People who have sex with multiple partners and men who have sex with men

are at highest risk of sexually transmitted HBV infection. Although the ability of latex

condoms to prevent HBV is not known for certain, their proper use may reduce the

chance of transmission.

Pregnant mothers infected with HBV:

Hepatitis B virus is found in breast milk. The virus can be transmitted from

mother to infant during birth through breast-feeding.

Synovial fluid (joint lubricant), Amniotic fluid, CSF, and Peritoneal fluid

(found in Abdominal cavity) can contain the HBV, but the risk of transmission to

workers is not known.

Faeces, nasal secretions, sputum, sweat, tears, urine and vomitus have not

been implicated in the spread of Hepatitis B.

Unless they are visibly contaminated with blood, the risk of getting Hepatitis

B from these fluids in the workplace is practically nonexistent.

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Tattooing/Body piercing:

Equipment, tattoo needles, body-piercing tools contaminated with infected

blood can easily transmit Hepatitis B infection.

Hepatitis B is not transmitted by casual contact. For example, hospital

employees who have no contact with blood and blood products or blood-

contaminated fluids are at no greater risk than the general public. However the

virus can spread through intimate contact with carriers in a household setting.

Why this happens is not completely understood. Somehow, the virus can find its

way into the bloodstream of fellow family members possibly because of frequent

physical contact with the small cuts or skin rashes. The virus can also spread

through biting and possibly by the sharing of toothbrushes or razors.

Table 47 Risks of occupational groups:

% Of people having

evidence of Hepatitis B

infection

Occupational Group

High (Over 20%) Pathologist’s, Biochemistry and hematology

laboratory personnel dialysis staff.

Intermediate (7-20%)

Hospital nurses, laboratory personnel other than those

in high-risk group, staff of institutions for the

developmentally handicapped, dentists.

Low (Less than 7%) Administrative hospital staff, medical and dental

students, healthy adults.

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PATHOLOGY

HEPATITIS B VIRUS REPLICATION87

After the virion enters the host cell, it is uncoated and its genome is delivered

to the nucleus. There the viral genome is converted to covalently closed circular

(CCC) DNA, a minichromosome that serves as the viral transcription template. From

this templete, RNA is translated to yield the viral proteins. In addition the 3.5 Kb

RNA serves as a pregenomic template for reverse transcription to negative strand

DNA which in turn becomes the template for transcription of positive stand DNA.

Nuclo capsid and envelope proteins are assembled around the viral genome to form

capsid that bud from the cell membrane.

Adding to the complexity of HBV is the fact that it has serotypes or genotypes

which vary in frequency among different populations.

Immunopathogenesis of Hepatitis-B87

:

The production of antibodies against HBsAg confers protective immunity and

can be detected in patients who have recovered from HBV infection or in those who

have been vaccinated. Antibody to HBsAg is detected in almost every patients with

previous exposure to HBV. The immunoglobulin, immunoglobulin M (IgM) subtype,

is indicative of acute infection or reactivation, while the immunoglobulin G (IGm)

subtype is indicative of chronic infection. With this marker alone, one cannot

understand the activity of the disease. Antibody to HBsAg is suggestive of a non-

replicative state and the antigen has been cleared.

The pathogenesis and clinical manifestations are due to the interaction of the

virus and the host immune system.

HBV is not cytotoxic but destroys liver cells indirectly by provoking an

immunology response. Kupffer cells endocytose viral antigens and present them

bound to MHC class II molecules to T-helper cells. These CD4 cells recognize the

antigens and release cytokines that direct B-cells and cytolytic T-cell (CTL) activity.

Stimulated B cells produce specific antibodies, including neutralizing

antibodies. CTLs recognize viral peptides bound to MHC class I molecules on

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hepatocyte surfaces, leading to destruction of infected hepatocytes. In persons who

fail to mount a sufficiently vigorous immune response to HBV during acute infection,

chronic infection develops, and the persistent, in effective immune response results in

progressive liver damage and fibrosis.

Histo pathology

Histo pathologically two predominant morphologic changes affect hepatocytes

in viral Hepatitis-B namely, ballooning and apoptosis. These are seen throughout the

acinus in various combinations and not all Hepatocytes in a given acinus are affected.

In some cases of Hepatitis-B ballooning tends to be more severe in Zone-3. Apoptosis

is a type of cell death that leads to elimination of dead cells; it results in fragmentation

of injuced hepatocyte. Recent studies have shown that it is induced by transforming

growth factor-1.

In ultrastructural studies of apoptosis the nuclear out line becomes convoluted

and the chromatin aggregates in dense sharply circumscribed masses that about on the

nuclear membrane. At the same time the condensed cytoplasm of the Liver cell

develops protuberances that separate and are released into spaces of Disse and

sinusoids while the nucleus breaks up in to discrete masses. Ballooning degeneration

refers to the swelling of hepatocytes, often to the several times to the normal size.

Affected cells have indistinct cell membrane and sometimes the membranes between

the adjacent hepatocytes disintegrate. The cytoplasm is rarefield, often with

perinuclear condensation of a small quantity of cytoplasmic remnants. There may be

bile retention in some ballooned hepatocytes in lysin, with disappearance or

“drooping-out”.

In addition to hepatocellular degeneration, the acute phase of viral Hepatitis is

characterized by pronounced hypertrophy and hyper plasia of Kupffer cells. These

cells also contain a light brown, finely granular pigment presumed to be phagocytosed

from necrotic hepatocytes, in addition to apoptotic bodies of various sizes. The portal

area in viral Hepatitis are usually heavily infiltered with inflammatory cells;

lymphocytes predominate, but a small number of plasma cells, eosinophillic

leukocytes and neutrophils may be present. Several Viral Hepatitis’s is associated

with sub massive necrosis. When necrosis occurs in Hepatitis-B it involves Zone-3,

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sometimes with extention in to Zone-2 of the hepatic acini, but causes of several viral

Hepatitis-A are characterized by necrosis predominantly involving Zone-1.

TABLE 48 SHOWING THE COMPARISON OF HISTOPATHOLOGICAL

CHANGES IN DIFFERENT TYPES OF VIRAL HEPATITIS

Histopathologic changes A B C D E

Spoty necrosis + + + + +

Zone 3 ballooning - + + + -

Zone 1 ballooning + - - - -

Panacinar ballooning - + - - -

Massive necrosis + + + + ?

Steatosis + + - + +

Pronounced cholestasis with or without pseudogl and

formation

+ - - - +

Kupffercell hypertrophy and Iron or lipofuscin or both + + + + -

Kupffer cell hypertrophy and bile accumulation + - - - +

Portal inflammation + + + + +

Types of inflammatory cells P

L

E

N

L

P

L

P

L

P

N

N

Ductular proliferation + + + + +

Bile duct degeneration - - + - -

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PRODROMAL SYMPTOMS

The prodromal symptoms of acute viral Hepatitis-B are systemic and quite

variable. Constitutional symptoms of anorexia, nausea and vomiting, fatigue,

malaise, arthalgia, myalgia, headache, photo phobia, pharyngitis, cough and coryza

and low grade fever between 100F -102F may precede the onset of jaundice by 1-2

weeks88

.

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PHASES OF ACUTE HEPATITIS B INFECTION

The most common consequence of Hepatitis B is acute inflammatory change

of the entire liver. Clinically acute Hepatitis B is categorized into 4 phases89

, they are

Incubation period

Pre - Icteric phase

Icteric phase

Post - Icteric phase

Incubation period:

The incubation period varies from 4 to 26 weeks. The patient remains

asymptomatic during the incubation period and the peak infectivity occurs during the

last asymptomatic days of the incubation period and the early days of acute

symptoms.

Pre-Icteric period:

This is marked by the non-specific constitutional symptoms. Malaise is

followed in few days by general fatigue, nausea and loss of appetite. Weight loss,

low-grade fever, headache, muscle and joint pain are inconstant symptoms.

Icteric phase:

In this phase following signs and symptoms are manifested.

1. Yellowish discoloration of sclera

2. High coloured urine

3. Pruritis

On examination,

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Liver is palpable with smooth and tender edge.

Spleenomegaly and cervical adenopathy are present in 10-20% of

patients.

Post-icteric phase:

The icteric phase lasting for about 1 to 4 weeks is followed by clinical and

bio-chemical recovery in 2 to 12 weeks. The recovery phase is more prolonged in

HBV compared to the other varieties of Viral Hepatitis. Up to 1% of causes may

develop Fulminant Hepatitis and 5-10% of cases may progress on to Chronic

Hepatitis and 10-20% of adults contracting Hepatitis - B develop carrier state.

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INVESTIGATIONS

Biochemical investigations are always very useful in confirming the disease.

Liver function tests are useful to confirm the clinical diagnosis and type of Jaundice

produced. LFT indicates whether hepatic cells or biliary tree is primarily involved, in

giving an indication of the extent of Liver damage and in assessing the progress of the

disease.

The entire LFT can be studied under following headings:

Tests to determine the synthetic function of Liver.

Tests to assess the bile secretive capacity.

Tests to assess the damage of Liver cells (Hepatocytes).

Serum Bilirubin:

The usual cause of Jaundice is large quantities of bilirubin in the extra cellular

fluid, either free bilirubin or conjugated bilirubin. Normally total serum Bilirubin is

0.2 to 0.8 mg/dl.

The common causes of Jaundice are:

Increased the destruction of red blood cells with rapid release of

bilirubin in to the blood and.

Obstruction of bile ducts or damage to the Liver cells so that even the

usual amount of bilirubin cannot be excreted into gastro intestinal tract.

Here total bilirubin is combination or a sum of conjugated and Unconjugated

bilirubin.

In Hyper Bilirubin condition

If conjugated bilirubin (direct Bilirubin) level is more than

Unconjugated bilirubin (Indirect bilirubin) level, then it suggest the

jaundice has resulted, either due to hepatic cause or due to post hepatic

cause.

If Un-conjugated bilirubin (Indirect bilirubin) level is more than

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conjugated bilirubin (Direct bilirubin level, then it suggest the Jaundice

has resulted due to prehepatic cause.

Serum Transaminases:

SGOT (Serum Glutamic oxaloacetic Transaminase) Or

AST (Aspartate Amino Transferase) and

SGPT (Serum Glutamic pyruvic Transaminase) OR

ALT (Alanine Amino Transferase)

SGOT – is a mitochondrial enzyme released from heart, Liver skeletal muscle

and kidney. Its normal serum level is 0-35 U/L.

SGPT is a cytosolic enzyme primarily present in the Liver. Its normal serum

level is 0-45 U/L.

SGOT and SGPT reflect inflammation and break down of Liver cells, but they

are not specific for the Liver because raised levels being found in other forms of

tissue damage such as myocardial infarction, muscle necrosis, haematemesis and

intravasclar heamolysis.

In these condition SGOT levels tends to be appreciably higher than SGPT

levels, whereas both enzymes tend to show similar rises in Liver diseases. An

exception to this is found in alcoholic Hepatitis where it is not uncommon to find

SGOT levels of several times, the upper limit of normal with SGPT levels, within the

normal range. Transaminase estimations are useful in the early diagnosis of viral

Hepatitis.

Alkaline Phosphatase:

Serum Alkaline Phosphatase is produced by many tissues especially bone

Liver, intestine and placenta and is excreted in the bile. Most of the serum alkaline

phosphatase (25-85 IU/dl) is derived from bone. Elevation of inactivity of the enzyme

can thus be found in diseases of bone, Liver and pregnancy.

In the absence of bone disease and pregnancy, an elevated serum alkaline

phosphatase levels generally reflect Hepato biliary diseases.

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The greatest elevation (3 to 10 times normal) occurs in biliary tract

obstruction. Slight to moderate increase is seen in parenchymal Liver disease such as

hepatitis and cirrhosis and in metastatic Liver disease.

Physiological elevations occur in children adolescence and the trimester of

pregnancy.

HBsAg:

(Hepatitis-B surface Antigen). This should be looked for in every patient with

the Liver disease in whom there is any uncertainty about the etiology.

Finding of HBsAg in the serum may be an important bearing on the aetiology

of the Liver disease since this is a marker of Hepatitis-B.

The Detection of antigen may have important implications with regard to

safety of healthy persons.

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DIFFERENTIAL DIAGNOSIS OF HEPATITIS-B

Positive and complete findings are the tools to arrive at a definite diagnosis, to

estimate the prognosis and to adopt appropriate line of treatment for the disease. A

correct diagnosis should be made to distinguish from one disease to another, which

will have the similar signs and symptoms. The term Sapeksha Nidana means

differential diagnosis of the disease.

In all types of Viral Hepatitis-B the presenting clinical features are almost

same. Clinical diagnosis in such condition is very difficult hence; with the help of

viral markers (Hepacard method) exact diagnosis is made. Following diseases can be

considered for the differential diagnosis of Hepatitis-B90

.

Viral Hepatitis A

Viral Hepatitis B

Viral Hepatitis C

Viral Hepatitis D

Viral Hepatitis E

Viral Hepatitis G

Alcoholic Hepatitis

Cholestatic Hepatitis

Obstructive Jaundice

Hemolytic Jaundice

Drug induced Hepatitis

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COMPLICATIONS OF HEPATITIS –B INFECTION

Many complications can occur but in practice serious complications are

uncommon. The common complications of viral hepatitis – B are as follows91

.

Fulminant hepatic failure,

Relapsing hepatitis,

Biochemical,

Clinical.

Cholestatic hepatitis,

Post hepatitis syndrome,

Connective tissue disease,

Eg. Polyarteritis nodosa.

Glomerulonephritis(Renal

failure)

Henoch–sehonlein purpura,

Papular acrodermatitis,

Chronic hepatitis,

Cirrhosis,

Hepatocellular carcinoma,

Asymptamatic carrierstate.

Fatalities are rare and are attributed to the development of fulminant hepatic

failure. Return of symptoms and signs of acute hepatitis during recovery are

characteristic of relapsing hepatitis and occur in 5 to 15% of patients. A symptomatic

“biochemical” relapses with increase of plasma amino transferase activity are even

more common. Relapsing hepatitis does not imply a worse prognosis, because it

resolves spontaneously.

Cholestatic viral hepatitis can develop from the onset or during the course of

illness, with more severe Jaundice of a clinically and biochemically obstructive type

which may follow a prolonged course. Debility for 2 –3 months is common following

clinical and biochemical recovery. Some times in anxious patients, there may be

prolonged malaise, anorexia, nausea and right hypochondrial discomfort without

clinical or biochemical evidence of Liver disease. This syndrome is known as post

hepatitis syndrome and is not due to Liver disease. Chronic Hepatitis and cirrhosis

developed when chronic Hepatitis-B infection occurs these chronic viral infections

predispose to Hepato cellular carcinoma.

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PREVENTION

Vaccines for the prevention of hepatitis B have been routinely recommended

for infants. Most vaccines are given in three doses over a course of months92

.

DESCRIPTION

Hepatitis - B vaccine (rDNA) is a non-infectious recombinant DNA Hepatitis

B vaccine. It contains purified surface antigen of the virus obtained by culturing

genetically-engineered Hansenula polymorpha yeast cells having the surface antigen

gene of the Hepatitis B virus. The Hepatitis-B surface antigen (HBsAg) expressed in

the cells of Hansenula polymorpha is purified through several chemical steps and

formulated as a suspension of the antigen adsorbed on aluminium hydroxide and

thiomersal is added as preservative. The vaccine does not contain any material of

human or animal origin.

INDICATIONS

Hepatitis-B Vaccination is indicated for active immunisation against Hepatitis-

B infection in subjects considered at risk of exposure to HBV-positive material.

Immunisation against hepatitis B is expected in the long term to reduce not only the

incidence of this disease, but also its chronic complications such as chronic active

Hepatitis-B and Hepatitis-B associated cirrhosis and primary hepatocellular

carcinoma.

In areas of low prevalence of Hepatitis-B, immunisation with Hepatitis-B vaccine is

recommended for neonates/infants and adolescents as well as for subjects who are, or

will be, at increased risk of infection such as.

Health Care Personnel.

Patients receiving frequent blood products.

Personnel and residents of institution.

Persons at increased risk due to their sexual behavior.

Illicit users of addictive injectable drugs.

Travelers to areas with a high endemicity of HBV.

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Infants born of mothers who are HBV carries.

Persons originating from areas with a high endemicity of HBV.

Others: Police personnel, fire brigade personnel, armed forces personnel and

anybody who through their work or personal lifestyle may be exposed to

HBV.

Household contacts of any of the above groups and of patients with acute or

chronic HBV infection.

In areas of intermediate or high prevalence of Hepatitis-B, with most of the

population at risk of acquiring the disease, immunisation should be offered to all

neonates and young children. Immunisation should also be considered for adolescents

and young adults.

The vaccine can be safely and effectively given simultaneously but at different

injection site with DTP, DT, TT, BCG, Polio vaccine (OPV and IPV) and yellow

fever vaccine.

CONTRAINDICATIONS

Hepatitis-B vaccine should not be administered to subjects with known

hypersensitivity to any component of the vaccine, or to subjects having shown signs

of hypersensitivity after previous Hepatitis-B Vaccine administration.

IMMUNISATION SCHEDULE

Primary Immunisation : A series of three intramuscular injections is required

to achieve optimal protection.

Two primary immunisation schedules can be recommended:

A rapid schedule, with immunisation at 0, 1 and 2 months, will confer protection

more quickly and is expected to provide better patient compliance.

Schedules which have more time between the second and third doses, such

as immunisation at 0, 1 and 6 months, may take longer to confer protection,

but will produce higher anti-HBs antibody titres.

The immunisation schedule may be adapted to meet local immunisation

recommendations.

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The following timing of injections gives general guidance :

1st dose at elected date

2nd dose 4 to 10 weeks after the 1st dose

3rd dose 1 to 5 months after the 2nd dose

BOOSTER DOSE.

It would seem advisable to recommend a booster dose when the anti-HBs

antibody titre falls below 10 IU/L, particularly for all people at risk.

After the 0, 1, 2 month primary immunisation schedule a booster dose is

recommended 12 months after the first dose. The next booster may be required

after 8 years.

After the 0, 1, 6 month primary immunisation schedule a booster dose may be

required after 5 years after the primary course.

METHOD OF ADMINISTRATION

Hepatitis-B Vaccine should be injected intramusculary in the deltoid region in

adults and children or in the anterolateral thigh in neonates, infants and young

children. The vaccine may be administered subcutaneously in patients with

thrombocytopenia or bleeding disorders. The vaccine should be well shaken before

use. Only sterile needle and syringes should be used for each injection.

STORAGE

Hepatitis-B should be stored between 2° to 8°C. Not to be frozen. Discard if

vaccine has been frozen.

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TREATMENT

Early antiviral treatment may be required in fewer than 1% of people, whose

infection takes a very aggressive course (fulminant hepatitis) or who

are immunocompromised. On the other hand, treatment of chronic infection may be

necessary to reduce the risk of cirrhosis and liver cancer. Chronically infected

individuals with persistently elevated serum alanine aminotransferase, a marker of

liver damage, and HBV DNA levels are candidates for therapy. Treatment lasts from

six months to a year, depending on medication and genotype93

.

Although none of the available drugs can clear the infection, they can stop the

virus from replicating, thus minimizing liver damage. As of 2008, there are seven

medications licensed for treatment of hepatitis B infection.

Theseinclude antiviral drugs lamivudine (Epivir), adefovir (Hepsera), tenofovi

r (Viread), telbivudine (Tyzeka) and entecavir (Baraclude), and the two immune

system modulators interferon alpha-2a and PEGylated interferon alpha-2a (Pegasys).

Hepatitis B virus infection may be either acute (self-limiting) or chronic (long-

standing). Persons with self-limiting infection clear the infection spontaneously within

weeks to months.

Children are less likely than adults to clear the infection. More than 95% of

people who become infected as adults or older children will stage a full recovery and

develop protective immunity to the virus. However, this drops to 30% for younger

children, and only 5% of newborns that acquire the infection from their mother at

birth will clear the infection. This population has a 40% lifetime risk of death

from cirrhosis or hepatocellular carcinoma. Of those infected between the age of one

to six, 70% will clear the infection.

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DIET

Calories94

:

In an adult of 60kg/body/wt, in severe and moderately severe Jaundice about

1500 to 2000 Kcal is to be provided.

Proteins:

The quantity of protein, which can be given in the diet, depends on the

severity of the disease. In severe Jaundice where serum Bilirubin is over 15 mg/dl an

intake of about 40gm perday is permissible. But a higher intake of protein may

precipitate coma and in cases where the Jaundice is mild, 60 to 80 gm to proteins are

permitted.

Fat:

Intake of fatty acid either in saturated form or in unsaturated form is to be

totally contraindicated in patients suffering from Viral Hepatitis and Jaundice. But

there are some controversies regarding the amount of fat consumed by the patient in

acute or chronic Hepatitis.

In some of the medical texts it is explained that Fat intake depends on the

severity of the disease. In severe jaundice, about 30 gm, of fat daily is permissible.

Even then fatty acids shock and Fulminant Hepatitis were reported after the intake of

very little amount of fat in acute and severe Hepatitis. In mild to moderate Jaundice

about 50 to 60 gm, of fat may be permissible.

Carbohydrates:

Carbohydrates are the main source of calories in the diets of snuggest setting

from viral Hepatitis-B.

In severe Jaundice, fruit juice, porridage and puddings containing sugar can be

administered. In mild to moderate Jaundice, cereals can form the main source of

carbohydrates.

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Vitamins:

A multivitamin tablet providing the daily requirement of all the vitamins and

vitamin C (500 mg), should be administered parentally.

Minerals:

The serum levels of sodium and potassium should be maintained at normal

levels by adding these salts to the food.

Hepatotoxic drugs : Cyclophosphamide, methotrexate, prednisolone

Alcohol: Alcoholics who also have chronic HBV have a greater risk of

developing cirrhosis (severe liver scarring) and primary liver cancer (hepatocellular

carcinoma.

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PROGNOSIS

Hepatitis B virus infection may either be acute (self-limiting) or chronic

(long-standing). Persons with self-limiting infection clear the infection

spontaneously within weeks to months.

Children are less likely than adults to clear the infection. More than 95% of

people who become infected as adults or older children will stage a full recovery and

develop protective immunity to the virus. However, this drops to 30% for younger

children, and only 5% of newborns that acquire the infection from their mother at

birth will clear the infection. This population has a 40% lifetime risk of death from

cirrhosis or hepatocellular carcinoma. Of those infected between the age of one to

six, 70% will clear the infection.

Reactivation:

Hepatitis B virus DNA persists in the body after infection, and in some

people the disease recurs. Although rare, reactivation is seen most often following

alcohol or drug use, or in people with impaired immunity. HBV goes through cycles

of replication and non-replication. Approximately 50% of overt carriers experience

acute reactivation. Males with baseline ALT of 200 UL/L are three times more likely

to develop a reactivation than people with lower levels. Although reactivation can

occur spontaneously, people who undergo chemotherapy have a higher risk.

Immunosuppressive drugs favor increased HBV replication while

inhibiting cytotoxic T cell function in the liver. The risk of reactivation varies

depending on the serological profile; those with detectable HBsAg in their blood are

at the greatest risk, but those with only antibodies to the core antigen are also at risk.

The presence of antibodies to the surface antigen, which are considered to be a

marker of immunity, does not preclude reactivation. Treatment with prophylactic

antiviral drugs can prevent the serious morbidity associated with HBV disease

reactivation.

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DRUG REVIEW

The drugs selected for Virechana, Nasya, Shamana and Amapachana were studied in

detail, Rasa, Guna, Veerya, Vipaka, Doshaghnata and other actions of each drugs were

noted.

TABLE 49 JEEMOOTAKA PHALA FOR NASYA

Sanskrit

Name

Latin

Name

Rasa Guna Virya Vipaka Doshagnata Karma

Jeemootaka

Phala

Luffa

echinata

Roxb

Tikta Laghu,

Ushna

Ushna Katu KaphaVatagna Krimighna,Sramsa

na

TABLE 50 PATOLAMOOLADI KASHAYA FOR VIRECHANA

Sanskrit

Name

Latin

Name

Rasa Guna Virya Vipaka Doshagnata Karma

Patola Trichosa

nthes

dioica

Roxb.

Tikta

Laghu,

Snigdha

Ushna

Katu

Kaphaghna Jwaraghna,

Balya,

Vrishya,

Vishaghna

Katuki Picrorhiz

a kurroa

Katu,

Tikta

Laghu,

Ruksha

Ushna Katu Pittahara Hridya ,

Deepini,

Bhedini,

Jwarahara

Haritaki Terminal

ia

chebula

Retz.

Madhura,

Amla,

Katu,

Tikta,

Kashaya

Laghu,

Rooksha

Ushna Madhura Sarvadosapra

samana

Chakshush

ya,

Deepana,

Hridya,

Medhya

Viibhitaki Terntinal

ia

belerica

Roxb.

Kashaya

Laghu,

Ruksha

Ushna Madhura Kaphapittajit

h

Chakshush

ya, Kesya

Amalaki Emblica

officinali

s Gaertn

Madhura,

Amla,

Katu,

Tikta,

Kashaya.

Laghu,

Ruksha

Seeta

Madhura Tridoshajit Chakshush

ya,

Rasayana, ,

Vrisya

Visala Trichosa

nthes

bracteata

(Lam.)

Katu.

Thikta

Laghu,

Ruksha

Laghu,

Ruksha

Ushna Katu

KaphaPittaha

ra

Vamaka,

Visagna,

Prasutikrut

a

Brahmi Bacopa

monnieri

(Linn.)

Madhur,

Tikta,

Kashaya

Laghu,

Sara

Seeta

Madhura Kapha

Vatahara,

Medhya,

Rasayana,

Swarya,

Visahara,

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Shunti Zingiber

officinale

Roxb.

Katu

Laghu,

Snigdha

Ushna

Madhura

Vata

kaphapaha

Anuloma,

Deepana,

Hridya,

Pachana

TABLE 51 NIMBATWAKADI KASHAYA AS SHAMANA AUSHADI

Sanskrit

Name

Latin

Name

Rasa Guna Virya Vipaka Doshagnata Karma

Nimba Azadira

chta

indica

Tikta

Laghu

Seeta Katu

Kaphahara,

Pittahara

Kandugna,

Ruchya,

Deepana,

Visagna,

Vrinashoda

na

Haritaki Termina

lia

chebula

Retz.

Madhura,

Amla,

Katu,

Tikta,

Kashaya

Laghu,

Rooksha

Ushna Madhura Sarvadosapras

amana

Chakshush

ya,Deepana

, Hridya,

Medhya

Viibhitaki Terntina

lia

belerica

Roxb.

Kashaya

Laghu,

Ruksha

Ushna Madhura Kapha

pittajith

Chakshush

ya,Kesya

Amalaki Emblica

officinal

is

Gaertn

Madhura,

Amla,

Katu,

Tikta,

Kashaya.

Laghu,

Ruksha

Seeta

Madhura Tridoshajit Chakshush

ya,Rasayan

a, Vrisya

Patola Trichosa

nthes

dioica

Roxb.

Tikta

Laghu,

Snigdha

Ushna

Katu

Kaphaghna Jwaraghna,

Balya,

Vrishya,

Vishaghna

Rajani Curcum

a longa

Linn.

Katu,

Tikta

Ruksha

Ushna

Katu

Kaphapittanut Krimigna,

Varnya,

Visagna, ,

Pramehanas

a

Vasa Adhatod

a vasica

Nees

Tikta,

Kashaya

Laghu

Seeta Katu

Kapha

pittahara

Hridya,

Raktasangr

ahika,

Kasagna

Guduchi Tinospo

ra

cordifoli

a

Tikta,

Kashaya

Laghu Ushana

Madhura

Tridoshasama Balya,

Deepana,

Rasayana,

Sangrahi, ,

Raktasodha

ka,

Jwaragna

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Sariva Hemide

smus

indicus

(Linn.)

Madhura

Guru,

Snigda

Seeta Madhura

Tridoshanasa Raktasodha

ka,

Visagna, ,

Deepana,

Amanasana

, Jwarahara

Trivrt Operculi

na

turpethu

m

(Linn.)

Madhura,

Katu,

Tikta,

Kashaya

Laghu,

Ruksha,

Tikshana

Uahna

Katu Kapha

pittahara

Pittahara,

Vatala,

Virechana,

Sukhavirec

haka,

Jwarahara

Palasa Butea

monosp

erma

Katu,

Tikta,

Kashaya

Sara,

Snigdha

Ushna Katu

Kapha

vatasamaka,

Vrishya,

Agnideepak

a, Saraka

Bala Sida

cordifoli

a Linn.

Madhura

Laghu,

Snigdha,

Pichila

Seeta Madhura

Vata-Pittahara Balya,

Brahmana,

Vrishya

Neeli Indigofe

ra

tinctoria

Linn.

Katu,

Tikta

Sara Ushna Katu

Kaphahara,

Vatahara

Kesya,

Rechani, ,

Bhrama

Mohahara

Yashti-

madhu

Glycyrr

hiza

glabra

Linn

Madhura

Guru,

Snigdha

Sita

Madhura

Vatapittajith Balya,

Chakshush

ya,

Vrishya,

Varnya, ,

Raktaprasa

da

Sthira Desmod

ium

gangetic

um

Madhura,

Tikta

Guru

Ushna

Madhura Tridoshahara Balya,

Vrishya,

Visahara,

Angamarda

prasamana,

Sukhaprasa

vakara,

Sarva

doshahara

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TABLE 52 HAREETAKYADI CHOORNA FOR AMAPACHANA

Sanskrit

Name

Latin

Name

Rasa Guna Virya Vipaka Doshagnata Karma

Haritaki Termina

lia

chebula

Retz.

Madhura,

Amla,

Katu,

Tikta,

Kashaya

Laghu,

Rooksha

Ushna Madhura Sarvadosa

prasamana

Chakshus

hya,

Deepana,

Hridya,

Medhya

Amalaki Emblica

officinal

is

Gaertn

Madhura,

Amla,

Katu,

Tikta,

Kashaya.

Laghu,

Ruksha

Seeta

Madhura Tridoshajit Chakshus

hya,

Rasayana,

, Vrisya

Vacha Acarus

calamus

Linn.

Katu Tikta Laghu

Tikshna

Ushna Katu

Kaphahara Deepani,

Medhya,

Vatahara,

Malamootr

a Shodini,

Vamaka

Vidanga Embelia ribes Burm

Katu, Tikta Laghu Ruksha Tikshna

Ushna Katu Vatakaphapaha

Anulomana

, Deepana,

Kriminasan

a,

Rajani Curcuma

longa

Linn.

Katu,

Tikta

Ruksha

Ushna

Katu

Kaphapittanut Krimigna,

Varnya,

Visagna, ,

Pippali Piper longum Linn.

Katu

Laghu Rooksha

Ushna Katu

Kaphahara, Vatahara

Deepana, ,

Pachana,

Ruchya, ,

Vatanulom

ana

Shunti Zingiber

officinal

e Roxb.

Katu

Laghu,

Snigdha

Ushna

Madhura

Vatakaphap

aha

Anuloma,

Deepana,

Hridya,

Pachana Saindhava

Lavana

Sodi

chloridiu

m

Lavana Laghu,

Snigdha,

Tikshna

Sheeta Lavana Tridoshasham

aka

Agnideepa

na,

Pachana,

Ruchya,

Netriya,

Hridya,

Vrishya

Guda Jaggery Madhura Guru,

Snigdha

Seeta Madhura Kaphakara,

Vatahara

Vrishya,Pa

chana,Ruch

ya

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MATERIALS AND METHODS

Ayurveda is a rich science but its mysteries are yet to be untapped. It is well

known that the drug study is complete only after the clinical trial. In the pursuit of

knowledge, this clinical study was taken up to evaluate the effect of drugs in the

Management of Hepatocellular B Virus induced Jaundice.

MATERIALS:

A group (Nasya)

1. Hareetakyadi Yoga for Amapachana

2. Jimutak Phala Swarasa for Nasya

3. Nimbatwakadi Kashaya as Shamanoushadhi

B group (Virechana):

1. Hareetakyadi Yoga for Amapachana

2. Patolamooladi Kashaya for Virechana

3. Nimbatwakadi Kashaya as Shamanoushadhi

Hareetakyadi Yoga for Amapachana:

For the purpose of Amapachana in the present study Hareethakyadi yoga was

prepared in the department of Rasashastra and Bhaishajya Kalpana of Ayurveda

Mahavidyalaya, Hubli.

Patolamooladi Kashaya for Virechana:

For the purpose of Virechana Karma, in the present study Patolamooladi

Kashaya was prepared in the department of Rasashastra and Bhaishajya Kalpana of

Ayurveda Mahavidyalaya, Hubli as per Ashtanga Hridaya, Kalpa sthana. Patola

Mooladi Kashaya consists of mainly Patolamoola, Katurohini, Triphala, Visala,

Brahmi, and Nagara.

Nimbatwakadi Kashaya as Samana oushadhi:

The Samana Oushadi given was Nimbatwakadi Kashaya, described in

Sahasrayoga as Kamalahara. It consists of the drugs, Nimbatwak, Triphala, Patola,

Rajani, Vasa, Amruta, Sariba, Syama, Amalaki, Palasha, Bala, Neeli, Yashti, and

Sthira.. These drugs were collected and Yavakuta churna was prepared.

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Method of preparation of Kashaya:

These drugs made into choorna and mixed with four times quantity of water

and boiled and reduced to one-fourth to make kashaya. Everyday fresh kashaya was

prepared and given to the patients.

Nasya:

Jimutaka phala Majja Swarasa were used for the Nasya.

Procedure of Preparation of Jimutaka Nasya:

Jimutaka phala Majja crushed in milk properly and filtered it and administered

into the nostrils of subjects suffering from Kamala (HBV Induced Jaundice).

Methods

Sampling:

30 patients of Hepatocellular-B virus induced Jaundice were selected from the

Post- Graduation outpatient Department of Ayurveda Mahavidyalaya and Hospital,

Hubli. They were divided into two groups 15 patients each.

Methods of collection of Data

a. A clinical survey of subjects attending the OPD and IPD of Post

Graduate Department of Panchakarma, Ayurveda Mahavidyalaya

Hospital, Hubli was made and subjects fulfilling the criteria of

diagnosis as per the proforma were selected for the study.

b. A clinical evaluation of patients was done by collection of data through

information obtained by history, physical examination, laboratory tests

and USG Abdomen etc.

c. Review of literature was done from Post Graduate Library, Department

of Panchakarma, Ayurveda Mahavidyalaya, Hubli, and from Authentic

Research Journals, Websites and Digital Publications etc.

d. The drugs required for the clinical study were procured and prepared in

the department of Rasa Shastra and Bhaishajya Kalpana, Ayurveda

Maha Vidyalaya, Hubli.

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Criteria for Selection of cases:

The main criteria for selection of patients were symptomatology and

laboratory evidence of serum HBsAg positive and deranged liver function test values.

Inclusion Criteria

1. Subjects of age between 15-50 years of both Sexes were included.

2. Subjects with HBsAg Test positive and Jaundice (features of Kamala)

were included.

3. Subjects fit for Nasya Karma and Virechana Karma were taken for study.

4. Subjects with Sr. Bilirubin level till 13mg/dl.

Exclusion Criteria

1. Subjects with any systemic metabolic disorders, T.B and HIV positive.

2. Subjects who were HBsAg negative, Pregnant, Children and Old age.

3. Subjects with Cirrhosis of liver, Alcoholic liver disease and Portal

Hypertension were excluded.

4. Subjects of HBV induced Jaundice with serious complications.

5. Subjects of HBV carriers who were asymptomatic.

Parameters of Study:

Subjective Parameters:

On disease

1. Ictrus (Netra Peetata)

2. Yellowish discoloration of urine (Mootra Peetata)

3. Yellowish discoloration of skin, nails etc. (Twak ,Nakha Peetata)

4. Dark coloured stools (Krishna Peeta varchas)

5. Weakness (Daurbalyam)

6. Loss of appetite (Agnimandya,Aruchi)

7. Fever, Headache and undue fatigue.

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On Procedure

NASYA

1. Laghuta of Siras

2. Sukha Swapna

3. Indriya Visudhi

4. Nasa Srava

VIRECHANA

Lakshanas of Samyak Virechana.

1. Vegiki

2. Maniki

3. Antiki

4. Laingiki

Objective Parameters:

On disease

1. Investigation for HBV by Hepacard method (HbsAg positive blood test).

2. Yellowish discoloration of the eyes, skin, tongue and urine.

3. Tenderness in the liver region.

On procedure

FOR NASYA

1. Blood pressure before and after Nasya Karma.

2. Respiratory rate before and after Nasya karma.

3. Pulse before and after Nasya.Karma.

4. Temperature of Nasya Dravya before administration.

5. Kshudha Pravruti, Mala Pravruti etc. on the day of Nasya Karma.

6. Dose (Matra) of the Dravya used in Nasya Karma.

FOR VIRECHANA

1. Blood pressure before and after of Virechana Karma.

2. Respiratory rate before and after Virechana karma.

3. Pulse before and after Virechana.Karma.

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4. Dose (Matra) of the Dravya used for Virechana Karma

Investigations:

Following investigations were carried out.

Blood analysis

Sr.Bilirubin – Total, Direct, Indirect

SGOT

SGPT

Alkaline phosphate

HBsAg

Albumin level

Prothrombin time

Urinalysis

Investigation for Bile Pigment and

Bile Salt.

USG Abdomen (If required)

Assignment:

Study / Research Design: A Comparative Clinical Study.

Sample size: A Minimum of 30 subjects diagnosed as Hepatitis B Virus induced

Jaundice were selected incidentally and randomly categorized into two groups

consisting 15 subjects in each group.

Group – A (Nasya)

Amapachana with Hareetakyadi Yoga (5-10 gms) for 3-5 days.

Mukhabhyanga with Murchita Tila Taila and Baashpa sweda was performed

initially as Poorva Karma.

Nasya with Jeemoothaka Phala Swarasa for 7 days initially followed by 14

days of Parihara Kala. Then one more course of Nasya with the same Swarasa

for 7 days after which 14 days of Parihara Kala was followed again.

During course of Parihara Kala internally Nimbatwakadi Kashaya(45-60ml),

was given as Shamanoushadhi.

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Group – B: (Virechana)

Amapachana with Hareetakyadi Yoga (5-10 gms) for 3-5 days.

Kaphoanuthklishtakara Ahara (Eshad Pramana of Goghrita along with Ahara)

was adviced for 3 days as a part of Poorva Karma. Bahya Prayoga of Murchita

Tila Taila in the form of Mrudu Abhyanga was suggested to the patients.

Sukhoshna Jala Snana was followed later as a part of Parisheka Sweda.

Virechana with Patolamooladi Kashaya(60-90 ml) and Samsarjana Krama

initially followed by 14 days of Parihara Kala. Then one more course of

Virechana with the same medicine and Samsarjana Krama for 3 days after

which 14 days of Parihara Kala was followed again.

During the course of Parihara Kala internally Nimbatwakadi Kashaya(45-

60ml), was given as Shamanoushadhi.

Duration: 45 days.

Follow-up:

After 45 days of treatment , follow-up was done for 3 months an interval of

30 days.

Nasya Karma:

Nasya karma is one of the major procedures of classical Pancha karma, of

Shodhana Chikitsa. Individually or in collaboration with other Karmas, Panchakarma

includes certain procedures either to expel the Doshas from the body through various

route or to administer the medicine with certain media carriers through nearest route.

Definition:

Aoushadhamoushadha siddho va sneho nasikabhyam diyatha eti Nasyam

Nasya is a term to be applied generally for medicines or medicated oil

administered through the nasal passage.

According to Bhavaprakasha all drugs and measures that can be administered

through the nasal passage are called „Nasya‟ (Bha.P.Pu.Kha).

In the classical text as well as in any one of the available literature, the method

of Administration of Jimutaka Nasya, its dosage (matra) and duration (kala) is not

explained. But some Tribal Vaidya practice Jimutaka Apakwa Phala Rasa Nasya

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some others instill Jimutaka pakwa phala (Shushka phala) along with Beeja and Majja

crushed with either Stanya (Breast milk) or Dugdha..

Pilot Study:

In order to fix the proper dosage of method of administration of Jimutaka

Nasya pilot study was carried out. It was observed that after the administration of

Aoushadhi dravya in to nostril usually after one to two hours, severe irritation in nasal

mucosa, and throat were developed. Patient developed severe congestion followed by

secretion of an yellowish coloured fluid through the nasal orifice and even yellowish

salivary secretions were also observed. Some of the patients developed throat pain

and difficulty in swallowing.

Since the condition like nasal irritation, burning sensation in nose was

temporary, next day again the same karma was followed but no chance of bleeding

through the nasal orifice was observed (Reported).

Hence it was planned to administered the Aoushadha dravya in the form of

Nasya at a dosage of 2 – 6 drops in each nostrils for 5 to 7 days.

The procedure of giving Nasya therapy is classified into the following three headings:

1. Poorva Karma

2. Pradhana Karma

3. Paschat Karma

Poorva Karma:

Before giving Nasya prior arrangement of the material and equipments were

made in a special room free from atmospheric effects like direct blow of air and dust

etc.

i. Nasya asana: A cot for lying purpose.

ii. Nasya Aoushadhi: Jimutaka Phala Majja and Milk in sufficient

quantity were used for Nasya.

iii. Nasya Yantra: For Pratimasha Nasya a dropper was used.

Besides this spitting measures pot, bowel, napkin and cotton were there.

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Selection of Patients:

The patients were selected according to indication and contraindication of

Nasya described in classics.

Preparation of Patients:

According to Sushruta‟s descriptions following regimens were given to

patients to prepare him for Nasya karma.

Patient passed his natural urges like urine, stool.

Completed his routine activities like tooth brushing, bath etc.

After patient was ready for Nasya karma, he was made to lie down on Nasya

table. Before Nasya, Mukhabhyanga with Murchita Tila Taila and Baashpa

sweda was performed initially as Poorva Karma.

In Kamala roga Swedana karma is Varjya but as part of Poorva karma the

following measures were carried.

According to Ayurvedic texts Swedana should not be given to the head.

Mrudu Swedana may be given for elimination of dosha and liquification of dosha.

Baashpa Sweda was given on Siras, Mukha bhaga, Nasa, Manya pradesha, Greeva

pradesha and Kantha region.

For this purpose cloth dipped in hot water and used for Mrudu Sweda. Some

patients were even advised to get exposed to sunlight (aatapa) instead of receiving the

Swedana karma. After Swedana smooth massage was adviced to patient on regions of

Gala, Kapola and Lalat pradesha. Hence the Swedana karma performed as a pre

requisite measure was not uniform. Either Aatapa Snana or Mrudu Swedana

according to Yukti were adopted.

Pradhana karma:

As described by Charaka, Vagbhata and Sushruta the following procedure

were adopted for performing the Nasya karma.

Patients were made to lie down in supine position on Nasya table.

Siras (Head) was kept „Pralambita‟ (lowered i.e. hanging down) and foot part

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was slightly raised.

Head was excessively flexed or extended.

The head is not lowered the nasal medication may not reach to the desired

distinction and it is lowered too much, there may be the danger of getting the

medication to be lodged in brain.

After covering the eyes with clean cotton cloth, raised the tip of patients nose

with left thumb and with the right hand Jimutaka and Nasya given.

The drug was neither less nor more in the dose i.e. was used proper quantity.

It was neither very hot nor very cold.

Since Nasya karma is an invasive technique proper care was taken, hand

gloves were used instruments were sterilized properly.

Paschat Karma:

As described by Charaka, Ashtanga Hridaya and Sushruta following regimen

were followed.

After administration of medication through nasal passage patient was made to

lie supine (Uttana) for about 2 minutes. After administration of Nasya, inorder to get

proper passage of medicine through nostrils; cheeks, nose etc were given massage.

The patient was advised not to swallow of Nasya dravya and other Strava

(Secretions).

Patient was directed to spit the Aoushadha dravya, which comes to the

oropharynx.

Patient was made to stay at place devoid of breeze. Light meal (Laghu ahara)

and Luke warm water (Sukoshana Jala) was given. It was observed that patient

developed mucosal discharge through the mucosa. Sometimes expulsion of

yellowish coloured fluid as Nasa Strava and Lala Strava were also light yellow

in colour.

Advised to avoid dust, smoke, sunshine, alcohol, hot bath, riding anger, excess

fat and liquid diet. Day sleeping and cold water for any purpose like Pana,

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Snana etc. were avoided after Nasya karma.

VIRECHANA KARMA:

The Ayurvedic management of diseases in general, can be broadly grouped in to

Shodhana and Shamana treatments.

The former is intended to eliminate excessively vitiated Dosha out of the body

and thereby eradicating disease as a whole, while the later is directed towards palliation

of vitiated Dosha. However Ayurvedic classics unequally give paramount importance to

the Shodhana therapy, owing to its credential of providing a complete cure. Acharya

Charaka says that Doshas treated by Langhana and Pachana therapies may get provoked

some times, but if treated by shodhana therapy there is seldom possibility of such

recurrence.

The Shodhana has got no parlance in the modern medicine, but we can say

that the toxins and metabolic toxic products responsible for the disease are eliminated

from the body.

It is worth mentioning that Virechana Karma unlike the modern purgative is

not merely an act to open the bowel, it is a complete therapeutic measure, which has

systemic as well as local effects. This fact is further supported by the word

“Virechana”.

Definition:

Tatradoshaharanam Adhobhagam Virechana Sanjnakam |

The act of expelling Dosha through Adhobhaga is known as Virechana. Here

the meaning of Adhobhaga is Guda as commented by Chakrapani.

Procedure of Virechana Karma:

Prior to Virechana karma following preparations should be done-

It should be decided earlier whether the patient is suitable for Virechana or not.

If the patient is suffering from both Virechana Yogya and Ayogya disease then the

karma may be done if the Virechana Yogya disease is more Guru than the Ayogya one.

All necessary equipments should be arranged. All necessary drugs as Deepana

Pachana drugs, Virechana yoga, Drugs for emergency such as Karpur rasa,

Sutashekhar, Kutajaghana vati etc. should be collected in sufficient quantity according

to Atura and Roga.

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Prior to procedure the detailed examination of the patient is required according

to Dosha, Desha, Kala, Bala, Shareera, Ahara, Satmya, Satva, Prakruti and Vaya.

When the symptoms of Bahudosha are present then Shodhana is indicated.

When it is associated with Ama than Shodhana can only be done after Pachana of

Ama. Which can be doing by Deepana, Pachana.

POORVA KARMA

Prakyat Kriyate tat Poorva karmam |

Procedure, which is necessary prior to pradhana karma, is known as Poorva

karma. Patients were given deepana and pachana drugs internally before Pradhana

Karma.

Patients suffering from Kamala taken for trial were administered Deepana,

Pachana drugs as Amapachaka and to increase the Agni bala of the Rogi.

Amapachana Chikitsa adopted for a period of 3 to 5 days with Hareethakyadi

Choorna 5 to 10gms along with Sukoshana Jala as Anupana as a simple measure of

Ama Chikitsa. Since the Kamala and Pandu Rogi are listed as “Nati Snigdhan

Virechayet”| Here the Hepatocellular B virus cause Hepato toxicity, inflammation in

the Hepatocytes. Hence administration of fatty acids may cause adverse reactions.

Administration of Sneha in large quantity is not advisable. As liver is the

storage organ, the major function of the liver is to digest Phospholipids. Whether

Sneha is Aoushadhasiddha or Accha by looking into the roga avastha and

complication of HBV induced Jaundice according to Yukti pramana, Snigdha bhojana

(Eshad pramana of Goghrita along with Ahara) only for 3 days were advised as a part

of Poorva Karma.

Bahya Prayoga of Murchita Tila Taila in the form of Mrudu Abhyanga was

suggested to the patients. Since Abhyanga is an invasive technique. Patients were

suggested to perform the same by their own.

Sukhoshna Jala Snana was followed later as a part of Parisheka Sweda.

PRADHANA KARMA:

The Virechana yoga (Patolamooladi Kashaya ,60-90 ml) was given to patients

.

While the patient was cheerful, slept well and had fully digested his

previous meal.

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After assessing the psychological condition of the patient.

Virechana was performed on empty stomach.

Regarding the time of giving Virechana, Vagbhata said “Sleshma

Kalagate” which means Virechana should be given after Sleshma Kala.

Just after administration of Virechana yoga cold water was sprinkled on

the face to prevent vomiting.

The patient was asked to gargle with hot water.

Patients were protected from direct cold wind.

Patients were advised to avoid Pravahana.

Hot water was given frequently to the patient to prevent Vibhanda.

Due to its Vatanulomana and Yogavahi action Virechana vega attained.

Observation:

Ausadha Jirna Lakshana:

Ausadha Jirna Lakshana are Vatanulomana, Svasthya, Ksudha Trisna,

Urjamanasvita, Indriya Laghuta.

ANULOMO---------JIRNOSADHAMA.

PASCHAT KARMA:

Samsarjan Krama:

After Virechana karma, patient develops Agnimandhya. So Peyadi krama was

recommended to increase the Agni gradually upto the normal level. In the Peyadi

krama Peya, Vilepi, Akruta yush, Kruta yush, Akruta Mamsa Rasa and Kruta Mamsa

Rasa were given for 3, 2 and 1 Anna kala for Pravara, Madhyama and Avara Shuddhi

patients respectively.

Acharya Sushruta mentioned Kulatha, Mudga, Jangala mamsa rasa inspite of

Peyadi krama. Dalhana commented on it that in Ksheena Kapha Peya should be

given.

In our Clinical trial laja, saktu, vilepi mudgayusha etc. were given in different

Annakala according to Agnibala and according to type of Shuddhi attained.

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The assessment and Scoring of Symptoms:

For the purpose of assessment two criteria were considered. The first criteria

was the relief of symptoms and the second criteria included changes in the

biochemical values or LFT and reactivity of HBsAg.

Symptoms for assessment:

Peeta netrata, Mootra peetata, Krishna peeta purisha, Peeta jivha, Peeta nakha,

Peeta twacha, Jwara in 0F, Agnimandya, Aruchi, Chardi, Kandu, Udara shoola and

Sandhi shoola

The bio-chemical assessment was done before the commencement of the

treatment and 90th

day after the commencement of treatment, which was the post test

assessment.

The Serum bilirubin was estimated immediately after Nasya karma in Group

A and the blood was tested for Serum bilirubin immediately after Virechana Karma in

Group B.

The Urine was tested for the presence of Bile salts and Bile pigments before

and after the treatment period in both the Groups.

Observation of Signs and Symptoms , before and after Nasya were noted to

assess the shuddhi given by Nasya.

Observation of Signs and Symptoms of Samyak and Asamyak Virechana

lakshanas along with Vagiki, Laingiki, Manaki and Antaki lakshana were noted to

assess type of Shuddhi.

The assessment criteriae are totally based on the changes in symptoms scores

of Kamala, observed before and after vamana and virechana karma.

The subjective and Objective parameters were graded and scorings (grading)

were given in the following manner.

Subjective parameters:

Score – 02 indicating presence of symptoms before treatment

Score – 01 indicating Improvement by the treatment

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Score – 00 indicating Absence of the symptoms (relief of symptoms)

after treatment

Objective parameters:

Test for HBsAg (Hepacard method)

Liver function Tests (LFT):

SGOT -

SGPT -

Sr. Alkaline Phosphatase –

Sr.Bilirubin -

Urine for Bile salts -

Urine for Bile pigment

For all the Objective Parameters, the Values of each criterion were noted and

BT and AT Values were compared statistically.

The findings after treatment were noted and analysed in the following manner.

Assessment criteria:

Changes in Subjective and objective features of Jaundice (Kamala) were assessed

before and after the treatment. The result will be recorded as;

Marked relief - Above 75% Improvement

Moderate relief - 50%-75% Improvement

Mild relief - 25%-50% Improvement

Unchanged - Below 25% Improvement

The data which obtained by the clinical trial were statistically analyzed by

applying Student„t‟ test.

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OBSERVATIONS AND RESULTS

OBSERVATIONS

A detailed case sheet (Case record form) was prepared, subject’s vital data

were recorded systematically and the following observations were made. Consent

paper was also systematically prepared and given to the subjects, written consent for

their willingness in receiving the therapy was obtained.

Table No. 53 - Showing the incidence of Sex in the subjects of HBV induced

Jaundice:

Sl.

No. Sex

Group A Group B Total

No. of

Subjects %

No. of

Subjects %

No. of

Subjects %

1 Male 12 80% 11 73.33% 23 76.67%

2 Female 3 20% 4 26.67% 7 23.33%

12 subjects (80%) were males and 3 (20%) were females in Group A and

11(73.33%) subjects were males and 4 (26.67%) females in Group B.

Table No.54 - Group A - Showing the incidence of Age in the subjects of HBV

induced Jaundice

Sl.

No. Age

Total No. of

Subjects Male Female

No.of

Subjects %

No.of

Subjects %

No.of

Subjects %

1 15 – 20 1 6.67% 0 0% 1 33.33%

2 21 – 30 2 13.33% 2 16.67% 0 0%

3 31 – 40 5 33.33% 3 25% 2 66.67%

4 41 – 50 7 46.67% 7 58.33% 0 0%

1 subject (6.67%) had between in age group 15 – 20 years, 2 (13.33%)

subjects were between 21 – 30 years in that 2 (16.67%) were males only. 5 (33.33%)

subjects were between 31 – 40 years of age, out of that 3 (25%) were males and 2

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(66.67%) were females. 7 (46.67%) subjects were between 41 – 50 years of age, out

of that 7 (58.33%) were males onlyin Group A.

Table No.55 - Group B - Showing the incidence of Age in the subjects of HBV

induced Jaundice

Sl.

No. Age

Total No. of

Subjects Male Female

No. of

Subjects %

No. of

Subjects %

No. of

Subjects %

1 15 – 20 0 0% 0 0% 0 0%

2 21 – 30 6 40% 5 45.45% 1 25%

3 31 – 40 2 13.33% 1 9.09% 1 25%

4 41 – 50 7 46.67% 5 45.45% 2 50%

No subjects were between the age group 15 – 20 years .6 (40%) subjects were

between 21 – 30 years of age out of that 5 (45.45%) were males and 1 (25%) was

female. 2 (13.33%) subjects were between 31 – 40 years of age, in that 1 9.09%) was

male and 1 (25%) was female. 7 (46.67%) subjects were between 41 – 50 years of

age, in that 5 (45.45%) were males and 2 (50%) ware females in Group B.

Total No.56- Showing the incidence of AGE in the subjects of HBV induced

Jaundice

Sl.

No. Age

Total No. of

Subjects Male Female

No. of

Subjects %

No. of

Subjects %

No. of

Subjects %

1 15 – 20 1 3.33% 0 0% 1 14.28%

2 21 – 30 8 26.67% 7 30.43% 1 14.28%

3 31 – 40 7 23.33% 4 17.39% 3 42.86%

4 41 – 50 14 46.67% 12 52.17% 2 28.57%

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1 subject (20%) were between age group of 15 – 20 years out of this 4

(13.33%) were males and 2 (06.67%) were females. 9 (30%) subjects were between

the age group of 21 – 30 years in that 7 (23.33%) were males and 2 (06.67%) were

females. 10 (33.33%) subjects were between 31 – 40 years of age, in that 7 (23.33%)

were males and 3 (10%) were females. 5 (16.67%) subjects were between 41 – 50

years of age, in that 3 (10%) were males and 2 (06.67%) were females in Toto.

Table No.57 - Showing the incidence of Religion in the subjects of HBV induced

Jaundice:

Sl.

No. Religion

Group A Group B Total

No. of

Subjects %

No. of

Subjects %

No. of

Subjects %

1 Hindu 14 93.33% 13 86.67% 27 90%

2 Muslim 1 6.67% 1 6.67% 2 6.67%

3 Christian 0 0% 1 6.67% 1 3.33%

14 (93.33%) subjects belonged to Hindu religion, whereas 1 (6.67%) subjects

belonged to Muslim community in Group A. 13 (86.67%) subjects belonged to Hindu

religion , 1 (6.67%) subjects belonged to Muslim community and 1 (6.67%) subjects

belonged to Christian community in Group B.

Table No. 58 - Showing the incidence of Marital status in the subjects of HBV

induced Jaundice:

Sl.

No.

Marital

Status

Group A Group B Total

No. of

Subjects %

No. of

Subjects %

No. of

Subjects %

1 Married 12 80% 12 80% 24 80%

2 Unmarried 3 20% 3 20% 6 20%

These distribution shows that 12 (80%) subjects were married, whereas 3

(20%) subjects were unmarried in Group A and in Group B.

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Table No.59 - Showing the incidence of Habitat in the subjects of HBV induced

Jaundice:

Sl.

No. Habitat

Group A Group B Total

No. of

Subjects %

No. of

Subjects %

No. of

Subjects %

1 Urban 9 60% 8 53.33% 17 56.67%

2 Rural 6 40% 7 46.67% 13 43.33%

9 (60%) subjects belonged to Urban area whereas 6 (40%) subjects belonged

to Rural area in Group A. 8 (53.33%) subjects belonged to Urban area and 7 (46.67%)

subjects belonged to Rural area in Group B.

Table No.60 - Showing the incidence of Food Habits in the subjects of HBV

induced Jaundice:

Sl.

No. Food Habit

Group A Group B Total

No. of

Subjects %

No. of

Subjects %

No. of

Subjects %

1 Vegetarian 11 73.33% 10 66.67% 21 70%

2 Mixed 4 26.67% 5 33.33% 9 30%

11 (73.33%) subjects were consuming vegetarian diet whereas 4 (26.67%)

subjects belonged to Mixed diet catogory in Group A. 10 (66.67%) subjects belonging

to vegetarian category and 5 (33.33%) subjects belonged to Mixed diet in Group B.

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Table No.61 - Showing the incidence of Duration of Illness the subjects of HBV

induced Jaundice:

Sl.

No.

Duration

after the

Onset of

Disease

Group A Group B Total

No. of

Subjects %

No. of

Subjects %

No. of

Subjects %

1 15 – 45 days 11 73.33% 9 60% 20 66.67%

2 46 – 75 days 4 26.67% 6 40% 10 33.33%

The duration of illness were recorded according to the statement of the

subjects from the onset of the symptoms of Jaundice.

11 (73.33%) subjects were giving the history of onset of the disease between

15-45 days after the onset of the Jaundice, whereas 4 (26.67%) subjects were giving

the history of onset of disease between 46-75 days duration in Group A. 9 (60%)

subjects were giving the history of onset of disease between 15-45 days duration after

the onset of the Jaundice whereas 6(40%) subject had given history of onset of

disease between 46-75 days duration in Group B.

Table No.62 - Showing the incidence of Socio-Economic status in the subjects of

HBV induced Jaundice:

Sl.

No.

Socio-

Economic

Status

Group A Group B Total

No. of

Subjects %

No. of

Subjects %

No. of

Subjects %

1 Poor 3 20% 3 20% 6 20%

2 Middle 11 73.33% 12 80% 23 76.67%

3 Rich 1 6.67% 0 0% 1 3.33%

Study of the socio-economic status of the subjects revealed that 3 (20%)

subjects in group A and in group B were poor.11 (73.33%) subjects in group A and 12

(80%) subjects in group B were Middle class. 1 (6.67%) subject in group A was from

Rich class.

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Table No.63 - Showing the incidence of History of previous treatment received in

the subjects of HBV induced Jaundice:

Sl.

No.

History of previous

treatment received

Group A Group B Total

No. of

Subjects %

No. of

Subjects %

No. of

Subjects %

1 Received 5 33.33% 7 46.67% 12 40%

2 Not received 10 66.67% 8 53.33% 18 60%

Study on the incidence of history of previous treatment received in the

subjects revealed that 5 (33.33%) subjects in group A and 7 (46.67%) subjects in

group B received previous treatment. 10 (66.67%) subjects in group A and 8 (53.33%)

subjects in group B did not receive any previous treatment.

Table No.64 - Showing the History of Hepatitis B vaccine received in the subjects

of HBV induced Jaundice:

Sl.

No.

History of

Hepatitis B

Vaccine received

Group A Group B Total

No. of

Subjects %

No. of

Subjects %

No. of

Subjects %

1 Received 3 20% 2 13.33% 5 16.67%

2 Not received 12 80% 13 86.67% 25 83.33%

Study on the history of Hepatitis B vaccine received in the subjects revealed

that 3 (20.00%) subjects in group A and 2 (13.33%) subjects in group B received

Hepatitis B vaccine. 12 (80.00%) subjects in group A and 13 (86.67%) subjects in

group B did not receive Hepatitis B vaccine.

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Table No.65- Showing the incidence of Education in the subjects of HBV induced

Jaundice:

Sl.

No. Education

Group A Group B Total

No. of

Subjects %

No. of

Subjects %

No. of

Subjects %

1 Primary 7 46.67% 7 46.67% 14 46.67%

2 High school 4 26.67% 5 33.33% 9 30%

3 Graduate 2 13.33% 2 13.33% 4 13.33%

4 Post

Graduate 2 13.33% 1 6.67% 3 10%

7 (46.67%)subjects in group A and in group B were having Primary education.

4 (26.67%)subjects in group A and 5 (33.33%) subjects in group B had High school

education. 2 (13.33%) subjects in both group A and in group B were having

Graduation and 2 (13.33%) subjects in group A, 1 (6.67%) subject in group B had

Post Graduate education.

Table No.66- Showing the incidence of Habits in the subjects of HBV induced

Jaundice:

Sl.

No. Habits

Group A Group B Total

No. of

Subjects %

No. of

Subjects %

No. of

Subjects %

1 Only Alcohol 2 13.33% 1 6.67% 3 10%

2 Only

Smoking/tobacco 7 46.67% 8 53.33% 15 50%

3 Alcohol and

Smoking 1 6.67% 3 20% 4 13.33%

4 Tea/Coffee 5 33.33% 3 20% 8 26.67%

2 (13.33%) subjects in group A and 1 (6.67%) subject in group B, were having

the habit of drinking Alcohol only. 7 (46.67%) subject in group A and 8 (53.33%)

subjects in group B were having only Smoking or Chewing Tobacco as habit. 1

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(6.67%) subject in group A and 3 (20%) subjects in group B, were having the habits

of Alcohol and Smoking together. 5 (33.33%) subjects in group A and 3 (20%)

subjects in group B were having the habits of drinking Tea/Coffee.

Table No.67 - Showing the incidence of State of Agni in the subjects of HBV

induced Jaundice:

Sl.

No. State of Agni

Group A Group B Total

No. of

Subjects %

No. of

Subjects %

No. of

Subjects %

1 Mandagni 7 46.67% 6 40% 13 43.33%

2 Vishamagni 6 40% 7 46.67% 13 43.33%

3 Teekshanagni 2 13.33% 2 13.33% 4 13.33%

In-group A, 7 (46.67%) subjects were having Mandagni, 6 (40%) Subjects

were having Vishamagni and 2 (13.33%) Subjects were having Teekshnagni. In-group

B 6 (40%) subjects were having Mandagni and 7 (46.67%) subjects were having

Vishamagni and 2 (13.33%) Subjects were having Teekshnagni.

Table No. 68- Showing the incidence of Nature of Koshta in the subjects of HBV

induced Jaundice:

Sl.

No. Koshta

Group A Group B Total

No. of

Subjects %

No. of

Subjects %

No. of

Subjects %

1 Madhyam 6 40% 4 26.67% 10 33.33%

2 Mrudhu 1 6.67% 3 20% 4 13.33%

3 Kroora 8 53.33% 8 53.33% 16 53.33%

In total 10 (33.33%) subjects were having Madhyam Koshta and 4 (13.33%)

Subjects were having Mrudhu Koshta and 16 (53.33%) subjects had Kroora Koshta.

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Table No. 69. Showing Dominent Rasa wise diet of 30 subjects of Kamala

Rasa Group A Group B Total %

Madhura 6 4 10 33.33%

Amla 9 10 19 63.33%

Lavana 7 6 13 43.33%

Katu 8 9 17 56.67%

Tikta 0 1 1 3.33%

Kasaya 0 0 0 0

Amla Rasa consumers were maximum 19(63.33%) subjects, followed by Katu

Rasa 17(56.67%) subjects, Lavana Rasa 13(43.33%) subjects and Madhura Rasa

10(33.33%) subjects and Tikta Rasa 1(3.33%) subject.

Table No 70 :Showing Dominent Guna wise diet of 30 subjects of Kamla

Guna Group A Group B Total %

Guru 4 4 8 26.67%

Laghu 1 3 4 13.33%

Ruksha 10 6 16 53.33%

Snigdha 1 1 2 6.67%

Ushna 4 7 11 36.67%

Sheeta 2 0 2 6.67%

Thikshna 7 8 15 50%

16(53.33%)subjects were consumers of Rooksha Guna and 50% ie 15 subjects

were consuming Teekshna Guna Pradhana Ahara, followed by Ushna Guna

11(36.67%), Guru 8(26.67%) ,Laghu Guna 4(13.33%) and finally Snigdha Guna and

Sheeta Guna 2(6.67%)subjects each.

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Table No. 71 - Showing the incidence of Deha prakruti in the subjects of HBV

induced Jaundice:

Sl.

No. Deha Prakruti

Group A Group B Total

No. of

Subjects %

No. of

Subjects %

No. of

Subjects %

1 Kapha pitta 5 33.33% 3 20% 8 26.67%

2 Vata pitta 5 33.33% 6 40% 11 36.67%

3 Vata kapha 5 33.33% 6 40% 11 36.67%

8 (26.67%) subjects were having Kapha pitta prakruti, 11 (36.67%) Subjects

were having Vata pitta prakruti and 11 subjects (36.67%) were having Vata kapha

prakruti.

Table No.72- Showing the incidence of Aetiological factors in the subjects of

HBV induced Jaundice:

Sl.

No

.

Etiology

Group A Group B Total

No. of

Subject

s

%

No. of

Subject

s

% No. of

Subjects %

1 Blood transfusion 1 6.67% 1 6.67% 2 6.67%

2 Contaminated

needles/syringe 10

66.67

% 8

53.33

% 18 60%

3 Sexual exposure 6 40% 7 46.67

% 13 43.33%

4 Dental surgery 3 20% 2 13.33

% 5 16.67%

2 (6.67%) subjects were giving the history of Blood transfusions, 18 (60%)

Subjects were giving history of received injections. 13 (43.33%) subjects were given

positive history of Sexual exposure and 5 (16.67%) subjects had given history of

Dental surgery.

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Table No. 73 - Showing the incidence of Occupation in the subjects of HBV

induced Jaundice:

Sl.

No. Occupation

Group A Group B Total

No. of

Subjects %

No. of

Subjects %

No. of

Subjects %

1 Housewife 3 20% 4 26.67% 7 23.33%

2 Agriculture 4 26.67% 4 26.67% 8 26.67%

3 Student 2 13.33% 2 13.33% 5 16.67%

4 Businessman 3 20% 3 20% 5 16.67%

5 Private/Govt.

Employee 3 20% 2 13.33% 6 20%

3 (20%) subjects were Housewife’s, 4 (26.67%) Subjects were Agriculturist. 2

(13.33%) subjects were Students, 3 (20.00%) subjects were Businessman and 3

(20.00%) subjects were Private/Government Employees in Group A.

4 (26.67%) subjects were Housewife’s, 4 (26.67%) Subjects were

Agriculturist. 2 (13.33%) subjects were Students, 3 (20%) subjects were

Businessmen and 2 (13.33%) subjects were Private/Government Employees in Group

B.

Table No.74 - Showing the incidence of Poorva roopa in the subjects of HBV

induced Jaundice:

Sl.

No. Poorva roopa

Group A Group B Total

No. of

Subjects %

No. of

Subjects %

No. of

Subjects %

1 Aruchi 14 93.33% 15 100% 29 96.67%

2 Agnimandya 12 80% 13 86.67% 25 83.33%

3 Dourbalya 9 60% 9 60% 18 60%

4 Parswarthi 3 20% 4 26.67% 7 23.33%

5 Kasa 2 13.33% 1 6.67% 3 10%

6 Jwara 11 73.33% 12 80% 23 76.67%

In Group A, 14 (93.33%) of subjects were having Aruchi as poorvaroopa, 12

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(80%) had Agnimandya as poorvaroopa,11 (73.33%) subjects had Jwara, 9(60%)

subjects had Dourbalya, 3 (20%) subjects had Parswarthi and 2(13.33%) had Kasa as

Poorvaroopa. In Group B, 15 (100%) of subjects were having Aruchi as

poorvaroopa, 13 (86.67%) had Agnimandya as poorvaroopa,12 (80%) subjects had

Jwara, 9(60%) subjects had Dourbalya, 4 (26.67%) subjects had Parswarthi and

1(6.67%) had Kasa as Poorvaroopa.

Table No.75 - Showing the incidence of Symptomatology (Roopa) in the subjects

of HBV induced Jaundice:

Sl.

No. Symptomatology

Group A Group B Total

No. of

Subjects %

No. of

Subjects %

No. of

Subjects %

1 Netra peetata 15 100% 15 100% 30 100%

2 Mootra peetata 15 100% 15 100% 30 100%

3 Twak peetata 5 33.33% 5 33.33% 10 33.33%

4 Nakha peetata 12 80% 12 80% 24 80%

5 Jihva Peetata 5 33.33% 5 33.33% 10 33.33%

6 Krishna peeta

purisha 13 86.67% 13 86.67% 26 86.67%

7 Daurbalya 11 73.33% 11 73.33% 22 73.33%

8 Agnimandya 11 73.33% 11 73.33% 22 73.33%

9 Aruchi 14 93.33% 14 93.33% 28 93.33%

10 Jwara 12 80% 12 80% 24 80%

11 Chardi 5 33.33% 6 40% 11 36.67%

12 Kandu 12 80% 12 80% 24 80%

13 Udara shola 7 46.67% 7 46.67% 14 46.67%

Netrapeetata and Mootrapeetata were found as symptom in all the subjects

ie.30 (100%) subjects. Aruchi was found in 28( 93.33%) of subjects. Krishnapeeta

Purisha was found in 26 (86.67%) subjects. Jwara, Kandu and Nakha peetata was

found in 24(80%) of subjects. Krishnapeeta Purisha was found in 26 (86.67%)

subjects. Naka Peetata was found as a symptom in 22(73.33%) of subjects. Daurbalya

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and Agnimandya was found as a symptom in 22(73.33%) of subjects. Udarasoola was

found as a symptom in 14(46.47%) of subjects. Chardi was found as a symptom in 11

(36.67%) of subjects. Jihva Peetata and Twak Peetata were seen in 10(33.33%) ,

Table No. 76. Showing the incidence of Objective Parameters / Invetigations in

the subjects of HBV induced Jaundice

Objective

parameter Group A Total

Average Group B

Total

Average

Sr. Bilirubin 55.1 mg/dl 3.67 mg/dl 61.3 mg/dl 4.08 mg/dl

SGOT 1028iu/L 68.53 iu/L 1118 iu/L 74.53 iu/L

SGPT 1103 iu/L 73.53 iu/L 1166 iu/L 77.73 iu/L

Alk. Phosp. 1422 iu/L 94.8 iu/L 1865 iu/L 124.33 iu/L

Urine BS 22 1.46 25 1.67

HBsAg Positive 15 15

The observation on the Objective parameters/investigation shows an average

of 3.67 mg dl for Serum Bilirubin Total, 68.53IU/L for SGOT, 73.53IU/L for SGPT,

94.8IU/L for Alk. Phosp. In Group A and the observation on the Objective

parameters/investigation shows an average of 4.08 mg dl for Serum Bilirubin Total,

74.53IU/L for SGOT, 77.73IU/L for SGPT, 124.3IU/L for Alk. Phosp. In Group B.

HBsAg was Positive in all of the Subjects

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NASYA KARMA OBSERVATION

Table No. 77 Nasya Karma Observation Chart in 15 Subjects Of Kamala

01 Average Dose Of Jeemootaka

Phalaswarasa Given For Nasya of subjects

In Each Nostrils

7 Drops

02 Average Temprature Of Nasya Dravya

On Administration

390c

Table No.78 Parameters of Nasya observed in 15 subjects of Kamala

Parameters of Nasya Total

Percentage

Laghuta of Siras 12 80%

Sukha Swapna 13 86.67%

Indriya Visudhi 12 80%

Nasa srava 10 66.67%

Parameters of Nasya - Laghuta of Siras was found in 12(80%) of the subjects, Sukha

Swapna was observed in 13(86.67%), Indriya Vishudhi was observed in 12(80%),

and Nasa Srava was complained by 15 (100%) of the subjects.

Table No.79 Complication observed in Nasya Karma in 15 subjects of Kamala

Complication

No. of subjects Percentage

Nasa Srava 15 100%

Weakness 12 80%

Sira shola 14 93.33%

Complication observed in Nasya -On the day of Nasya 15(100%) of the subjects had

Nasaarava and ShiraSoola was observed in 14(93.33%) of the subjects and Weakness

was in 12(80 %) of the subjects.

Table No. 80 Average time taken to relieve Complication observed in Nasya

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Karma in 15 subjects of Kamala

Complication

Time taken for

Full Relief

% Relief after 5

hrs

% Relief after 10

hrs

Nasa Srava 10 hrs 50% 100%

Weakness 12hrs 30% 90%

Sira shola 8.5hrs 50% 100%

Nasasrava was relived in 10hrs in most cases, Weakness was relieved in 12 hrs

in most cases and Sirasoola was relieved in 8.5 hrs after the administration of Nasya

Dravya.

Table No.81 Showing B.P and Pulse reported before and after Nasya Karma

Before Nasya Avg After Nasya Avg

B.P mmHg Systolic 122 130

Diastolic 80 84

Pulse/Min 72 70

Resp Rate/Min 20 18

Blood Pressure was decreased after Nasya from Average 122 to 130 Systolic

and from 80 to 84 diastolic blood pressure. Pulse rate was decreased after Nasya from

average 72 to 70 per minute and respiratory rate was decresed from 20 per minitue to

18 per minute. .

VIRECHANA OBSERVATION

Table No.82 Virechana Karma observation chart in 15 subjects of Kamala

01 Average dose of Patolamooladi Kashaya

given

60ml

02 Average time taken for the beginning of

First Vega

1½ hr

03 Average no of vega 13

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management of HBV induced Jaundice

Table No.83 Assessment of Virechana in 15 Subjects of Kamala

VAIGIKI ANTIKI LAINGIKI

Average no of vega 13 Malanta - Indriya Prasad 13

Kaphanta 9

Pittanta 3 Laghuta 12

Vatanta 3 Vatanulomana 12

Daurbalya 10

Aruchi 08

Table No. 84 Virechana Sudhi Lakshanas wise distribution of 15 subjects of

Kamala

Nature of Sudhi No. of subjects Percentage

Pravar 01 6.67%

Madhyama 12 80%

Avara 02 13.33%

Virechana Sudhi - In maximum number of subjects i.e. 12(80%) had seen

Madhyama sudhi followed by 02(13.33%) subjects Avara sudhi, while 01(6.67%)

subjects were Pravara sudhi in Virechana.

Table No. 85 Complication observed in Virechana Karma in 15 subjects of

Kamala

Complication

No. of subjects Percentage

Vomitting 02 13.33%

Weakness 01 6.67%

Abdominal pain 02 13.33%

Complication observed in Virechana -On the day of Virechana 03(20%) of the

subjects had weakness and vomiting was observed in 02(13.33%) of the subjects and

abdominal pain was in 01(6.67 %) of the subjects.

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Table No.86 Samyak Virechana Lakshan observed in 15 subjects of Kamala

SamyakVirechana Lakshan Total

Percentage

Indriya Prasad 13 86.67%

Laghuta 12 80%

Vatanulomana 12 80%

Daurbalya 10 66.67%

Aruchi 08 53.33%

Samyak Virechana Lakshana - Indriya Prasad was found in 13(86.67%) of the

subjects, Laghuta was observed in 12(80%), Vatanulomana was observed in 12(80%),

Daurbalya was noticed in 10(66.67%) of the subjects, and Aruchi was complained by

08(53.33%) of the subjects.

Table No.87 B.P and Pulse reported before and after Virechana Karma

Before Virechana Avg After Virechana Avg

B.P mmHg Systolic 130 120

Diastolic 84 76

Pulse/Min 72 70

Resp Rate/Min 20 18

Blood Pressure was decreased after Virechana from Average 120 to 110

Systolic and from 80 to 72 diastolic pressure. Pulse rate was decreased after

Virechana from average 72 to 70 per minute .

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management of HBV induced Jaundice

GRAPHS

Graph 1- Showing the incidence of Sex in the subjects of HBV induced Jaundice:

Graph 2 Group A - Showing the incidence of Age in the subjects of HBV induced

Jaundice

Graph 3 Group B - Showing the incidence of Age in the subjects of HBV induced

Jaundice

0

2

4

6

8

15 – 20 21 – 30 31 – 40 41 – 50

No

. of

Pat

ien

ts

Group A - Showing the incidence of Age in the subjects

Total No. of Patients

Male

Female

0

1

2

3

4

5

6

7

15 – 20 21 – 30 31 – 40 41 – 50

No

. of

Pat

ien

ts

Group B - Showing the incidence of Age in the subjects

Total No. of Patients

Male

Female

0

5

10

15

20

25

Group A Group B Total

No

. of

Pat

ien

ts

Showing the incidence of Sex in the subjects of HBV induced Jaundice

Male

Female

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management of HBV induced Jaundice

Graph 4 Showing the incidence of Age in the subjects of HBV induced Jaundice

Graph 5 Showing the incidence of Religion in the subjects of HBV induced

Jaundice:

Graph 6 Showing the incidence of Marital status in the subjects of HBV induced

Jaundice:

0

2

4

6

8

10

12

14

16

11 – 20 21 – 30 31 – 40 41 – 50

No

. of

Pat

ien

ts

Showing the incidence of Age in the subjects

Total No. of Patients

Male

Female

0

5

10

15

20

25

30

Group A Group B Total

No

. of

Pat

ien

ts

Showing the incidence of Religion in the subjects

Hindu

Muslim

Christian

0

5

10

15

20

25

30

Group A Group B Total

No

. of

Pat

ien

ts

Showing the incidence of Marital status in the subjects

Married

Unmarried

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management of HBV induced Jaundice

Graph 7 Showing the incidence of Habitat in the subjects of HBV induced

Jaundice:

Graph 8 Showing the incidence of Food Habits in the subjects of HBV induced

Jaundice:

Graph 9 Showing the incidence of Duration of Illness the subjects of HBV

induced Jaundice:

0

5

10

15

20

Group A Group B Total

No

. of

Pat

ien

ts

Showing the incidence of Habitat in the subjects

Urban

Rural

0

5

10

15

20

25

Group A Group B Total

No

. of

Pat

ien

ts

Showing the incidence of Food Habits in the subjects

Vegetarian

Mixed

0

5

10

15

20

25

Group A Group B Total

No

. of

Pat

ien

ts

Showing the incidence of Duration of Illness the subjects

15 – 45 days

46 – 75 days

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Graph 10 Showing the incidence of Socio-Economic status in the subjects of HBV

induced Jaundice:

Graph 11 Showing the incidence of History of previous treatment received in the

subjects of HBV induced Jaundice

Graph 12 Showing the History of Hepatitis B vaccine received in the subjects of

HBV induced Jaundice:

0

5

10

15

20

25

Group A Group B Total

No

. of

Pat

ien

ts

Showing the incidence of Socio-Economic status in the subjects

Poor

Middle

Rich

0

5

10

15

20

Group A Group B Total

No

. of

Pat

ien

ts

Showing the incidence of History of previous treatment received in the subjects

Received

Not received

0

5

10

15

20

25

30

Group A Group B Total

No

. of

Pat

ien

ts

Showing the History of Hepatitis B vaccine received in the subjects

Received

Not received

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Graph 13 Showing the incidence of Education in the subjects of HBV induced

Jaundice:

Graph 14 Showing the incidence of Habits in the subjects of HBV induced

Jaundice:

Graph 15 Showing the incidence of State of Agni in the subjects of HBV induced

Jaundice

0

2

4

6

8

10

12

14

16

Primary High school Graduate Post Graduate

No

. of

Pat

ien

ts

Showing the incidence of Education in the subjects

Group A

Group B

Total

0

5

10

15

20

Only Alcohol OnlySmoking/tobacco

Alcohol andSmoking

Tea/Coffee

No

. of

Pat

ien

ts

Showing the incidence of Habits in the subjects

Group A

Group B

Total

0

2

4

6

8

10

12

14

Group A Group B Total

No

. of

Pat

ien

ts

Showing the incidence of State of Agni in the subjects

Mandagni

Vishamagni

Teekshanagni

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Graph 16 Showing the incidence of Nature of Koshta in the subjects of HBV

induced Jaundice

Graph 17 Showing Dominent Rasa wise diet of 30 subjects of Kamala

Graph 18 Showing Dominent Guna wise diet of 30 subjects of Kamla

0

5

10

15

20

Group A Group B Total

No

. of

Pat

ien

ts

Showing the incidence of Nature of Koshta in the subjects

Madhyam

Mrudhu

Kroora

0

5

10

15

20

Guru Laghu Ruksha Snigdha Ushna Sheeta Thikshna

Nu

mb

er

of

Sub

ject

s

Showing Dominent Guna wise diet of 30 subjects of Kamlaa

Group A

Group B

Total

02468

101214161820

Madhura Amla Lavana Katu Tikta Kasaya

Nu

mb

er

of

Sub

ject

s

Group A

Group B

Total

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management of HBV induced Jaundice

Graph 19 Showing the incidence of Deha prakruti in the subjects of HBV

induced Jaundice

Graph 20 Showing the incidence of Aetiological factors in the subjects of HBV

induced Jaundice

Graph No 21 - Showing the incidence of Occupation in the subjects of HBV

induced Jaundice:

0

2

4

6

8

10

12

Group A Group B Total

No

. of

Pat

ien

ts

Showing the incidence of Deha prakruti in the subjects

Kapha pitta

Vata pitta

Vata kapha

0

5

10

15

20

Blood transfusion Contaminatedneedles/syringe

Sexual exposure Dental surgery

No

. of

Pat

ien

ts

Showing the incidence of Aetiological factors in the subjects

Group A

Group B

Total

0

2

4

6

8

10

Showing the incidence of Occupation in the subjects of HBV induced Jaundice

Group A No. of Subjects

Group B No. of Subjects

Total No. of Subjects

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Graph No.22- Showing the incidence of Poorva roopa in the subjects of HBV

induced Jaundice

Graph No. 23- Showing the incidence of Symptomatology (Roopa) in the subjects

of HBV induced Jaundice

0

5

10

15

20

25

30

35

Aruchi Agnimandya Dourbalya Parswarthi Kasa Jwara

No

. of

Pat

ien

ts

Showing the incidence of Poorva roopa in the subjects

Group A

Group B

Total

0

5

10

15

20

25

30

35

Group A

Group B

Total

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Graph No 24: Parameters of Nasya observed in 15 subjects of Kamala

Graph 25: Complication observed in Nasya Karma in 15 subjects of Kamala

0

5

10

15

Laghuta of Siras Sukha Swapna Indriya Visudhi Nasa srava

Total

Total

0

5

10

15

20

Nasa Srava Weakness Sira shoola

No. of subjects

No. of subjects

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Graph 26: Virechana Sudhi Lakshanas wise distribution of 15 subjects of

Kamala

Graph 27: Complication observed in Virechana Karma in 15 subjects of Kamala

Graph 28: Samyak Virechana Lakshan observed in 15 subjects of Kamala

7%

80%

13%

No. of subjects

Pravar

Madhyama

Avara

0

0.5

1

1.5

2

2.5

Vomitting Weakness Abdominal pain

No. of subjects

No. of subjects

0

2

4

6

8

10

12

14

Indriya Prasad Laghuta Vatanulomana Daurbalya Aruchi

Total

Total

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RESULTS

SUBJECTIVE PARAMETERS:

Table No.88 - Results of symptom relief in Group A (Nasya):

Sl.

No. Lakshana BT AT

X

(Mean) % SD SE T P Remarks

1 Netra

peetata 2 0.27 1.73 86.67 0.45 0.11 14.66 <0.001 H.S

2 Mootra

peetata 2 0.33 1.67 83.33 0.48 0.12 13.22 <0.001 H.S

3 Twak

peetata 0.67

0.2

0.47 70 0.74 0.19 2.43 <0.10 S

4 Nakha

peetata 1.6 0.2 1.4 87.5 0.82 0.21 2.54 <0.05 S

5 Jihva

Peetata 0.67 0.13 0.53 80 0.83 0.22 2.47 <0.10 S

6

Krishna

peeta

purisha

1.73 0,4 1.33 76.92 0.72 0.18 7.13 <0.001 H.S

7 Daurbalya 1.47 0.47 1 68.18 0.75 0.19 5.12 <0.001 H.S

8 Agnimandya 1.47 0.4 1.06 72.72 0.79 0.20 5.17 <0.001 H.S

9 Aruchi 1.87 0.53 1.33 71.42 0.61 0.15 8.36 <0.001 H.S

10 Jwara 1.6 0.13 1.47 91.67 0.83 0.21 6.81 <0.001 H.S

11 Chardi 0.67 0 0.67 100 0.95 0.25 2.64 <0.02 S

12 Udara shola 1.6 0.4 1.2 75 0.77 0.20 6 <0.001 H.S

13 Kandu 0.93 0.2 0.73 78.51 0.88 0.22 3.21 <0.02 S

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Group A (Nasya):

Netra peetata:

All the subjects presented with Netra Peetata. The mean value of B.T. and

A.T. was 2 and .27 respectively, which gives the relief of 86.67% and statistically

Highly Significant at t = 14.66 and P <0.001. (Table No. )

Mootra peetata:

All the subjects presented with Mootra peetata. The mean value of B.T. and

A.T. was 2 and 0.33 respectively, which gives the relief of 83.33% and statistically

Highly Significant at t = 13.22 and P is less than 0.001. (Table No. )

Twak peetata:

5 subjects presented with this symptom, the mean value of B.T. and A.T. was

0.67 and 0.2 respectively which provides 70% relief which is statistically Significant

at t = 2.43 and P <0.10. (Table No. )

Nakha peetata:

12 subjects presented with this symptom, the mean value of B.T. and A.T. was

1.6 and 0.2 respectively which provides 80% relief which is statistically Highly

Significant at t = 4.67 and P <0.05. (Table No. )

Jihva peetata:

5 subjects presented with this symptom, the mean value of B.T. and A.T. was

0.67 and 0.13 respectively which provides 80% relief which is statistically

Significant at t = 2.47 and P <0. 10. (Table No. )

Krishna Peeta purisha:

13 subjects presented with this symptom, the mean value of B.T. and A.T. was

1.73 and 0.4 respectively which provides 76.92% relief which is statistically Highly

Significant at t = 7.13 and P < 0.001 (Table No. )

Daurbalya:

11 subjects presented with this symptom, the mean value of B.T. and A.T. was

1.47 and 0.47 respectively which provides 68.18% relief which is statistically Highly

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Significant at t = 5.12 and P < 0.001 (Table No. )

Agnimandya:

11 subjects presented with this symptom, the mean value of B.T. and A.T. was

1.47 and 0.4 respectively which provides 72.72% relief which is statistically Highly

Significant at t = 5.17 and P < 0.001 (Table No. )

Aruchi:

14 subjects presented with this symptom, the mean value of B.T. and A.T. was

1.87 and 0.53 respectively which provides 71.42% relief which is statistically Highly

Significant at t = 8.36 and P < 0.001 (Table No. )

Jwara:

Totally 12 subjects presented with Jwara in this group. The mean value of B.T.

and A.T. was 1.6 and 0.13 respectively which shows 91.67% relief and statistically

H.S. at t = 6.81 and P<0.001 (Table No. )

Chardi:

5 subjects presented with this symptom, the mean value of B.T. and A.T. was

0.67 and 0 respectively which provides 100% relief which is statistically Significant

at t = 2.64 and P < 0.02 (Table No. )

Udarashoola:

12 subjects presented with this symptom, the mean value of B.T. and A.T. was

1.6 and 0.4 respectively which provides 75% relief which is statistically Significant at

t = 6 and P < 0.001 (Table No. )

Kandu:

Totally 7 subjects presented with Kandu. The mean value B.T. and A.T. was

0.93 and 0.2 respectively which gives 78.51% relief and is statistically Significant at t

= 3.21 and P <0.02 (Table No. )

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Table No.89 Results of symptom relief in Group B (Virechana):

Sl.

No. Lakshana BT AT

X

(Me

an)

% SD SE T P Rema

rks

1 Netra

peetata 2 0.33 1.67 83.33 0.48 2.11 13.22 <0.001 H.S

2 Mootra

peetata 2 0.27 1.73 86.67 0.45 0.11 14.65 <0.001 H.S

3 Twak

peetata 0.67 0.13 0.53 80 0.83 0.21 2.47 <0.10 S

4 Nakha

peetata 1.6 0.13 1.47 91.67 0.83 0.21 6.81 <0.001 H.S

5 Jihva

Peetata 0.67 0.06 0.6 90 0.91 0.24 2.55 <0.10 S

6

Krishna

peeta

purisha

1.73 0.33 1.4 80.76 0.74 0.19 7.35 <0.001 H.S

7 Daurbalya 1.47 0.4 1.06 72.72 0.79 0.20 5.17 <0.001 H.S

8 Agnimand

ya 1.57 0.33 1.13 77.27 0.83 0.21 5.26 <0.001 H.S

9 Aruchi 1.87 0.46 1.41 75 0.63 0.16 8.57 <0.001 H.S

10 Jwara 1.6 0.2 1.4 87.5 0.82 0.21 6.55 <0.001 H.S

11 Chardi 0.8 0 0.8 100 1.01 0.26 3.05 <0. 05 S

12 Udara

shola 1.6 0.27 1.33 83.33 0.81 0.21 6.32 <0.001 H.S

13 Kandu 0.93 0.13 0.8 85.71 0.94 0.24 3.29 <0.02 S

Group B (Virechana):

Netra peetata:

All the subjects presented with Netra Peetata. The mean value of B.T. and

A.T. was 2 and 0.33 respectively, which gives the relief of 83.33% and statistically

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Highly Significant at t = 13.22 and P <0.001. (Table No. )

Mootra peetata:

All the subjects presented with Mootra peetata. The mean value of B.T. and

A.T. was 2 and 0.27 respectively, which gives the relief of 86.67% and statistically

Highly Significant at t = 14.65 and P is less than 0.001. (Table No. )

Twak peetata:

5 subjects presented with this symptom, the mean value of B.T. and A.T. was

0.67 and 0.13 respectively which provides 80% relief which is statistically Significant

at t = 2.47 and P <0.10. (Table No. )

Nakha peetata:

12 subjects presented with this symptom, the mean value of B.T. and A.T. was

1.6 and 0.13 respectively which provides 91.67% relief which is statistically Highly

Significant at t = 6.81 and P <0.001. (Table No. )

Jihva peetata:

5 subjects presented with this symptom, the mean value of B.T. and A.T. was

0.67 and 0.06 respectively which provides 90% relief which is statistically

Significant at t = 2.55 and P <0.10. (Table No. )

Krishna Peeta purisha:

13 subjects presented with this symptom, the mean value of B.T. and A.T. was

1.73 and 0.33 respectively which provides 80.76% relief which is statistically Highly

Significant at t = 7.35 and P < 0.001 (Table No. )

Daurbalya:

11 subjects presented with this symptom, the mean value of B.T. and A.T. was

1.47 and 0.4 respectively which provides 72.72% relief which is statistically Highly

Significant at t = 5.17 and P < 0.001 (Table No. )

Agnimandya:

11 subjects presented with this symptom, the mean value of B.T. and A.T. was

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1.47 and 0.33 respectively which provides 77.27% relief which is statistically Highly

Significant at t = 5.26 and P < 0.001 (Table No. )

Aruchi:

14 subjects presented with this symptom, the mean value of B.T. and A.T. was

1.87 and 1.46 respectively which provides 75% relief which is statistically Highly

Significant at t = 8.57 and P < 0.001 (Table No. )

Jwara:

Totally 12 subjects presented with Jwara in this group. The mean value of B.T.

and A.T. was 1.6 and 0.2 respectively which shows 87.50% relief and statistically

H.S. at t = 6.54 and P<0.001 (Table No. )

Chardi:

6 subjects presented with this symptom, the mean value of B.T. and A.T. was

0.8 and 0 respectively which provides 100% relief which is statistically Significant at

t = 3.05 and P < 0.05 (Table No. )

Udarashoola:

12 subjects presented with this symptom, the mean value of B.T. and A.T. was

1.6 and 0.27 respectively which provides 83.33% relief which is statistically Highly

Significant at t = 6.32 and P < 0.001 (Table No. )

Kandu:

Totally 7 subjects presented with Kandu. The mean value B.T. and A.T. was

0.93 and 0.13 respectively which gives 85.71% relief and is statistically Significant at

t = 3.29 and P <0.02 (Table No. )

OVERALL RESPONSE ON TOTAL SYMPTOM SCORE:

Group A:

Out of 15 subjects the Total symptom score B.T. and A.T. was 246 and 43

respectively, which provided 82.52% relief. (Table No. )

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Group B:

Out of 15 subjects the Total symptom score B.T. and A.T. was 262 and 55

respectively, which provided 79.01 % relief. (Table No. )

Table No.90 - Results of Biochemical and other Objective parameters in Group

A (Nasya):

Sl.

No

.

Objectiv

e

paramete

r

BT AT

X

(Mean

)

% SD SE T P Remark

s

1 Sr.

Bilirubin 3.67 1.04 2.63 71.69 1.35 0.35 7.50

<0.00

1 H.S

2 SGOT 68.5

3

33.5

3 35 51.07

17.2

7 4.45 7.84

<0.00

1 H.S

3 SGPT 73.5

3

36.4

6 36.89 50.40

15.0

4 3.88 9.53

<0.00

1 H.S

4 Alk.

Phosp. 94.8

53.2

6 41.54 43.81

42.6

0

11.0

1 3.77 <0.01 S

5 Urine BS 1.47 0.06 1.41 95.45 .50 .13 10.6

9

<0.00

1 H.S

6 Urine BP 1.67 0.47 1.2 88 0.51 0.13 11 <0.00

1 H.S

RESULTS ON BIO-CHEMICAL AND OTHER OBJECTIVE PARAMETERS OF GROUP A

(NASYA):

Sr.Bilirubin:

The mean Sr.Bilirubin B.T. and A.T. was 3.67 and 1.04 respectively, which

gives the relief of 71.69% and statistically Highly Significant at t = 7.50 and P

<0.001.

SGOT:

The mean SGOT level B.T. and A.T. was 68.53 and 33.53 respectively, which

gives the relief of 51.04% and statistically Highly Significant at t = 7.84 and P

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<0.001.

SGPT:

The mean SGPT value B.T. and A.T. was 73.53 and 36.46 respectively, which

gives the relief of 50.40% and statistically Highly Significant at t = 9.53 and P

<0.001.

Alkaline Phosphatase:

The mean Alkaline Phosphatase value B.T. and A.T. was 94.80 and 53.26

respectively, which gives relief of 43.81% and statistically Significant at t = 3.77 and

P <0.01.

Urine Bile salt

The mean value for Urine BS, B.T. and A.T. was 1.47 and 0.06 respectively,

which gives relief of 95.45% and statistically Highly Significant at t = 10.69 and P

<0.001.

Urine Bile Pigment:

The mean value for Urine BP, B.T. and A.T. was 1.67 and 0.47 respectively,

which gives relief of 88% and statistically Highly Significant at t = 11 and P <0.001.

Table No. 91 - Results of Bio-chemical and other Objective parameters in Group

B (Virechana):

Sl.

No

.

Objectiv

e

paramete

r

BT AT

X

(Mean

)

% SD SE T P Rem

arks

1 Sr.

Bilirubin 4.09 1.14 2.95

72.1

0 2.32 0.59 4.91

<0.00

1 H.S

2 SGOT 74.53 33.3

3 41.2

55.2

7

22.5

5 5.82 7.07

<0.00

1 H.S

3 SGPT 77.73 36.5

3 41.2

53.0

1

27.5

5 7.11 5.79 <0.01 S

4 Alk.

Phosp.

124.3

3 61.4 62.93

50.6

1

84.2

2

21.7

4 2.89 <0.01 S

5 Urine BS 1.66 0.2 1.46 88 0.51 0.13 11 <0.00

1 H.S

6 Urine BP 1.46 0.06 1.4 95.4

5 .50 .13

10.6

9

<0.00

1 H.S

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RESULTS ON BIO-CHEMICAL AND OTHER OBJECTIVE PARAMETERS OF GROUP B

(VIRECHANA):

Sr.Bilirubin:

The mean Sr.Bilirubin B.T. and A.T. was 4.09 and 1.14 respectively, which

gives relief of 72% and statistically Highly Significant at t = 4.91 and P <0.001.

SGOT:

The mean SGOT level B.T. and A.T. was 74.53 and 33.33 respectively, which

gives relief of 72.10% and statistically Highly Significant at t = 7.07 and P <0.001.

SGPT:

The mean SGPT value B.T. and A.T. was 77.73 and 36.53 respectively, which

gives relief of 53.01% and statistically Significant at t = 5.79 and P <0.01.

Alkaline Phosphatase:

The mean Alkaline Phosphatase B.T. and A.T. was 124.33 and 61.4

respectively, which gives relief of 50.61% and statistically Significant at t = 2.89 and

P <0.01.

Urine Bile salt:

The mean value for Urine BS, B.T. and A.T. was 1.66 and 0.2 respectively,

which gives relief of 88% and statistically Highly Significant at t = 11 and P <0.001.

Urine Bile Pigment

The mean value for Urine BP, B.T. and A.T. was 1.46 and 0.06 respectively,

which gives relief of 95.45% and statistically Highly Significant at t = 10.69 and P

<0.001.

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Table No.92 - Results of test for HBsAg (HBV) by Hepacard method in Group A

(Nasya) and Group B (Virechana):

Results

on

HBsAg

Group A (Nasya) Group B (Virechana)

B.T. A.T. %

relieved

B.T. A.T. %

relieved

Positive 15 7 53.33% 15 9 60%

Negative 0 8 0 6

Group A (Virechana) HBsAg:

Out of 15 HBsAg positive subjects 8 subjects were found HBsAg negative

after treatment. It shows 53.33% relief and it can be said that 8 subjects were fully

cured.

Group B (Nasya) HBsAg:

Out of 15 HBsAg positive subjects 9 subjects were found HBsAg negative

after treatment. It shows 60% relief and it can be said that 9subjects were fully cured.

Table No.93 – Group A showing Sr.Bilirubin (Total) Before and After Nasya :

Sl. No. B.T. A.T. X (Mean) Percentage

1 7.3 2.2 5.1 69.86%

2 3.4 0.8 2.6 76.47%

3 2.6 0.9 1.7 65.38%

4 5.4 1.1 4.3 79.62%

5 1.9 1 0.9 47.36%

6 3.6 0.9 2.7 75%

7 2.4 0.8 1.6 66.67%

8 2.1 0.7 1.4 66.67%

9 5.4 1.2 4.2 77.78%

10 3.6 0.9 2.7 75%

11 4.8 0.8 4 83.33%

12 2.2 1 1.2 54.54%

13 5.1 1.3 3.8 74.50%

14 1.9 0.9 1 52.63%

15 3.4 1.1 2.3 67.64%

Total 55.1 15.6 39.5 71.69%

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Table No.94 –Group B showing Sr.Bilirubin (Total) Before and After Virechana:

Sl. No. B.T. A.T. X (Mean) Percentage

1 11.2 2.4 8.8 78.57%

2 5.4 1.3 4.1 75.92%

3 2.8 0.9 1.9 67.85%

4 2.2 0.8 1.4 63.63%

5 2.3 1.1 1.2 52.17%

6 3.3 1.2 2.1 63.63%

7 7.6 1.8 5.8 76.31%

8 3.1 1 2.1 67.74%

9 2 0.9 1.1 55%

10 4.1 0.8 3.3 80.48%

11 3.8 1.2 2.6 68.42%

12 2.4 0.9 1.5 62.50%

13 7.4 1.2 6.2 83.78%

14 2.1 0.8 1.3 61.90%

15 1.6 0.8 0.8 50%

Total 61.3 17.1 44.2 72.10%

Table No. 95 - Total Response of Therapy (Objective parameters) in Group A

and Group B:(Comparison between Group A and Group B)

Prameters Group A Group B

Percentage Percentage

HBsAg 53.33% 60%

Sr.Bilirubin 71.69%% 72.10%

SGOT 51.07 55.27

SGPT 50.40 53.01

Alk.Phosp 43.81 50.61

Urine Bile Salt 95.45 88.00

Urine Bile Pigment 88 95.45

Overall comparison of the results in Group A and Group B (Objective

parameters)

HBsAg:

In Group A, subjects showed 53.33% response and subjects in Group B 60%

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response.

Sr. Bilirubin:

In Group A, subjects showed 71.69% response and subjects in Group B 55.27%

response.

SGOT:

In Group A, subject showed 51.07% response and subjects in Group B showed

55.27% response.

SGPT:

In Group A, subjects showed 50.40% response and subjects in Group B

showed 53.01% response.

Alkaline Phosphatase:

In Group A, subjects showed 43.81% response and subjects in Group B

showed 50.61% response.

Urine for Bile Salts:

In Group A, subjects showed 95.45% response and subjects in Group B

showed 88% response.

Urine for Bile Pigments:

In Group A, subjects showed 88% response and subjects in Group B showed

95.45% response.

Table No. 96 Comparative Efficacy of Therapies on Assessment Parameters in

Group A and Group B using Unpaired Student ‘t’ test:

Subjective

Parameters

Group A

Group B

Unpaired ‘t’ test

(Group A vs Group B)

Remark

Mean S.D S.E Mean S.D S.E S.D S.E ‘t’ P

Netra peetata 1.73 0.45 0.11 1.67 0.48 2.11 0.93 0.17 0.35 >0.05 NS

Mootra

peetata 1.67 0.48 0.12 1.73 0.45 0.11

0.93 0.17 0.35 >0.05 NS

Twak peetata 0.47 0.74 0.19 0.53 0.83 0.21 1.54 0.49 0.12 >0.05 NS

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Nakha peetata 1.4 0.82 0.21 1.47 0.83 0.21 1.61 0.33 0.21 >0.05 NS

Jihva Peetata 0.53 0.83 0.22 0.6 0.91 0.24 1.62 0.51 0.13 >0.05 NS

Krishna peeta

purisha 1.33 0.72 0.18 1.4 0.74 0.19

1.47 0.29 0.24 >0.05 NS

Daurbalya 1 0.75 0.19 1.06 0.79 0.20 1.50 0.32 0.18 >0.05 NS

Agnimandya 1.06 0.79 0.20 1.13 0.83 0.21 1.59 0.34 0.20 >0.05 NS

Aruchi 1.33 0.61 0.15 1.41 0.63 0.16 1.21 0.23 0.34 >0.05 NS

Jwara 1.47 0.83 0.21 1.4 0.82 0.21 1.66 0.34 0.20 >0.05 NS

Chardi 0.67 0.95 0.25 0.8 1.01 0.26 1.87 0.40 0.85 >0.05 NS

Udara shola 1.2 0.77 0.20 1.33 0.81 0.21 1.56 0.32 0.40 >0.05 NS

Kandu 0.73 0.88 0.22 0.8 0.94 0.24 1.83 0.49 0.14 >0.05 NS

Objective

Parameter

Group A

Group B

Unpaired ‘t’ test

(Group A vs Group B)

Remark

Mean S.D S.E Mean S.D S.E S.D S.E ‘t’ P

Sr. Bilirubin 2.63 1.35 0.35 2.95 2.32 0.59 20.7 0.69 0.46 >0.05 NS

SGOT 35 17.2

7 4.45 41.2

22.5

5 5.82

40.1

4

7.33 0.84 >0.05 NS

SGPT 36.89 15.0

4 3.88 41.3

27.5

5 7.11

44.3

6

8.10 0.54 >0.05 NS

Alk. Phosp. 41.54 42.6

0

11.0

1 62.93

84.2

2

21.7

4

133.

42

24.3

6

0.88 >0.05 NS

Urine BS 1.41 .50 .13 1.46 0.51 0.13 0.98 0.18 0.27 >0.05 NS

Urine BP 1.2 0.51 0.13 1.4 .50 .13 1.04 0.19 1.08 >0.05 NS

Comparative Efficacy of the Therapies in Group A and Group B:

The Mean Score of the parameter ‘Netrapeetata’ in Group A was 1.73, S.D is

0.45 and S.E is 0.11. In Group B, The Mean Score of parameter ‘Netrapeetata’ was

1.67, S.D is 0.48, S.E is 2.11. The Comparative Efficacy of Group A with Group B

was Statistically Not Significant (p<0.01) with S.D 0.93, S.E 0.17 and ‘t’ value of

0.35.

The Mean Score of the Subjective Parameter ‘Mootrapeetata’ in Group A

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was 1.67, S.D is 0.48 and S.E is 0.12. In Group B, The Mean Score of Subjective

Parameter ‘Mootrapeetata’ was 1.73, S.D is 0.45, S.E is 0.11. The Comparative

Efficacy of Group A with Group B was Statistically Not Significant (p>0.05) with

S.D 0.93, S.E 0.17 and ‘t’ value of 0.35.

The Mean Score of the Subjective Parameter ‘Twakpeetata’ in Group A was

0.47, S.D is 0.74 and S.E is 0.19. In Group B, The Mean Score of Subjective

Parameter ‘Twakpeetata’ was 0.53, S.D is 0.83, S.E is 0.21. The Comparative

Efficacy of Group A with Group B was Statistically Not Significant (p>0.05) with

S.D 1.54, S.E 0.49 and ‘t’ value of 0.12.

The Mean Score of the Subjective Parameter ‘Nakapeetata’ in Group A was

1.4, S.D is 0.82 and S.E is 0.21. In Group B, The Mean Score of Subjective Parameter

‘Nakapeetata’ was 1.47, S.D is 0.83, S.E is 0.21. The comparative efficacy of Group

A with Group B was Statistically Not Significant (p>0.05) with S.D 1.61, S.E 0.33

and ‘t’ value of 0.21.

The Mean Score of the Subjective Parameter ‘Jihvapeetata’ in Group A was

0.53, S.D is 0.83 and S.E is 0.22. In Group B, The Mean Score of Subjective

Parameter ‘Jihvapeetata’ was 0.6, S.D is 0.91, S.E is 0.24. The Comparative Efficacy

of Group A with Group B was Statistically Not Significant (p>0.05) with S.D 1.62,

S.E 0.51 and ‘t’ value of 0.13.

The Mean Score of the Subjective Parameter ‘KrishnaPeeta Purisha’ in

Group A was 1.33, S.D is 0.72 and S.E is 0.18. In Group B, The Mean Score of

Subjective Parameter ‘KrishnaPeeta Purisha’ was 1.4, S.D is 0.74, S.E is 0.19. The

Comparative Efficacy of Group A with Group B was Statistically Not Significant

(p>0.05) with S.D 1.47, S.E 0.29 and ‘t’ value of 0.24.

The Mean Score of the Subjective Parameter ‘Daurbalya’ in Group A was 1,

S.D is 0.75 and S.E is 0.19. In Group B, The Mean Score of Subjective Parameter

‘Daurbalya’ was 1.06, S.D is 0.79, S.E is 0.20. The Comparative Efficacy of Group

A with Group B was Statistically Not Significant (p>0.05) with S.D 1.50, S.E 0.32

and ‘t’ value of 0.18.

The Mean Score of the Subjective Parameter ‘Agnimandya’ in Group A was

1.06, S.D is 0.79 and S.E is 0.20. In Group B, The Mean Score of Subjective

Parameter ‘Agnimandya’ was 1.13, S.D is 0.831, S.E is 0.21. The Comparative

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Efficacy of Group A with Group B was Statistically Not Significant (p>0.05) with

S.D 1.59, S.E 0.34 and ‘t’ value of 0.20.

The Mean Score of the Subjective Parameter ‘Aruchi’ in Group A was 1.33,

S.D is 0.61 and S.E is 0.15. In Group B, The Mean Score of Subjective Parameter

‘Aruchi’ was 1.41, S.D is 0.63, S.E is 0.16. The Comparative Efficacy of Group A

with Group B was Statistically Not Significant (p>0.05) with S.D 1.21, S.E 0.23 and

‘t’ value of 0.34.

The Mean Score of the Subjective Parameter ‘Jwara’ in Group A was 1.47,

S.D is 0.83 and S.E is 0.21. In Group B, The Mean Score of Subjective Parameter

‘’Jwara’ was 1.4, S.D is 0.82, S.E is 0.21. The Comparative Efficacy of Group A

with Group B was Statistically Not Significant (p>0.05) with S.D 1.66, S.E 0.34 and

‘t’ value of 0.20.

The Mean Score of the Subjective Parameter ‘Chardi’ in Group A was 0.67,

S.D is 0.95 and S.E is 0.25. In Group B, The Mean Score of Subjective Parameter

‘Chardi’ was 0.80, S.D is 1.01, S.E is 0.26. The Comparative Efficacy of Group A

with Group B was Statistically Not Significant (p>0.05) with S.D 1.87, S.E 0.40 and

‘t’ value of 0.85.

The Mean Score of the Subjective Parameter ‘UdaraShoola’ in Group A was

1.2, S.D is 0.77 and S.E is 0.20. In Group B, The Mean Score of Subjective Parameter

‘Udarashoola’ was 1.33, S.D is 0.81, S.E is 0.21. The Comparative Efficacy of

Group A with Group B was Statistically Not Significant (p>0.05) with S.D 1.56, S.E

0.32 and ‘t’ value of 0.40.

The Mean Score of the Subjective Parameter ‘Kandu’ in Group A was 0.73,

S.D is 0.88 and S.E is 0.22. In Group B, The Mean Score of Subjective Parameter

‘Kandu’ was 0.80, S.D is 0.94, S.E is 0.24. The Comparative Efficacy of Group A

with Group B was Statistically Not Significant (p>0.05) with S.D 1.83, S.E 0.49 and

‘t’ value of 0.14.

The Mean Score of the Objective Parameter ‘Serum Bilirubin Total’ in

Group A was 2.63, S.D is 1.35 and S.E is 0.35. In Group B, The Mean Score of

Objective Parameter ‘Serum Bilirubin Total’ was 2.95, S.D is 2.32, S.E is 0.59. The

Comparative Efficacy of Group A with Group B was Statistically Not Significant

(p>0.05) with S.D 20.7, S.E 0.69 and‘t’ value of 0.46.

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The Mean Score of the Objective Parameter ‘SGOT’ in Group A was 35, S.D

is 17.27 and S.E is 4.45. In Group B, The Mean Score of Objective Parameter

‘SGOT’ was 41.2, S.D is 22.55, S.E is 5.82. The Comparative Efficacy of Group A

with Group B was Statistically Not Significant (p>0.05) with S.D 40.14, S.E 7.33 and

‘t’ value of 0.84.

The Mean Score of the Objective Parameter ‘SGPT’ in Group A was 36.89,

S.D is 15.04 and S.E is 3.88. In Group B, The Mean Score of Objective Parameter

‘’SGPT’ was 41.3, S.D is 27.55, S.E is 7.11. The Comparative Efficacy of Group A

with Group B was Statistically Not Significant (p>0.05) with S.D 44,36, S.E 8.10 and

‘t’ value of 0.54.

The Mean Score of the Objective Parameter ‘Alkaline Phospatase’ in Group

A was 41.54, S.D is 42.60 and S.E is 11.01. In Group B, The Mean Score of

Objective Parameter ‘Alkaline Phospatase’ was 62.93, S.D is 84.22, S.E is 21.74.

The Comparative Efficacy of Group A with Group B was Statistically Not Significant

(p>0.05) with S.D 133.42, S.E 24.36 and ‘t’ value of 0.88..

The Mean Score of the Objective Parameter ‘Urine Bile Salt’ in Group A was

1.41, S.D is 0.50 and S.E is 0.13. In Group B, The Mean Score of Objective

Parameter ‘Urine Bile Salt’ was 1.46, S.D is 0.51, S.E is 0.13. The Comparative

Efficacy of Group A with Group B was Statistically Not Significant (p>0.05) with

S.D 0.98, S.E 0.18 and ‘t’ value of 0.27.

The Mean Score of the Objective Parameter ‘Urine Bile Pigment’ in Group A

was 1.2, S.D is 0.51 and S.E is 0.13. In Group B, The Mean Score of Objective

Parameter ‘Urine Bile Pigment’ was 1.4, S.D is 0.50, S.E is 0.13. The Comparative

Efficacy of Group A with Group B was Statistically Not Significant (p>0.05) with

S.D 1.04, S.E 0.19 and ‘t’ value of 1.08.

Overall Response on Subjective Parameters:

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Table No.97-Total Response of Therapy (Subjective parameters) in Group A and

Group B:

(Comparison between Group A and Group B)

Response of Therapy

Group A Group B

No. of

Subjects % No. of Subjects %

Excellent >75% 8 53.33% 6 40%

Good 50 – 75% 4 26.67% 5 33.33%

Moderate 25 – 50% 3 20% 4 26.67%

No Response 0 – 25% 0 0% 0 0%

Out of 15 subjects in Group A, 8 (53.33%) subjects showed Excellent

response. 4 (26.67%) subjects showed Good response and 3 (20%) subject showed

moderate response to therapy. Out of 15 subjects in Group B, 6 (40%) subjects

showed Excellent response. 5 (33.33%) subjects showed Good response to therapy

and 4 (26.67%) subjects showed moderate response to therapy.

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DISCUSSION

Ayurveda is based on scientific ways of its kind. Facts mentioned in Ayurvedic

classics are not merely stands on imaginations or logical interpretations but are written after

careful investigations, observations and experimentations. Ancient research methodology

has also accepted the importance of discussion prior coming to any conclusion. A theory is

accepted only after the proper reasoning hence; discussion is a critical part of any scientific

research.

This section includes the following

1. Discussion on Literary review

2. Discussion on Materials and Methods

3. Discussion on Observations

4. Discussion on results

1. DISCUSSION ON LITERARY REVIEW

Hepatitis B is an infectious inflammatory illness of the liver caused by the hepatitis

B virus (HBV) that affects hominoidea, including humans. Charaka and Vagbhata have

opined that the nomenclature of the diseases need not be over emphasized. Instead,

management is more stressed on the basis of Dosha and Dushya. Ayurveda documented

that infectious disease in the form of Agantuka rogas or Sankramaka rogas. The

Symptomatology of HBV induced jaundice resembles that of Kamala roga.

Different Acharyas has mentioned a wide range of Nidana for Kamala Roga.The

entire nidana aspect of Kamala can be broadly divided into 5 headings as Kamala as a

nidanarthakara vyadhi of Pandu and other diseases, Pittala ahara vihara sevana by

pittolbana purisha, Specific nidana of Shākhasrita Kamala, Specific nidanas of both the

types of Kamala and Indirect nidana of Kamala. Caraka and Vagbhata have stated that

Kamala is Rakta pradoshaja and is due to Rakta vaha sroto dusti respectively.

Considering the Samprapti of Kamala, the Ranjaka Pitta deviated from its

normal path gets into Rakta Dhatu (circulation). This condition may be viewed as the

hyper Bilirubinaemia present in Jaundice. Ranjaka Pitta, which is circulated along

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with the blood, gets settled in Twak, Dhatu and other areas in loose elastic tissues,

which also constitute shakha. This is the actual stage of manifestation of disease,

which can also be called the Icteric phase of the Hepatocellular Jaundice in general

and Hepatitis in particular. The Ranjaka Pitta just deposited results in the symptoms

such as peetata of netra, mootra, twak, rakta and purish etc.

Specific Poorvarupas for Kamala have not been mentioned either in Brihatrayi or in

Laghutrayi. Vagbhata defined Poorvarupa as Alpavyaktatvam and hence the rupa with less

intensity (Alpabala) can be considesed as Poorva Roopa of Kamala (Swatantraja).

Considering Roopa of Kamala, Charaka Samhita stated Haridra netrata, Haridra

mootra, Haridra twak, Tila Pishta Nibha Varchas , Aatopa , Vishtambha , Guruna hridayena

, Dourbalya , Alpagni, Parswarthi, Hikka, Kasa , Aruchi,and Jwara.

Charaka samhita classified the disease kamala into two types as Koshta shakhashrita

kamala, and Shakhashrita kamala. Koshta Shakhashrita kamala is a paratantra vyadhi. It

manifests as a sequel to panduroga, or due to some other disease. Charaka samhita has used

the term ‘Bahupitta kamala’ as a synonym to the Koshta Shakhashrita kamala. Shakhashrita

kamala is ‘Swatantra vyadhi’. Chakrapani termed this kamala as ‘Alpapitta kamala’.

Sushrutasamhita has stated that, kamala is a later stage of Pandu roga or any other disease.

Kumbha kamala, Lagharaka, Alasa and Haleemaka are its different stages.

Samanya Chikitsa sutra of Kamala explained in different classics

differently.Kamala can be treated by Snehana, Mrudu, Virechana and

Shamanaoushadhi.Astanga Hridaya opines to adopt Pittahara chikitsa along with the above

measures. Even he is in favor of Anjana Chikitsa. In Sushruta samhita, Kamala is

considered as one of the varieties of Panduroga and Panduroga Chikitsa sutra is indicated

for Kamala. In Yoga Ratnakar clear Chikitsa krama is mentioned for Kamala. They are

Snehana, Virechana and he has also indicated Anjana and Nasya along with the above

measures.From the above classical references we can frame the line of treatment of Kamala

as Deepana and Pachana, Snehana, Virechana, Nasya, Anjana and Shamanoushadhi.

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2. DISCUSSION ON MATERIALS AND METHODS

MATERIALS:

I. Hareetakyadi Yoga for Amapachana

II. Jimutak Phala Swarasa for Nasya (Group A)

III. Patolamooladi Kashaya for Virechana (Group B)

IV. Nimbatwakadi Kashaya as Shamanoushadhi

I. Hareetakyadi Yoga for Amapachana

Hareetakyadi yoga consists of Haritaki, Amalaki, Vacha, Vidanga, Rajani, Pippali

Shunti, Saindava Lavana,and Guda. The drugs of the combination have predominantly

Thikta, Katu,Lavana,rasa and has got excellent Amapachana and Deepana Property.

Amapachana is should be done before any Shodana Therapy for 3 to 5 days.

II. Jimutaka Phala Swarasa for Nasya (Group A)

The clear description regarding the mode of action of Nasya karma is not available

in Ayurvedic classics. Jimutakaa is Teekshna, Ashukari, Vyavayi and Vikasi in property. It

produces irritation in the nasal mucosa.

It is an experimentally proved fact that where any type of irritation takes place in

any part of the body, the local circulation is always increased. This is the result of natural

protection, function of the body. Because of irritation a thin serous secretion starts from the

nasal cavity. Even it is practically observed in our clinical trial.

In Jaundice due to the affinity of Bilirubin towards elastic tissue on sclera, Bilirubin

gets deposited. Jimutakaa phala Nasya irritates in the nasal mucosa, then as stated above

circulation increases. So as a result of natural protection, function of the body increases the

lacrimal secretion.

When provocation of Doshas takes place in Shiras due to irritating effect of

administered drug resulting increase the blood circulation of brain. So extra accumulated

morbid doshas are expelled out from small blood vessels. Ultimately the morbid doshas are

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thrown out along with the nasal discharge, tears and by salivation.

Through lacrimal secretion Bilirubin, which is deposited is eliminated (excreted).

Here along with the lacrimation even drugs may be helping in the removal of Bilirubin

from sclera and circulation.

The Vyavayi guna of drug is responsible for quick absorption. The Vikasi guna

causing Mrudutva and Shithilatva (softening and Loosing) of the strotovibandha i.e. Dosha

dushya sammurchana. Due to Ushna guna, the Dosha sanghata (compactness)

vishyandhana is getting Vilayana (Liquefied). Action of Tikshna guna is to break the mala

and dosha in microforms. Due to Sukshma guna, by reaching in micro-channels,

disintegrates endogenic toxins, which are then excreted through micro-channels

(Anupravana bhava).

It is also observed that the drug belongs to Cucurbitaciae family (Luffa species),

and some of the Upavisha dravyas are getting absorbed from a particular site in the body

and getting resecreted from the same site. Jimutaka is a magic drug if instilled through the

nostrils getting absorbed through the mucosa of nasopharynx and getting resecreted from

the same site along with mucopolypeptides, bile and other accumulated enzymes.

III. Patolamooladi Kashaya For Virechana( Group B)

Patola

Patola consists of the root of Trichosanthes dioica Roxb.. (Fam. Cucurbitaceae);

Root is a drastic purgative and useful in jaundice, anasarca and ascites. The important

chemical constituent is Glucoside (Picrorhizin). It has got Rasa – Tikta, Guna - Laghu,

Snigdha, Veerya – Ushna, Vipaka – Katu. It does the Karmas Vedanasthapana, Keshya,

Vranashodhana, Vranaropana, Deepana, Pachana, Anulomana, Rechana, Pittasaraka,

Trishnanigrahana, Krirnighna, Raktashodhaka, Hridya, Shothahara, Kaphaghna,

Kushthaghna, Jwaraghna, Balya, Vrishya, Vishaghna.

Due to its Predominant Tikta Rasa property, it is Pittashamaka and acts as Kamala

samaka. Due to its Pittasaraka Karma it increases sara guna of Pitta Dosa, and removes

Pitta from body by its Rechana Karma.

Katuki

Katuki consists of the dried rhizome with root of Picrorhiza kurroa Royle ex Benth.

(Fam. Scrophulariaceae); a perennial, more or less hairy herb common on the northwestern

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Himalayas from Kashmir to Sikkim. Rhizome is cut into small pieces and is used in

formulations. The important chemical constituent is Glucoside (Picrorhizin). It has got Rasa

: Katu, Tikta, Guna: Laghu, Virya: Ushna, Vipaka: Katu. It does the Karmas : Hridya ,

Pittahara, Deepini, Bhedini, Jwarahara

Katuki is Pittahara, and Kamalahara due to its Tikta rasa. It is Bhedhini and leads to

Virechana karma.

Haritaki

Haritaki consists of the pericarp of mature fruits of Terminalia chebula Retz.(Fam.

Combretaceae), a moderate sized or large tree found throughout India. The important

chemical constituents are Tannins, anthraquinones and polyphenolic compounds.It has got

Rasa: Madhura, Amla, Katu, Tikta, Kashaya, Guna: Laghu, Rooksha, Virya: Ushna,

Vipak: Madhura. It does the Karmas :Chakshushya, Deepana, Hridya, Medhya,

Sarvadosaprasamana, Rasayana, Anulomana.

Due to its Madhura rasa and Vipaka It is Pitta nasaka. It has got all Rasas with

exception of lavana Rasa and acts as Sarvadosha samaka also. It is anulomana in Karma

and acts as Virechana oushada.

Vibhitaki

Viibhitaki consists of pericarp of dried ripe fruits of Terntinalia belerica Roxb.

(Fam. Combretaceae),and is a large deciduous tree. The important chemical constituents

are Gallic acid, tannic acid and glycosides. It has got Rasa : Kashaya, Guna : Laghu,

Ruksha, Virya : Ushna Vipaka : Madhura. It does the Karmas : Chakshushya, Kesya,

Kaphapittajith, Bhedaka, Kriminasana, Kasahara.

In Vipaka, Vibhitaki is Madhura and acts as Pittasamaka, and due to its Bhedana

karma it acts as Virechana Oushada.

Amalaki

Amalaki consists of pericarp of dried mature fruits of Emblica officinalis Gaertn.

Syn. Phyllanthus emblica Linn. (Fam. Euphorbiaceae). The important chemical constituents

are Ascorbic acid and gallotannins. It has got Rasa: Madhura, Amla, Katu, Tikta, Kashaya.

Guna : Laghu, Ruksha. Virya : Seeta. Vipaka : Madhura. It does the Karmas :

Chakshushya, Rasayana, Tridoshajit, Vrisya.

Due to its Madhura rasa, Tikta rasa, Madhura Vipaka, Seeta veerya, Amalaki acts

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as Pitta samaka and thus is kamala nasaka.

Visala

Visala consists of dried root of Trichosanthes bracteata (Lam.) Voigt (Fam.

Cucurbitaceae), and is a large perennial. The important chemical constituents are Saponins,

trichosanthin. It has got Rasa : Katu. Thikta, Guna : Laghu, Ruksha, Virya : Ushna, Vipaka

: Katu. It does the Karmas : Kaphahara, Pittahara, Vamaka, Visagna, Prasutikruta.

Visala is Thikta Rasa and acts as Pitta Kapha samaka, thus acts as Kamala samaka.

Brahmi

Brahmi consists of dried whole plant of Bacopa monnieri (Linn.) Wettst., Syn.

Herpestis monnieria (LiM.) H.B.& K. (Fam. Scrophulariaceae); a glabrous, succulent,

small, prostrate or creeping annual herb, found throughout India in wet and damp places.

The important chemical constituent is Alkaloids. It has got Rasa : Madhur, Tikta, Kashaya,

Guna : Laghu, Sara, Virya : Seeta, Vipaka : Madhura. It does the Karmas: Kaphahara,

Medhya, Rasayana, Swarya, Vatahara, Visahara, Ayushya, Matiprada, Prajnasthapana,

Mohahara.

Due to its Madhura, Tikta Rasa, Seeta Virya, and Madhura Vipaka, Brahmi is

Pittasamaka, and thus Kamalanasaka. Due to its Sara Guna, it acts as Virechaka.

Shunti

Shunti consists of dried rhizome of Zingiber officinale Roxb. (Fam. Zinglberaceae),

widely cultivated in India, rhizomes dug in January-February, buds and roots removed,

soaked overnight-in water, decorticated, and some times treated with lime and dried. The

important chemical constituents are Essential oil, pungent constituents (gingerol and

shogaol), resinous matter and starch. It has got Rasa : Katu, Guna : Laghu, Snigdha, Virya :

Ushna, Vipaka : Madhura. It does the Karmas: Anuloma, Deepana, Hridya, Pachana,

Vatakaphapaha, Asmadosahara.

Due to its Katu Rasa it is Amapachana. Madhura Vipaka makes it Pittashamaka, Its

Anulomana Karma makes it a good constituent of Patolamooladi kashaya for virechana.

Action of Patolamooladi Kashaya

Most of the Drugs in Patolamooladi Kashaya have Madhura, Katu Thikta Rasa,

Ushna Veerya, Laghu, Snigdha, Sara, Vikashi, Tikshna Guna, and Madhura Vipaka. Most

of the Drugs are Raktashodaka, Pithasaraka,and Deepana. Patola, Brahmi Katuki, Visala,

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and Hareetaki which are present in Kashaya have Bhedana property which are the main

drugs acting in Virechana Karma. All the other drugs are supporting drugs in Amapachana

or Pithasamana.

Mode of action of Virechana In Kamala

Virechana is the main treatment for pitta predominant Vyadhi. Kamala being one,

Virechana has importance in its management. Virechana drug (Patolamooladi Kashaya)

gets absorbed and because of its Veerya, it reaches Hridaya, from hridaya to Dhamanis and

thereafter reaches to Sthula and Anustrotas i.e. macro and micro channels of the body

(Anupravana bhava)

The Vyavayi guna of drug is responsible for quick absorption.

The Vikasi guna causing Mrudutva and Shithilatva (softening and Loosening) of the

strotovibandha – Dosha dushya sammurchana.

Due to Ushna guna, the Dosha sanghata (compactness) vishyandhana is getting

Vilayana (Liquified)

Action of Tikshna guna is to break the mala and dosha in microforms. According to

Dalhana it is responsible for quick excretion, secretion and discharge of sanchita

mala.

Due to Sukshma guna, by reaching in micro-channels, disintegrates endogenic

toxins, which are then excreted through micro-channels (Anupravana bhava)

Due to its Ashukari nature it spreads quickly all over the body and immediate effect

is attained.

Due to Prabhava mainly and also due to predominance of Pruthvi and Jala

mahabhuta, finally Virechana occurs. This is the evacuation action.

Apakarshana is one of the major Karma attained by the Virechana dravya. Naturally

Patola Mooladi Kashaya causes Dosha apakarshana, Malapakarshana and even

Apakarshana of Krimi. Though in Viral Hepatitis the Krimi (virus) is in invisible form. The

principle of Krimi chikitsa benefits a lot. Virechana dravya generally due to its krimihara

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and krimishodhana nature, removes the virus deposited in the Liver and present in the

biliary secretion, seen in circulation and which is observed in the body fluids.

Due to the prerequisite procedure like Mridusnehana and Swedana an atmosphere is

created in the Sharira, which prepares Shariragata dushita dosha and mala to come out.

Virechaka dravya are mainly irritants. They induce mild inflammatory changes on

the digestive mucosa and localized tissues. Owing to the increased permeability of the

membranes the transportation and excretion of the waste materials takes place easily.

IV. Nimbatwakadi Kashaya as Shamana Aushadi

Nimba

Nimba consists of dried root bark of Azadirachta indica A. Juss. syn.

Meliaazadirachta Linn. (Fam. Meliaceae), a medium to large evergreen tree. The important

chemical constituents are Tetranortriterpenoids, margocin, nimbidiol, nimbolicin,

azadirinin. It has got Rasa : Tikta, Guna : Laghu, Virya : Seeta, Vipaka : Katu. It does the

Karmas : Kandugna, Kaphahara, Pittahara, Ruchya, Deepana, Visagna, Vrinashodana.

Due to its tikta rasa, Seeta Virya, Nimba acts as Pitta Samaka. Its Visagna and

Vrinashodana Karmas shows its action on Raktavaha Srotas , which is the site of desease

pathology in Kamala, thus making it an excellent drug of choice in the treatment of

Kamala/Hepatitis B.

Haritaki

Haritaki consists of the pericarp of mature fruits of Terminalia chebula Retz.(Fam.

Combretaceae), a moderate sized or large tree found throughout India. The important

chemical constituents are Tannins, anthraquinones and polyphenolic compounds.It has got

Rasa: Madhura, Amla, Katu, Tikta, Kashaya, Guna: Laghu, Rooksha, Virya: Ushna,

Vipak: Madhura. It does the Karmas :Chakshushya, Deepana, Hridya, Medhya,

Sarvadosaprasamana, Rasayana, Anulomana

Due to its Madhura rasa and Vipaka It is Pitta nasaka. It has got all Rasas with

exception of lavana Rasa and acts as Sarvadosha samaka also. It is anulomana in Karma

and acts as Virechana oushada.

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Vibhitaki

Viibhitaki consists of pericarp of dried ripe fruits of Terntinalia belerica Roxb.

(Fam. Combretaceae),and is a large deciduous tree. The important chemical constituents

are Gallic acid, tannic acid and glycosides. It has got Rasa : Kashaya, Guna : Laghu,

Ruksha, Virya : Ushna Vipaka : Madhura. It does the Karmas : Chakshushya, Kesya,

Kaphapittajith, Bhedaka, Kriminasana, Kasahara.

In Vipaka, Vibhitaki is Madhura and acts as Pittasamaka, and due to its Bhedana

karma it acts as Virechana Oushada.

Amalaki

Amalaki consists of pericarp of dried mature fruits of Emblica officinalis Gaertn.

Syn. Phyllanthus emblica Linn. (Fam. Euphorbiaceae). The important chemical constituents

are Ascorbic acid and gallotannins. It has got Rasa: Madhura, Amla, Katu, Tikta, Kashaya.

Guna : Laghu, Ruksha. Virya : Seeta. Vipaka : Madhura. It does the Karmas :

Chakshushya, Rasayana, Tridoshajit, Vrisya.

Due to its Madhura rasa, Tikta rasa, Madhura Vipaka, Seeta veerya, Amalaki shown

to be Pitta samaka and thus is kamala nasaka.

Patola

Patola consists of the root of Trichosanthes dioica Roxb.. (Fam. Cucurbitaceae);

Root is a drastic purgative and useful in jaundice, anasarca and ascites. The important

chemical constituent is Glucoside (Picrorhizin). It has got Rasa – Tikta, Guna - Laghu,

Snigdha, Veerya – Ushna, Vipaka – Katu. It does the Karmas Vedanasthapana, Keshya,

Vranashodhana, Vranaropana, Rochana, Deepana, Pachana, Anulomana, Rechana,

Pittasaraka, Trishnanigrahana, Krirnighna, Raktashodhaka, Hridya, Shothahara,

Kaphaghna, Kushthaghna, Jwaraghna, Balya, Vrishya, Vishaghna.

Patola is Tikta rasa and is Pitta shamaka. Katu vipaka gives amapachana property.

Its Vedanasthapana Karma makes it effective in relieving Abdominal pain and tenderness.

It is Jwaragna and helps in relieving fever which is a preliminary symptom of Hepatitis B.

It is raktashodaka and acts in blood, which is the site of pathology in Hepatitis and helps in

reducing viral load and thus relieving Hepatitis infection.

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Rajani

Rajani consists of the dried and cured rhizomes of Curcuma longa Linn. (Fam.

Zingiberaceae), a perennial herb extensively cultivated in all parts of the country, when

lower leaves turn yellow rhizomes carefully dug up with hand-picks between October-April

and cured by boiling and dried. The important chemical constituents are Essential oil and a

colouring matter (curcumin). It has got Rasa : Katu, Tikta, Guna :Ruksha, Virya : Ushna,

Vipaka : Katu. It does the Karmas: Krimigna, Varnya, Visagna, Kaphapittanut,

Pramehanasaka.

Rajani is Krimigna, Varnya and Visagna, which shows action on Raktavaha srotas.

It has got a proved Anti –Viral action which is the main property that makes it an excellent

drug of choice in kamala/ hepatitis B.

Vasa

Vasa consists of fresh, dried, mature leaves of Adhatoda vasica Nees (Fam.

Acanthaceae), a sub-herbaceous bush, found throughout the year in plains and sub-

Himalayan tracts in India. The important chemical constituents are Alkaloids and essential

oil. It has got Rasa : Tikta, Kashaya, Guna : Laghu, Virya : Seeta, Vipaka :Katu. It does the

Karmas: Hridya, Kaphapittahara, Raktasangrahika, Kasagna.

Vasa is Tikta rasa, Seeta Virya and acts as Pitta shamaka and helps in reducing

dushta pitta circulating in blood and thus relieves Kamala.

Guduchi

Guduchi consists of dried, matured pieces of stem of Tinospora cordifolia (Willd.)

Miers. (Fam, Menispermaceae), a perennial climber found throughout Tropical India. The

important chemical constituents are Terpenoids and alkaloids. It has got Rasa :Tikta,

Kashaya, Guna :Laghu, Virya : Ushana , Vipaka :Madhura. It does the Karmas :Balya,

Deepana, Rasayana, Sangrahi, Tridoshasamaka, Raktasodhaka, Jwaragna.

Guduchi is Tikta rasa and Madhura Vipaka and thus Pittasamaka. It is Balya and

Rasayana and helps in relieving general weakness of Kamalarogi. It is Raktasodhaka and

helps to remove Viral load of Hepatitis B virus. Its Jwaragna Karma helps to relieve Fever

and chills shown to be presenting complaints of HBV induced Jaundice Patients.

Sariva

Sariva consists of root of Hemidesmus indicus (Linn.) R. Br. (Fam.

Asclepiadaceae), a prostrate or semi-erect shrub found throughout India from upper

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Gangetic plains east-wards to Assam, throughout Central, Western and Southern India upto

an elevation of 600 m. The important chemical constituents are Easential oil, saponin, resin,

tannins, sterols and glucosides. It has got Rasa :Madhura, Guna: Guru, Snigda, Virya

:Seeta, Vipaka : Madhura. It does the Karmas: Raktasodhaka, Visagna, Tridoshanasa,

Deepana, Amanasana, Jwarahara.

Sariva is Madhura rasa, Seeta virya, and Madhura Vipaka, Making it Pithasamaka.

It also acts as Raktasodhaka and Visagna showing its action in reducing HBV Viral load. It

also acts as Jwaragna.

Trivrut

Trivrt consists of dried root of Operculina turpethum (Linn.) Silva Manso Syn.

Ipomoea turpethum R. Br. (Fam. Convolvulaceae); a large perennial twiner with milky

juice and fleshy roots, found growing wild nearly throughout the country. The important

chemical constituents are Resinous Glycosides. It has got Rasa : Madhura, Katu, Tikta,

Kashaya. Guna : Laghu, Ruksha, Tikshana. Virya :Uahna. Vipaka : Katu. It does the

karmas : Kaphapittahara, Pittahara, Vatala, Virechana, Sukhavirechaka, Jwarahara.

Trivrut is Madhura, tikta rasa making it Pittahara. It is Sukhavirechaka in Karma,

making it to help body to remove excess pitta dosha present in Kamala rogi without excess

excertion or fatique. It is also Jwarahara in Karma.

Palasa

Palasa consists of dried stem bark of Butea monosperma (Lam.) Kuntze (Fam.

Fabaceae); a medium sized tree with somewhat crooked trunk. The important chemical

constituents are Kinotannic acid and Gallic acid. It has got Rasa : Katu, Tikta, Kashaya,

Guna : Sara, Snigdha, Virya : Ushna, Vipaka : Katu. It does the Karmas: Vrishya,

Kaphavtasamaka, Agnideepaka, Saraka.

Palasa is Katu,Titkta rasa, Ushna Virya, and Katu Vipaka making it Amapachana

and Agnideepaka which helps in relieving Aruchi, and Agnimandya present in Kamala

Rogi.

Bala

Bala consists of dried roots of Sida cordifolia Linn. (Fam. Malvaceae), an erect

annual or perennial undershrub, 1.5 m high, distributed throughout the country especially in

moist regions, ascending to an altitude of 1800 m in the Himalayas. The important

chemical constituent is Alkaloids (ephedrine). It has got Rasa : Madhura, Guna : Laghu,

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Snigdha, Pichila, Virya : Seeta, Vipaka : Madhura. It does Karmas: Vata-Pittahara, Balya,

Brahmana, Vrishya.

Bala is Madhura rasa, Seeta virya, Madhura Vipaka, and Laghu Snigda, Pichila in

Guna making it Pittahara and Vatahara. It is Balya and helps in relieving general weakness

present in Kamala rogi.

Neeli

Neeli consists of dried root of Indigofera tinctoria Linn. (Fam. Fabaceae); a shrub,

1.2-1.8 m high, found throughout and widely cultivated in many parts of the country. The

important chemical constituent is Glycoside (Indican). It has got Rasa : Katu, Tikta, Guna :

Sara, Virya : Ushna, Vipaka: Katu. It does the Karmas: Kaphahara, Kesya, Rechani,

Vatahara, Bhrama Mohahara.

Neeli being Katu Tikta rasa, Sara guna, Katu Vipaka, helps in amapachana. Sara

guna helps to liquify Dosha and Its Rechana Karma helps to remove it through Gudamarga,

helping Kamala rogi to relive the disease.

Yashtimadhu

Yashti consists of dried, unpeeled, stolon and root of Glycyrrhiza glabra Linn,

(Fam. Leguminosae) , a tall perennial herb, upto 2 m high found cultivated in Europe.

Persia, Afghanistan and to little extent in some parts of India. The important chemical

constituents are Glycyrrhizin, glycyrrhizic acid, glycyrrhetinic acid, asparagine, sugars,

resin and starch. It has got Rasa : Madhura, Guna : Guru, Snigdha, Virya : Sita, Vipaka :

Madhura. It does the Karmas : Balya, Chakshushya, Vrishya, Varnya, Vatapittajith,

Raktaprasadana.

Yashtimadhu is Madhura rasa, Seeta virya and Madhura Vipaka, making it

Pithasamaka. It is Balya and Helps to relieve weakness.

Sthira

Sthira consists of dried root of Desmodium gangeticum DC. (Fam. Fabaceae), a

nearly erect under shrub, 0.6 -1.2 m high, growing wild almost throughout India in the

plains and Western Ghats, and upto 1500 m in the north upto Sikkim. The important

chemical constituent is Alkaloids. It has got Rasa : Madhura, Tikta, Guna : Guru,Virya :

Ushna, Vipaka : Madhura. It does Karmas: Balya, Tridoshahara, Vrishya, Visahara,

Angamardaprasamana, Sukhaprasavakara, Sarvadoshahara, Vatadoshajit, Rasayani,

Bhramahara, Santapanasini.

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Sthira is Madhura Thikta rasa and Madhura Vipaka and thus Vatadoshajith and

pithahara. It has got action in raktavahasrotas.

Mode of action of Nimbatwakadi Kashaya

Nimbatwakadi kashaya consists of Nimba, Hareetaki, Vibhitaki, Amalaki, Patola,

Rajani, Vasa, Guduchi, Sariva, Trivrut, Palasa, Bala, Neeli, Yashtimadhu, and Sthira. Of

which Nimba, Hareetaki, Vibhitaki, Amalaki, Vasa, Guduchi, Sariva, Trivrut,

Yashtimadhu, and Sthira are Pitta Samaka due to Madhura Tiktha rasa and sheeta veerya

predominance. It helps in relieving Pittadosha Pradana symptoms like Netra peetata,

Mootrapeetata, Jihwa, Twak and Naka Peetata. Nimba, patola, rajani, vasa, guduchi and

sariva has got action on raktavahasrothas, ie rakthasodhaka action, with the exception of

vasa which has raktasthambana Karma. These drugs help in purification of blood and

removal of viral debris. Bala and yashtimadhu are balya and helps to relive weakness due

to Kamala. Guduchi , patola and,trivrut are Jwarahara. Guduchi and Rajani are

hepatoprotective in function. Palasa, Patola, and Hareetaki are deepana and Pachana helps

to relieve agnimandya in Kamala. Patola is vedanasthapana in Karma and helps to relieve

abdominal Pain and tenderness. Hareetaki, Amalaki, Guduchi, and Sthira are Rasayana in

Karma, helps in rejuvenation of damaged Hepatic cells in Liver. Rajani is anti viral and its

action on Viral disorders are proved to be excellent.

Trivrut is sukhavirechaka, Neeli and Patola are Rechaka, Vibhitaki is Bhedaka, and

Haritaki is Anulomaka which helps in removing pitha dosha through gudamarga. Giving

Nimbatwakadi Kashaya as SamanaOushadi thus helps in Pradidina Mruduvirechana. Thus

it helps in removing Malavarodha and Pittadosha from body, leading to relief in kamala.

Thus Nimbatwakadi Kashaya is an excellent combination of drugs which are

hepatoprotective, Pithadosha samana, and anti-viral. It is highly potent enough to give relief

to all of the symptoms of the HBV induced Jaundice-Kamala.

3. DISCUSSION ON OBSERVATIONS

1. Discussion on Incidence of Sex in the subjects of HBV induced Jaundice:

12 subjects (80%) were males and 3 (20%) were females in Group A and 11

(73.33%) subjects were males and 4 (26.67%) females in Group B.

The observed incidence of sex shows more males are affected in the vicinity than

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females may be correlated to more exposure of disease to males than females.

2. Discussion on Incidence of AGE in the subjects of HBV induced Jaundice

1 subject (20%) were between age group of 15 – 20 years out of this 4 (13.33%)

were males and 2 (06.67%) were females. 9 (30%) subjects were between the age group of

21 – 30 years in that 7 (23.33%) were males and 2 (06.67%) were females. 10 (33.33%)

subjects were between 31 – 40 years of age, in that 7 (23.33%) were males and 3 (10%)

were females. 5 (16.67%) subjects were between 41 – 50 years of age, in that 3 (10%) were

males and 2 (06.67%) were females in Total.

The subjects were included in study from 15 to 50 yrs of age. Maximum incidence

was from age group 31 to 40 ie 10 subjects and 21 to 30 ie 9 subjects. Age has got no much

importance in the incidence of HBV induced Jaundice, but the result shows that the

working age group especially males, were infected, may be correlated to more exposure to

the disease.

3. Discussion on Incidence of Religion in the subjects of HBV induced Jaundice:

14 (93.33%) subjects belonged to Hindu religion, whereas 1 (6.67%) subject

belonged to Muslim community in Group A. 13 (86.67%) subjects belonged to Hindu

religion , 1 (6.67%) subjects belonged to Muslim community and 1 (6.67%) subjects

belonged to Christian community in Group B.

The incidence rate of subjects according to religion expresses only the geographical

predominance of communities in the locality, were study was conducted.

4. Discussion on Incidence of Marital status in the subjects of HBV induced

Jaundice:

These distribution shows that 12 (80%) subjects were married, whereas 3 (20%)

subjects were unmarried in Group A and in Group B.

Sexual exposure is one of the major causes of Hepatitis B Virus induced jaundice.

Comparatively married subjects are having more incidence here shows no significance in

the present study as in most married subjects partners were uninfected.

5. Discussion on Incidence of Habitat in the subjects of HBV induced Jaundice:

9 (60%) subjects belonged to Urban area whereas 6 (40%) subjects belonged to

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Rural area in Group A. 8 (53.33%) subjects belonged to Urban area and 7 (46.67%)

subjects belonged to Rural area in Group B.

The observation on incidence of Habitat in subjects shows that more incidence was

from urban area, shows more subjects were from locality, as the vicinity of study was urban

area.

6. Discussion on Incidence of Food Habits in the subjects of HBV induced Jaundice:

11 (73.33%) subjects were consuming vegetarian diet whereas 4 (26.67%) subjects

belonged to Mixed diet catogory in Group A. 10 (66.67%) subjects belonging to vegetarian

category and 5 (33.33%) subjects belonged to Mixed diet in Group B.

Non- vegetarian diet is a supporting factor for the disease manifestation. But in the

observation, it is shown that incidence of subjects were more from the Vegetarian group,

shows the food habit pattern of the population studied.

7. Discussion on Incidence of Duration of Illness the subjects of HBV induced

Jaundice:

The duration of illness were recorded according to the statement of the subjects

from the onset of the symptoms of Jaundice. 11 (73.33%) subjects were giving the history

of onset of the disease between 15-45 days after the onset of the Jaundice, whereas 4

(26.67%) subjects were giving the history of onset of disease between 46-75 days duration

in Group A. 9 (60%) subjects were giving the history of onset of disease between 15-45

days duration after the onset of the Jaundice where as 6(40%) subject had given history of

onset of disease between 46-75 days duration in Group B.

Most subjects will be coming for Ayurvedic treatment, when the symptoms of

Kamala are well-defined like that of Netrapeetata and Mootrapeetata. In most cases

symptoms will be shown within the period of 15 to 45 days. So as observation shows,

incidence of subjects was more from 15 to 45 days after the onset of disease. Less number

of subjects turned up after 45 days, as they may seek other contemporary treatments, and

thereafter turned to Ayurvedic treatment.

8. Discussion on Incidence of Socio-Economic status in the subjects of HBV induced

Jaundice:

Study of the socio-economic status of the subjects revealed that 3 (20%) subjects in

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group A and in group B were poor.11 (73.33%) subjects in group A and 12 (80%) subjects

in group B were Middle class. 1 (6.67%) subject in group A was from Rich class.

This observation shows the demographic pattern of socio-economic status in the

vicinity of study.

9. Discussion on Incidence of History of previous treatment received in the subjects

of HBV induced Jaundice:

Study on the incidence of history of previous treatment received in the subjects

revealed that 5 (33.33%) subjects in group A and 7 (46.67%) subjects in group B received

previous treatment. 10 (66.67%) subjects in group A and 8 (53.33%) subjects in group B

did not receive any previous treatment.

Most population of the locality is aware of the fact that Ayurveda do possess

effective treatment in the management of Kamala. The observation underlines the fact as

most subjects did not receive any previous treatment. In the rural areas some subjects

received folklore medicine, which was not effective in curing the disease fully.

10. Discussion on History of Hepatitis B vaccine received in the subjects of HBV

induced Jaundice:

Study on the history of Hepatitis B vaccine received in the subjects revealed that 3

(20.00%) subjects in group A and 2 (13.33%) subjects in group B received Hepatitis B

vaccine. 12 (80.00%) subjects in group A and 13 (86.67%) subjects in group B did not

receive Hepatitis B vaccine.

Most of the subjects were not undergone Hepatitis B vaccination Schedule. The

subjects who received also did not take the full course of vaccination Schedule. So the

Observation did not express lacuna of Vaccination schedule.

11. Discussion on Incidence of Education in the subjects of HBV induced Jaundice:

7 (46.67%) subjects in group A and in group B were having Primary education. 4

(26.67%) subjects in group A and 5 (33.33%) subjects in group B had High school

education. 2 (13.33%) subjects in both group A and in group B were having Graduation

and 2 (13.33%) subjects in group A, 1 (6.67%) subject in group B had Post Graduate

education.

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Literacy rate and Education rate has got no impact on the incidence of disease. Lack

of knowledge about cleanliness, hygene, mode of transmission of disease, etc may affect

the incidence of disease.

12. Discussion on Incidence of Habits in the subjects of HBV induced Jaundice:

2 (13.33%) subjects in group A and 1 (6.67%) subject in group B, were having the

habit of drinking Alcohol only. 7 (46.67%) subject in group A and 8 (53.33%) subjects in

group B were having only Smoking or Chewing Tobacco as habit. 1 (6.67%) subject in

group A and 3 (20%) subjects in group B, were having the habits of Alcohol and Smoking

together. 5 (33.33%) subjects in group A and 3 (20%) subjects in group B were having the

habits of drinking Tea/Coffee.

Chewing tobacco was a common habit in every range of people in the vicinity of

study. Alcaholism was also much common. Even though these habbits are not the direct

cause of HBV induced Jaundice, they act as vitiating factors which will increase the

severity and duration of symptoms of disease.

13. Discussion on Incidence of State of Agni in the subjects of HBV induced Jaundice:

In-group A, 7 (46.67%) subjects were having Mandagni, 6 (40%) Subjects were

having Vishamagni and 2 (13.33%) Subjects were having Teekshnagni. In-group B 6

(40%) subjects were having Mandagni and 7 (46.67%) subjects were having Vishamagni

and 2 (13.33%) Subjects were having Teekshnagni.

Mandagni and Vishamagni may be considered as the root cause of most diseases.

After the manifestation of HBV induced Jaundice, subjects developed Agnimandya and it

leads to expression of other symptoms of disease like Jwara, Chardi, Aruchi etc.

14. Discussion on Incidence of Nature of Koshta in the subjects of HBV induced

Jaundice:

In total 10 (33.33%) subjects were having Madhyam Koshta and 4 (13.33%)

Subjects were having Mrudhu Koshta and 16 (53.33%) subjects had Kroora Koshta.

Koshta as such does not correlate any pathogenesis in this study.

15. Discussion on Dominent Rasa wise diet of 30 subjects of Kamala

Amla Rasa consumers were maximum 19(63.33%) subjects, followed by Katu Rasa

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17(56.67%) subjects, Lavana Rasa 13(43.33%) subjects and Madhura Rasa 10(33.33%)

subjects and Tikta Rasa 1(3.33%) subject.

This observation shows that most of the subjects were consuming Amla-Katu Rasa

Pradana Ahara. Amla Katu Rasa Pradana Ahara Sevana leads to vitiation of Pitta dosha and

causes aggravation of symptoms of Kamala.

16. Discussion on Dominent Guna wise diet of 30 subjects of Kamlaa

16(53.33%)subjects were consumers of Rooksha Guna and 50% ie 15 subjects were

consuming Teekshna Guna Pradhana Ahara, followed by Ushna Guna 11(36.67%), Guru

8(26.67%) ,Laghu Guna 4(13.33%) and finally Snigdha Guna and Sheeta Guna

2(6.67%)subjects each.

This observation shows that most of the subjects were consuming Rooksha and

Theekshna Guna pradana Ahara. Rooksha and Theekshna Guna pradana Ahara sevana also

leads to vitiation of Pitta Dosha and aggravation of symptoms of Kamala Roga.

17. Discussion on Incidence of Deha prakruti in the subjects of HBV induced

Jaundice:

8 (26.67%) subjects were having Kapha pitta prakruti, 11 (36.67%) Subjects were

having Vata pitta prakruti and 11 subjects (36.67%) were having Vata kapha prakruti.

KaphaPitta Prakruti Purusha are prone to get Kapha and Pitha Predominant

disorders. As Kamla is a Pitha Predominant disorder, the chance of getting this Disease is

more in case of Pitta predominant Purusha. Study requires a wider range of subjects for the

correct assessment of relation between Deha Prakruti and Manifestation of Kamala.

18. Discussion on Incidence of Aetiological factors in the subjects of HBV induced

Jaundice:

2 (6.67%) subjects were giving the history of Blood transfusions, 18 (60%) Subjects

were giving history of received injections. 13 (43.33%) subjects were given positive history

of Sexual exposure and 5 (16.67%) subjects had given history of Dental surgery.

As currently understood, this disease is mainly transmitted through infected blood

and blood products and other physiological and pathological secretions. The observations

of the study also support this view.

19. Discussion on Incidence of Occupation in the subjects of HBV induced Jaundice:

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3 (20%) subjects were Housewife’s, 4 (26.67%) Subjects were Agriculturist. 2

(13.33%) subjects were Students, 3 (20.00%) subjects were Businessman and 3 (20.00%)

subjects were Private/Government Employees in Group A.

4 (26.67%) subjects were Housewife’s, 4 (26.67%) Subjects were Agriculturist. 2

(13.33%) subjects were Students, 3 (20%) subjects were Businessmen and 2 (13.33%)

subjects were Private/Government Employees in Group B.

The occupational incidence of Hepatitis B is considered to be more in the

professionals like laboratory workers, dentists, surgeons, parental drug abusers and people

engaging in high risk of sexual activity. However, as the sample size in the present study

was small, the impact of occupation on the disease cannot be predicted.

20. Discussion on Incidence of Poorva roopa in the subjects of HBV induced

Jaundice:

In Group A, 14 (93.33%) of subjects were having Aruchi as poorvaroopa, 12 (80%)

had Agnimandya as poorvaroopa,11 (73.33%) subjects had Jwara, 9(60%) subjects had

Dourbalya, 3 (20%) subjects had Parswarthi and 2(13.33%) had Kasa as Poorvaroopa.

In Group B, 15 (100%) of subjects were having Aruchi as poorvaroopa, 13

(86.67%) had Agnimandya as poorvaroopa,12 (80%) subjects had Jwara, 9(60%) subjects

had Dourbalya, 4 (26.67%) subjects had Parswarthi and 1(6.67%) had Kasa as

Poorvaroopa.

As per the Observation on incidence on Poorvaroopa, most subjects experienced

one or more Poorva roopa of the disease. Amoung the Poorvaroopa of Kamala, Aruchi,

Agnimandya and Jwara were predominant showing intial phase of Koshtasrita dosha

dooshya sammorchana.

21. Discussion on Incidence of Symptomatology (Roopa) in the subjects of HBV

induced Jaundice:

Netrapeetata and Mootrapeetata were found as symptom in all the subjects

ie.30 (100%) subjects. Aruchi was found in 28( 93.33%) of subjects. Krishnapeeta Purisha

was found in 26 (86.67%) subjects. Jwara, Kandu and Nakha peetata was found in 24(80%)

of subjects. Krishnapeeta Purisha was found in 26 (86.67%) subjects. Naka Peetata was

found as a symptom in 22(73.33%) of subjects. Daurbalya and Agnimandya was found as a

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symptom in 22(73.33%) of subjects. Udarasoola was found as a symptom in 14(46.47%) of

subjects. Chardi was found as a symptom in 11 (36.67%) of subjects. Jihva Peetata and

Twak Peetata were seen in 10(33.33%).

Hepatitis B is a disease, which mainly gives rise to a good number of somatic

symptoms mainly involving the symptoms of digestive system. Yellowish discoloration of

sclera, urine, skin, tongue, and stools are other cardinal features of the disease. In this study

the above symptoms were present in all the patients.

22. Discussion on Incidence of Objective Parameters / Invetigations in the subjects of

HBV induced Jaundice

In Kamala Roga, Liver function test results will be deranged. The observation on

the Objective parameters/investigation shows an average of 3.67 mg dl for Serum Bilirubin

Total, 68.53IU/L for SGOT, 73.53IU/L for SGPT, 94.8IU/L for Alk. Phosp. In Group A

and the observation on the Objective parameters/investigation shows an average of 4.08 mg

dl for Serum Bilirubin Total, 74.53IU/L for SGOT, 77.73IU/L for SGPT, 124.3IU/L for

Alk. Phosp. In Group B. HBsAg was Positive in all of the Subjects

DISCUSSION ON NASYA KARMA OBSERVATION

Parameters of Nasya observed in 15 subjects of Kamala

Siro Laghuta was found in 12 , Sukha Swapna was found in 13, Indriya Visudhi in

12 and Nasa srava was complained in 15 of subjects. Jeemotaka Nasya was a Theekshna

Virechana Nasya. Nasal irritation and resulting Sirogurutwa, and Nasa srava will persist for

long after Nasya karama. So all of the subjects did not experienced Samyak Nasya

Lakshanas.

Complication observed in Nasya Karma in 15 subjects of Kamala

On the day of Nasya 15(100%) of the subjects had Nasaarava and ShiraSoola was

observed in 14(93.33%) of the subjects and Weakness was in 12(80 %) of the subjects.

Due to the Teekshanatha of Jeemutaka Phala Nasya, the Complictions observed were

anticipated and proper medication was administered to relieve the same.

Average time taken to relieve Complication observed in Nasya Karma in 15 subjects

of Kamala

Nasasrava was relived in 10hrs in most cases, Weakness was relieved in 12 hrs in

most cases and Sirasoola was relieved in 8.5 hrs after the administration of Nasya Dravya.

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Almost all the complications relieved after 12 hrs or in same day of administration of

Nasya and thus was able to continue treatment on next day.

B.P and Pulse reported before and after Nasya Karma

Blood Pressure was increased after Nasya from Average 122 to 130 Systolic and

from 80 to 84 diastolic Blood Pressure. Pulse rate was decreased after Nasya from average

72 to 70 per minute and respiratory rate was decresed from 20 per minitue to 18 per minute.

Jeemoothaka Phala Nasya being Irritation to the Nasal Passage, as a response to

body mechanism, BP was increased at first. Later the BP was reduced to Normal.

DISCUSSION ON VIRECHANA OBSERVATION

Assessment of Virechana in 15 Subjects of Kamala

Average number of Vega in Virechana was 13.Antiki Observation on Virechana

Shows 9 subjects had Kaphanta virechana and 3 subjects each as Pittanta and Vatanta

virechana. Laingiiki Observations on Virechana showed Indriya Prasada in 13 subjects,

Vatanulomana and Laghuta in 12 subjects each, Daurbalya in 10 and Aruchi in 08 subjects.

Virechana Sudhi Lakshanas wise distribution of 15 subjects of Kamala

In maximum number of subjects i.e. 12(80%) had seen Madhyama sudhi followed

by 02(13.33%) subjects Avara sudhi, while 01(6.67%) subjects were Pravara sudhi in

Virechana.

Complication observed in Virechana Karma in 15 subjects of Kamala

On the day of Virechana 03(20%) of the subjects had weakness, and vomiting was

observed in 02(13.33%) of the subjects and abdominal pain was in 01(6.67 %) of the

subjects. After the Virechana, fluid loss from body was more in some subjects leading to

weakness. Vomiting happened in some subjectsas complication because of the rejection of

Virechana aushada, due to excess dose, or mridu koshta of the subjects. Abdominal pain

was present in one subject, because of lesser dose of aushada and resulting amolpatti.

Samyak Virechana Lakshan observed in 15 subjects of Kamala

Indriya Prasad was found in 13(86.67%) of the subjects, Laghuta was observed in

12(80%), Vatanulomana was observed in 12(80%), Daurbalya was noticed in 10(66.67%)

of the subjects, and Aruchi was complained by 08(53.33%) of the subjects. These

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observations shows the proper elimination of doshas in Virechana

B.P and Pulse reported before and after Virechana Karma

Blood Pressure was decreased after Virechana from Average 120 to 110 Systolic

and from 80 to 72 diastolic pressure. Pulse rate was decreased after Virechana from average

72 to 70 per minute .

4. DISCUSSION ON RESULTS:

SUBJECTIVE PARAMETERS:

Discussion on Results of symptom relief in Group A (Nasya):

Netra peetata:

All the subjects presented with Netra Peetata. The mean value of B.T. and A.T. was

2 and .27 respectively, which gives the relief of 86.67% and statistically Highly Significant

at t = 14.66 and P <0.001.

Jihva peetata:

5 subjects presented with this symptom, the mean value of B.T. and A.T. was 0.67

and 0.13 respectively which provides 80% relief which is statistically Not Significant at t =

2.47 and P <0. 10.

Netra peetata and Jihwa Peetata shows localized manifestation of pitta dosha over

Netra and Jihwa. Jeemootaka Nasya shows excellent result in eliminating Jathru

Oordwagata Pitta dosha especially from Netra but less from Jihwa.

Mootra peetata:

All the subjects presented with Mootra peetata. The mean value of B.T. and A.T.

was 2 and 0.33 respectively, which gives the relief of 83.33% and statistically Highly

Significant at t = 13.22 and P is less than 0.001.

Kleda nirvahana is the Karma of Mootra. Mootra peetata shows removal of

Sakagata Pitta dosha and Kleda through Mootra as the part of body mechanism. Relief in

Mootra peetata shows reduction in Sakagata Pitta dosha ie in circulation. Thus the result

shows Jeemootaka Phala Nasya has got systemic effect on circulation in removing excess

Pitta dosha and thus relieving the disease.

Twak peetata:

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5 subjects presented with this symptom, the mean value of B.T. and A.T. was 0.67

and 0.2 respectively which provides 70% relief which is statistically Significant at t = 2.43

and P <0.10.

Nakha peetata:

12 subjects presented with this symptom, the mean value of B.T. and A.T. was 1.6

and 0.2 respectively which provides 80% relief which is statistically Highly Significant at t

= 4.67 and P <0.05.

Twak and Naka peetata shows Sakagata Pitta sthanasamsraya in Twak and Naka..

Nasya was not significant enough to remove Pitta, which is deposited over Twak and Naka.

Krishna Peeta purisha:

13 subjects presented with this symptom, the mean value of B.T. and A.T. was 1.73

and 0.4 respectively which provides 76.92% relief which is statistically Highly Significant

at t = 7.13 and P < 0.001

The Krishna Peeta Purisha is caused by the effect of disease on raktavaha sroto

moolam ie.Yakrut. Purisha get its normal colour and consistency as a result of normal

functioning of Yakrut. The excellent result shows Jeemootaka Phala Nasya has got

regenerative action over yakrut and its functions.

Daurbalya:

11 subjects presented with this symptom, the mean value of B.T. and A.T. was 1.47

and 0.47 respectively which provides 68.18% relief which is statistically Highly Significant

at t = 5.12 and P < 0.001

Daurbalya shows lack of proper nutrition. As a result of improper functioning of

yakrut, the appetite will be less and the food consumed will not be digested properly. So

nourishing will be improper leading to Daurbalya. This excellent result shows the action of

Jeemootaka Phala nasya over Yakrut and its functional aspects.

Agnimandya:

11 subjects presented with this symptom, the mean value of B.T. and A.T. was 1.47

and 0.4 respectively which provides 72.72% relief which is statistically Highly Significant

at t = 5.17 and P < 0.001

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Agnimandya can be correlated to lack of digestive enzymes. The production of

these enzymes are mainly carried out in Yakrut. The result on agnimandya underlines the

action of Jeemootaka Phala nasya over Yakrut and its functional aspects.

Aruchi:

14 subjects presented with this symptom, the mean value of B.T. and A.T. was 1.87

and 0.53 respectively which provides 71.42% relief which is statistically Highly Significant

at t = 8.36 and P < 0.001

Asya and Jihwa Upalepatham will be present in Kamala. Due to this Upalepatwam,

Aruchi may occur. Jeemoothaka Phala Nasya shows excellent result in the removal of

Upalipta Doshas from Asya and Jihwa.

Jwara:

Totally 12 subjects presented with Jwara in this group. The mean value of B.T. and

A.T. was 1.6 and 0.13 respectively which shows 91.67% relief and statistically H.S. at t =

6.81 and P<0.001

Chardi:

5 subjects presented with this symptom, the mean value of B.T. and A.T. was 0.67

and 0 respectively which provides 100% relief which is statistically Significant at t = 2.64

and P < 0.02

Jwara and Chardi occurs due to Amasayagata Amolpathi. Jeemootaka Phala Nasya

preceeded by Amapachana in present study shows excellent result in removing Ama and

Dushta Pitha from body.

Udarashoola:

12 subjects presented with this symptom, the mean value of B.T. and A.T. was 1.6

and 0.4 respectively which provides 75% relief which is statistically Significant at t = 6 and

P < 0.001

The Udarasoola can be correlated to the pain and tenderness of abdominal region

especially over liver. As said earlier, the Jeemootaka Phala Nasya has got Action over

Liver (Yakrut), it helps in relieving pain and tenderness over liver region.

Kandu:

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Totally 7 subjects presented with Kandu. The mean value B.T. and A.T. was 0.93

and 0.2 respectively which gives 78.51% relief and is statistically Significant at t = 3.21

and P <0.02

Kandu may be caused by the deposition of Kleda over skin. As stated earlier the

systemic or circulatory action of the Jeemootaka Phala nasya is underlined in the result on

Kandu.

Discussion on Results of symptom relief in Group B (Virechana):

Netra peetata:

All the subjects presented with Netra Peetata. The mean value of B.T. and A.T. was

2 and 0.33 respectively, which gives the relief of 83.33% and statistically Highly

Significant at t = 13.22 and P <0.001

Netra peetata shows localized manifestation of pitta dosha over Netra. Virechana

being primary Pittahara Shodana Chikitsa, removes Sakagata Pittadosha through

gudamarga and showed excellent result in Netra peetata.

Mootra peetata:

All the subjects presented with Mootra peetata. The mean value of B.T. and A.T.

was 2 and 0.27 respectively, which gives the relief of 86.67% and statistically Highly

Significant at t = 14.65 and P is less than 0.001

Mootra peetata shows removal of Sakagata Pitta dosha and Kleda through Mootra

as the part of body mechanism. Relief in Mootra peetata shows reduction in Sakagata Pitta

dosha ie in circulation. Thus the excellent result shows Virechana with Patolamooladi

Kashaya is potent to bringing excess Pittadosha circulating in body to Koshta and removing

it through Gudamarga.

Twak peetata:

5 subjects presented with this symptom, the mean value of B.T. and A.T. was 0.67

and 0.13 respectively which provides 80% relief which is statistically Significant at t = 2.47

and P <0.10.

Nakha peetata:

12 subjects presented with this symptom, the mean value of B.T. and A.T. was 1.6

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and 0.13 respectively which provides 91.67% relief which is statistically Highly Significant

at t = 6.81 and P <0.001.

Twak and Naka peetata shows Sakagata Pitta Sthanasamsraya in Twak and Naka.

The the excellent result shows Virechana with Patolamooladi Kashaya is potent to bringing

Sakagata Pittadosha to Koshta and removing it through Gudamarga. Even though the action

of Virechana on Twak peetata is shown to be Not Significant, Percentage relief shown was

not ignorable.

Jihva peetata:

5 subjects presented with this symptom, the mean value of B.T. and A.T. was 0.67

and 0.06 respectively which provides 90% relief which is statistically Not Significant at t =

2.55 and P <0.10.

Jihwa peetata is due to the Sthanasamsraya of Pittadosha over Jihwa Pradesha.

Virechana being the main Pittahara shodana Chikitsa, was able to remove excess pitha from

body. The excellent percentage relief underlines this fact even though result was not

statistically significant.

Krishna Peeta purisha:

13 subjects presented with this symptom, the mean value of B.T. and A.T. was 1.73

and 0.33 respectively which provides 80.76% relief which is statistically Highly Significant

at t = 7.35 and P < 0.001

The Krishna Peeta Purisha may be caused due to improper function of ranchaka

pitha and Pachaka Pitha. Removing Dushta Pitta from Koshta through GudaMarga in

Virechana makes the Vitiation of Pitha dosha to come down and regains the Mala

Ranchana Karma and Pachana of Ahara. The result on Krishna Peeta varchas shows this

action.

Daurbalya:

11 subjects presented with this symptom, the mean value of B.T. and A.T. was 1.47

and 0.4 respectively which provides 72.72% relief which is statistically Highly Significant

at t = 5.17 and P < 0.001

Daurbalya shows lack of proper nutrition. The excellent result on Daurbalya shows

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the action of Virechana over Yakrut and its functional aspects in improving digestion and

Nourishing of body.

Agnimandya:

11 subjects presented with this symptom, the mean value of B.T. and A.T. was 1.47

and 0.33 respectively which provides 77.27% relief which is statistically Highly Significant

at t = 5.26 and P < 0.001

Removal of Dushta Pitha present in Koshta was done by Virechana. Samsargana

Krama helps to relive the Agnimandya and improve Jadaragni slowly. The excellent result

on Agnimandya after Virechana followed by Samsargana Krama highlights this aspect.

Aruchi:

14 subjects presented with this symptom, the mean value of B.T. and A.T. was 1.87

and 1.46 respectively which provides 75% relief which is statistically Highly Significant at

t = 8.57 and P < 0.001

Virechana helps in relieving Pitha Upalepatwa over jihwa and Aasya present in

Kamala roga. The excellent result on Aruchi underlines this aspect.

Jwara:

Totally 12 subjects presented with Jwara in this group. The mean value of B.T. and

A.T. was 1.6 and 0.2 respectively which shows 87.50% relief and statistically H.S. at t =

6.54 and P<0.001

Pitta dosha is the main dosha involved in Jwara. The excess Pitta dosha will be

removed by Virechana. The Excellent result of Virechana on Jwara highlights this aspect.

Chardi:

6 subjects presented with this symptom, the mean value of B.T. and A.T. was 0.8

and 0 respectively which provides 100% relief which is statistically Significant at t = 3.05

and P < 0.05

Amatwa was removed from Koshta by Virechana. This helps in relief of Chardi in

subjects. The result also underlines this fact.

Udarashoola:

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12 subjects presented with this symptom, the mean value of B.T. and A.T. was 1.6

and 0.27 respectively which provides 83.33% relief which is statistically Highly Significant

at t = 6.32 and P < 0.001

The Udarasoola can be correlated to the pain and tenderness of abdominal region

especially over liver. As the channels of Yakrut is blocked by Klada in Kamla Rogi, the

Yakrut became enlarged leading to Yakrutodara and in later stage leads to Jalodara. The

pain over the region of Yakrut goes on increasing on accumulation of more and more

Kleda. Virechana helps in removing Kleda through Guda marga after bringing it to Koshta.

The excellent result over Udarasoola by Virechana Highlights this aspect.

Kandu:

Totally 7 subjects presented with Kandu. The mean value B.T. and A.T. was 0.93

and 0.13 respectively which gives 85.71% relief and is statistically Significant at t = 3.29

and P <0.02

As circulating Kleda is removed by Virechana, diposition of Kleda over Twak is

reduced and thereby Kandu is reduced or relieved. The excellent result over Kandu by

Virechana shows this aspect.

DISCUSSION ON OVERALL RESPONSE ON TOTAL (SUBJECTIVE PARAMETERS )SYMPTOM

SCORE:

Group A:

Out of 15 subjects the Total symptom score B.T. and A.T. was 246 and 43

respectively, which provided 82.52% relief.

Group B:

Out of 15 subjects the Total symptom score B.T. and A.T. was 262 and 55

respectively, which provided 79.01 % relief.

Kamala roga is predominantly due to Pitha dosha. Virechana is the main treatment

for pithanirharana. But in the study, the relief of total symptom score is shown more in case

of Nasya. Even though Pitha nirharana may be more in Virechana Karma, Jeemootaka

Phala Nasya Karma has got more specific action over symptoms and the sites studied in

this thesis.

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DISCUSSION ON COMPARISON OF RESULTS ON BIO-CHEMICAL AND OTHER OBJECTIVE

PARAMETERS BETWEEN GROUP A (NASYA) AND GROUP B ( VIRECHANA):

Sr.Bilirubin:

In group A the mean Sr.Bilirubin B.T. and A.T. was 3.67 and 1.04 respectively,

which gives the relief of 71.69% and statistically Highly Significant at t = 7.50 and P

<0.001

In group B the mean Sr.Bilirubin B.T. and A.T. was 4.09 and 1.14 respectively,

which gives relief of 72% and statistically Highly Significant at t = 4.91 and P <0.001.

Both groups showed almost same results which are statistically highly significant.

SGOT:

In group A the mean SGOT level B.T. and A.T. was 68.53 and 33.53 respectively,

which gives the relief of 51.04% and statistically Highly Significant at t = 7.84 and P

<0.001.

In group B the mean SGOT level B.T. and A.T. was 1118 and 500 respectively,

which gives relief of 72.10% and statistically Highly Significant at t = 7.07 and P <0.001.

Both groups showed statistically highly significant results. The percentage

improvement was more in case of Group B (Virechana).

SGPT:

In group A the mean SGPT value B.T. and A.T. was 73.53 and 36.46 respectively,

which gives the relief of 50.40% and statistically Highly Significant at t = 9.53 and P

<0.001.

In group B the mean SGPT value B.T. and A.T. was 77.73 and 36.53 respectively,

which gives relief of 53.01% and statistically Significant at t = 5.79 and P <0.01.

Both groups showed almost same results which are statistically highly significant.

Alkaline Phosphatase:

In group A the mean Alkaline Phosphatase value B.T. and A.T. was 94.80 and

53.26 respectively, which gives relief of 43.81% and statistically Significant at t = 3.77 and

P <0.01.

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In group B the mean Alkaline Phosphatase B.T. and A.T. was 124.33 and 61.4

respectively, which gives relief of 50.61% and statistically Significant at t = 2.89 and P

<0.01.

Both groups showed statistically significant results. The percentage improvement

was more in case of Group B (Virechana).

Urine Bile salt

In group A the mean value for Urine BS, B.T. and A.T. was 1.47 and 0.06

respectively, which gives relief of 95.45% and statistically Highly Significant at t = 10.69

and P <0.001.

In group B the mean value for Urine BS, B.T. and A.T. was 1.66 and 0.2

respectively, which gives relief of 88% and statistically Highly Significant at t = 11 and P

<0.001.

Both groups showed statistically highly significant results. The percentage

improvement was more in case of Group A (Nasya).

Urine Bile Pigment:

In group A the mean value for Urine BP, B.T. and A.T. was 1.67 and 0.47

respectively, which gives relief of 88% and statistically Highly Significant at t = 11 and P

<0.001.

In group B the mean value for Urine BP, B.T. and A.T. was 1.46 and 0.06

respectively, which gives relief of 95.45% and statistically Highly Significant at t = 10.69

and P <0.001.

Both groups showed statistically highly significant results. The percentage

improvement was more in case of Group B (Virechana).

HBsAg:

Out of 15 HBsAg positive subjects in Group A, 8 subjects were found HBsAg

negative after treatment. It shows 53.33% relief and it can be said that 8 subjects were fully

cured.

Out of 15 HBsAg positive subjects in Group B, 9 subjects were found HBsAg

negative after treatment. It shows 60% relief and it can be said that 9subjects were fully

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cured.

Both groups showed almost similar results in parameter of HBsAg.

Discussion on Overall Response on Parameters of study:

Total Response of Therapy (Subjective parameters) in Group A and B:

(Comparison between Group A and Group B)

Out of 15 subjects in Group A, 8 (53.33%) subjects showed Excellent response. 4

(26.67%) subjects showed Good response and 3 (20%) subject showed moderate response

to therapy.

Out of 15 subjects in Group B, 6 (40%) subjects showed Excellent response. 5

(33.33%) subjects showed Good response to therapy and 4 (26.67%) subjects showed

moderate response to therapy.

Discussion on Comparative Efficacy of the Therapies in Group A and Group B:

This Result on comparative efficacy of the therapies in group A and group B shows

both groups are have statistically similar results in all parameters of study.

Comparing the total response of Therapy and Parameters of both groups in this

study, Group A and Group B showed similar results. The mean difference and

corresponding percentage reduction shows Nasya and Virechana are highly effective in the

treatment of Hepatitis B Virus induced Jaundice.

Thus it can be stated that Jeemootaka Nasya and Virechana with Patolamooladi

kashaya along with Nimbatwakadi Kashaya as Shamana Aushadi are excellent methods of

managing Hepatitis Virus induced Jaundice.

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CONCLUSION

The dissertation ‘Comparative clinical study to evaluate the efficacy of

Nasya and Virechana in the management of HBV induced Jaundice’ were carried

out in 30 patients with 2 groups, each consisting of 15 subjects for duration of 45 days

From the literally review it is found that HBV induced Jaundice has get

clinical co-relation with Rogavastha explained in association with the Kamala vyadhi.

It can be said that the signs and symptoms observed in HBV induced Jaundice can be

called as Swatantra Kamala but majority of the Lakshanas can be compared with the

Koshta Shakhashrita Kamala. But even the features of the Ruddhapatha Kamala are

seen in a mild intensity.

Religion, Educational status, Marital status, Socio-economic status and

Habitat was not found influential in the incidence of HBV induced Jaundice.

Addicted (Alcoholic), middle aged, male patients are more prone to Viral

Hepatitis. Unprotected sex , contaminated needles and injections, Blood transfusions

are the mode of transmission of the disease.

Non-vegetarian diet predominant of Katu amla Rasa and theekshna and ushna

guna may aggravate the disease and leads to long standing of the disease.

Vaccination on Hepatitis B Virus induced Jaundice has got much importance

in the prevention of disease.

From the clinical trial it was observed that by the administration of

Hareetakyadi Choorna as amapachana drug, there was minimal reduction in Sr.

Bilirubin

In Group A, patients received Jimutaka Nasya were responded very well, but

minimal signs of irritation in nasal mucosa, throat congestion ,Headache, oozing from

nose were the Vyapat observed in subjects. The Nasya yoga in HBV induced Jaundice

has a definite role in the reduction of bio-chemical parameters, other objective

parameters and symptomatology.

Group B patient received Virechana Karma with Patolamooladi kashaya

responded very well. There was reduction in Sr. Bilirubin level after Virechana.

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Hence, it can be stated that Virechana Karma is an effective Chikitsa krama and the

virus causing the infection may be getting inactive and may be driven away through

the rectal route.

It was observed that Amapachana followed by Virechana and Shamana yoga

and Amapachana followed by Nasya along with Shamanoushadhi Nimbatwakadi

kashaya is very effective and highly significant in reducing the symptoms (subjective

parameters) and also in reducing the bio-chemical parameters, and other objective

parameters.

After treatment in both of the groups all the bio-chemical parameters were

within physiological range and maximum of the 30 patients of either groups become

negative (Sero negative) for HBsAg. There was a 57% response of the therapy.

Hence it can be said that the overall therapy Amapachana-Shodhana therapy-

Shamanoushadhi is effective and statistically highly significant in the management of

HBV induced Jaundice.

After completion of follow up period for 3 months, it was found that the

symptoms of Jaundice were not relapsing and the bio-chemical parameters were not

increasing and the HBsAg (Hepacard method) test found negative were not turned

positive in both of the groups.

The combination of Rasayana dravya (immuno-modulators), anti-microbials

(krimighna) Pitta shamaka, Pitta virachaka, Yakrut uttejaka dravya, Amapachana,

Shodhana and Shamana contributed in the overall response.

Hepatitis B is one of the words most common viruses and one of the top ten

killers. Unlike much else in our often gloom-filled world, it looks likely that HBV

will be effectively controlled and possibly eradicated within the next decade.

RECOMMENDATION FOR FURTHER STUDY:

Further clinical study is proposed with a large sample size and for a long

period. Hence combined therapy is more beneficial and it can be tried in a large

number of subjects to come out with more comprehensive results and for wide

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acceptance of therapy.

Viral load estimation, Liver biopsy, HBV DNA test and assessment of core

antigen should be the parameters. .

Drugs having anti-viral property and anti-microbial property should be

thoroughly studied, analysed and administered along with Rasayana aoshadhi yoga

(immuno-modulator).

The drug Jimutaka should be experimentally proved, its dosage should be

standardized and toxic effects if any should be properly assessed before the

administration.

The Aoushadhi dravya belonging to the Cucurbitaceae family of Luffa species

should be identified, analysed and administered.

Present study can be continued as further with different parameters.

To study the various changes in the bio-chemical value accompanying the

treatment, various viral markers indicative of the presence of HBV infections such as

Igm, anti HBc, IgG, anti HBc, anti HBe can be incorporated in the assessment of the

treatment.

A coordinate research work to the Pharmaco-dynamics and Pharmaco-kinetics

of Nimbatwakadi kashaya can be carried out. Studies to evaluate the properties and

mode of action of each individual drug may be carried out.

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SUMMARY

The present clinical study, “Comparative clinical study to evaluate

the efficacy of Nasya and Virechana in the management of HBV induced

Jaundice” highlights both the conceptual and practical aspects of HBV induced

Jaundice/Kamala in Modern and Ayurvedic perspective.

This study comprises of Introduction, Conceptual Study, Drug Review,

Materials and Methods, Observations, Results, Discussion, Summary and

Conclusion.

The Literary Review consist of Historical Review of Virecnana and Nasya,

Virechana and Nasya Nirukti, Karma, Bhedas, Purva Karma, Pradhan Karma and

Paschat Karma, Complications, Its Management etc, then Historical Review of

Kamala, Functional Anatomy and Physiology of Liver, Etymology and

Derivations, Nidana Panchakas, Bheda, Sadhyasadhyata, Chikitsa, Pathyaapathya

of Kamala, Modern review of HBV Induced Jaundice.

The Methodology consists of Materials and Methods. The detailed

description of all the Materials and Methods used in the study were included

which includes Drug review on Hareetakyadi Choorna, Patolamooladi Kashaya,

Jeemoothaka Phala and Nimbatwakadi Kashaya.

Observations obtained from the study have been explained. The General

Observations and Clinical Observations made in this study have been presented

table wise and the results obtained were analyzed statistically and were presented

with the details.

The Effect of Therapies on Various Assessment Parameters of Kamala

such as Netrapeetata Mootrapeetata, Daurbalya Aruchi, Jwara, Agnimandya, etc

and modern Objective Parameters like SGOT, SGPT, Alkaline Phosphatase,Urine

BP and BS has been statistically analyzed.

The Therapy under Group A Provided Relief Ranging Average of 82.52%,

whereas The Therapy under Group B Provided Relief Average of 79.01%.

In the study Out of 30 subjects, 14 (46.66%) subjects showed Excellent

response.9(30%) subjects showed Good response and 7 (23.33%) subject showed

moderate response to therapy.

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Later, the results obtained from all the groups have been discussed. In the

last part i.e. Conclusion and also gives information regarding Limitations and

Recommendations for Future Studies.

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