dr. jeevan k. jose.pdf
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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
L I S T O F F I G U R E S P a g e | XIV
Comparative clinical study to evaluate the efficacy of Nasya and Virechana in the management of
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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Comparative clinical study to evaluate the efficacy of Nasya and Virechana in the
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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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Comparative clinical study to evaluate the efficacy of Nasya and Virechana in the
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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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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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management of HBV induced Jaundice
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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management of HBV induced Jaundice
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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management of HBV induced Jaundice
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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management of HBV induced Jaundice
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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management of HBV induced Jaundice
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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management of HBV induced Jaundice
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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management of HBV induced Jaundice
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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management of HBV induced Jaundice
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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