pathogenesis of tuberculosis

Case Report

Tuberculosis with Marasmus

SUPERVISOR : Dr. Hj. Sri Sofyani M. Ked (Ped), Sp. A(K)

PRESENTATOR : Renuka Gunasagaran 110100421

Golda Asina Miranda 100100

DEPARTMENT OF CHILD HEALTH

MEDICAL FACULTY NORTH SUMATRA UNIVERSITY

H. ADAM MALIK GENERAL HOSPITAL

MEDAN

2015

ACKNOWLEDGMENTS

We are greatly indebted to the Almighty One for giving us blessing to finish this case

report,“Tuberculosis and Marasmus”. This case report is a requirement to complete the

clinical assistance program in Department of Child Health in H. Adam Malik General

Hospital, Medical Faculty of North Sumatra University.

We are also indebted to our supervisor and adviser, dr.Hj. Sri Sofyani for much spent

time to give us guidances, comments, and suggestions. We are grateful because without her

this case report wouldn’t have taken its present shape.

This case report has gone through series of developments and corrections. There were

critical but constructive comments and relevants suggestions from the reviewers. Hopefully

the content will be useful for everyone in the future.

Medan, th November 2015

Presentator

TABLE OF CONTENTS

COVER ............................................................................................................ i

ACKNOWLEDGMENT………………………………………………………ii

TABLE OF CONTENT ............................................................................... ..3

CHAPTER I INTRODUCTION ....................................................................4

CHAPTER II LITERATURE REVIEW ...................................................... 62.1. Definition ....................................................................................62.2. Classification ............................................................................. 62.3. Etiology .......................................................................................72.4. Pathogenesis and Pathophysiology ……………………………. 92.5. Clinical Manifestation .................................................................132.6.Diagnosis ……….............................................................................132.7. Treatment and Management ……………………………………...142.8. Complications ................................................................................ 15

CHAPTER III CASE REPORT .....................................................................163.1 Objective ......................................................................................... 163.2 Case ..................................................................................................163.3 Follow Up ....................................................................................... .22

CHAPTER IV DISCUSSION ..........................................................................30

CHAPTER V SUMMARY .............................................................................. 31

REFERENCES ............................................................................................32

CHAPTER 1

1.1. Introduction

Tuberculosis (TB), one of the oldest recorded human afflictions, is still one of the biggest

killers among the infectious diseases, killing two million people each year, despite the

worldwide use of attenuated vaccine and antibiotics. In 1993, the World Health Organization

(WHO) declared TB to be a global public health emergency. Tuberculosis can present in

various forms, including one that attacks bone and causes skeletal deformities. Bones can be

preserved for thousands of years, allowing the identification of individuals with bone TB who

died more than 4,000 years ago. Similarly deformed bones in various sites in Italy, Denmark,

and countries in the Middle East also indicates that TB was found throughout the world up to

4,000 years ago.

The origin of M. tuberculosis, is thought that the bacteria in the genus Mycobacterium, like

other actimomycetes, were initially found in soil and that some species evolved to live in

mammals. The domestication of cattle, thought to have occurred between 10,000 and 25,000

years ago, might have allowed the passage of a mycobacterial pathogen from domestic

livestock to humans. It has been hypothesized that M. bovis, which causes a TB-like disease

in cattle, is the evolutionary precursor of M. Tuberculosis.

Globally, the World Health Organization (WHO) reports more than 9 million new cases of

tuberculosis (TB) occur each year.The incidence of TB ranges from less than 10 per 100,000

in North America to 100 to 300 per 100,000 in Asia and Western Russia to over 300 per

100,000 in Southern and Central Africa. There is one death from TB every 15 s (over two

million per year), and eight million people develop TB every year. The annual risk of TB

infection in Southeast Asia is 1-2.5%, representing an upward trend for the region. In

Indonesia, there are roughly 500,000 new cases of TB annually and 175,000 deaths.

Tuberculosis is the second major killer of adults after cardiovascular disease.

1.2 Objective

This paper is one of the requirements to fulfill the senior clinical assistance programs

in the Pediatric Department of Haji Adam Malik General Hospital, University of Sumatera

Utara. This paper was written to report a case of a 1 year 11 months old girl with the

diagnosis of Marasmus + Tuberculosis.

CHAPTER 2

LITERATURE REVIEW

Definition

Tuberculosis is an infectious disease caused by Mycobacterium Tuberculosis. The common

form is Tuberculosis of the lungs, but the more severe form of Tb affects other organs, such

as brain, and bones.Tuberculosis of the lungs usually results in no or minimal symptoms in its

early stages. In most persons the primary infection is contained by the body's immune

system. In others the disease may break out again and become active years later, usually

when the body's immune defenses are weak. Symptoms of the disease include cough, sputum,

bleeding from the lungs, fever, night sweats, loss of weight, decreased appetite and weakness.

Tuberculosis occuring before the age of 15 is known as paediatric tuberculosis.

Etiology and classification

There are 5 types Mycobacterium that causes an infection. M. Tuberculosis,M. Bovis, M.

Africanum, M. Microti dan M. Canetti. The most common bacilli that infects humans is

M. Tuberculosis. M tuberculosis is an aerobic, non-spore-forming, nonmotile, slow-growing

bacillus with a curved and beaded rod-shaped morphology. It is a very hardy bacillus that can

survive under adverse conditions. Humans are the only known reservoirs for M tuberculosis.

Pulmonary tuberculosis (TB) may manifest itself in several forms, including endobronchial

TB with focal lymphadenopathy, progressive pulmonary disease, pleural involvement, and

reactivated pulmonary disease. Symptoms of primary pulmonary disease in pediatrics are

often meager. Fever, night sweats, anorexia, nonproductive cough, failure to thrive, and

difficulty gaining weight may occur. Signs of disease depend on the site involved.

a) Endobronchial TB with lymphadenopathy

Endobronchial disease with enlargement of lymph nodes is the most common variety of

pulmonary TB.. Enlargement of lymph nodes and persistent cough may result in signs

suggestive of bronchial obstruction or hemidiaphragmatic paralysis, whereas difficulty

swallowing may result from esophageal compression. Vocal cord paralysis may be suggested

by hoarseness or difficulty breathing and may occur as a result of local nerve compression.

Dysphagia due to esophageal compression may also be observed.

b) TB pleural effusion

Pleural effusions due to TB usually occur in older children and are rarely associated with

miliary disease. The typical history reveals an acute onset of fever, chest pain that increases

in intensity on deep inspiration, and shortness of breath. Fever usually persists for 14-21

days. Signs include tachypnea, respiratory distress, dullness to percussion, decreased breath

sounds, and, occasionally, features of mediastinal shift.

c) Progressive primary TB

Progression of the pulmonary parenchymal component leads to enlargement of the caseous

area and may lead to pneumonia, atelectasis, and air trapping. This is more likely to occur in

young children than in adolescents. The child usually appears ill with symptoms of fever,

cough, malaise, and weight loss.This condition presents with classic signs of pneumonia,

including tachypnea, nasal flaring, grunting, dullness to percussion, egophony, decreased

breath sounds, and crackles.

d) Reactivation TB

Reactivation of TB disease usually has a presentation with weight loss, fever, cough, and,

rarely, hemoptysis. This condition typically occurs in older children and adolescent and is

more common in patients who acquire TB at age 7 years and older.

Epidemiology

In 1993, the World Health Organization (WHO) declared TB to be a global public health

emergency. The incidence of TB ranges from less than 10 per 100,000 in North America to

100 to 300 per 100,000 in Asia and Western Russia to over 300 per 100,000 in Southern and

Central Africa. There is one death from TB every 15 people (over two million per year), and

eight million people develop TB every year. The annual risk of TB infection in Southeast

Asia is 1-2.5%, representing an upward trend for the region. In Indonesia, there are roughly

500,000 new cases of TB annually and 175,000 deaths. In devaloping countries, incidence of

TB below 15 years olds totals to 15% of total Tb occurances, while in devaloped countries,

the percentage is lower,at 5-7%.

Pathogenesis

Tuberculosis (TB) occurs when individuals inhale bacteria aerosolized by infected persons.

The organism is slow growing,where it may remain metabolically inert for years before

reactivation and disease. The main determinant of the pathogenicity of TB is its ability to

escape host defense mechanisms, such as macrophages and delayed hypersensitivity

responses.

Mycobacterium tuberculosis, contained in aerosol droplets, deposits onto lung alveolar

surfaces, where its first contact is thought be with resident macrophages. Dendritic cells act

as antigen presenters and play a key role in activating T cells with specific M.

tuberculosis antigens. Since dendritic cells are migratory, they cause the dissemination of

M.tuberculosis.

On entry into a host macrophage, M. tuberculosis initially reside in an endocytic vacuole

called the phagosome. When phagosome-lysosome fusion occurs, these bacteria encounter a

hostile environment that includes acid pH, reactive oxygen intermediates (ROI), lysosomal

enzymes, and toxic peptides. An interesting finding is that Ca2+ signaling is inhibited

when M. tuberculosis enters human macrophages. Ca2+ stimulates many host responses to

infection, e.g., NO and cytokine production. Thus, preventing increases in Ca2+ levels would

help M. tuberculosis avoid these host defense mechanisms. Virulence factors in the

mycobacterial cell wall are the cord factor, lipoarabinomannan (LAM). LAM inhibits

macrophage activation by interferon (IFN)-gamma and induces macrophages to secrete TNF-

alpha, which causes fever, weight loss, and tissue damage.

Infected macrophages in the lung, through their production of chemokines, attract

inactivated monocytes, lymphocytes, and neutrophils none of which kill the bacteria very

efficiently . Granulomatous focal lesions composed of macrophage-derived giant cells and

lymphocytes begin to form. As cellular immunity develops, macrophages loaded with bacilli

are killed, and this results in the formation of the caseous center of the granuloma,

surrounded by a cellular zone of fibroblasts, lymphocytes, and monocytes. Unable to multiply

within this caseous tissue due to its acidic pH, the low availability of oxygen, and the

presence of toxic fatty acids, some organisms may remain dormant for decades. The strength

of the host cellular immune response determines whether an infection is arrested here or

progresses to the next stages. The granulomas subsequently heal, leaving small fibrous and

calcified lesions. This is referred to as latent or persistent TB and persist throughout a

person's life in an asymptomatic and nontransmissible state.

However, if an infected person cannot control the initial infection in the lung or if a latently

infected person's immune system becomes weakened, the granuloma center becomes

liquefied by and then serves as a rich medium in which the now the bacteria replicates in an

uncontrolled manner. At this point, M. tuberculosis escapes from the granuloma and spread

within the lungs (active pulmonary TB) and even to other tissues via the lymphatic system

and the blood (miliary or extrapulmonary TB). When this happens, the person becomes

infectious.

Clinical Manifestation

Tuberculosis in peadiatric lacks clinical symptoms,thus known as a clinically silent

disease.Symptoms of primary pulmonary disease in the pediatric population are often

meager. Fever longer than 2 weeks, night sweats, anorexia, nonproductive cough, failure to

thrive,persistant diarrhoea and difficulty gaining weight may occur.

Tb with pleural effusion.

Pleural effusions due to TB usually occur in older children.The typical history reveals an

acute onset of fever, chest pain that increases in intensity on deep inspiration, and shortness

of breath. Fever usually persists for 14-21 days. Signs include tachypnea, respiratory distress,

dullness to percussion, decreased breath sounds, and, occasionally, features of mediastinal

shift.

Progressive primary TB

Enlargement of the caseous area may lead to pneumonia, atelectasis, and air trapping. This is

more likely to occur in young children than in adolescents. The child usually appears ill with

symptoms of fever, cough, malaise, and weight loss.

This condition presents with classic signs of pneumonia, including tachypnea, nasal flaring,

grunting, dullness to percussion, egophony, decreased breath sounds, and crackles.

Reactivation TB

Reactivation of TB disease usually presents with weight loss, fever, cough, and, rarely,

hemoptysis. This condition typically occurs in older children and adolescent and is more

common in patients who acquire TB at age 7 years and older.

Physical examination results may be normal or may reveal posttussive crackles.

Diagnosis

The tuberculin skin test (TST) is a widely used diagnostic test for evaluation of patients who

have symptoms of tuberculosis (TB) or in whom infection with M tuberculosis is suspected.

The sensitivity and the specificity of the TST is approximately 90%. Interferon gamma

release assays (IGRA) are now replacing the TST as the preferred test for screening and

testing for tuberculosis. According to the American Academy of Pediatrics (AAP), immediate

skin testing is indicated for the following children

Those who have been in contact with persons with active or suspected TB

Immigrants from TB-endemic countries (eg, Asia, Middle East, Africa, Latin America)

or children with travel histories to these countries

Those who have radiographic or clinical findings suggestive of TB

An annual TST is indicated for the following children:

Children who are infected with human immunodeficiency virus (HIV) or those living

in a household with persons infected with HIV

Incarcerated adolescents

The dosage of 0.1 mL or 5 tuberculin units [TU] of purified protein derivative (PPD) should

be injected intradermally into the volar aspect of the forearm A detergent called Tween 80 to

prevent loss of efficacy on contact and adsorption by glass stabilizes the PPD. A wheal should be

raised and should measure approximately 6-10 mm in diameter.

Skilled personnel should always read the test 48-72 hours after administration. Measure the

amount of induration and not erythema. This should be measured transverse to the long axis

of the forearm.

Interpretation of TST results

The Centers for Disease Control and Prevention (CDC) and the AAP provided

recommendations regarding the size of the induration created by the TST that is considered a

positive result and indicative of disease. The TST is interpreted on the basis of 3 "cut points":

5 mm, 10 mm, and 15 mm.

Induration of 5 mm or more is considered a positive TST result in the following

children

Children having close contact with known or suspected contagious cases of the

disease, including those with household contacts with active TB whose treatment

cannot be verified before exposure

Children with immunosuppressive conditions (eg, HIV) or children who are on

immunosuppressive medications

Children who have an abnormal chest radiograph finding consistent with active TB,

previously active TB, or clinical evidence of the disease

Induration of 10 mm or more is considered a positive TST result in the following

children

Children who are at a higher risk of dissemination of TB disease, including those

younger than 5 years or those who are immunosuppressed because of conditions such

as lymphoma, Hodgkin disease, diabetes mellitus, and malnutrition

Children with increased exposure to the disease, including those who are exposed to

adults in high-risk categories (eg, homeless, HIV infected, users of illicit drugs,

residents of nursing homes,); those who were born in or whose parents were born in

high-prevalence areas of the world; and those with travel histories to high-prevalence

areas of the world

Induration of 15 mm or more is considered a positive TST result in children aged 5

years or older without any risk factors for the disease.

False-positive and false-negative results

False-positive reactions and false-negative results can have various causes. False-positive

reactions are often attributed to asymptomatic infection by environmental non-TB

mycobacteria (due to cross-reactivity).

False-negative results may be due to vaccination with live-attenuated virus, anergy,

immunosuppression, immune deficiency, or malnutrition. Other factors that may cause a

false-negative result include improper administration (eg, subcutaneous injection, injection of

too little antigen), improper storage, and contamination. PPD has been recognized to have an

initial false-negative rate of 29%.

Previous BCG vaccination

Some important points regarding administering the TST to previous recipients of the bacille

Calmette-Guérin (BCG) are briefly discussed.Immunization with BCG is not a

contraindication to the TST. BCG vaccination is used in many parts of the world, especially

in developing countries.Differentiating tuberculin reactions caused by vaccination with BCG

versus reactions caused by infection with M tuberculosis is difficult. History of contact with a

person with contagious TB or emigration from a country with a high prevalence of TB

suggests that the positive results are due to infection with M tuberculosis.However, multiple

BCG vaccinations may increase the likelihood that the positive TST result is due to the BCG

vaccination.

A previous BCG vaccination does not affect interpretation of a TST result for a person who is

symptomatic or in whom TB is strongly suspected.

Specimen Collection for Analysis

The initial step in detection of the mycobacterium is to obtain appropriate specimens for

bacteriologic examination. Examination of sputum, gastric lavage, bronchoalveolar lavage,

lung tissue, lymph node tissue, bone marrow, blood, liver, cerebrospinal fluid (CSF), urine,

and stool may be useful, depending on the location of the disease.

Sputum specimens

Sputum specimens may be used in older children, but not in very young children (< 6 y), who

usually do not have a cough deep enough to produce sputum for analysis. In those younger

than 6 years, gastric aspirates are used.

Nasopharyngeal secretions and saliva are not acceptable. In older children, bronchial

secretions may be obtained by the stimulation of cough by an aerosol solution of propylene

glycol in 10% sodium chloride.

Gastric aspirates

Gastric aspirates are used in children younger than 6 years.. An early morning sample should

be obtained before the child has had a chance to eat or ambulate, because these activities

dilute the bronchial secretions accumulated during the night.

Initially, the stomach contents should be aspirated, and then a small amount of sterile water is

injected through the orogastric tube. This aspirate should also be added to the specimen.

Because gastric acidity is poorly tolerated by the tubercle bacilli, neutralization of the

specimen should be performed immediately with 10% sodium carbonate or 40% anhydrous

sodium phosphate. Even with careful attention to detail and meticulous technique, the

tubercle bacilli can be detected in only 70% of infants and in 30-40% of children with

disease.

Acid Fast Bacilli Staining

Because M tuberculosis is an acid-fast bacilli (AFB), AFB staining provides preliminary

confirmation of the diagnosis. Staining can also give a quantitative assessment of the number

of bacilli being excreted (eg, 1+, 2+, 3+). This can be of clinical and epidemiologic

importance in estimating the infectiousness of the patient

Mycobacterium cultures

Culture of mycobacterium is the definitive method to detect bacilli. It is also more sensitive

than examination of the smear. Approximately 10 acid-fast bacilli (AFB) per millimeter of a

digested concentrated specimen are sufficient to detect the organisms by culture.

Another advantage of culture is that it allows specific species identification and testing for

recognition of drug susceptibility patterns. However, because M tuberculosis is a slow-

growing organism, a period of 6-8 weeks is required for colonies to appear on conventional

culture media.

Radiology

General radiological features that suggest Tuberculosis are:

Enlargement of glands at the hilus or paratracheal with or without infiltrate.

Lobar/segemental consolidation

Milliary

Calcifications with infiltrate

Atelectasis

Cavity

Pleural Effusion

Tuberculoma

Treatment and Management

In 2006 the World Health Organisation (WHO) carried out a review of TB drug treatment for

children and produced a set of recommendations about the amount of different TB drugs that

should be provided per kg of a child’s body weight. In 2010 the recommendations were

changed with the amount of each TB drug in general being increased.

Anti-TB medications kill mycobacteria, preventing further complications of early primary

disease and progression of disease. However, disappearance of caseous or granulomatous

lesions does not occur even with therapy. These drugs are classified as first-line and second-

line drugs. First-line drugs have less toxicity with greater efficacy than second-line drugs. All

first-line agents are bactericidal with the exception of ethambutol.

First line agents include rifampin, isoniazid, pyrazinamid, and streptoycin. Second-line agents

are capreomycin, ciprofloxacin, cycloserine,ethionamide, kanamycin,ofloxacin, levofloxacin,

and para-aminosalicylic acid.

INH and rifampin are effective against bacilli in necrotic foci and intracellular populations of

mycobacteria. Streptomycin, aminoglycosides, and capreomycin have poor intracellular

penetration. Multidrug-resistant (MDR) TB is defined as resistance to at least INH and ri.

Recommendations for the treatment of pulmonary tuberculosis (TB) include a 6-month

course of isoniazid (INH) and rifampin, supplemented during the first 2 months with

pyrazinamide. Ethambutol (or streptomycin in children too young to be monitored for visual

acuity) may need to be included in the initial regimen until the results of drug susceptibility

studies are available.

Another treatment option is a 2-month regimen of INH, rifampin, and pyrazinamide daily,

followed by 4 months of INH and rifampin twice a week. Effective treatment of hilar

adenopathy when the organisms are fully susceptible is a 9-month regimen of INH and

rifampin daily or a 1-month regimen of INH and rifampin once a day, followed by 8 months

of INH and rifampin twice a week.

Another initiative recently launched by the World Health Organization (WHO) is the DOTS-

plus strategy, which is based on finding appropriate treatment strategies for MDR TB and

drug susceptibility testing, as well as judicious usage of second-line drugs. This initiative also

focuses on community involvement and a good recording and reporting system.

Adverse Drug Effects

Monthly monitoring of hepatic function tests in the following patients: those with severe or

disseminated TB;those with concurrent or recent hepatic disease; those receiving high daily

doses of INH (10 mg/kg/d) in combination with rifampin, pyrazinamide, or both; women

who are pregnant or within the first 6 weeks postpartum; those with clinical evidence of

hepatotoxic effects; and those with hepatobiliary tract disease from other causes.

Extrapulmonary Tuberculosis.

Most cases of extrapulmonary tuberculosis (TB), including cervical lymphadenopathy, can be

treated with the same regimens used to treat pulmonary TB. Exceptions include bone and

http://reference.medscape.com/drug/levaquin-levofloxacin-systemic-levofloxacin-342532

http://reference.medscape.com/drug/kantrex-kanamycin-342693

http://reference.medscape.com/drug/trecator-sc-ethionamide-342695

http://reference.medscape.com/drug/seromycin-cycloserine-342660

http://reference.medscape.com/drug/cipro-xr-ciprofloxacin-342530

http://reference.medscape.com/drug/capastat-capreomycin-342552

joint disease, miliary disease, and meningitis. For these severe forms of drug-susceptible

disease, the recommendation is a regimen of 2 months of isoniazid (INH), rifampin,

pyrazinamide, and streptomycin once a day, followed by 7-10 months of INH and rifampin

once a day.

Another recommended regimen is 2 months of INH, rifampin, pyrazinamide, and

streptomycin, followed by 7-10 months of INH and rifampin twice a week. Streptomycin

may be administered with initial therapy until drug susceptibility is known. Consider

administering capreomycin or kanamycin instead of streptomycin in patients who may have

acquired TB in areas in which resistance to streptomycin

Effectiveness of therapy is evaluated by improvements of clinical symptoms, radiological

features, or an erythrocyte sediment rate.

Complications

Miliary disease and tubercular (TB) meningitis are the earliest and most deadly complications

of primary TB. Pulmonary complications include the development of pleural effusions and

pneumothorax. Complete obstruction of a bronchus can result if caseous material extrudes

into the lumen. This can lead to atelectasis of the involved lung. Bronchiectasis, stenosis of

the airways, bronchoesophageal fistula, and endobronchial disease caused by penetration

through an airway wall are other catastrophes that may occur with primary TB.

Perforation of the small bowel, obstruction, enterocutaneous fistula, and the development of

severe malabsorption may complicate TB of the small intestine.Pericardial effusion can be an

acute complication or can resemble chronic constrictive pericarditis. Renal complications

including hydronephrosis and autonephrectomy usually do not occur in children. Paraplegia

may complicate Pott disease of the spine (ie, TB spondylitis)

Preventing TB

The key method of preventing tuberculosis (TB) is prompt identification and treatment of

patients with TB. Other strategies include patient education, treatment of latent infection, and

vaccination.

The World Health Organization (WHO) launched the Stop TB strategy in 2006 (modelled

after the directly observed theraphy [DOT] strategy) and the core components include

pursuing high-quality DOT expansion and enhancement; addressing TB and human

immunodeficiency (HIV) infection, multidrug-resistant (MDR) TB, and other challenges;

contributing to health system strengthening; engaging all care providers; empowering people

with TB; and enabling and promoting research.

CHAPTER III

CASE REPORT

3.1 ObjectiveThe objective of this paper is to report a case of a 1 year 11 month old girl with the diagnosis of Pulmonary Tuberculosis with Malnutrition Class III.

3.2 Case

NS, a 1 year 11 month old girl, with BW of 4,5 kg and height of 68 cm, came to Haji Adam

Malik General Hospital Medan on 26th October,with chief complaint low body mass.

History of disease:

NS, a 1 year 11 month old girl, with BW of 4.5 kg and 66 cm long, came to Haji Adam

Malik General Hospital Medan on 26th October with low body mass as chief complaint.The

patient has been underwight since she was 2 months old. Patients mother claims NS has

difficulity in gaining weight. The heaviest NS weighed was 5.5 kg. NS also has a pooappetite

and vomits after eating. NS has been having dry cough for 1 year. Fluctuating fever was also

experienced for a year, with very high temperatures 3 days ago. Fever subsided upon

consumption of anti pyretics. Chills or seizures was not found.

NS has been having diarrhoea for the past 2 days, with the frequency of 3 times per day.

Diarrhoea with a very watery consistency, without mucus or blood. Episodes of diarrhoea in

the past was denied.

History of contact with coughing adult was found. NS’s neighbour has been coughing for a

year.

History of medication:

Anti Tuberculosis Drugs for 8 months, completed by NS. At the moment, NS is consuming

Rifampicin and Isoniazid 1x50mg, and vitamin B complex 1x1 tablet.

History of family:

Family history of similar symptoms and disease were not found.

History of parent’s medication:

Not found

History of pregnancy:

Patient’s mother was 31 years old during pregnancy. She regularly goes for control. No

history of complication neonate and maternal problem. Consumtion of herbal medication (-)

History of birth:

Patient is the only child to her parents. Gestational age was preterm (28 weeks). Body weight

was 1200 gram, body length was not measured. Birth was assisted by a midwife. Baby was

born normally and cried spontaneously. Cyanosis was not found.

History of immunization:

Not complete

History of growth and development:

Patient’s mother claims NS is underwight. She is not able to crawl and sit appropriately

according to her age.

Physical Examination:

Present status:

Sensorium : CM, body temperature: 38,0°C, HR: 120 bpm, RR: 36 x/i, BW: 4,5 kg, BH: 68

cm, BW/A: Z score < -3 SD , BL/A: Z score < -3 SD, BW/BL: -1< Z score < -2, anemic (-),

icteric (-), dyspnea (-), cyanosis (-), edema (-).

Localized status: Head :Face: Old Man Face

Eyes: light reflex +/+, isochoric pupil, pale inferior palpebral conjunctiva -/-, superior

and inferior palpebra edema-/-

Ears: within normal range

Nose:normal

Mouth : within normal range

Neck : lymph node enlargement (-)

Thorax: Symmetrical fusiform, intercostal and epigastric retraction (-) HR: 120 bpm,

regular, murmur (-)

-RR: 38x/i, regular, ronchi (+/+), wheezing (-/-)

Abdomen: Symmetric, supple, normal peristaltic, liver and spleen: normal

Extremities : pulse 120 bpm regular, adequate p/v, felt warm, CRT < 3”

Working diagnosis :Pulmonary Tuberculosis and Marasmus

Laboratory findings

Complete blood analysis ( 26 th October 2015 )

Test Result Unit ReferencesHemoglobin 11.70 g% 11.3-14.1Erythrocyte 4.04 106/mm3 4.40-4.48Leucocyte 14.07 103/mm3 6.0-17.5Thrombocyte 318 103/mm3 217-497Hematocrite 33.50 % 37-41Eosinophil 0.00 % 1-6Basophil 0.200 % 0-1Neutrophil 47.00 % 37-80Lymphocyte 41.70 % 20-40Monocyte 11.10 % 2-8Neutrophil absolut 6.76 103/µL 1.9-5.4Lymphocyte absolut 6.04 103/µL 3.7-10.7Monocyte absolute 1.61 103/µL 0.3-0.8Eosinophil absolute 0.00 103/µL 0.20-0.50Basophil absolute 0.03 103/µL 0-0.1MCV 82.90 Fl 81-95MCH 34.90 Pg 25-29MCHC 34.90 g% 29-31

Clinical chemistry (26th October 2015 )Test Result Unit ReferencesBlood Glucose 88.10 mg/Dl 40-60Ureum mg/dL < 50Calcium 6.7 mg/dL 8.4-10.4Natrium 132 mEq/L 135-155Potassium 3.5 mEq/L 3.6-5.5Chloride 103 mEq/L 96–106Procalcitonin 0.2 ng/mL <0.05

Urinalysis (30 th October 2015)

Immunoserology and Immunophenotyping (29 th October 2015)

Result s of Chest Radiology

Color -Clear yellow - YellowGlucose Negative - NegativeBilirubin Negative - NegativeKeton Negative - NegativeSpesific gravity 1.005 - 1.005-1.030pH 5.0 - 5-8Protein Negative - NegativeUrobilinogen Negative - -Nitrite Negative - NegativeLeucocyte Postive - -Blood Negative - -Urine sedimentErythrocyte 2-3 HPF <3Leucocyte 1-3 HPF <6Epithelial 1-3 HPF -Casts Negative HPF NegativeCrystal Negative HPF -

Anti HIV- 3 Method: Anti HIV Rapid 1

Non reactive Non reactive

CD4 % 20 % 31-60CD 4 Absolute 626 Cell/ul 410-1590

- Both costophrenic sinuses are sharp. Diafragm is smooth- Infiltrate on bilateral suprahiler.- No cardiomegaly (CTR 45%)- Trachea in middle- Bones and soft tissues :normal

Conclusion : Pulmonary tuberculosis

Therapy:

D10% 50cc /per oral

Cotrimoxazole 2x120mg

Paracetamol 3x50mg

Resomal 25cc/30 minutes for 2 hours

Vitamin A 1x160.000 IU

Diet 75cc/3 jam

NGT

Follow Up

26th October 2015 (1700)

S Malnutrition

O -Sensorium: CM, Temp: 38 °C, BW: 4,5 kg, BH: 68cm

-Head : Fontanella Major was closed

Eye : Light reflex (+/+), isochoric pupil, pale inferior conjunctiva

palpebra (-/-), sclera icteric (-/-)

Ear : normal

Nose : normal

Mouth : normal

-Neck : lymph node enlargement (-)

-Thorax : symmetrical fusiform, retraction (-) intercostal, epigastric

HR: 120 bpm, regular, murmur (-)

RR : 36x/i, regular, ronchi (+/+), wheezing(-/-)

-Abdomen : supple, peristaltic (+)N, Liver and Spleen: not palpable

-Extremities : pulse 120 bpm, regular, adequate p/v , felt warm, CRT < 3”

A DD/Pulmonary tuberculosis + Marasmus + Susp Sepsis

P Resomal 25 cc/30minutes for 2 hours

Paracetamol 3x 50 mg

F75 Diet 55cc/2 hours + 1.5 cc mineral mix


Folate 1x5mg

Vitamin B complex 1x1

Vitamin C 1X 100mg

Advice from dr. Hj iangsa Sembiring M.Ked (Peads) SpA.K:

-Ampicilin Inj 250mg/6hours/iv

-Gentamycin Inj 25mg/24hours/iv

-IVFD D5% NacL 0.225%- 4cc/hour

27th October 2015 (0600)

S Diarrhoea, Fever

O Sensorium: CM T= 39,3 °C

Thorax: Simetris Fusiformis, epigastrial retraction (-)

HR: 120x/i, reg, murmur (-)

RR: 40x/i, reg, stridor (-), ronchi (+)

P IVFD D5% NacL 0.225%- 4gtt/minute micro

Ampicilin Inj 250mg/6hours/iv



Folate 1x5mg


Resomal 50cc/diarrhoea or vomit


F75 Diet 55cc/3 hours + 1.5 cc mineral mix

R Check blood gas analysis, LFT,RFT, Blood culture, Urine culure,

Consult to Respiralogy.

27th October 2015 (Nurition and Metabolic Module)

S Diarrhoea (+) frequency of 5 times. Fever(+).

O Sensorium: CM, Temp: 38°C,

BBM: 5.25kg PB:68cm BB/U: z score < -3Sd

BBS:5.25kg HA: 7 ½ years PB/ U: z score <-3sd

BBI: 7.8kg LLA: 10.5cm BB/PB: z score: <-3sd

-Head : Face: old man face +



Ear : within normal range

Nose : NGT

Mouth : within normal range.

-Neck : Normal

-Thorax : symmetrical fusiform, retraction (-) intercostal, epigastric,

protruding ribs +,


RR : 30x/i, regular, ronchi (+/+), wheezing(-/-)

Abdomen : supple, peristaltic (+)N, Liver and Spleen: not palpable

Extremities : pulse 132 bpm, regular, adequate p/v , felt warm, CRT <

3”,muscle hypertrophy +, thinning subcutaneous fats +, baggy pants -.

A Marasmus + Pulmonary TB+Susp sepsis

P Diet F 75 55cc/hour + Min.Mix 1.1cc

IVFD D5% NacL 0.225%- 4gtt/minute micro




Folate 1x5mg




Consult Respirology, Urine and Feces and Blood Culture, septic work up.

28th October2015 –Nutrition and Metabolic Module

S Diarrhoea (+)

O Sensorium: CM, Temp: 37,7°C, BW: 5,25 kg, BH: 68 cm




Head : Face: old man face +




Nose : NGT


-Neck : Normal


protruding ribs +,


RR : 32x/i, regular, ronchi -/-), wheezing(-/-)



3”,muscle hypertrophy +, thinning subcutaneous fats +, baggy pants -.

-


P Diet F 75 55cc/hour + Min.Mix 1.1cc




OAT 1x1 (RHZ, INH)


Folate 1x5mg



Routin Feses:

Macroscopic: Microscopic:

Consistency: Watery Parasite eggs:-

Blood:- Amoeba:-

Mucus:- Erythrocyte:0-1

Leucocyte:0-1

29thOctober 2015

S Diarrhoea +, vomit +, fever +

O Sensorium: CM, Temp: 37,8°C, BW: 5,25 kg, BH: 68 cm

BW: 5.25kg BL:68cm





Nose : NGT


-Neck : Normal


protruding ribs +,





3”,muscle hypertrophy +, thinning subcutaneous fats +, baggy pants +


P Diet F 75 85cc/ 3 hour + Min.Mix 1.7cc




OAT 1x1 (RHZ, INH)


Vitamin c 1x100mg

Paracetamol 4x60mg

Folate 1x5mg



Chest Xray Consultation, washout 3 days, Consult Allergy and Immunology

department, HIV scrining

29thOctober 2015 Nutrition and Metabolic Module (1700)

S Diarrhoea +, vomit -, fever +









Nose : NGT


-Neck : Normal


protruding ribs +,











OAT 1x1 (RHZ, INH)


Vitamin c 1x100mg

Paracetamol 4x60mg

Folate 1x1mg



Chest Xray Consultation, washout 3 days, Consult Allergy and Immunology

department, HIV screening

Immunoserology Lab results:

Immunodeficiency profile:

Anti HIV 3 methode:

Anti HIV rapid d : NON REACTIVE

Immunophenotyping:

cd4 : 20% (Range 31-60)

Absolute cd4: 626 cell/ul (range 41-=1590)

Urine dipstick

30thOctober 2015 Nutrition and Metabolic Module (0600)

S Diarrhoea + x4, vomit -, fever -, reddish anus

O Sensorium: CM, Temp: 36.8°C,








Nose : NGT


-Neck : Normal


protruding ribs +,











OAT 1x1 (RHZ, INH)


Vitamin c 1x100mg

Paracetamol 4x60mg

Folate 1x1mg



1st November 2015

S Diarrhoea +, vomit +,






Nose : NGT


-Neck : Normal


protruding ribs +,





3”,muscle hypertrophy +, thinning subcutaneous fats +, baggy pants -






OAT 1x1 (RHZ, INH)


Vitamin c 1x100mg

Folate 1x1mg



2nd November 2015

S Diarrhoea +

O Sensorium: CM, Temp: 36.9°C,





Nose : NGT


-Neck : Normal


protruding ribs +,











OAT 1x1 (RHZ, INH)


Vitamin c 1x100mg

Paracetamol 4x60mg

Folate 1x1mg



2nd November 2015 Nutrition and Metabolic Module (1700)

S Diarrhoea +,









Nose : NGT


-Neck : Normal


protruding ribs +,











OAT 1x1 (RHZ, INH)


Vitamin c 1x100mg

Folate 1x1mg



pathogenesis of tuberculosis

Documents

case report wouldnt

case reporttuberculosis

chapter v summary

marasmus supervisor

sri sofyani

ak presentator

relevants suggestions

constructive comments