1

Case Report Presented at Child Health Department

Respirology subdivision Tuesday, Nov 10th 2009

HEPATIC TUBERCULOSIS IN CHILDREN

Sadiyah M.T.
PEDIATRIC DEPARTMENT- MEDICAL FACULTY of HASANUDDIN UNIVERSITY
Wahidin Sudirohusodo Hospital, Makassar

BACKGROUND
Tuberculosis can affect almost all organs but mostly the lung and rarely liver. The
overall incidence of tuberculosis (TB) is declining in the Western world where the major
risk factors now include immunosuppression (including AIDS), intravenous drug abuse,
cirrhosis, steroid therapy, diabetes, neoplasia, and immigration from endemic areas. 1,2,3,4
But lately, it is shown a reverse trend after the increasing rate of AIDS. 2,3,4 In developing
countries TB still constitutes a major health problem, being associated with malnutrition
and poor socio-economic status. In children the mortality is high if additional
kwashiorkor or measles coexist.1
Tuberculosis remains one of the major diseases afflicting children throughout the
world. Although the exact number of annual cases of childhood tuberculosis is
unknown, the World Health Organization (WHO) has estimated approximately 1 million
new cases and 400,000 deaths per year in children due to tuberculosis. Many of these
cases went undiagnosed and untreated and many of these children could be cured if
only improvements in diagnosis and treatment were available for children.5
Despite tuberculosis as the most common and well documented infectious
disease, hepatic tuberculosis is considered to be a rare disease.1,2,3,6,7,8 A study from
South Africa showed that liver tuberculosis accounted for only 1.2% of all cases of
tuberculosis diagnosed at a general hospital. However, even in developing countries,
liver tuberculosis accompanied by local symptoms is an uncommon entity. Liver
involvement in tuberculosis is usually clinically silent. Occasionally, local signs and
symptoms may be prominent in hepatic tuberculosis, and may constitute the initial or
sole presenting feature of the disease. 2,3,6,7 Lack of familiarity with this condition was
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apparently responsible for the diagnosis of hepatic tuberculosis being made at autopsy
or surgery in the past.

The nomenclature of hepatic tuberculosis is confusing and there’s no a uniformly

acceptable classification and nomenclature, yet, but broadly speaking, hepatic
tuberculosis presents in three forms,6,7,9 as either described by Alvarez.10
1. Diffuse hepatic involvement with pulmonary or miliary tuberculosis (seen along with
pulmonary or miliary tuberculosis) is the most common form, also called miliary
hepatic tuberculosis.
2. Diffuse hepatic infiltration without recognizable pulmonary involvement is the second
form. This forms is also called granulomatous hepatitis or granulomatous liver
disease. The tubercle lesions were ≤ 2mm in diameter.
3. Focal or nodular lesion in the liver which may be multiple or solitary and present as
tuberculoma or abcess. This is the rarest form. The tubercle lesions were >2 mm in
diameter.
The diagnosis is often overlooked because hepatic tuberculosis can have a
relatively nonspecific clinical presentation. 6,7,8,9 High fever, weight loss, right
hypochondrium pain, and hepatomegaly are the most frequently observed clinical
findings and may mimic malignancy.1,3,7,9,10 As is true for tuberculous involvement of
other organs, the final diagnosis of hepatic tuberculosis rests on histopathologic
evidence of caseating granuloma or demonstration of AFB on smear or culture of biopsy
specimen.6,7 Prompt diagnosis and early treatment will give a better result.
This paper will report a case of hepatic tuberculosis in a ten-year-old girl.

CASE REPORT
History taking
A girl, ten-year-old was admitted into the surgery department of the hospital referred by
Palu general hospital on September 14 th 2009 with diagnosis of hepatic malignancy. The
main complaint was a mass on her belly and in both sides of her neck noted since 1
year before admission. There was history of frequent subfebrile episodes, abdominal
pain, neck pain, and night sweating. Body weight decreased despite her good appetite.
She was weakened and not able to sit and walk since 6 months before admission.
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History of exposure to tuberculosis patient wasn’t confirmed. History of immunization

was none. History of malignant disease in the family was denied. History of
hospitalization in Palu general hospital for 1 week with radiographic examination
revealed bronchopneumonia and USG showed hepatomegaly with nodular hyperechoic
suspected of nodular degerative hyperplasia differentialy diagnosed as fibrolamelar
carcinoma and metastatic carcinoma and afterward referred to surgery department of
Wahidin Sudirohusodo hospital. During hospitalization in surgery department, the
laboratory examination (complete blood count, renal function test, liver function test,
HBsAg, Anti-HCV, random blood sugar, coagulation profile, and stool examination),
abdominal USG and CT-Scan were performed. The results were normal for laboratory
examination except for the hemoglobin level revealed a mild hypochromic micrositic
anemia. The abdominal USG result was hepatomegaly suspect of malignancy and
abdominal CT-scan revealed hepatomegaly with calcification due to suspected parasite
invasion. She underwent lymphnodes FNA, lymphnodes excision and liver biopsy and
the pathology results were specific granulomatous inflammation due to tuberculosis on
biopsy. On October 17th, 2009, she was then referred to pediatric department due to
suspected hepatic and lymphadenitis
tuberculosis.
Physical examination
General condition : moderately ill/under
nourish/conscious (BW:
17 kg, BH 117 cm,
ideal body weight 21
kg)
Vital sign : BP 100/60 mmHg, PR
124/m, RR 28/m, t
37,50C
Muscles tone and turgor were normal.
Head : normocephal, fontanel was closed
Ear : within normal limit
Eyes : Pupil was isokor with Ø of 3 mm, reflex to light was positive
Mouth : within normal limit
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Throat : within normal limit

Neck : there were enlarged,
tender, firm, well-defined,
and matted lymphnodes
with Ø of 3 cm on the left
neck and dry excision
wound on the right neck.
Chest : symmetric, left ICS equal
to right ICS
Heart : normal heart sound
Lung : sonor, vesicular breath sound and no adventitious breath sound.
Abdomen : dry excision wound on the abdominal wall, prominent veins and
liver was palpable 4 cm below costal margin, hard consistency,
rough surface, dull margin, tender on palpation. There was no
spleen enlargement.
Ekstremities : there was no edema nor pathologic reflexes. Physiologic
reflexes, muscles tone, and the movements were normal
Skin : no BCG scar
Mantoux test revealed a turgid 15mm induration
Working diagnosis :
Hepatic tuberculosis
Lymphadenitis tuberculosis
Under nourish
Post biopsy excision.
Therapy :
Isoniazide 1 x 100 mg
Rifampicin 1 x 200 mg
Pirazinamide 1 x 400 mg
Ethambutol 1 x 250 mg
Vitamin BC/C 2x1 tab & Regular food (1300 kcal, protein 50 g)
Planning :
CBC, urinalysis, stool examination
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AFB staining of sputum

Blood culture and gastric aspirate culture
Chest X-ray AP/LAT

Follow-up
Treatment day-3 (Okt 19th, 2009)
GC : weak, VS were in normal limit. No cough but sub-febrile at night. There was neck
pain and headache but micturation and bowel movement were normal. Her appetite was
good. On physical examination there was no jaundice. Lymphadenopathies in left side
of her neck about 3 cm, mobile, firm, matted and tender. Peristaltics were normal, liver
was palpable 4 cm bcm, tender and hard. BW 17 kg
Laboratory results :
- AFB staining : negative
- Urinalysis : pH 5,0, yellow, specific gravity 1,025, protein ++100, glucose
negative, bilirubin (-), urobilinogen (+1), keton (-), nitrite (-), blood (-), sediment :
leukocite 2/HPF, erythrocyte (-), thorax (-), crystal Ca. oxalate 3-5/LPF, epithelial
cells 2/ul.
- Stool ex : soft, yellow, no blood nor mucous, neither worm eggs

Chest X-ray AP/LAT :

- Symmetric view, appropriate condition and inspiration
- Coarse bronchovascular feature with infiltrate patches on bilateral parahilar and
paracordial accompanied by density on both hillus, mainly on the right hillus,
- Heart : within normal limit
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- Higher right diaphragm, both sinus and left diaphragm are normal
- Bones are intack
Conclusion :
Duplex bronchopneumonia with lymphadenopathy suspect of specific process
Right diaphragm elevation (probably an intra-abdominal process)
Therapy :
continued

Follow-up
Treatment day-7 (Okt 23th, 2009)
GC : weak, vital signs were in normal limit. No cough but sub-febrile at night. There was
neck pain and headache but micturation and bowel movement were normal. Her
appetite was good. On physical examination there was no jaundice.
Lymphadenopathies in left side of her neck about 3 cm, matted, mobile, firm, and
tender. Peristaltics were normal. Liver was palpable 5 cm bcm, tender and hard. BW
16,5 kg
Therapy : continued

Follow-up
Treatment day-12 (Okt 28th, 2009)
GC : weak, VS were in normal limit. No cough but sub-febrile at night. There was neck
pain and headache but micturation and bowel movement were normal. On physical
examination there was no jaundice. Lymphadenopathies in left side of her neck about 3
cm, mobile, firm, and tender. Peristaltics were normal, liver was palpable 6 cm bcm,
tender and hard. BW 17 kg
Laboratory results :
- Complete blood count
Hb 11 gr/dl, leukocyte 9000/mm3, erythrocyte 4.540.000/mm3, Hm 31,3%, platelet
440.000/mm3, MCV 69 fl, MCH 24,2 g/dl, MCHC 35,1 g/dl, RDW 19,9%, Neutr
68,9%, lymph 23,3%, monocyte 6,1%, Eos 1,3%, Bas 0,4%.
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- Urinalysis : pH 6,5, kuning, bilirubin (-), urobilinogen (-), sedimen : leukosit 3-4/LPB,
erytrocite 0-1/LPB
- Stool ex : soft, yellow, no blood nor mucous, neither worm eggs
- other blood examinations :
Ureum 16 mg/dl, creatinin 0,24 mg/dl, SGOT 24 u/l, SGPT 12 u/l, alkali phosphatase
393 u/l (N < 240 u/l), Gamma GT 139 u/l (N 7-32 u/l)
Therapy : continued

Follow-up
Treatment day-14 (Okt 30th, 2009)
GC : weak, VS were in normal limit. No cough but sub-febrile at night. There was neck
pain and headache but micturation and bowel movement were normal. On physical
examination there was no jaundice. Lymphadenopathies in left side of her neck about 3
cm, mobile, firm, and tender. Peristaltics were normal, liver was palpable 7 cm bcm,
tender and hard. BW 16 kg
Laboratory results :
- PCR : negative
Therapy : continued

Follow-up
Treatment day-16 (Nov 1th, 2009)
GC : weak, VS were in normal limit. No cough but sub-febrile at night. There was neck
pain and headache but micturation and bowel movement were normal. On physical
examination there was no jaundice. Lymphadenopathies in left side of her neck about 3
cm, mobile, firm, and tender. Peristaltics were normal, liver was palpable 8 cm bcm,
tender and hard. Spleen was palpable S1. BW 16kg
Therapy : continued

Follow-up
Treatment day-20 (Nov 5th, 2009)
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GC : weak, VS were in normal limit. No cough but sub-febrile at night. There was neck
pain and headache but micturation and bowel movement were normal. On physical
examination there was pallor & slightly jaundice. Lymphadenopathies in left side of her
neck about 3 cm, mobile, firm, and tender. Peristaltics were normal, liver was palpable 8
cm bcm, tender and hard. Spleen was palpable S1. BW 17kg
Therapy : continued
Planning :
CBC, SGOT, SGPT, total bilirubin, direct bilirubin, ALP, GGT

Follow-up
Treatment day-21 (Nov 6th, 2009)
GC : weak, VS were in normal limit, no fever nor cough. There was neck pain and
headache but micturation and bowel movement were normal. On physical examination
there was pallor & slightly jaundice. Lymphadenopathies in left side of her neck about 3
cm, mobile, firm, and tender. Peristaltics were normal, liver was palpable 8 cm bcm,
tender and hard. Spleen was palpable S1.
Laboratory results :
Total bilirubin 1,6 mg/dl, direct bilirubin 0,97 mg/dl, SGOT 26 u/l, SGPT 14 u/l, alkali
phosphatase 407 u/l (N < 240 u/l), Gamma GT 223 u/l (N 7-32 u/l)
Therapy :
continued

Definitive diagnosis
Lung tuberculosis
Hepatic tuberculosis
Lymphnodes tuberculosis
Under nutrition

Prognosis
Qua ad vitam: dubia
Qua ad sanationem: dubia
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DISCUSSION
Fever is the commonest symptom (63% - 99%) in tubercular hepatic
granulomatosis followed by weight loss (50%-84%) and abdominal pain (46%-70%).
Hepatomegaly is present in more than half the patients whereas splenomegaly is
present in one third.6,7 Other literatures described right upper quadrant abdominal pain
as the commonest symptom while hepatomegaly and splenomegaly are the commonest
findings,6,7,10 being present in 70%- 96% and 25%-55% of patients respectively. In our
case, the patient endure episodes of sub-febrile particularly at night-time, episodes of
abdominal pain, and weight loss. The hepatic symptom on this patient present as
hepatomegaly, and she had a splenomegaly on the 50 th day hospitalization. Her
appetite was good.
As is true for tuberculous involvement of other organs, the final diagnosis of
hepatic tuberculosis rests on histopathologic evidence of caseating granuloma or
demonstration of AFB on smear or culture of biopsy specimen.2,6,7 In this patient, at the
first day of hospitalisation, she was misdiagnosed as having a hepatomegaly due to
malignancy on the basis of clinical symptoms (hard consistency and dull margin
hepatomegaly). Those symptoms can present also in hepatic tuberculosis but oftenly
overlooked. Ultrasonically, a tuberculoma may be seen as a hypoechoic lesion without a
distinct wall resulting from the conglomeration of numerous small tubercles or as a low
density lesion. In this patient, the ultrasonography conclusion was hepatomegaly
suspect of malignancy because it was showed a nodular form with calcification,as in
hepatic tuberculosis may revealed the same image. Abdominal CT-Scan in hepatic
tuberculosis most commonly revealed a hypoechoic lesion. On CT scan, liver
tuberculoma appears as an unenhancing, central, low density lesion due to caseation
necrosis with a slightly enhancing peripheral rim corresponding to surrounding
granulation tissue. In this case, it was revealed otherwise because the calcification
process. These findings, though suggestive of tuberculosis, have also been seen in
necrotic tumours, such as metastatic carcinoma and primary hepatocellular
carcinoma2,6,9,10.
Acid fast bacilli were negative in three times examination, so were the culture
and PCR result. Examinations results which supporting the diagnosis of hepatic
tuberculosis in our case, aside from the clinical symptoms (frequent subfebrile episodes,
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weight loss, abdominal pain, hepatomegaly, and lymphadenopathy) and the abdominal
CT-Scan, were chest X-Ray which revealed a specific process, mantoux test with turgid
induration of 15 mm, and pathology result which revealed a granulomatous
inflammation as the gold standard. A granulomatous inflammation, actually, can be
caused by other disease such as sarcoidosis, primary biliary cirrhosis and fungal
disease. But in endemic area, such as Indonesia, tuberculosis has to be the first
diagnosis to consider, particularly when caseating granuloma is present. 6,7,9 As for the
negative results of PCR, AFB staining and culture, they probably due to inappropriate
source of samples, which were taken from gastric aspirate. The probability for positive
results might be higher if only the samples were taken from the tissue on biopsy. PCR
result only positive in 57% cases, while in AFB staining only 0-59% gave a positive
results, especially in endemic area, and particularly difficult in children. Cytology and
histopathology are the established mode of diagnosis of hepatic tuberculosis without the
need for demonstrating AFB and/or culturing tubercle bacilli, 2 as in our case.
Tubercle bacillly reach the liver by way of hematogenous dissemination : the
portal of entry in the case of miliary tuberculosis is through hepatic artery, whereas in
the case of focal liver tuberculosis is via portal vein. Irrespective of mode of entry, the
response is granuloma formation. Tuberculous granuloma are most frequently found in
the periportal ares (zone 1 of Rappaport zone) but may occasionally occure in zone 3.
Both caseating and noncaseating granulomas are seen. In focal tuberculosis, various
tuberculoma may coalesce to form a large tumor-like tuberculoma. A tuberculoma that
has undergone extensive casseation and liquefaction necrosis form a tubercular
abscess.6,9 The form of hepatic tuberculosis in our case was considered as miliary
hepatic tuberculosis based on the presence of pulmonary tuberculosis. The source of
infection in this case is thought to be the lung as the site of primary infection and spread
haematogenously or hematolymphogenously into the liver. 1,7,9
Since tuberculosis remains a potentially curable disease, an awareness of its
protean manifestations is very essential. 6,7 Therefore a prompt diagnosis and treatment
is very important to give a better result. This patient were treated with four regiments
oral anti-tuberculosis,4,7,9,10,11 planning for 12 months and has been followed-up for the
response until now by observing the clinical manifestations, laboratory results especially
liver function test and USG. There was progressive liver enlargement and she was
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slightly jaundice. Jaundice can be caused by cholestasis jaundice (due either to porta
hepatis nodes causing biliary compression or to pericholangitis or the rupture of a
tuberculous granuloma into the bile ducts)3,9,10 or parenchymatous (by the adverse effect
of oral anti-tuberculosis or by the disease process itself). In this case, even though the
symptoms developed during the early treatment accompanied by the high level of alkali
phosphatase and gamma glutamil transferase, but because the transaminase enzyme
still within normal limit so the progress of the liver enlargement and jaundice were
considered due to cholestasis process. But it still under observation when this report
was made.
The prognosis of hepatic tuberculosis in children is unclear. The worst prognosis
may be in neonatally acquired infection.4 Untreated abdominal tuberculosis carries a
50% mortality rate,1,7 whereas with appropriate treatment will give a very good
prognostic.1,6,9 Poor prognostic factors of hepatic tuberculosis include an age less than
20 years old, miliary tuberculosis, acute hepatic involvement, chronic renal failure,
diabetes, liver failure, steroid medication, prolonged prothrombin time, and severe
caseous necrosis.6,8 The prognosis of qua ad vitam and qua ad sanationem in our case
are dubia due to young age, the delayed of theraphy (the patient was late to seek for
medication) and the wide spread of the caseous necrosis.

SUMMARY
A case of tuberculosis affected liver, lung and lymphnodes and under-nutrition in
a ten-year-old girl was reported. The diagnosis was based on history taking, physical
examinations, and supported by pathology results of liver and lymphnodes biopsy. She
was treated with oral anti-tuberculosis and was still in observation when this case report
was made. The prognosis of this patient in term of quo ad vitam and quo ad sanationem
were dubia.
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(1)
1) USG showed hepatomegaly with nodular hyperechoic. 2) liver seems enlarged,
(2)
nodular form with calcification, no vascular/bile duct dilatation.

Liver enlargement with hyperdense lesions spreading in left and right lobes of the liver.
.
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Biopsy results of the liver : shows caseating necrosis, epitheloid granuloma, spreads of Datia
Langhans cells and mature lymphocytes,

Biopsy results of the lymphnodes : shows irregular lymphnode structure with Datia Langhans cells

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Boca Raton. 1994.
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