Keywords
abdominal tuberculosis - ascites - diagnostic laparotomy - loss of appetite
Introduction
Tuberculosis (TB) continues to remain a major public health problem in the Southeast
Asian countries, including the Indian subcontinent, and is resurfacing as a major
health issue in developed countries due to the HIV pandemic and immunosuppressive
therapies. It can virtually affect any human organ and has a varied presentation,
posing a diagnostic challenge to the clinicians. The burden of extrapulmonary TB is
estimated to range from 15 to 20% of all TB cases in HIV-negative patients, while
in HIV-positive subjects, it accounts for 40 to 50% of new TB cases.[1] India is an endemic area with an increasing incidence of multidrug-resistant TB.[2] Abdominal TB, defined as an infection of the peritoneum, hollow or solid abdominal
organs, and abdominal lymphatics with Mycobacterium tuberculosis, is the sixth most frequent site of extrapulmonary involvement, with the ileocecal
region being the most common site affected followed by ascending colon, jejunum, appendix,
duodenum, stomach, esophagus, sigmoid colon, and rectum.[3]
Abdominal TB is thought to occur due to reactivation of a dormant focus. It may also
be caused by swallowed bacilli traversing through the Peyer's patches of the intestinal
mucosa and being transported by macrosphages through the lymphatics to the mesenteric
lymph nodes.[4] Due to its varied presentations, abdominal TB remains a diagnostic dilemma. The
disease may mimic several other conditions such as lymphoma, Crohn's disease, amebiasis,
and even adenocarcinoma amongst others. Imaging findings are not pathognomonic but
may be highly suggestive of the disease if considered in conjunction with clinical
findings, laboratory tests, immunological status, and demographic origin of the patient.[5]
This study was done to characterize the clinical, imaging, and endoscopic profile
of patients presenting with abdominal TB at a tertiary care center.
Subjects and Methods
This was a prospective observational study conducted at Meenakshi Medical College
Hospital, Kanchipuram, over a 3-year period extending from March 2011 to February
2014. A total of 76 patients were diagnosed with abdominal TB based on their clinical,
pathological, endoscopic, and radiological features. A meticulous history and physical
examination with complete blood count, HIV status, chest X-ray, ultrasound of the
abdomen, upper endoscopy, and colonoscopy was performed. Barium study, ascitic fluid
analysis, and contrast-enhanced computed tomography (CECT) of the abdomen and pelvis
with peritoneal biopsies where need be were also performed. All the patients received
antituberculosis treatment (AKT) under close surveillance and monitoring.
Results
Demographics
Of the total 76 patients, 40 were males and 36 females with age ranging from 18 to
75 years and majority of our patients were in the age group of 18 to 30 years (42.1%).
A history of pulmonary Koch's was elicited in 28 patients of whom 17 had defaulted
on AKT. While three patients tested positive for HIV, one was a chronic hepatitis
B surface antigen carrier but not on any antivirals for the same. A history of close
contact with a family member who was diagnosed with pulmonary Koch's was noted in
16 patients ([Fig. 1]).
Fig. 1 Age distribution of study population.
Clinical Features
Abdominal pain, either localized or generalized, was the most common symptom noted
in 70 patients followed by loss of appetite/weight loss in 52, fever in 48, constipation
in 28, abdominal distention/ascites in 14, diarrhea in 6 patients, and 2 patients
presented with intestinal obstruction requiring emergency laparotomy (one patient
showed evidence of abdominal cocooning on CT and the other showed peritoneal tubercles
with stricture at the ileocecal junction) ([Table 1]).
Table 1
Symptom profile of study population
Symptoms
|
Number of patients (%)
|
Pain abdomen
|
70 (92.1)
|
Loss of appetite/weight loss
|
52 (68.4)
|
Fever
|
48 (63)
|
Constipation
|
28 (37)
|
Abdominal distention
|
14 (18.4)
|
Diarrhea
|
6 (7.9)
|
Acute intestinal obstruction
|
2 (2.6)
|
Fever was the most common clinical finding noted in 42 patients followed by anemia
in 35, ascites in 26, abdominal tenderness in 22, and palpable abdominal mass in 10
patients ([Table 2]).
Table 2
Clinical features/findings of study population
Signs
|
Number of patients (%)
|
Fever
|
42 (55.26)
|
Pallor
|
35 (46)
|
Ascites
|
26 (34.2)
|
Abdominal tenderness
|
22 (28.9)
|
Abdominal mass
|
10 (13.15)
|
Laboratory Findings
An elevated erythrocyte sedimentation rate (ESR) (>30 mm) was noted in 46 patients.
The other laboratory findings included anemia in 38 and hypoalbuminemia (serum albumin
<3.5 g/dL) in 26 patients. Ultrasound-guided ascitic fluid analysis was undertaken
in 30 patients who had clinical and/or ultrasound evidence of ascites. Apart from
calculating serum ascites albumin gradient (SAAG), ascitic fluid was analyzed for
adenosine deaminase (ADA), AFB smear, and acid fast bacilli (AFB) culture. All 30
patients showed high protein and low SAAG ascites; while ADA was elevated in 23 patients
(>33 U/L), 2 patients showed AFB on smear but none of them grew AFB on culture ([Table 3]).
Table 3
Laboratory findings
Investigation
|
Number of patients (%)
|
Abbreviations: HIV, human immunodeficiency virus; HBsAg, epatitis B surface antigen;
SAAG, serum ascites albumin gradient; ADA, Adenosine deaminase; AFB, acid fast bacilli;
CBC, complete blood count; ESR, erythrocyte sedimentation rate
|
CBC
|
|
Anemia
|
38 (50)
|
Raised ESR (>30 mm/h)
|
46 (60.5)
|
Hypoalbuminemia
|
26 (34.2)
|
Normocytic normochromic anemia
|
20 (26.3)
|
HIV (ELISA)
|
3
|
HBsAg
|
1
|
Ascitic fluid analysis
|
30
|
High protein, low SAAG ascites
|
30
|
ADA (>33 U/L)
|
23
|
Smear positive for AFB
|
2
|
Radiological Findings
A chest X-ray was done in all the patients with 8 showing stigmata of previous infection
(fibrosis, pleural thickening, etc.), 14 showing parenchymal consolidation, 6 with
miliary TB, and 5 showing pleural effusion ([Table 4]).
Table 4
Radiological/imaging findings
Imaging study
|
Number of patients
|
Abbreviation: CECT, contrast-enhanced computed tomography.
|
Chest X-ray (n = 76)
|
|
Consolidation
|
14
|
Miliary tuberculosis
|
6
|
Stigmata of healed tuberculosis (pleural thickening, upper zone fibrosis, etc.)
|
8
|
Pleural effusion
|
5
|
Ultrasound abdomen (n = 76)
|
|
Ascites
|
30
|
Abdominal lymphadenopathy
|
58
|
Peritoneal thickening
|
20
|
Bowel wall thickening
|
18
|
Barium meal follow-through (n = 8)
|
|
Deformed and pulled up cecum
|
6
|
Multiple strictures
|
2
|
CECT abdomen (n = 42)
|
|
Abdominal lymphadenopathy
|
34
|
Ascites
|
39
|
Deformed and pulled up cecum
|
31
|
Abdominal cocoon
|
1
|
Splenic/liver tuberculosis
|
1
|
Enlarged mesenteric and para-aortic lymph nodes were the most common ultrasound finding
noted in 58 patients followed by ascites in 30 patients. Thickening of the mesentery
and peritoneum was noted in 20 patients and thickened ileocecal region was reported
in 18 patients. CECT was done in 42 patients with abdominal lymphadenopathy followed
by ascites and ileocecal thickening with pulled-up and deformed cecum as the most
common finding reported. One patient who tested positive for HIV had miliary TB on
chest X-ray ([Fig. 2]
[3]
[4]) and showed similar lesions in the liver and spleen (miliary tubercles) ([Fig. 5]). All our patients were subjected for colonoscopy and biopsies were obtained if
any mucosal abnormality was noted ([Fig. 6]).
Fig. 2 barium meal follow-through (BMFT) showing pulled up and distorted cecum with straightening
of ileocecal junction
Fig. 3 Computed tomography scan of the abdomen showing moderate free fluid in the abdomen
with conglomerate of several small bowel loops within occupying the center of the
abdomen
Fig. 4 Diffuse circumferential wall thickening noted in the terminal ileum, cecum, and ascending
colon causing significant luminal narrowing with paracolic and pericecal fat stranding
Fig. 5 Chest X-ray showing military tuberculosis in a human immunodeficiency virus positive
patient
Fig. 6 Multiple hypoattenuating lesions in the liver and spleen
Endoscopic/Colonoscopic Findings
The most common site of involvement in the gastrointestinal (GI) tract was the ileocecal
region with deformed ileocecal (IC) valve, and ulcers in the ileocecal region were
noted in 58 patients ([Fig. 7]), 5 of them had either ulcers or strictures in the ascending colon ([Fig. 8]), and 2 showed transverse ulcers with luminal narrowing in the transverse colon.
One patient on gastroscopy was noted to have nodular lesion of the antrum ([Fig. 9]) which was biopsied and histology was consistent with TB (caseating granuloma with
AFB). Twenty-two patients who underwent colonoscopic biopsies showed the histological
features diagnostic of TB ([Table 5]).
Fig. 7 Colonoscopy showing deformed and narrowed IC valve with ulcers and polypoidal lesions
in the cecum and ascending colon
Fig. 8 Colonoscopy showing a stricture due to ulceroproliferative lesion in the ascending
colon mimicking malignancy. Histology showed casesating granuloma with numerous AFBs
Fig. 9 Esophagogastroduodenoscopy showing a nodular lesion in the stomach which was subsequently
diagnosed to be tubercular in origin
Table 5
Endoscopic/colonoscopic findings
Anatomic site of affection
|
Number of patients
|
IC, ileocecal valve
|
Ileocecal region with deformed IC valve and transverse ulcers, polypoidal/nodular
mucosa
|
58
|
Ascending colon ulcers/strictures
|
5
|
Transverse colon ulcers
|
2
|
Multiple ulcers throughout the colon
|
1
|
Antral nodules
|
1
|
Treatment and Follow-up
All patients enrolled in this study were initiated on ATT (weight-based regimen) with
close follow-up of liver function tests. Patients with miliary TB were treated with
an extended 9-month regimen, and the remaining patients were initiated on 6-month
ATT regimen. Six patients were lost to follow-up, of whom three could not be traced.
Treatment was interrupted in eight of the patients due to drug-induced hepatotoxicity
of whom seven tolerated sequential reinitiation of AKT and one patient developed acute
liver failure and had to be referred to a tertiary liver center. Fortunately, this
patient survived and had to be treated with second-line AKT and went on to complete
12 months of treatment with any further untoward events.
Discussion
It is estimated that the Indian subcontinent is home to ~25% of the world's TB cases.[2] The primary site of TB is usually lung, from where it can get disseminated to other
parts of the body. Abdominal TB which is the sixth most common extrapulmonary site
of TB is usually diagnosed late due to its nonspecific symptoms.[6] Hence, a high index of suspicion by an astute clinician helps in early diagnosis
and timely treatment to prevent long-term morbidity and mortality from the disease.
The ileocecal region is the most common site of infection due to rich lymphatic tissue,
physiological stasis, and limited digestive activity.[7]
Of the 76 patients in our study, there was a slight preponderance of male patients
who constituted 52.6% of the subjects and 47.3% were females. Studies have shown that
abdominal TB is predominantly a disease of young adults at the peak of their productive
life, and about two-thirds of the affected patients are in the second to fourth decades
of their lives. The same observation was reflected in our study, wherein abdominal
TB was more prevalent in patients aged 18 to 40 years (n = 50) who constituted 66% of the study population.[8]
[9]
Pain abdomen was the most common symptom noted in 70 (92.1%) of the patients; the
same was also reported in previous studies.[6]
[10]
[11] Loss of appetite with weight loss, fever, pyrexia of unknown origin (PUO), constipation,
abdominal distention, and diarrhea were the other symptoms noted in descending order
of frequency.
In our study, 25 patients (32.8%) showed concomitant pulmonary findings, while previous
studies have documented ~15 to 25% of cases with abdominal TB to have coexisting pulmonary
TB.[12]
[13] Due to financial constraints, CECT was done only in 42 patients (55.56%) in our
study, with the most common finding being mesenteric lymphadenopathy in isolation
or with involvement of other GI organs and peritoneum. Similar findings were demonstrated
by Suri et al, who reported mesenteric lymph nodes as the most common site of affection
in abdominal TB.[14] Other findings included mural thickening of the ileocecal region and peritoneal
involvement ([Figure 4]).
Although short-course (6-month) chemotherapy with ATT is usually well tolerated, drug-induced
hepatotoxicity is the most common culprit, leading to interruption of treatment.[15]
[16] The reported incidence of antituberculosis drug-induced liver injury is ~8 to 36%
in India.[17] Acute viral hepatitis should be ruled out, especially in countries like India that
are endemic for it. In our study, eight patients (10.5%) developed hepatotoxicity
due to ATT, seven out of whom tolerated either sequential reinitiation of AKT or modified
ATT. One patient had to be referred to a tertiary liver center due to the development
of ALF.
In patients with compatible ileocecal lesions and a history of exposure to TB, strong
positive PPD skin test, evidence of TB on chest X-ray, or those originating from an
endemic region, Wagner et al favored initiation of antituberculosis therapy.[18] We followed our clinical instincts and started five patients on empiric AKT as there
was diagnostic dilemma due to discordance in clinical and laboratory findings, and
fortunately, all five patients showed a dramatic response with ATT with complete resolution
of their symptoms at the end of 6 months of treatment.
Conclusions
Abdominal TB presents with a wide variety of nonspecific symptoms and hence requires
a high index of suspicion for timely diagnosis and treatment. Early diagnosis and
initiation of ATT are essential to prevent morbidity and mortality associated with
this multisystem infectious disease. Chemotherapy is same as for pulmonary TB with
surgery reserved for life-threatening obstructive features. A therapeutic trial of
ATT is appropriate in cases of diagnostic dilemma. Although drug-induced hepatotoxicity
remains a dreaded complication, close monitoring of liver function tests and regular
follow-up with alteration in therapy offers an effective cure.
Financial Support and Sponsorship
Nil.