Secondary Logo

Journal Logo

Original Studies

Abdominal Involvement in Children With Bacteriologically Confirmed Tuberculosis

A Five-year Experience From Cape Town, South Africa

Sartoris, Giulia MD*,†; Seddon, James A. PhD*,‡; Rabie, Helena PhD*; Nel, Etienne D. MMed*; Losurdo, Giuseppe MD; Schaaf, H. Simon MD (Paed)*

Author Information
The Pediatric Infectious Disease Journal: October 2020 - Volume 39 - Issue 10 - p 914-919
doi: 10.1097/INF.0000000000002749


Tuberculosis (TB) remains one of the major causes of mortality in children less than 5 years worldwide. It is estimated that 1 million children younger than 15 years of age develop TB each year,1 with an estimated mortality of 240,000 children; many of these children are undiagnosed and untreated.2 Previous studies have shown that abdominal TB occurs in approximately 1%–3% of all pediatric TB cases and represents ≈10% of extrapulmonary disease in children younger than 15 years.3–6 However, it is unclear how many children develop isolated abdominal TB and how many children with pulmonary or other types of extrapulmonary TB have additional abdominal involvement. This is likely due to the nonspecific and insidious presentation of abdominal TB that could go unnoticed in the presence of pulmonary or other extrapulmonary disease.

However, diagnosing abdominal TB is important for appropriate management. Children with severe extrapulmonary drug-susceptible TB (including abdominal TB) are recommended to receive a 4-drug regimen during the intensive treatment phase, as opposed to the usual 3-drug regimen that is advised for children with uncomplicated drug-susceptible TB.7 Children also may have complications secondary to abdominal involvement which may require further investigation, intervention and follow-up.

Bacteriologic or histologic confirmation of abdominal TB is often not achieved,8–11 as obtaining specimens can be challenging. Blood tests, such as full blood count, electrolytes, inflammation indexes and liver function tests are frequently used, but their role in diagnosis is not clear.9 Radiologic imaging therefore plays an important role in the diagnosis. Of these, ultrasonography (US) is likely the initial imaging method of choice in suspected abdominal TB in children.12,13

The aim of this study was to describe the presenting and diagnostic characteristics of children with bacteriologically confirmed TB and abdominal involvement seen at Tygerberg Hospital, Cape Town, with a focus on US imaging.


Setting and Study Population

This retrospective study was done at Tygerberg Hospital, a referral hospital in Cape Town, Western Cape province, South Africa. This hospital serves as secondary referral hospital for the surrounding suburbs and tertiary referrals for about half the province. The Western Cape had a TB notification rate of 681 of 100,000 population in 2015, and the HIV prevalence for the whole population of the Western Cape was 6.8% in 2018.14

As part of an ongoing drug resistance surveillance study, all children less than 13 years of age with positive bacteriology for Mycobacterium tuberculosis on culture or Xpert MTB/RIF (Cepheid, Sunnyvale, CA) at Tygerberg Hospital are prospectively identified and recorded in a database. From this database, which also captures clinical data including type of TB, all children who also received a diagnosis of abdominal TB by the managing clinicians from January 1, 2014, through December 31, 2018, were included in this substudy. We reviewed their medical records and their imaging reports.

Case Definitions

For this study, “abdominal TB” refers to abdominal involvement in patients with either pulmonary or extrapulmonary TB. Abdominal TB was defined as TB involving the gastrointestinal system from the distal esophagus to the rectum, the peritoneum and the intraperitoneal organs (liver and spleen), the pancreas and their lymph nodes. The diagnosis was based on (1) imaging findings interpreted by a radiologist (abdominal US, computed tomography [CT] and/or magnetic resonance imaging [MRI] scan) and/or (2) laparoscopy/laparotomy findings and/or (3) M. tuberculosis confirmation through smear microscopy, culture or Xpert in abdominal specimens (ascites, liver aspirate, abdominal lymph node or tissue biopsy during laparoscopy/laparotomy). Dependent on the site affected, we classified abdominal TB into 4 types: intra-abdominal lymph node-related type, solid organ involvement type, peritoneal type and intestinal type. Children could have more than 1 type. Intra-abdominal lymph node-related type: This was based on the findings of lymph nodes described as enlarged according to the radiologist on abdominal US, CT or MRI scan. Solid organ involvement/visceral type: This included children with spleen and/or liver abscesses, spleen calcifications or findings consistent with liver granulomas. It also included children with focal liver hyperechogenicity or diffuse coarse echogenicity on US. Children who had only hepatosplenomegaly were excluded because this finding may be due to many other conditions. Intestinal type: This included all children with dilated and/or thickened bowel loops and those with intestinal complications such as perforations, extensive bowel necrosis and intussusception. Peritoneal type: All children with ascites demonstrated radiologically. Those with exclusive involvement of the genitourinary tract or psoas abscesses were excluded.

Data Collection

Demographic and Clinical Data

Age (in months), sex, symptoms and signs on presentation, history of TB contact, weight at diagnosis (with weight-for-age Z scores calculated), sites of TB, tuberculin skin test results and HIV status were collected. HIV status was considered positive if 2 different enzyme-linked immunosorbent assay tests in children >18 months were positive, or an HIV DNA polymerase chain reaction test was positive in younger or breast-fed children. The immunologic status for HIV-positive children was classified according to their CD4 counts. CD4 counts and HIV viral loads were not necessarily done at diagnosis; we accepted results obtained within a window period of 6 months before and 1 month after admission to Tygerberg Hospital. Tuberculin skin test (Mantoux, 2 tuberculin units injected intradermally; purified protein derivative RT23, Statens Serum Institut) induration of ≥10 mm was considered positive in HIV-negative children and ≥5 mm in HIV-positive or severely malnourished children.

Laboratory Investigations

Full blood count, electrolytes, urea, creatinine and liver function tests results were collected. When possible, we collected the first blood test results undertaken at diagnosis, but as these were not necessarily done simultaneously, we accepted blood tests taken in the first 2 weeks after admission. The biochemical characteristics of the ascitic fluid are reported including cells (neutrophils and lymphocytes), total protein, albumin, serum-ascites albumin gradient, adenosine deaminase (ADA) and lactate dehydrogenase. Bacteriologic confirmation results for M. tuberculosis by culture, smear microscopy for acid-fast bacilli (AFB) or Xpert, in abdominal and extra-abdominal specimens were collected.

Imaging Findings and Invasive Investigations

Chest radiographs (CRs) were done in all patients and reviewed by an experienced pediatrician (H.S.S.) using a standardized radiologic classification.15 Abdominal US, as well as CT and MRI imaging, was reviewed by radiologists in an academic tertiary hospital. Radiologists were aware that they were looking for evidence of abdominal TB. Laparoscopy and laparotomy findings, when done, were collected.

Statistical Analysis

Descriptive data are presented as total numbers and their respective percentages, means (with respective standard deviations) and medians (when the data were not parametrically distributed, together with respective interquartile ranges [IQRs]). Comparisons were drawn between HIV status (positive vs. negative) and age (<5 years vs. ≥5 years) with abdominal US findings and type of abdominal TB and between CR findings and abdominal US findings, using χ2 test and odds ratio (OR) with 95% confidence interval (CI). Missing data were excluded from analysis. When comparing proportions, the χ2 test was used to determine P values. This retrospective study was approved by the Health Research Ethics Committee of Stellenbosch University (N19/04/046) with approval for waiver of individual informed consent.


A total of 966 children were diagnosed with bacteriologic confirmed TB at Tygerberg Hospital over the 5-year study period. One hundred eleven (11.5%) were diagnosed with abdominal TB by the managing clinicians. Sixteen patients were excluded from further analysis due to lack of data. The remaining 95 (9.8%) patients were included in the analysis (Fig. 1).

Schema of patient inclusion into the study.

Clinical Profile

Of the 95 children studied, 47 (49.5%) were boys. The median age of all the 966 bacteriologically confirmed TB cases was 30 months (IQR: 13–74), while the median age of the 95 children with abdominal TB was 43 months (IQR: 20–94) with 54 (56.8%) children younger than 5 years of age. Of the total 966 patients, 96 (9.9%) were HIV positive, while among the 95 patients with abdominal TB, 26 (27.4%) were HIV positive (OR: 4.31; 95% CI: 2.58–7.20; P < 0.001); of the 26 HIV-positive children, 13 (50%) had severe immunosuppression. The demographic and clinical features of the children with abdominal TB are summarized according to HIV status in Table, Supplemental Digital Content 1, Sixty-five (68.4%) had intra-abdominal lymph node TB, 52 (54.7%) had solid organ involvement, 22 (23.2%) peritoneal type and 10 (10.5%) had intestinal type abdominal TB.

Laboratory Findings

The laboratory findings are summarized in Table 1, including full blood count, liver function tests and ascitic analyses. All patients had a confirmed diagnosis by culture, smear microscopy for AFB or Xpert, mainly from respiratory or extra-abdominal specimens (Table, Supplemental Digital Content 2, Abdominal specimens were collected and evaluated for M. tuberculosis in 15 patients (15.8%); 13 (86.7%) were positive. Ascites was bacteriologically positive in 8 of 9 patients (88.9%). Of these 8 children with positive microbiology, Xpert was positive in 3 of 8 (37.5%) and culture in 7 of 8 (87.5%). A liver aspirate was performed in 2 children. One child had a positive Xpert result but was negative for culture and AFB microscopy. The other child had negative microbiology. An abdominal lymph node biopsy was performed in 2 children: one was culture positive and the other Xpert positive. Two other intra-abdominal laparotomy tissue specimens were collected; both were culture positive, and one was Xpert positive (Table, Supplemental Digital Content 2,

TABLE 1. - Laboratory Findings of Children (<13 Years) Diagnosed With Abdominal Tuberculosis Among Bacteriologically Confirmed Cases at Tygerberg Hospital From 2014 to 2018 Including Bloods and Ascitic Features
Laboratory Tests (Number Done) Results
Blood tests
 WBC (95/95)
  Mean (×109 /L), SD 13.8 ± 8
  Within normal range for age 51/95 (53.7%)
  Leucopenia for age 10/95 (10.5%)
  Leukocytosis for age 34/95 (35.8%)
  % Neutrophils mean (84/95), SD 65.1 ± 15
  % Lymphocytes mean (83/95), SD 25.4 ± 14
 Hb (95/95)
  Mean (g/dL) 9,3 ± 7 SD
  Within normal range for age 15/95 (15.8%)
  Anemia for age 77/95 (81.0%)
  MCV mean (SD) 77.5 (±1)
  MCH mean (SD) 23.2 (±4)
 PLT (95/95)
  Mean (×109 /L), SD 409 ± 239
  Within normal range (180–440 × 109 /L) 36/95 (37.9%)
  PLT below range 20/95 (21.1%)
  PLT above range 39/95 (41.1%)
 Liver function (mean), SD
  Albumin (g/L) (71/95) 27 ± 8
  AST (U/L) (69/95) 69 ± 69
  ALT (U/L) (79/95) 33 ± 31
  gGT (U/L) (57/95) 95.4 ± 103
  ALP (U/L) (56/95) 189 ± 148
  Total bilirubin (54/95) 15.6 ± 26
 Proteins mean (g/L), SD 38 ± 22
 Proteins > 25 g/L 4/7 (57.1%)
 Albumin mean (g/L), SD 20 ± 12
 SAAG < 11 g/L 3/5 (60%)
 ADA mean (IU/L), SD 47,7 ± 27
 ADA > 30 IU/L 6/8 (75%)
 LDH mean, SD 1584 ± 1391
 Predominance of neutrophils 2/4 (50%)
 Predominance of lymphocytes 2/4 (50%)
*Ascites detected by US in 22, but ascetic tap only done in 10 cases.
ALP indicates alkaline phosphatase; ALT, alanine aminotransferase; AST, aspartate aminotransferase; gGT, gamma-glutamyl transferase; Hb, hemoglobin; LDH, lactate dehydrogenase; MCH, mean corupuscular hemoglobin; MCV, mean corpuscular volume; PLT, platelets; SAAG, serum-ascites albumin gradient; SD: standard deviation; WBC, white blood cells.


The imaging findings, including CR, abdominal US, CT and MRI scans, are summarized in Table 2. CRs were performed in all 95 patients. Eight (8.4%) had a normal CR, and among the 87 remaining children with an abnormal CR, 21 (24.1%) had a military picture. Abdominal US was performed in 90 patients, and abdominal lymphadenopathy was the most common findings, present in 61 (67.6%) children and usually described as increased lymph node size with a central hypoechogenic area due to necrosis and liquefaction. Splenic and liver abscesses were usually described as millimetric hypoechoic lesions in the parenchyma, while findings consistent with splenic and hepatic granulomas were described as hyperechogenic.

TABLE 2. - Imaging Findings (Ultrasound, Computed Tomography, Magnetic Resonance Imaging and Chest Radiographs) of Children With Confirmed Tuberculosis and Abdominal Tuberculosis
Imaging Modality Imaging Findings Total Patients
Abdominal US (90/95) Abdominal Lymphadenopathy 61/90 (67.7%)
 Para-aortic 22/60 (36.7%)
 Mesenteric 13/60 (21.7%)
 Porta hepatis 12/60 (20%)
 Peripancreatic 12/60 (20%)
 Perisplenic 11/60 (18.3%)
 Periportal 5/60 (8.3%)
 Aortocaval 2/60 (3.3%)
 Perirenal 2/60 (3.3%)
 Retroperitoneal 2/60 (3.3%)
 Retrocaval 1/60 (1.7%)
 Ileocecal 1/60 (1.7%)
 Nonspecified (intra-abdominal) 10/60 (16.6%)
Spleen involvement
 Splenic abscesses 37/90 (41.1%)
 Splenic calcifications 5/90 (5.5%)
 Spleen coarse echo structure 1/90 (1.1%)
Liver involvement
 Liver abscesses 13/90 (14.4%)
 Liver granulomas 3/90 (3.3%)
 Liver coarse echo structure 2/90 (2.2%)
 Liver focal hyperechogenicity 2/90 (2.2%)
Hepatomegaly 19/90 (21.1%)
Splenomegaly 15/90 (16.7%)
Hepatosplenomegaly 7/90 (7.8%)
Ascites 22/90 (24.4%)
Complicated (septations, debris) 5/22 (22.7%)
Bowel loop abnormalities 7/90 (7.8%)
CT (9/95) Spleen abscesses 2/9 (2.2%)
Liver abscesses 6/9 (6.7%)
Intra-abdominal LN 6/9 (6.7%)
Loop abnormalities 1/9 (1.1%)
MRI (3/95) Intra-abdominal LN 3/3 (100%)
Spleen granuloma 1/3 (33.3%)
Chest radiograph (95/95) Normal CR 8/95 (8.4%)
Mediastinal lymph nodes 55/95 (57.9%)
Large airways compression 16/95 (16.8%)
Alveolar opacification 61/95 (64.2%)
Expansile pneumonia 5/95 (5.3%)
Bronchopneumonic opacification 13/95 (13.7%)
Miliary 21/95 (22.1%)
Ghon focus 2/95 (2.1%)
Cavities 19/95 (20%)
Pleural effusion 19/95 (20%)
Pericardial effusion 7/95 (7.4%)
Calcifications 4/95 (4.2%)
LN indicates lymph node.

We compared US findings and type of abdominal TB by HIV status as well as by age. Splenic abscesses seen on US were more common in HIV-positive children (OR: 6.93; 95% CI: 2.45–19.3; P < 0.001). Solid organ type abdominal TB was also more common in HIV-positive children (OR: 3.85; 95% CI: 1.38-10.7; P = 0.0079). Abdominal lymphadenopathy (detected by US) was seen more commonly in children older than 5 years (OR: 2.71; 95% CI: 1.04–7.06; P = 0.038), as was lymph node-related abdominal TB (detected also by CT and MRI) (OR: 3.60; 95% CI: 1.36–9.56; P = 0.008; Table 3).

TABLE 3. - Comparisons Between HIV Status and Age of Child and US Findings and Type of Abdominal TB
All Patients (n = 90) HIV Negative (n = 64) HIV Positive (n = 26) P Value Odds Ratio (95% CI)
US findings
Abdominal LN 61/90 (67.8%) 43/64 (67.2%) 18/26 (69.3%) 0.85 1.09 (0.41–2.93)
 Splenic abscesses 37/90 (41.1%) 18/64 (28.1%) 19/26 (73.1%) <0.001 6.93 (2.45–19.3)
 Liver abscesses 13/90 (14.4%) 10/64 (15.6%) 3/26 (11.5%) 0.62 0.70 (0.17–2.79)
 Splenic calcifications 5/90 (55.5%) 4/64 (6.2%) 1/26 (3.8%) 0.65 0.60 (0.06–5.63)
 Liver granulomas 3/90 (3.3%) 3/64 (4.7%) 0/26 (0%) 0.26 0.57 (0.06–5.41)
 Loop abnormalities 7/90 (7.8%) 6/64 (9.3%) 1/26 (3.8%) 0.38 0.38 (0.04–3.38)
 Ascites 22/90 (24.4%) 15/64 (23.4%) 7/26 (26.9%) 0.73 1.21 (0.42–3.41)
Type of abdominal TB
Abdominal LN-related type 65/95 (68.4%) 47/69 (68.1%) 18/26 (69.2%) 0.91 1.05 (0.39–2.79)
 Solid organ involvement 52/95 (54.7%) 32/69 (46.3%) 20/26 (76.9%) 0.0079 3.85 (1.38–10.7)
 Peritoneal type 22/95 (23.2%) 15/69 (21.7%) 7/26 (26.9%) 0.60 1.30 (0.46–3.68)
 Intestinal type 10/95 (10.5%) 9/69 (13.0%) 1/26 (3.8%) 0.19 0.27 (0.03–2.21)
All Patients (n = 90) Under 5 Years (n = 51) Over 5 Years (n = 39) P Value Odds Ratio (95% CI)
US findings
Abdominal LN 61/90 (67.8%) 30/51 (58.8%) 31/39 (79.5%) 0.038 2.71 (1.04–7.06)
 Splenic abscesses 37/90 (41.1%) 21/51 (41.2%) 16/39 (41.0%) 0.98 0.99 (0.43–2.32)
 Liver abscesses 13/90 (14.4%) 9/51 (17.6%) 4/39 (10.2%) 0.33 0.53 (0.15–1.88)
 Splenic calcifications 5/90 (55.5%) 4/51 (7.8%) 1/39 (2.6%) 0.18 0.31 (0.03–2.88)
 Liver granulomas 3/90 (3.3%) 2/51 (3.9%) 1/39 (2.6%) 0.73 0.42 (0.04–4.21)
 Loop abnormalities 7/90 (7.8%) 2/51 (3.9%) 5/39 (12.8%) 0.12 3.60 (0.66–19.6)
 Ascites 22/90 (24.4%) 14/51 (27.4%) 8/39 (20.5%) 0.45 0.74 (0.35–1.60)
Type of abdominal TB
Abdominal LN-related type 65/95 (68.4%) 31/54 (57.4%) 34/41 (82.9%) 0.0084 3.60 (1.36–9.56)
 Solid organ involvement 52/95 (54.7%) 30/54 (55.5%) 22/41 (53.6%) 0.85 0.93 (0.41–2.09)
 Peritoneal type 22/95 (23.2%) 14/54 (25.9%) 8/41 (19.5%) 0.46 0.67 (0.25–1.80)
 Intestinal type 10/95 (10.5%) 3/54 (5.5%) 7/41 (17.1%) 0.06 3.5 (0.84–14.48)
LN indicates lymph node.

We did not find associations, either in the whole cohort or in HIV-positive children between a miliary pattern on CR and splenic/liver abscesses on abdominal US (P = 0.41 and P = 0.11, respectively); nor between chest lymphadenopathy and abdominal lymphadenopathy (P = 0.84) nor between pleural/pericardial effusion and ascites (P = 0.53 and P = 0.90, respectively).


Abdominal TB is considered an uncommon form of TB in children younger than 15 years of age, constituting approximately 10%–12% of extrapulmonary disease and 1%–3% of all TB.3–6 However, we found that of the 966 confirmed TB pediatric cases in a 5-year period at Tygerberg Hospital, 12% had abdominal involvement. Consistent with other South African studies, most of our patients were <5 years on admission and no sex predilection was shown.16–18 The majority of cases of abdominal TB in children are seen in those <5 years and this seems to be largely due to the fact the that the majority of TB disease is seen in young children, as described in observational studies from the prechemotherapy era. Young children are also more likely to develop disseminated or extrapulmonary TB disease. However, we found that the median age of children with abdominal involvement (43 months) was higher than the median age of all 966 bacteriologic confirmed TB cases (30 months). The incidence of abdominal TB is reported to be similar in HIV-positive and HIV-negative patients.19,20 In our series, about a third of children with abdominal TB were HIV positive, in contrast to only 10% among the total 966 patients with bacteriologic confirmed TB in the study period. We found that blood tests were frequently in the normal range, suggesting a limited role in the diagnosis of abdominal TB in children. This is consistent with other studies of abdominal TB in children.9

Abdominal lymph node disease type, together with peritoneal TB, is reported to be the most common presentation of abdominal TB in children (45%–80%).21–24 In our series, the abdominal lymph node-related type was the most common presentation, followed by solid organ involvement, peritoneal and intestinal type. We found that abdominal lymphadenopathy/lymph node type abdominal TB was more common in children >5 years. This is contrary to what is seen in the lungs where lymph node disease occurs mainly in children <5 years of age. Solid organ involvement was present in about half of our children, with splenic abscesses as the most common feature. Similar to another study, we found that splenic abscesses and solid organ involvement were significantly more common in HIV-positive children. This suggests the need to routinely exclude, using US, abdominal solid organ involvement in HIV-positive children with TB. Contrary to what we expected, we did not see an association between miliary TB on CRs and visceral abdominal TB.

Splenic and liver microabscesses were described by our radiologists as millimetric multiple hypoechoic lesions at US and hypointense at CT throughout the parenchyma. In general, splenic abscesses are considered an uncommon entity with a reported incidence of less than 1% in autopsy studies. The prevalence in children is unclear.25–27M. tuberculosis is reported as the causative agent of splenic abscesses in up to 36% of cases among adults even in low TB burden settings.25,28–30 US is the imaging method of choice for early diagnosis of patients with suspected splenic abscesses,31 usually showing hypoechoic lesions, but it should be considered that some malignancies can mimic splenic abscesses on US. A differential diagnosis between lymphoma and small spleen abscesses, such as those due to M. tuberculosis, can be difficult even with contrast-enhanced US.32 Evaluation of clinical data, together with a combination of investigations, is essential.

Performing a fine-needle aspiration biopsy (FNAB) of the spleen in case of suspected TB abscesses is not routine in endemic countries, considering the abundant vascularization of the organ; the fear of complication like bleeding, rupture and pneumothorax; and the need for the patient to cooperate. Nevertheless, different studies showed that spleen FNAB is quite a safe procedure for tissue diagnosis reporting a complication rate of <1% cases in children and adults. Tarantino et al33 reported a yield of 100% for both microscopy for AFB and culture from splenic FNAB in the diagnosis of disseminated mycobacterial disease in adult patients with HIV disease. Further research is needed to establish the role of splenic FNAB in children, especially in low prevalence regions and in microbiologically unconfirmed cases in which a more definitive diagnosis should be pursued.

US is better than CT for detecting ascites.13 In this series, ascites was detected by US in 22 of 90 children and showed septations or debris in a quarter. The peritoneal fluid was collected in 10 children and was mainly exudative. A predominance of lymphocytes is described in the literature, but cell count analysis from ascitic fluid in TB peritonitis can either show neutrophil or lymphocyte predominance. Indeed, in our study, we found a predominance of neutrophils or lymphocytes at the same frequencies. An elevated ADA level on ascitic fluid has a high positive predictive value for TB, and a cutoff of ≥30 IU/L is usually considered reliable.9,18,34,35 An ADA level cutoff ≥39 IU/L has been shown to be associated with a sensitivity of 100% and a specificity of 97.2% for peritoneal TB in systematic review of mainly adult patients.36 In our study, we found an ADA level >30 IU/L in three quarters of cases, suggesting that, even if expensive, it remains a useful tool while awaiting results of mycobacterial cultures or biopsies. However, these results demonstrate that a high ADA or lymphocyte predominance is not always seen in abdominal TB. All 10 patients who underwent ascitic fluid collection were HIV negative, so we could not verify any differences in the composition by HIV status. The reported yields of microscopy for AFB on ascitic fluid are low,8,10,11,37,38 and ascitic cultures are usually negative in the majority of cases. We found similar results for microscopy (AFB were positive in 12.5%), yet in our study culture results were positive in 87.5%. This figure is much higher than reported in other studies, but this may be due to the more severely ill patients with ascites having had a diagnostic ascitic tap done.

This study has several limitations. This was a retrospective study with incomplete data, leading to exclusion of some cases and inability to evaluate factors such as treatment regimens/duration and treatment outcome. The study included only children with bacteriologically confirmed TB, precluding any calculation of the true prevalence of abdominal TB in children. Although all children had confirmed TB, the diagnosis of abdominal involvement was made using a combination of radiology, clinical and laboratory characteristics and it is possible that in some of these children, these features were caused by etiologies other than TB. Another limitation is that abdominal US was not performed systematically in all children with bacteriologically confirmed TB, and HIV-positive children with confirmed TB may have had more abdominal US done and that this could have led to bias; therefore, we could not define the real prevalence of abdominal involvement in these children. Abdominal US was performed by several different staff members, potentially leading to differences in definitions and findings.

Consequently, with this study, we cannot conclusively define the role of abdominal US in children with pulmonary TB. A more routine use of abdominal US in children with pulmonary TB, regardless of gastrointestinal symptoms, could be useful to define the proportion with abdominal involvement. Abdominal samples for bacteriologic confirmation of TB were collected only in 15 patients, precluding confirmation of the etiology in most patients diagnosed with abdominal TB. Except for ascites, collection of other samples is not part of the routine assessment of suspected TB in endemic countries, as it is neither feasible nor cost-effective. However, a strength of this study is that all children were bacteriologically confirmed. The presence of abdominal findings on US in children in a nonendemic area or in children with microbiologically nonconfirmed TB may have different implications. It may be that clinicians should strive harder for a definitive diagnosis and follow up carefully to rule out other diagnoses.

Abdominal involvement in children with TB appears to be underestimated, and although a prospective study would be necessary to define the true prevalence, our study suggests that abdominal involvement is common. More frequent use of abdominal US and the collection of abdominal samples to be tested by Xpert may increase the frequency that abdominal involvement is diagnosed. Abdominal TB should always be considered in a child presenting with nonspecific abdominal symptoms or signs, especially where TB is part of the differential diagnosis.


1. World Health Organization, Geneva, Switzerland. Global Tuberculosis Report. 2018Available at: Accessed December 10, 2018.
2. Dodd PJ, Yuen CM, Sismanidis C, et al. The global burden of tuberculosis mortality in children: a mathematical modelling study. Lancet Glob Health. 2017;5:e898–e906.
3. Schaaf HS, Garcia-Prats AJ. Diagnosis of the most common forms of extrathoracic tuberculosis in children. In: Handbook of Child and Adolescent Tuberculosis. 2015:New York: Oxford University Press; 16–21.
4. Basu S, Ganguly S, Chandra PK, et al. Clinical profile and outcome of abdominal tuberculosis in Indian children. Singapore Med J. 2007;48:900–905.
5. Shah I, Uppuluri R. Clinical profile of abdominal tuberculosis in children. Indian J Med Sci. 2010;64:204–209.
6. Sheer TA, Coyle WJ. Gastrointestinal tuberculosis. Curr Gastroenterol Rep. 2003;5:273–278.
7. World Health Organization, Geneva, Switzerland. Guidance for national tuberculosis programme on the management of tuberculosis in children (Second edition). 2014Available at: Accessed June 11, 2018.
8. Dinler G, Sensoy G, Helek D, et al. Tuberculous peritonitis in children: report of nine patients and review of the literature. World J Gastroenterol. 2008;14:7235–7239.
9. Sartoris G, Seddon JA, Rabie H, et al. Abdominal tuberculosis in children: challenges, uncertainty, and confusion. J Pediatric Infect Dis Soc. 2020;9:218–227.
10. Shakil AO, Korula J, Kanel GC, et al. Diagnostic features of tuberculous peritonitis in the absence and presence of chronic liver disease: a case control study. Am J Med. 1996;100:179–185.
11. Kiliç Ö, Somer A, Hançerli Törün S, et al. Assessment of 35 children with abdominal tuberculosis. Turk J Gastroenterol. 2015;26:128–132.
12. Scheepers S, Andronikou S, Mapukata A, et al. Abdominal lymphadenopathy in children with tuberculosis presenting with respiratory symptoms. Ultrasound. 2011;19:134–139.
13. Andronikou S, Wieselthaler N. Modern imaging of tuberculosis in children: thoracic, central nervous system and abdominal tuberculosis. Pediatr Radiol. 2004;34:861–875.
14. Low M, MacDonell S. Graphs that tell the story of HIV in South Africa’s provinces. Available at: Accessed February 27, 2020.
15. Marais BJ, Gie RP, Schaaf HS, et al. A proposed radiological classification of childhood intra-thoracic tuberculosis. Pediatr Radiol. 2004;34:886–894.
16. Nel ED. Schaaf HS, Zumla AI. Abdominal tuberculosis in children. In: Tuberculosis: A Comprehensive Clinical Reference. 2009:London: Saunders, Elsevier Publishers; 432–437.
17. Davies MR. Abdominal tuberculosis in children. S Afr J Surg. 1982;20:7–19.
18. Saczek KB, Schaaf HS, Voss M, et al. Diagnostic dilemmas in abdominal tuberculosis in children. Pediatr Surg Int. 2001;17:111–115.
19. Harisinghani MG, McLoud TC, Shepard JA, et al. Tuberculosis from head to toe. Radiographics. 2000;20:449–470; quiz 528.
20. Jadvar H, Mindelzun RE, Olcott EW, et al. Still the great mimicker: abdominal tuberculosis. AJR Am J Roentgenol. 1997;168:1455–1460.
21. Tinsa F, Essaddam L, Fitouri Z, et al. Abdominal tuberculosis in children. J Pediatr Gastroenterol Nutr. 2010;50:634–638.
22. Johnson CA, Hill ID, Bowie MD. Abdominal tuberculosis in children. A survey of cases at the Red Cross War Memorial Children’s Hospital, 1976-1985. S Afr Med J. 1987;72:20–22.
23. Talwar BS, Talwar R, Chowdhary B, et al. Abdominal tuberculosis in children: an Indian experience. J Trop Pediatr. 2000;46:368–370.
24. Sharma AK, Agarwal LD, Sharma CS, et al. Abdominal tuberculosis in children: experience over a decade. Indian Pediatr. 1993;30:1149–1153.
25. Nelken N, Ignatius J, Skinner M, et al. Changing clinical spectrum of splenic abscess. A multicenter study and review of the literature. Am J Surg. 1987;154:27–34.
26. Lawhorne TW Jr, Zuidema GD. Splenic abscess. Surgery. 1976;79:686–689.
27. Chun CH, Raff MJ, Contreras L, et al. Splenic abscess. Medicine (Baltimore). 1980;59:50–65.
28. Ooi LL, Leong SS. Splenic abscesses from 1987 to 1995. Am J Surg. 1997;174:87–93.
29. Chang KC, Chuah SK, Changchien CS, et al. Clinical characteristics and prognostic factors of splenic abscess: a review of 67 cases in a single medical center of Taiwan. World J Gastroenterol. 2006;12:460–464.
30. Llenas-García J, Fernández-Ruiz M, Caurcel L, et al. Splenic abscess: a review of 22 cases in a single institution. Eur J Intern Med. 2009;20:537–539.
31. Rudick MG, Wood BP, Lerner RM. Splenic abscess diagnosed by ultrasound in the pediatric patient. Report of three cases. Pediatr Radiol. 1983;13:269–271.
32. Caremani M, Occhini U, Caremani A, et al. Focal splenic lesions: US findings. J Ultrasound. 2013;16:65–74.
33. Tarantino L, Giorgio A, De Stefano G, et al. Disseminated mycobacterial infection in AIDS patients: abdominal US features and value of fine-needle aspiration biopsy of lymph nodes and spleen. Abdom Imaging. 2003;28:602–608.
34. Dwivedi M, Misra SP, Misra V, et al. Value of adenosine deaminase estimation in the diagnosis of tuberculous ascites. Am J Gastroenterol. 1990;85:1123–1125.
35. Sathar MA, Simjee AE, Coovadia YM, et al. Ascitic fluid gamma interferon concentrations and adenosine deaminase activity in tuberculous peritonitis. Gut. 1995;36:419–421.
36. Riquelme A, Calvo M, Salech F, et al. Value of adenosine deaminase (ADA) in ascitic fluid for the diagnosis of tuberculous peritonitis: a meta-analysis. J Clin Gastroenterol. 2006;40:705–710.
37. Singh MM, Bhargava AN, Jain KP. Tuberculous peritonitis. An evaluation of pathogenetic mechanisms, diagnostic procedures and therapeutic measures. N Engl J Med. 1969;281:1091–1094.
38. Muneef MA, Memish Z, Mahmoud SA, et al. Tuberculosis in the belly: a review of forty-six cases involving the gastrointestinal tract and peritoneum. Scand J Gastroenterol. 2001;36:528–532.

tuberculosis; children; abdominal; ultrasound; spleen abscesses

Supplemental Digital Content

Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.