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Liver Abscess in Children-experience From a Single Tertiary Care Center of North India

Etiology, Clinical Profile and Predictors of Complications

Lal, Sadhna Bhasin MD, DM*; Venkatesh, Vybhav MD, DM*; Kumar, Aditi MD, DM*; Anushree, Neha MD*; Seetharaman, Keerthivasan MD*; Aneja, Aradhana MD, DM*; Chaluvashetty, Sreedhara B. MD; Sehgal, Rakesh MD

Author Information
The Pediatric Infectious Disease Journal: May 2021 - Volume 40 - Issue 5 - p e179-e184
doi: 10.1097/INF.0000000000003053
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Liver abscess (LA) in children, although uncommon in developed countries is still a frequently encountered problem, in developing countries, especially in the tropics, resulting in significant morbidity. Pyogenic LA (PLA) followed by amebic LA (ALA) account for majority of cases, a minority being attributed to fungal and tubercular etiology.1,2 PLA has been reported to account for 11–140 cases per 100,000 pediatric admissions across various countries.3–5Staphylococcus aureus, Klebsiella pneumoniae and Escherichia coli account for majority of cases of PLA both in developed and developing nations.1,6 ALA occurs in approximately 5%–7% of patients after an amebic infestation of the intestinal tract. Higher incidence of ALA has been reported from endemic regions like the Indian subcontinent, Africa and Brazil.7–9 India is among the countries with a high prevalence of amebiasis; reported rates vary from 11% to 60% based on the different methods used for estimating prevalence.10–13 However, despite this endemicity, PLA is perceived to be the commonest cause of LA even in Indian children, resulting in a standard policy of using prolonged antibiotics, presuming a pyogenic etiology of LA.1,5,14

Antibiotics coupled with either single time aspiration or percutaneous catheter drainage (PCD) is now the first line of management, owing to a high success rate and fewer complications with this approach.1,15 With improved management techniques, mortality rates in children with LA have come down from 15% to 40% in yesteryears to less than 0.8% nowadays.4,16,17 The literature on pediatric LA mostly describes the clinical, etiological, management profiles; data regarding predictors of complications in children with LA is lacking. This study aimed to relook at the etiology, presentation and complications of pediatric LA in the current context with an emphasis on exploring the risk factors for complications in children with LA treated in a Pediatric Gastroenterology center of North India.


A retrospective medical record review of all consecutive children with LA managed in the Division of Pediatric Gastroenterology, Hepatology and Nutrition of the Post Graduate Institute of Medical Education and Research, Chandigarh from September 2017 to August 2020 was performed. Along with the demographic data, the presenting clinical features, imaging findings, details of blood investigations and the management procedures were recorded. Complications (impending rupture, rupture, vascular thrombosis, pleural effusion/consolidation, peritonitis, septic shock, death) due to LA, if any, were also recorded. Details of immunodeficiency workup, if any, were also recorded (HIV serology, nitroblue tetrazolium test and immunoglobulin profile). Those with incomplete clinical and radiologic details and those lost to follow-up after treatment were excluded. The study was approved by the Institute Ethics Committee.


All children had an initial ultrasonography (USG) imaging and the details of LA such as the site, size, number and features of impending rupture (<1 cm liver parenchyma between the abscess cavity and liver margin) and rupture, if any, were noted. Chest radiograph was done to look for features of pleural effusion and consolidation. A computed tomography scan of the abdomen was done in cases with a diagnostic dilemma or for better anatomic delineation of abdominal or extra-abdominal complications.


  1. As per the standard protocol, all children initially received empirical intravenous antibiotic regimen comprising ceftriaxone, cloxacillin and metronidazole in weight-appropriate doses. Those managed with antibiotics alone without any drainage procedure were classified into “conservative” management category.
  2. In those with ALA, antibiotics were stopped after 2 weeks, and no luminal amebicide was given. Those with PLA and mixed infection LA received antibiotics for a total duration of 6 weeks.
  3. Drainage procedures, if required, were performed, with strict asepsis, after informed consent, under USG guidance and using intravenous sedation with midazolam (0.1 mg/kg) and ketamine (1 mg/kg). “Percutaneous needle aspiration (PNA)” was done using 18G spinal needle for smaller abscesses (<5 cm). Response to PNA was monitored by USG, and a repeat PNA was done if necessary (liquefied abscess contents, persistent symptoms). The aspirated pus was sent for Gram stain, culture and sensitivity and polymerase chain reaction (PCR) for detection of Entamoeba histolytica DNA. Antibiotics were modified according to the culture sensitivity report.
  4. Amebic PCR: DNA isolated from axenically grown E. histolytica (HM-1: IMSS) was used as control. After isolating DNA from clinical samples using the standard phenol:chloroform:isoamyl alcohol method, they were amplified using the primers 5′-ATGCACGAGAGCGAAAGCAT-3′ and 5′-GATCTAGAAACAATGCTTCTCT-3′ in a standard PCR assay as described previously.18
  5. For larger abscesses (>5 cm), PCD, was performed, wherein, after aspiration as described above, appropriate sized percutaneous catheter (8–12 French) was placed using the Seldinger technique and attached to a collection bag. An additional PCD was placed in case of multiple noncommunicating large LAs.
  6. Before drainage, children with deranged coagulogram (prothrombin time [PT] prolongation more than 3 seconds above the upper limit normal) were transfused with fresh frozen plasma to correct the coagulation abnormality.
  7. Post drainage, drain output was monitored daily, and when it reduced to less than 10 mL for 3 consecutive days, a repeat USG was performed for assessing the residual abscess cavity. If the abscess had organized with no residual liquefied contents, PCD was removed, whereas catheter repositioning was done if there was significant residual liquefied content to facilitate further drainage. Any complications during the procedure were noted.
  8. Children with pleural effusion were managed conservatively, and only in symptomatic patients (respiratory distress, persistent fever), pleural tap and placement of intercostal chest drain (ICD) were done. The monitoring of output from ICD, response assessment and removal was done in a similar manner as described above with PCD.

Etiologic Categorization of LA

LA was classified as follows:

  1. ALA: a) Positive amebic PCR in the pus with
    • b) Negative pus Gram stain and
    • c) Sterile culture from pus/blood.
  2. PLA: a) Negative amebic PCR in the pus with/without
    • b) Positive pus Gram stain or
    • c) Positive culture from pus/blood.
  3. Mixed: a) Positive amebic PCR in the pus with
    • b) Positive pus Gram stain or
    • c) Positive culture from pus/blood.

Pus and blood cultures were done both for aerobic and anerobic organisms.

Follow-up and Response

Post drainage, all the children were followed up for resolution, clinically as well as radiologically, by serial USG imaging. Following clinical recovery, some children were discharged with PCD in situ, who were assessed weekly by USG on outpatient basis for reduction in liquefied content of the LA and removal of PCD. All the children post removal of PCD were monitored using serial USG every 3–4 weekly for complete resolution of abscess (organized abscess with no liquid component or complete disappearance of altered echogenicity) or recurrence.


Analysis was performed using Statistical Package for Social Sciences software version 20.0 (SPSS Inc, Chicago, IL). Normality of the data was tested using Shapiro-Wilk test and visual inspection of Q-Q plots. Median and interquartile range was used to describe continuous variables. χ2 test was used to compare categorical data between groups. Mann-Whitney U test (for 2 groups) and Kruskal-Wallis (for more than 2 groups) were used to compare continuous variables like age, length of hospital stay, etc. Spearman correlation coefficient was used to determine if there was any correlation between 2 continuous variables. A binary logistic regression was done to predict the factors like age, type, site and size of abscess, etc., associated with complicated LA. All tests were 2 tailed and a P value of <0.05 was considered statistically significant.


Clinical and Etiologic Details

A total of 86 children with LA were managed in our unit from September 2017 to August 2020. After exclusion (inadequate details-1; lost to follow-up after PCD-3; tubercular abscess-1), a total of 81 children (median age 7; range 1–12 years, 53% boys) were included in the final analysis. The triad of fever, hepatomegaly and right upper quadrant tenderness was seen in 65 (80.2%) children. PT prolongation >3 times upper limit normal was seen in 60 (77%) and biochemical jaundice in 12 (14.8%) children. ALA, PLA and mixed infection LA were diagnosed in 40 (49.4%), 32 (39.5%) and 9 (11.1%) children, respectively. Single LA was present in 71.6% and right lobe involvement predominated (69%). The demographic, clinical, investigative and management profiles of the whole cohort and among different etiologies are summarized in Table 1. There were no significant differences in these parameters among different etiologies of LA except for the management profiles (P = 0.04). Although 10 (12.3%) children had a positive pus Gram stain (Gram-positive cocci-7, Gram-negative bacilli-2, both-1); culture positivity was seen in only 6 (7.4%) children (blood-2 [1-Salmonella, 1-coagulase-negative Staphylococcus]; pus-4 [1-E. coli, 2-S. aureus, 1-Enterococcus]). In majority, no predisposing factor for LA was identified: only 2 children (2.5%) had underlying hyper IgE syndrome. Initial USG was suggestive of LA in all and a computed tomography was done in 29 children (35.8%) with suspected rupture/caudate lobe LA to better delineate the lesion (Fig. 1A–C) before drainage.

TABLE 1. - Clinical and Laboratory Profile of Whole Group of Children With Liver Abscess and According to the Etiology
Characteristics Whole Group (n = 81) Pyogenic LA (n = 32) Amebic LA (n = 40) Mixed Infection LA (n = 9)
Age (yr, median [IQR]) 7 (3–9.5) 5.5 (2–9) 7 (5–10) 5 (2–7)
Gender (boys, n [%]) 43 (53) 15 (47) 21 (52.5) 7 (77.8)
Presenting complaints (n [%])
 Fever 77 (95.1) 31 (96.9) 37 (92.5) 9 (100)
 Abdominal pain 70 (86.4) 25 (78.1) 38 (95) 7 (77.8)
 Abdominal distension 33 (40.7) 14 (43.8) 15 (37.5) 4 (44.4)
 Vomiting 18 (22.2) 6 (18.8) 11 (27.5) 1 (11.1)
 Jaundice 6 (7.4) 4 (12.5) 1 (2.5) 1 (11.1)
Signs (n [%])
 Pallor 47 (58) 20 (62.5) 20 (50) 7 (77.8)
 Hepatomegaly 81 (100) 32 (100) 40 (100) 9 (100)
 RUQ tenderness 74 (91.4) 27 (84.4) 39 (97.5) 8 (89)
 Ascites 13 (16) 8 (25) 4 (10) 1 (11.1)
 Pleural effusion/consolidation 27 (33.3) 9 (28.1) 13 (32.5) 5 (55.5)
Hemogram (median [IQR])
 Hemoglobin (g/dL) 8.8 (7.4–9.9) 8.7 (7.5–9.7) 9 (7.3–11) 8 (7.3–9.6)
 Total leukocyte count (×109/L) 17 (12.5–21.2) 15.5 (10.7–20.3) 18.1 (12.5–24.2) 18 (13.8–20.5)
 Platelet count (×109/L) 348 (261–514) 360 (227–549) 355 (267–509) 310 (282–448)
Liver function tests (median [IQR])
 Total bilirubin (mg/dL) 0.4 (0.1–0.7) 0.5 (0.1–1) 0.58 (0.1–0.6) 0.4 (0.2–0.8)
 Direct bilirubin (mg/dL) 0.1 (0.01–0.3) 0.1 (0.01–0.3) 0.1 (0.01–0.2) 0.1 (0.09–0.3)
 AST (U/L) 33 (26–61) 34 (26–72) 32 (25–54) 39 (20–90)
 ALT (U/L) 31 (20–61) 34 (19–62) 31 (20–61) 28 (18–69)
 ALP (U/L) 231 (178–290) 226 (181–283) 246 (181–332) 181 (152–225)
 Total protein (g/dL) 6.4 (5.6–7) 6.2 (5.2–7) 6.6 (5.9–7.3) 6.2 (5–7.1)
 Albumin (g/dL) 2.9 (2.3–3.4) 3 (2.1–3.5) 2.9 (2.4–3.3) 2.8 (2–3.5)
Coagulogram (median [IQR])
 Prothrombin time (s) 19.1 (17–21.5) 19 (16.7–21) 19.3 (17.3–22) 19 (17.4–23)
 INR 1.37 (1.2–1.5) 1.3 (1.2–1.5) 1.4 (1.2–1.5) 1.3 (1.2–1.6)
Characteristics of LA
 Single:multiple 58:23 22:10 32:8 4:5
 Right lobe/left lobe/both 56/16/9 21/7/4 28/8/4 7/1/1
 Size (maximum dimension in cm) 6.9 (5.7–8.1) 6.6 (5.1–7.8) 7 (6–7.8) 8 (6.5–10)
Complications (n [%]) 43 (53) 17 (53.1) 21 (52.5) 5 (55.6)
Management (n [%])
 Conservative 9 (11.1) 7 (21.8) 2 (5) 0 (0)
 Percutaneous needle aspiration 3 (3.7) 0 (0) 3 (7.5) 0 (0)
 Percutaneous catheter drainage 67 (82.7) 23 (71.9) 35 (87.5) 9 (100)
 Surgery 2 (2.5) 2 (6.3) 0 (0) 0 (0)
Duration of hospital stay (d, median [IQR]) 13 (7.5–18.5) 13.5 (7–20) 11.5 (7–18) 16 (12–21)
Time to resolution (d, median [IQR]) 48 (30–60) 46.5 (30–60) 48 (34–58.5) 52 (26–55)
ALP indicates alkaline phosphatase; AST, aspartate transaminase; IQR, interquartile range; RUQ, right upper quadrant.

Imaging features of liver abscess in children. Computed tomography scan of the abdomen showing (A) loculated abscess in right lobe with right pleural effusion, (B) single large abscess in left lobe, (C) 2 abscesses with impending rupture and (D) colonoscopy image at the level of ileocecal valve in a child with amebic liver abscess showing ulcers (arrows).


Complicated LA was seen in 43 (53.1%) children of which respiratory involvement (pleural effusion/consolidation) was the commonest (33.3%; 27/81) followed by rupture (29.6%; 24/81; pleural-14, subphrenic-7, abdominal-3), impending rupture (14.8%; 12/81), vascular thrombosis (8.6%; 7/81; inferior vena cava-2, hepatic veins-3, portal vein-1, hepatic and portal vein-1) and septic shock (1.2%; 1/81). ICD was required in 14 (32.5%) children. The comparison of various parameters between complicated and uncomplicated LA is depicted in Table 2. There was significant difference in alanine transaminase (ALT), PT/international normalized ratio (INR), serum total protein and albumin levels between complicated and uncomplicated LA subgroups. A logistic regression was performed to ascertain the effect of age, gender, ALT, PT/INR, albumin, site, size, type and number LA on the likelihood of complications. The regression model was significant χ2 (12) = 26.5 (P < 0.005). Of these parameters, children with serum albumin less than 3 g/dL had higher chance of having complicated LA compared with those with albumin levels >3 g/dL (odds ratio, 4.8; 95% confidence interval, 1.5 to 15; P = 0.008). Further, the duration of hospital stay had a negative correlation with serum albumin levels (r = –0.34, P = 0.002).

TABLE 2. - Comparison of Parameters Between Complicated and Uncomplicated Liver Abscess Groups
Characteristics Uncomplicated LA (n = 38) Complicated LA (n = 43) P
Symptoms and signs (n [%])
 Fever 37 (97.4) 40 (93) 0.6
 Abdominal pain 35 (92.1) 35 (81.4) 0.2
 Abdominal distension 7 (18.4) 27 (62.8) 0.001
 Pallor 20 (52.6) 27 (62.8) 0.3
 Ascites 1 (2.6) 12 (27.9) 0.002
Hemogram (median [IQR])
 Hemoglobin (g/dL) 8.9 (7.5–10) 8.5 (7.3–9.9) 0.34
 Total leukocyte count (×109/L) 18.4 (14.8–21.1) 15.4 (10.3–24.2) 0.21
 Platelet count (×109/L) 403 (309–591) 290 (211–460) 0.003
Liver function tests (median [IQR])
 Total bilirubin (mg/dL) 0.3 (0.1–0.6) 0.5 (0.1–0.9) 0.2
 Direct bilirubin (mg/dL) 0.1 (0.01–0.2) 0.1 (0.01–0.3) 0.7
 AST (U/L) 32 (24–49) 34 (26–96) 0.1
 ALT (U/L) 27 (19–38) 53 (26–85) 0.003
 ALP (U/L) 219 (180–256) 247 (177–320) 0.1
 Total protein (g/dL) 6.6 (6–7.2) 5.9 (5.2–7) 0.007
 Albumin (g/dL) 3.1 (2.8–3.5) 2.5 (2–3) 0.001
Coagulogram (median [IQR])
 Prothrombin time (s) 18.2 (17–21) 20.3 (18–23) 0.02
 INR 1.3 (1.2–1.5) 1.5 (1.2–1.6) 0.02
Etiology of LA (n [%]) 0.9
Pyogenic LA 15 (39.4) 17 (39.5)
 Amebic LA 19 (50) 21 (48.8)
 Mixed infection LA 4 (10.5) 5 (11.6)
Abscess characteristics
 Number (n [%]) 0.4
  Single 29 (76.3) 29 (67.4)
  Multiple 9 (23.7) 14 (32.6)
 Site 0.4
  Right lobe (n [%]) 25 (65.8) 31 (72)
  Left lobe (n [%]) 10 (26.3) 6 (14)
  Both lobes (n [%]) 3 (7.9) 6 (14)
 Size (maximum dimension in cm) (median [IQR]) 6.5 (5–7.7) 7 (6.5–8.6) 0.02
Management (n [%]) 0.4
 Conservative 5 (13.2) 4 (9.3)
 Percutaneous needle aspiration 2 (5.3) 1 (2.3)
 Percutaneous catheter drainage 31 (81.5) 36 (83.7)
 Surgery 0 (0) 2 (4.7)
Duration of hospital stay (d, median [IQR]) 10 (6–13) 18 (11–22) 0.001
Time to resolution (d, median [IQR]) 48 (30–55) 48 (30–60) 0.7
ALP indicates alkaline phosphatase; AST, aspartate transaminase; IQR, interquartile range.

Management and Outcome

Nine children (11.1%) responded to conservative management alone with intravenous antibiotics. Majority of the children were managed with PCD (82.7%, 67/81) followed by PNA (3.7%; 3/81). One child with a ruptured caudate lobe abscess was managed with endoscopic ultrasound (EUS) guided transgastric drainage using plastic stents and for the analysis purpose was included in the PCD category. Multiple pigtails (≥2) were required in 7 children. In those children who underwent PCD, after complete drainage of pus, 6 children (9%; 6/67) had bilious drain output, which resolved in all over a period of 11.1 ± 2.6 days. Mean PCD duration was 16.3 ± 9 days (range 4–60 days). Only 2 children (2.5%) required surgical drainage. Median duration of intravenous antibiotics and duration of hospital stay was 14 days (11–16 days) and 14 days (range 5–45 days), respectively. Median duration of follow-up was 2 months (range 1–12 months) and median time to resolution of LA post discharge was 48 days (range 24–88 days) and there were no recurrences.


LA continues to be a public health problem in the tropical countries. Clinical features like fever, abdominal pain, hepatomegaly, right upper quadrant tenderness in our study were comparable to the results from previous studies.5,14,15,17 We also found a higher proportion of children (77%) with deranged coagulogram at presentation as reported by Roy Choudhury et al.15 However, drainage procedure was not delayed pending correction of coagulopathy in cases of impending rupture.

Majority of our children had no predisposing factors for development of LA as seen in the developed countries as evinced by the negative immunologic work up in 79 of 81 cases. LA could be the first manifestation of chronic granulomatous disease in children, an important predisposing factor for LA.19 However, 92.5% of our children had a screening nitroblue tetrazolium test for chronic granulomatous disease, and none of them were positive.

The bacterial culture positivity rate was lower than previously reported. This may be due to the initiation of antibiotics before referral (43% in our cohort). ALA is a common form of invasive amebiasis caused by E. histolytica and can lead to significant morbidity among children in the endemic areas.5,20 Few studies from endemic regions report ALA accounting for more than 30% cases of pediatric LA.8,21 We observed a higher proportion of ALA (49.3%) compared with PLA in contrast to previous studies.5,14 This may be reflective of the poor level of sanitation and the endemicity of amebiasis in our region. Also, the higher detection of ALA in our cohort is because we used for the first time in children, the PCR technique for the detection of E. histolytica DNA in pus samples. This has a higher sensitivity (70%–100%) and specificity (95%–100%) for the diagnosis of ALA when compared with antibody-based serologic tests, which have low diagnostic value in endemic areas.22–27 It is important to differentiate between ALA and PLA to avoid unnecessary prolongation of antibiotic treatment to 6 weeks in all children with LA.

Similar to previous studies, we did not find any clinical parameters to differentiate ALA and PLA.14,15 Although ALA tends to be solitary, multiple abscesses have been reported up to 10%–30%.21,28,29 In our cohort, 20% of children with ALA had multiple abscesses. We had 9 (11.1%) children with mixed infection LA which is usually seen in endemic regions to the tune of 6%–20%.30,31 These children might be having ALA with superadded bacterial infection. Colonic involvement in ALA have been described in more than two-thirds of cases in adults.29,32 Although we did not perform colonoscopy in all the children with ALA, at least 2 children with ALA who underwent a colonoscopy showed amebic ulcers (representative image—Fig. 1D).

More than half of our patients had complicated LA irrespective of the etiology, with pleural effusions being the commonest complication. It has been observed that these are predominantly sympathetic effusions and resolve on their own. However, half of our patients with pleural effusions (51.8%; 14/27) required ICD due to symptoms similar to the results by few researchers.15,33 LA can predispose to thrombosis of nearby vessels.34,35 A significant proportion (16.2%) of our cohort had vascular complications leading to hepatic venous outflow tract obstruction and portal vein thrombosis. The 2 children with portal vein thrombosis on follow-up developed portal cavernoma and extra hepatic portal hypertension and are under follow-up for development of varices. These findings highlight the need for meticulous evaluation using Doppler USG at presentation as well as during follow-up in children with LA. Although there were no clinical and laboratory parameters to differentiate among the etiologies of LA in our study, we identified certain parameters which could predict complicated LA. Children with complicated LA presented with significantly higher frequency of abdominal distension and ascites (P < 0.05). Ileus and hypoalbuminemia could have accounted for these features in these children. Also, children with complicated LA had significantly higher levels of ALT, prolonged PT and INR and low levels of serum total protein and albumin. Moreover, a lower level of serum albumin significantly prolonged the hospital stay (P = 0.002).

There has been a paradigm shift in the management strategies of LA in children with PCD being increasingly used across various centers in combination with antibiotics.14,15,36,37 Open surgical drainage has been limited to a very few cases of complicated LA. PCD is found to be more effective than PNA by few researchers.14,37 Although a proportion of LA can be managed with antibiotics alone, majority would require drainage. Nearly 90% of our patients required a drainage procedure majority being PCD and surgical drainage only in 2.5%. PCD was found to be safe, feasible and effective in the management of LA in children in our study, as reported in previous studies.14,15 The complications associated with PCD include needle tract infection, bleeding, bile leak, biliary peritonitis and fistula formation.38,39 We observed bilious output in the pigtail drain in 9%, which is comparable to previous studies15 and can be managed conservatively. To overcome these complications, newer techniques like EUS guided LA drainage have been described in adults.40,41 We recently reported the first case of EUS guided ALA drainage in a child.42 Mortality rates in cases of LA have decreased to less than 1% in recent times, and we also did not observe any mortality on our cohort, despite the large fraction of children presenting with complicated LA.

To conclude, ALA is the commonest cause of pediatric LA in endemic regions, and there are no specific parameters to differentiate ALA and PLA clinically. PCD, combined with antibiotics, is safe and effective modality with minimal complications, for the management of LA in children, with the need for surgery only in a few cases. In patients with amebic LA, antibiotic treatment with metronidazole for 2 weeks is sufficient to effect a cure. Routine use of amebic PCR, as was done by us, can avoid an unnecessary prolongation of antibiotics in the majority of children with LA. This would also translate into a major reduction of treatment costs, from the public health perspective, in developing countries. Complicated LA is frequent in children but can be effectively managed. A higher ALT, prolonged PT/INR and low serum albumin levels (< 3 g/dL) would help in identifying complicated LA. Complicated LA significantly prolongs the duration of hospital stay and requires recognition for prompt and appropriate management.


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children; amebic; liver abscess; percutaneous drainage; pyogenic

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