A 2-year-old boy with abdominal pain and prolonged fever

Prepared by.........Nuthapong Ukarapol , M.D.
Thanyawee Puthanakit, M.D.
Virat Sirisanthana, M.D.
CC : Prolonged fever and abdominal pain for 3 weeks.

PI : The patient has had high grade fever and abdominal pain for 3 weeks prior to admission. The abdominal pain was confined over the right upper quadrant and epigastrium. He was treated as dyspepsia without clinical improvement. At the general hospital, physical examinations revealed abdominal distention and right upper quadrant tenderness. An ill-defined mass at RUQ was also noted. A complete blood count showed hematocrit 30% and WBC 7650/cumm with 44% PMN. Ultrasonography demonstrated a cystic lesion, 6x4x6 cm, locating anterior to the gallbladder. He was treated with ampicillin, gentamicin, and metronidazole intravenously, because of suspected infected choledochal cyst. He was then referred to Chiang Mai University Hospital.
PH: He was born at home. According to his past history, he was immunized once with unknown vaccine when he was 3 months old. There was no history of contact with tuberculosis patient.

Significant PE

BW=9.5 kg (less than 3rd percentile for Thai boy), Ht=82 cm (3rd percentile for Thai boy)
BP=110/70 mmHg, PR 110/min , RR=24/min , body temperature = 38-39 C (intermittent fever)
Moderately pale, no jaundice, few cervical lymph nodes=0.5 cm in diameter
Heart: regular rhythm, no murmur, increased P2.
Lungs: no retraction, normal breath sound.
Abdomen: Mild distension over upper abdomen with an ill-defined mass, sized 5x5 cm. Marked tenderness was noted over the mass. The liver edge was sharp, 5 cm from the right costal margin. There was no splenomegaly nor ascites.
Extremities: No edema

Problem lists

1. Prolonged fever.
2. Upper abdominal pain with RUQ mass
3. Malnutrition
4. Incomplete immunization

Investigations

CBC : Hb 10.1 gm/dl, Hct 30.3%, WBC=15,600 cell/cu.mm, PMN 49%, L 41%, Mono 9%, Eosinophil 1%, Platelet 636,000/cumm
Stool examination : positive for occult blood
Chest X-ray : perilhilar infiltration, hilar lymphadenopathy, and minimal right pleural effusion
LFTs : Albumin 3.0 gm/dL, globulin 2.9 gm/dL, cholesterol 89 mg/dL, alkaline phosphatase 153 IU/L, AST 25 IU/L, ALT 9 IU/L, total/ direct bilirubin 0.57/0.28 mg/dL
PT : 15.5 sec (12.0), PTT : 31.8 sec (30.9)

Figure 1. CT abdomen showed a 5x7 cm well-defined non enhancing hypodense lesion in the left sub hepatic region, anterior-inferior to the gallbladder, containing air-fluid level. Internal debris and calcification were noted. A tiny calcified nodules was seen in the hepatic region. Multiple enlarged mesenteric lymph nodes, some containing rim, punctate, and amorphous calcification, were noted.

Provisional diagnosis: Liver abscess.
Clinical course:

> The patient underwent percutaneous aspiration and drainage. Foul smell (fetid odor) cloudy fluid was obtained (Figure 2). Gram's stain revealed many PMNs and mixed organisms (Gram positive cocci, Gram positive bacilli, Gram negative cocci and Gram negative bacilli) (Figure 3-4). The specimen was sent for culture. It grew 2 stains of E. coli. .

Figure 2.
Figure 3.
Figure 4.
>The patient was treated as pyogenic liver abscess with cefotaxime, amikacin, and metronidazole for 3 weeks. Percutaneous drainage was left in place for one week. Follow up ultrasonography 3 weeks after the treatment showed complete resolution of the liver abscess.
> Since the patient had no history of BCG vccination and some of his findings, such as:
  • CXR finding (peri hilar infiltration, hilar lymphadenopathy, and minimal right pleural effusion)
  • Calcifications in the liver and mesenteric lymph nodes
  • Malnutrition
could not be explained solely by liver abscess. The tuberculosis was suspected, so the tuberculin skin test (PPD) was done. It was positive, 15 mm induration.
> Treatment with antituberculous drugs was then initiated and will be continued for 6-9 months.
Liver abscess
- Liver abcess is rare in children.
- Etiology The liver abscess can result from various microorganisms, including bacteria, amoeba, Ecchinococcus, M. tuberculosis, and fungus. The incidence of the last 3 etiologies is considerably low. For pyogenic liver abscess, gram-positive organisms (esp. Staphylococcus aureus) are the most common cause in children, followed by gram-negative organisms, e.g. E. coli, and Klebsiella sp., and anaerobic organisms. Fungal liver abscess should be considered in immunocompromised hosts.
- Symptoms and signs
In children, clinical manifestations are non-specific. Fever, abdominal pain, RUQ tenderness, and hepatomegaly comprise as clinical presentations. Chronic diarrhea might be noted in only half of patients with amebic liver abscess.
- Laboratory: Leukocytosis with predominant neutrophil can be seen in pyogenic liver abscess. Peripheral eosinophilia might be evident in hydratid cyst and amebic liver abscess. Liver function tests show mildly elevated alkaline phosphatase, transaminases, and bilirubin. Radiologic studies are required to establish diagnosis including, ultrasonography and CT scan. Percutaneous aspiration and drainage are necessary to identify microorganism and treatment. Serology tests for Entameba histolytica and Ecchinococcus are helpful in suspected cases.
- Treatment
Percutaneous or surgical drainage is required for a large abscess (>6-8 cm in diameter). Three-six week course of appropriate antibiotics should be prescribed.
Comment on causative bacteriology of the liver abscess in this case:

- Although the pus culture grew two strains of E. Coli (aerobe), a fetid odor of the specimen and Gram-stained smears which showed mixed organisms supported the presence of anaerobes in the sample. The liver abscess in this case is a mixed aerobic-anaerobic infection.
- The specimen was sent for anaerobic culture and there was no organism isolated. This was not uncommon, since special precautions are needed for appropriate collection and transport of specimens.
- Treatment of anaerobic infections may be difficult. Failure to provide antibacterial coverage against the anaerobes in a mixed aerobic-anaerobic infection may lead to an inadequate response.
- Resistance of anaerobic bacteria to antibacterial agents is increasing, and a number of antimicrobials have poor or no activity against anaerobes.
- Surgical management, particularly drainage is an important aspect of treatment of most anaerobic infections.

Suggested reading:
1. Pashankar DS, Schreiber RA. Postnatal infections of the liver: bacterial, parasitic, and other infections. In: Walker WA, et al. editors. Pediatric gastrointestinal disease. 3rd ed. Ontario: B.C. Decker Inc; 2000. p. 976-85.
2.Yeoh KG, Yap I, Wong ST, Wee A, Guan R, Kang JY. Tropical liver abscess. Postgrad Med J 1997;73:89-92.
3.Patanakar T, Prasad S, Armao D, Mukherji SK. Tuberculous abscesses of the liver. AJR 2000;174:1166-7.
4. Finegold SM. Anaerobic Bacteria : General Concepts. In Mandell GL, Bennett JE and Dorin R, eds. Principles and practice of infectious diseases, 5th ed. Philadelphia: Churchill Livingston; 2000:2519-2537.
Diagnosis : Pyogenic liver abscess and abdominal tuberculosis

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