Pediatr Surg Int (1994) 9:489-491

© Springer-Verlag 1994

Splenic abscess in children with sickle-cell disease Ahmed H. AI-Salem 1, Kolar Kadappa Mallapa 2, S. Qaisaruddinl, Ali A1-Jam'a3, and Ali Elbashir~ ~ Division of Pediatric Surgery, 2 Department of Surgery, 3 Department of Internal Medicine, 4 Department of Microbiology, Qatif Central Hospital, Qatif, Saudi Arabia Accepted 22 November 1993

Abstract. This paper reviews four cases of splenic abscess in children. All of them had sickle-cell disease and were treated by splenectomy covered by a course of antibiotics and pneumovax and made a rapid recovery. Of particular interest was the isolation of salmonella in two of our patients. Splenic abscess is a not u n c o m m o n complication of sickle-cell disease, and physicians caring for these children must be aware of this complication, its mode of presentation, and alternate forms of management.

Key words: Spleen - Abscess - Splenectomy - Sickle-cell disease

Introduction Splenic abscess is an u n c o m m o n condition and remains a diagnostic challenge. Several factors predisposing to splenic abscess have been suggested [5], the most c o m m o n being hematogenous spread of a pyogenic infection. Others include infection of a splenic hematoma following trauma and direct extension from an adjacent infectious process. Splenic abscess m a y also arise from hematogenous seeding in the presence of a splenic abnormality such as that seen in sickle-cell disease (SCD) [10, 11]. We report four cases of splenic abscess in children with SCD.

Fig. 1. CT scan showing splenic abscess with extension to abdominal wall of SCD was made by a positive sickling test and hemoglobin electrophoresis using Helena Laboratories, super Z electrophoresis kit. A drop of packed red blood cells was hemolyzed with hemolysate reagent, applied to a Titan III cellulose acetate plate, and electrophoresed in Supre Hemobuffer (pH 8.2 to 8.6) for 25 rain. The plate was stained in Poneeau S, cleared, and the pattern quantified using a Helena Quick-scan densitometer. Ultrasound (US) and CT scans of the abdomen were performed in all cases.

Results Patients and methods Four cases of splenic abscess were treated at Qatif Central Hospital, Saudi Arabia, over a 3-year period, June 1989-June 1992. The records were analyzed with regard to age, sex, symptoms and signs, radiologic and laboratory findings, as well as treatment and outcome. The diagnosis

Correspondence to: A. H. A1-Salem, R O. Box 18432, Qatif Central Hospital, Qatif 31911, Saudi Arabia

The relevant clinical data are summarized in Table 1. All patients presented with fever and had a tender, enlarged spleen. One (case 3) was found to have a large splenic abscess that had ruptured and extended subcutaneously (Fig. 1). Two patients (cases 1 and 2) also had left lower lobe pneumonia. Patients 1, 3, and 4 had thrombocytosis (Table 1) as well as Howell-Jolly bodies, indicating functional asplenia. Case 4 also had a sulfar colloid technetium scan that showed no uptake in the spleen. The chest radiographs were normal in cases 3 and 4. Plain abdominal

490 minor wound infection and case 2, who developed a minor wound infection. The bacteriology of the abscesses is summarized in Table 1. Blood cultures were negative in all cases; in case 4 there was no bacterial growth. The histopathology of all the specimens confirmed the diagnosis of splenic abscess. The residual splenic tissue showed infection, congestion with sickled red blood cells, chronic inflammation, and hemosiderin deposition. In case 3 there was cavitation and formarion of a tract leading to the splenic capsule and the abscess. A notable feature was the presence of numerous foam cells in two patients (cases 1 and 3), in keeping with the presence of salmonella.

Discussion Fig. 2. Abdominal CT scan demonstrating large splenic abscess

radiographs confirmed a left upper quadrant soft-tissue mass displacing the stomach shadow, consistent with splenomegaly. Both CT and US demonstrated splenomegaly with multiple irregular, large areas of cystic changes with fluid collection suggestive of a splenic abscess (Fig. 2). All patients received 0.5 ml prophylactic pneumococcal vaccine (PMU-Immune 23, Lederle) and underwent splenectomy. In case 3, the abscess had ruptured and penetrated the left l l t h intercostal space, entering the posterior subcutaneous tissue. Case 2 also had a cholecystectomy due to gall-stones and case 4 had an incidental appendectomy. The splenic bed was irrigated with warm saline and drained via a tube. All four patients received prophylactic antibiotics intravenously; penicillin, metronidazole, and gentamycin which were changed depending on the culture results. Postoperatively all the patients recovered well except for patient 1, who developed a subacute intestinal obstruction and

Sickle-cell disease is one of the commonly inherited hemoglobinopathies in the Eastern Province of Saudi Arabia [1, 15]. The disease has been reported to have a wide spectrum of clinical severity, but the clinical course is usually more benign here than in other countries [7, 14, 15]. This has been attributed to the high levels of hemoglobin F and the frequently associated alpha-thalassemia [2, 14, 15]; nevertheless, SCD causes significant morbidity [1, 3, 14, 15]. The spleen, which is commonly enlarged during the 1st decade of life, undergoes progressive atrophy due to repeated attacks of vaso-occlusion and infarction, but in some cases splenomegaly persists into adult life with the subsequent development of splenic infarction and, in the presence of bacteremia, predisposes to the development of splenic abscess. This is more likely in the presence of functional asplenia, which was demonstrated in three of our patients by the inability of the enlarged spleen to remove Howell-Jolly bodies and in one to take up colloid sulphur-labelled particles.

Table 1. Summary of the clinical and laboratory findings in a 4 children with splenic abscess Case Age Sex (Y)

Symptoms and signs

1

Temp.Hb WBC Plate(gldl) letes

Geno-Hb S Hb F Hb A2 Operative type procedure

Bacteriology Post-op of the abscess complications

4

M

Fever, 38.6 abdominal pain, enlarged tender spleen

9.6

23.4x 866,000 SS 103

83

14.3

2.8

Splenectomy Salmonella Group "D"

14

F

Fever,left 40 hypochondrial pain, enlarged tender spleen

9.0

ll.4x 103

76.5

20

3.5

Splenectomy Enterobacter Minor wound and Chole- cloacae and infection cystectomy Enterobacter Sakasaki

17

M

Fever,left back 38.5 pain, fullness, tenderness left renal area, enlarged tender spleen

6.3

20.3x 693,000 SS 103

87

10.9

2.1

Splenectomy Salmonella Group "D"

None

18

M

Left upper 38.3 10.2 12.4x 732,000 SS abdominal pain 103 and fever, tender enlarged spleen

Splenectomy No Growth and appendectomy

None

398,000 SS

86.3 13.7 -

SubacuteIntestinal Obstructions, Minor wound infection

491 Splenic abscess is an infrequent clinical entity that is rarely encountered in healthy individuals and is usually associated with pyogenic infections including subacute bacterial endocarditis, splenic trauma with super-infection, hemoglobinopathies, or spread from an adjacent infectious process [5, 6]. Our patients had SCD, in which there is a high incidence of splenic infarction in addition to the opportunity for bacteremia, especially in the presence of functional asplenia, which renders these patients prone to develop splenic abscess [10, 11]. The clinical presentation of splenic abscess is not specific, and a high. degree of clinical awareness is essential for early diagnosis.. The classic signs of fever and tender splenomegaly occurred in only one-half of the patients in one series [5] and 32% in another [13]. All our patients presented with fever and abdominal pain and were found to have a tender, enlarged spleen. US and CT are the most useful aids in :making the diagnosis; we found CT more reliable. It also allows more accurate anatomic localization. In two of our patients we found it difficult to differentiate between a splenic abscess and a large splenic infarction, which is also not uncoommon in patients with SCD. The diagnosis in these two cases was confirmed by needle aspiration under US guidance. Many organisms can cause splenic abscess~ the most frequently encountered are Staphylococcus aureus, streptococci, and gram-negative bacilli. Less c o m m o n pathogens include anaerobic organisms, Mycobacterium tuberculosis, Serratia marcescens, and Salmonella sp. which is a not u n c o m m o n finding in patients with SCD and various infections including septicemia, osteomyelitis, and septic arthritis due to salmonella [3]. Immune-suppressed patients are prone to fungal splenic abscess [5, 6]. The treatment of choice of splenic abscess is splenectomy and appropriate antibiotics [5, 17]. However, with advances in dJ[agnostic imaging and interventional radiologic techniques, recent reports have established the effectiveness of percutaneous abscess drainage (PAD) of splenic abscess in both adults and children, as preservation of splenic tissue is of value in regard to later susceptibility to overwhelming post-splenectomy infection [4, I2, 16]. The success of PAD depends on two factors, namely, the morphology and localization of the abscess and the availability of personnel skilled in PAD. Gerzot et al. [8, 9] achieved a success rate of 86% with PAD in unilocular lesions, but only 45% in multilocular or ill-defined lesions. PAD should be of value in children with SCD who are at high risk for general anasthesia and major surgery, how-

ever, we feel that as the presence of asplenia makes these patients prone to recurrent infections splenectomy together with prophylactic pneumococcal vaccination and antibiotics is the treatment of choice. Our patients were treated successfully with this management with no mortality and low morbidity.

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