| Abstract|| |
Enteric fever complicated by splenic abscess is a rare entity in pediatric age group. It is usually a part of disseminated infection. There can be single or multiple abscesses. Single abscess most commonly responds to conservative management with appropriate antibiotics and ultrasound-guided percutaneous drainage of the abscess. However, multiple abscesses require splenectomy. The child presented here had multiple splenic abscesses as a complication of enteric fever. There was no response to conservative management and hence he had to undergo splenectomy. So, in children with enteric fever, it is strong suspicion, which helps in identifying complications early and treating them accordingly. Salvaging the spleen is not possible in case of multiple splenic abscesses.
Keywords: Enteric fever, splenic abscess, splenectomy
|How to cite this article:|
Doddaiah N, Nagaraj R, Anil Kumar MG, Murthy RS. Enteric fever complicated by multiple splenic abscesses. Ann Trop Med Public Health 2012;5:534-6
|How to cite this URL:|
Doddaiah N, Nagaraj R, Anil Kumar MG, Murthy RS. Enteric fever complicated by multiple splenic abscesses. Ann Trop Med Public Health [serial online] 2012 [cited 2021 Apr 11];5:534-6. Available from: https://www.atmph.org/text.asp?2012/5/5/534/105157
| Introduction|| |
Splenic abscess is rare, with lesser than 500 cases reported in literature.  Enteric fever as a cause of this condition is even rarer.  Only about 38 cases are described in literature since 1977, with majority being solitary and a few of them, multiple abscesses. The clinical diagnosis of splenic abscess due to typhoid fever is difficult because it is rare, has an insidious onset and non-specific clinical features. , It, therefore, requires a very high index of suspicion. Ultrasonography and computed tomography (CT scan) help in achieving an early diagnosis. Splenectomy remains the mainstay of treatment with a success rate of 86-94%. ,, It is often fatal if left untreated.
| Case Report|| |
A 13-year-old boy presented to the pediatric emergency ward with history of continuous high grade fever and diffuse intermittent pain abdomen of eight days duration and nausea and loose stools of three days duration. There was no history of any other associated symptoms or significant past history. He was immunized to date according to the National Immunization Programme. On examination, he was conscious, oriented, pale, dehydrated, and in shock. He was resuscitated with 20 ml/kg of intravenous normal saline and oxygen supplementation by mask. His blood pressure improved, and he did not require inotropic support. His general examination also revealed pallor, with no icterus or edema or significant lymphadenopathy. He was poorly-built and nourished. There was no rash or bleeding tendency. Hess test was negative. His abdominal examination revealed diffuse tenderness with mild hepatosplenomegaly. Other systems were normal. His investigations revealed a hemoglobin percentage of 9.9 g/dl, total WBC count of 13,200/cmm, with neutrophilic predominance and absent eosinophils. Platelet count was 1.77 lakh/cmm and ESR of 15 mm/1 st hour. Peripheral blood smear showed microcytic hypochromic anemia. Urea, creatinine, and serum electrolytes were all within normal limits. Liver enzymes were mildly elevated with an AST of 214 U/L and ALT of 85 U/L and normal bilirubin level. Blood culture was sterile on two consecutive samples. Urine culture was sterile. Widal test did not show any significant titers or any significant rise in titers on subsequent samples. Dengue serology and QBC and peripheral smear for malarial parasite were negative. Ultrasound abdomen, however, revealed multiple splenic abscesses/splenic infarctions. Child was started on intravenous ceftriaxone initially, and following ultrasound, intravenous linezolid and metronidazole were added. Further investigations to look for the cause of splenic abscesses were done. Brucella More Details test was negative by slide agglutination, sickling test was negative, HIV ELISA was non-reactive, and 2D ECHO did not show any evidence of infective endocarditis. Therefore, ultrasound-guided aspiration of the splenic abscess was done, following CT scan of the abdomen [Figure 1], which confirmed multiple splenic abscesses with subcapsular fluid collection. The aspirate grew nalidixic acid-resistant Salmonella More Details typhi, which was sensitive to ceftriaxone, chloramphenicol, ampicillin, and tetracycline. So, Ceftriaxone was continued for 14 days. However, the child remained febrile, and pain abdomen persisted. Repeat CT abdomen showed persistence of the splenic abscesses. Since there was no response to conservative management, splenectomy was planned for. Child underwent splenectomy, following which he became afebrile on the second post-operative day. The splenectomized specimen revealed areas of abscess and infarcts [Figure 2]. Ceftriaxone was continued for seven more days, and the patient remained afebrile throughout the rest of his hospital stay. He was discharged in a stable condition.
|Figure 1: CT abdomen showing multiple splenic abscesses (arrows) and also subcapsular fluid collection (upper arrow on the left side)|
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|Figure 2: Splenectomized specimen showing an area of infarction (upper right arrow), and an area of abscess (lower left arrow)|
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| Discussion|| |
Splenic abscesses can occur due to systemic bacteremia originating in another site, such as endocarditis and intravenous drug abuse, superinfection of a spleen damaged by ischemia or infarction (as in hemoglobinopaties and sickle cell anemia), penetrating or blunt trauma with superinfection of a subcapsular hematoma, or other diseases (malaria, leukemia, and splenic cyst), immunodeficiency due to acquired immunodeficiency syndrome (AIDS), chemotherapy or long term steroid therapy, or from conditions that predispose to immunosuppresion such as diabetes mellitus and alcoholism and extension from a contiguous focus such as pancreatic, subphrenic, or perinephric abscess. 
Staphylococcus aureus, streptococci, and various aerobic and anaerobic intestinal flora and, rarely, fungi are important causes of splenic abscess. However, non-typhoidal salmonella are more frequently reported than Salmonella typhi.  Another rare cause, especially in the developing countries, is tuberculosis, in which the splenic abscess may be isolated or associated with a disseminated disease.  Reports show that in up to 20% of patients with splenic abscess, the pus is sterile while the blood culture isolates the organisms in 40-50% of cases.  A negative pus or blood culture probably results from the use of antibiotics as was seen in our patient. Diagnosis of splenic abscess, especially in the setting of enteric fever, requires a very high index of suspicion with the presenting symptoms being non-specific. The triad of fever, left upper quadrant pain, and a tender mass (suggested by Sarr and Zudeima) as an important presenting complex is seen in only about one-third of all patients.  Ultrasound abdomen helps in the preliminary diagnosis. CT scan is most useful in establishing the diagnosis and demonstrating the number and location of abscesses, besides showing any other concomitant disease or involvement of other organs. MRI gives some clues in the diagnosis by defining the extent and internal structure of splenic abscess because of its greater tissue resolution.  Single unilocular abscesses may respond well to percutaneous drainage. Multiple or loculated abscesses may respond to antibiotics alone, but splenectomy is the preferred treatment. In general, failure to respond to antibiotics with or without percutaneous drainage requires splenectomy.  This fact was evident in our patient.
| References|| |
|1.||Philips GS, Radosevich MD, Lipsett PA. Splenic abscess - another look at an old disease. Arch Surg 1997;132:1331-6. |
|2.||Shin PJ, Choi H, Bae CW, Choi YM, Yoon Y. Percutaneous drainage of splenic abscess in typhoid fever - a case report. J Kor Med Sc 1995;10:44-7. |
|3.||Ng KK, Lee TY, Wan YL, Tan CF, Lui KW, Cheung YC, et al. Splenic abscess: Diagnosis and management. Hepatogastroenterology 2002;49:567-71. |
|4.||Liang JT, Lee PH, Wang SM, Chang KJ. Splenic abscess: A diagnostic pitfall in the ED. Am J Emer Med 1995;13:337-43. |
|5.||Smyrniotis V, Kehagias D, Voros D, Fotopoulos A, Lambrou A, Kostopanagiotou G, et al. Splenic abscess - an old disease with new interest. Dig Surg 2000;17:354-7. |
|6.||Anuradha S, Singh NP, Agarwal SK. Splenic abscess - a diversity within. J Indian Aca Clin Med 2000;1:279-81. |
|7.||Elsayes KM, Narra VR, Mukundan G, Lewis JS, Menias CO, Heiken JP. MRI Imaging of the spleen: Spectrum of abnormalities. Radiographics 2005;25:967-82. |
|8.||Mehta SS, Gittes GK. Splenic Abscess. In: Ashcraft KW, Holcomb GW, Murphy JP editors. Pediatric Surgery. 4 th ed. Philadelphia: Elsevier Saunders; 2005. p. 652-3. |
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Source of Support: None, Conflict of Interest: None
[Figure 1], [Figure 2]