|LETTER TO THE EDITOR
|Year : 2017 | Volume
| Issue : 2 | Page : 140-141
Massive splenomegaly, acute kidney injury, and the challenges of diagnosing hyperractive malarial syndrome in a resource-limited setting
Department of Paediatrics, Aminu Kano Teaching Hospital/Bayero University Kano, Kano, Nigeria
|Date of Web Publication||15-Nov-2017|
Consultant Paediatrician, Department of Paediatrics, Aminu Kano Teaching Hospital, Kano
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Aliyu I. Massive splenomegaly, acute kidney injury, and the challenges of diagnosing hyperractive malarial syndrome in a resource-limited setting. J Med Trop 2017;19:140-1
|How to cite this URL:|
Aliyu I. Massive splenomegaly, acute kidney injury, and the challenges of diagnosing hyperractive malarial syndrome in a resource-limited setting. J Med Trop [serial online] 2017 [cited 2020 Jul 7];19:140-1. Available from: http://www.jmedtropics.org/text.asp?2017/19/2/140/218408
Massive splenomegaly may be associated with grave complications. Among these are anemia, leucopenia, and thrombocytopenia due to consumption of these blood elements by the enlarged spleen-hypersplenism. Similarly, such enlarged spleen may easily be subjected to trauma, resulting in splenic rupture, bleeding, and shock. Though splenic enlargement has been reported in patients with chronic kidney disease, its mechanism is poorly understood; however, the role of hemodailysis in red blood cell destruction and the influence of immunologic response to components of the hemodialysis such as ethylene oxide have been implicated. But the association of massive splenomegaly with acute kidney failure is a rare phenomenon. Therefore, the case of a 12-year-old boy is highlighted in this communication. He presented with complaint of recurrent abdominal swelling and pain for 5 months before presentation. The complaints were of insidious onset; he had associated weight loss; however, no history of cough, bleeding, or difficulty with breathing. He was not a sickle cell anemic child. There was no complaint of reduced urine volume; on examination, he was febrile and pale; however, there was no significant peripheral lymphadenopathy but he had peripheral and scrotal edema. There was tachycardia, pulse rate of 152/min, the blood pressure was 100/50 mmHg sitting right arm; the jugular venous pressure was elevated. He also had a displaced apex (sixth left intercostal space at the anterior axillary line); there were first, second, and third heart sounds with a basal ejection systolic murmur. He was tachypneic with respiratory rate of 34/min, with bilateral crepitations. He had splenomegaly of 16 cm and hepatomegaly of 8 cm. The full blood count revealed a packed cell volume of 12%, white blood cell count (WBC) of 1.5 × 109/L, platelet count of 50 × 109/L, and no leukemic cells were seen; the bone-marrow aspiration was not remarkable as no malignant cells were seen; the liver function test was essentially normal. The electrolyte and urea were normal at admission; however, on the 4th day on admission, he developed a urea of 39.7 mmol/L (1.7–9.1 mmol/L) and creatinine of 250 μmol/L (10–140 μmol/L); serology for viral studies such as hepatitis b surface antigen and hepatitis c viral antibody (HbsAg and anti-HCV) and malaria parasite test were negative. Abdominal ultrasound revealed normal-sized kidneys with increased parenchymal echogenicity with hepatosplenomegaly. The Mantoux test was nonreactive, his hemoglobin electrophoresis was adult haemoglobin (AA). However, immunoglobulin M (IgM) assay and liver biopsy were not done due to lack of facility for these tests.
The definition of massive splenomegaly has been associated with controversies. Zhu et al. “defines massive splenomegaly in children as a splenic margin below the umbilicus or anteriorly extending over the midline.” The exact incidence of hyperactive malaria syndrome is not known in most areas with endemic malaria infection; this is not surprising because most established criteria are cumbersome,; furthermore, the cost and expertise for making the diagnosis are also lacking in areas where this disease may be most prevalent due to absence of basic facilities. This is further compounded because other causes of massive splenomegaly are also prevalent in such areas. Therefore, clinicians are often at a loss on the way forward. To make progress, there is the need for an establishment of less cumbersome criteria which is applicable in resource poor areas.
Isolated splenomegaly is usually associated with good prognosis, but the index case died; the association of acute renal failure and massive splenomegaly in the index case is unclear; massive splenomegaly may be associated with anemia, resulting from red blood cell trapping in the spleen with associated red blood cell (RBC) destruction, or dilutional anemia, due to increased plasma volume; furthermore, the enlarged spleen may impinge on organs, resulting in obstruction such as hydronephrosis. Again, the reduced WBC may also increase the risk of severe bacterial infection; therefore, these outlined factors may have accounted for the renal failure witnessed in the index case.
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