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Spontaneous Splenic Rupture Complicating Severe P. falciparu | 56138

Jornal de Microbiologia e Imunologia

Abstrato

Spontaneous Splenic Rupture Complicating Severe P. falciparum Infection: A Case Report and Literature Review

Eltaib Saad, A. ElaminElasamani, G. WalidAbdelrahman

Malaria is a parasitic life-threatening endemic disease in over 100 tropics and subtropics [1].Malarial splenic rupture (MSR) is a rare but potentiallyfatal complication of severe malarial infection and hence it deserves special attention [2].The estimated incidence of MSR is 2% in acute malarial infections;however, the exact incidence is largely unknown due to the substantial under-reporting [2].A high index of clinical suspicion is warranted for the early diagnosis as delayed or missed diagnosis can be potentially fatal [3]. We report on a 32-year-old Sudanese male who was a resident from Plasmodium falciparum malaria-endemic area, who was diagnosed with severe P. falciparum infection as per WHO criteria [3]when he presented with an acute abdomen and hypovolemic shock due to spontaneous splenic rupture following five days of onset of characteristic febrile pattern of Plasmodium falciparum. The diagnosis of MSR was suspected clinically and confirmed by radiological imaging (ultrasonography and contrast-enhanced computed tomography (CT scan). He was managed conservatively with intravenous quinine therapy(a slow infusion of 600 mg every 8 hours) as per national malaria treatment protocol, intravenous fluids and blood transfusions and he had made a remarkable recovery after sever days. A repeat blood film smear on day 7 confirmed parasitic clearance, and quinine therapy was discontinued, and he was prescribed a 5 day course of doxycycline (100 mg once daily). A follow-up CT scan on day 10 revealed resolution of the subcapsularsplenic haematoma with no residual collections.A combination of three principalfactors, which ultimately result in a sub-capsular haematoma formation, is thought to be implicated in pathogenesis of MSR. These factors are (I) cellular hyperplasiaand venous-sinusoidal congestion leading to increased tension and stress on the capsule, (II) vascular occlusion of the reticuloendothelial cells resulting in thrombotic or ischemic events, and (III) episodic increase in intra-abdominal pressure accompanying coughing, sneezing, and laughing which add more stress on the diseased and friable spleen [2, 4].In the modern surgical practice era, a non-operative management can be safely followed for haemodynamically stable patients and splenectomy is indicated for haemodynamically unstable patients with ongoing shock as a critical life-saving surgery [2].