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Year : 2016  |  Volume : 2  |  Issue : 1  |  Page : 36-38

Multiple splenic infarctions with a rare etiology

Department of Medicine, SP Medical College, Bikaner, Rajasthan, India

Date of Submission18-Dec-2015
Date of Acceptance25-May-2016
Date of Web Publication16-Jun-2016

Correspondence Address:
Harish Kumar
Department of Medicine, S P Medical College, Bikaner, Rajasthan
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2455-3069.184127

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Malaria is the most common parasitic infection in tropical countries such as India, and it causing a major economic burden on the Asian and African countries. Splenic complication is common in Plasmodium falciparum infection, but splenic infarction itself is a rare clinical entity in P. falciparum infection. Herein, we are presenting a case report of an 18-year-old male patient who presented to the department of medicine with a complaint of pain abdomen. On the next day of admission, the patient had complained of fever with chills and rigor. Routine blood investigations including peripheral smear examination for malarial parasites were sent. Contrast-enhanced computed tomography (CECT) of the abdomen was performed to diagnose the cause of abdominal pain after the findings of infarction in ultrasonography. CECT showed multiple infarctions of spleen and peripheral blood film showed ring forms of P. falciparum. Hence, we should always rule out splenic complication in cases of malaria which present with fever and left hypochondrium pain.

Keywords: Abdominal pain, infarct, malaria, Plasmodium falciparum, rupture, spleen

How to cite this article:
Kumar H, Singh VB, Meena BL, Kumar R, Agrawal J. Multiple splenic infarctions with a rare etiology. J Curr Res Sci Med 2016;2:36-8

How to cite this URL:
Kumar H, Singh VB, Meena BL, Kumar R, Agrawal J. Multiple splenic infarctions with a rare etiology. J Curr Res Sci Med [serial online] 2016 [cited 2023 Mar 21];2:36-8. Available from: https://www.jcrsmed.org/text.asp?2016/2/1/36/184127

  Introduction Top

Splenic infarction is a rare clinical entity that usually goes undiagnosed in malaria; splenic complications, either as splenic rupture or splenic infarct, should be ruled out by imaging. Clinicians should be aware of this rare complication of malaria. Myelofibrosis, hematological neoplasms, thromboembolic disease from atrial fibrillation, systemic lupus erythematous, falciparum malaria, septic emboli in endocarditis, sickle cell disease, and Wegener's granulomatosis are some of the causes of splenic infarction. The clinical spectrum of malaria is varies from asymptomatic infections to complications such as splenic infarct, rupture, abscess, and hemoperitoneum. [1] Here, we are reporting a case who presented with pain in the left hypochondrium, diagnosed as acute splenic infarction due to Plasmodium falciparum malaria. This case report describes the splenic complications of acute malaria, as two different prognostic and treatment entities: splenic infarction and splenic rupture.

  Case report Top

An 18-year-old male patient was admitted to the department of medicine with a chief complaint of dull aching pain in the left upper quadrant of the abdomen for 2 days, which was nonradiating, accompanied by nausea and decreased appetite. Abdomen was soft and nontender. There was no history of vomiting, diarrhea, and constipation. After 1 day of admission, the patient had complained of high-grade fever with chills and rigor. Fever was relieved with sweating. He denied a history of cough and burning micturition.

Hemodynamically, the patient was stable with a pulse rate of 88 beats/min with regular good volume, blood pressure of 110/80 mmHg in the supine position in the left brachial artery. The patient was febrile with a temperature of 103°F in the axilla. He was anemic with no evidence of icterus, clubbing, lymphadenopathy, and pedal edema. Nontender palpable spleen, 6 cm below the left costal margin with smooth surface and firm in consistency, was present. Liver was normal on examination. There was no evidence of ascites, and bowel sounds were normal. Chest and cardiac examinations were normal on auscultation. Central nervous system examination was also in normal limits.

Blood investigation revealed hemoglobin of 8.5 g/dl, total lymphocyte count of 3200/mm 3 (polymorphs 68%, lymphocytes 22%, monocytes 6%, eosinophils 3%, and basophils 1%), and platelet count of 28,000/mm 3 . Liver and renal function tests were normal. No evidence of any abnormality was found in urine and stool examination. Card test for malaria antigen was positive for P. falciparum. Peripheral blood showed ring forms of P. falciparum with density of parasites at 100,000 parasites/μl. Card test and PBF were negative for Plasmodium vivax. Bleeding time was prolonged, but there were no bleeding episodes. Clotting time (CT), prothrombin time, and activated partial thromboplastin time (appt) were normal.

Tests for the underlying coagulation disorders such as protein C and protein S deficiency, Leiden mutation, and antithrombin III deficiency were negative. Antiphospholipid antibody levels, serum homocysteine levels, and hemoglobin electrophoresis were normal.

Ultrasonographic evaluation of the abdomen revealed multiple wedge-shaped hypo-echoic areas in the spleen, suggestive of infarction. Contrast-enhanced computed tomography of the abdomen revealed multiple wedge-shaped hypodense nonenhancing lesions consistent with splenic infarction [Figure 1] and [Figure 2].
Figure 1: Contrast-enhanced computed tomography of the abdomen showing multiple splenic infarction

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Figure 2: Contrast-enhanced computed tomography of the abdomen showing multiple splenic infarction

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The patient was treated with intravenous artesunate, analgesic, fluids, and other supportive measures for 5 days. Splenic infarction in malarial patients requires only symptomatic treatment. He became afebrile after 5 days and pain resolved completely after 10 days of oral treatment with analgesic. Splenic rupture or splenic abscess have been reported in cases of splenic infarction, but in the present case study, ultrasonography of the abdomen was repeated after 4 weeks, which showed complete resolution of the infarcted areas. He was discharged in stable condition and is on regular follow-up.

  Discussion Top

Malaria is the most common parasitic infection in tropical countries such as India. P. vivax is the most common cause of malaria followed by P. falciparum. P. falciparum infection is commonly complicated by cerebral malaria, acute renal failure, liver damage, and hemodynamic collapse. [2]

Although splenomegaly is frequently observed in malaria cases, there is no need of special attention, as it is not usually associated with any symptoms, and can be gradually resolved via standard antimalarial therapy. Splenic complication with malaria infection is not uncommon. Spleen is the second most common organ next to kidney where embolism and infarction occur. Infective endocarditis is the most common cause of splenic infarct. Malaria is a rare cause of infarction in spleen. [3] Clinicians should be aware that left hypochondrial pain occurring during treatment for acute malaria could be due to splenic infarction. [4] The pathophysiology of splenic infarction is different in P. vivax and P. falciparum malaria. In P. vivax infection, splenic infarction occurs probably secondary to ischemia induced by hyperplasia of reticuloendothelial system and tissue avascularity with hypoxia due to increased stickiness of parasitized RBC. [5],[6],[7],[8] While in P. falciparum malaria, high levels of parasitemia and microvascular sequestration of parasitized red blood cells, rouleaux formation by erythrocytes, infective embolism, low oxygen tension, and out-stripping of massive splenomegaly of its available blood supply can lead to splenic infarct. Sequestration occurs in the venules of the vital organs predominantly in the white matter of brain, heart, eyes, liver, kidney, adipose tissue, and least in skin. Spleen acts as a principal host defense against malarial parasite by destroying and filtering both uninfected and parasitized red cells. Wedge-shaped infarct of the spleen is the result of segmental occlusion of branches of splenic and short gastric artery. The wedge-shaped infarct has its apex toward the hilum and its base beneath the capsule. It is either segmental or global. The clinical presentation of infarction varies. One-third of the cases are asymptomatic and the rest present incidentally on radiological or postmortem studies, or in haemorrhagic shock as a result of splenic rupture. The most common symptom is the left upper quadrant abdominal pain along with nausea and vomiting. Laboratory tests are not diagnostic for splenic infarction. [9]

Ultrasonography or computed tomography is well defined, though computed tomography is the preferred imaging modality for making the diagnosis. [10] Ultrasonography can be used in the evaluation of splenomegaly, but this technique is less sensitive than CT during the acute stage of infarction. Splenic angiography, if performed, will show wedge-shaped regions of reduced perfusion corresponding to the infarction patterns observed on CT. Splenic abscess can be excluded by radiologic findings and clinical features, as an abscess is normally accompanied by systemic symptoms. Rupture of the spleen is more common than splenic infarction during malaria and is a diagnostic emergency, usually necessitating surgery. Few cases have reported that splenic infarction is complicated by splenic rupture. Splenic rupture or splenic abscess have been reported in the cases of splenic infarction. [11] For these reasons, splenic infarction must be considered as a complication distinct from splenic rupture in acute malaria, as both have different prognoses and treatment. This complication must be evoked whatever the Plasmodium species. [12],[13]

  Conclusion Top

Malaria though a rare cause of splenic infarct must be considered in the malaria-endemic areas such as India in patients presenting with upper abdominal pain and fever.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Contini S, Lewis HR. Spleen abscess as malaria complication. Emerg Infect Dis 2006;12:529-31.  Back to cited text no. 1
Dash AP, Valecha N, Anvikar AR, Kumar A. Malaria in India: Challenges and opportunities. J Biosci 2008;33:583-92.  Back to cited text no. 2
Hovette P, Lecoules S, Boete F, Imbert P, Touze JE, Laroche R. Splenic infarction during P. falciparum and P. vivax malaria. Presse Med 1994;23:1226.  Back to cited text no. 3
Singh BJ, Kumar A. Splenic infarctions in mixed infection with kala azar and falciparum malaria. J Assoc Physicians India 1991;39:293.  Back to cited text no. 4
Bonnard P, Guiard-Schmid JB, Develoux M, Rozenbaum W, Pialoux G. Splenic infarction during acute malaria. Trans R Soc Trop Med Hyg 2005;99:82-6.  Back to cited text no. 5
Osonuga OA, Osonuga A, Osonuga AA, Osonuga IO. Resolution pattern of jaundice among children presenting with severe malaria in rural South-West Nigeria. Asian Pac J Trop Biomed 2012;2:551-3.  Back to cited text no. 6
Jombo GT, Araoye MA, Damen JG. Malaria self medications and choices of drugs for its treatment among residents of a malaria endemic community in West Africa. Asian Pac J Trop Dis 2011;1:10-6.  Back to cited text no. 7
Guth AA, Pacheter HC. Splenic infarct. Med J 2002;3:1-11.  Back to cited text no. 8
Hershey FB, Lubitz JM. Spontaneous rupture of the malarial spleen: Case report and analysis of 64 reported cases. Ann Surg 1948;127:40-57.  Back to cited text no. 9
Goerg C, Schwerk WB. Splenic infarction: Sonographic patterns, diagnosis, follow-up, and complications. Radiology 1990;174(3 Pt 1):803-7.  Back to cited text no. 10
Miller LA, Mirvis SE, Shanmuganathan K, Ohson AS. CT diagnosis of splenic infarction in blunt trauma: Imaging features, clinical significance and complications. Clin Radiol 2004;59:342-8.  Back to cited text no. 11
Facer CA, Rouse D. Spontaneous splenic rupture due to Plasmodium ovale malaria. Lancet 1991;338:896.  Back to cited text no. 12
Patel MI. Spontaneous rupture of a malarial spleen. Med J Aust 1993;159:836-7.  Back to cited text no. 13


  [Figure 1], [Figure 2]


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