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LETTER TO EDITOR
Year : 2004  |  Volume : 50  |  Issue : 1  |  Page : 80-81

Persistent hypotension and splenic rupture in a patient with Plasmodium vivax and falciparum co-infection


1 Departments of Medicine, Christian Medical College, Vellore, Tamilnadu - 632004, India
2 Departments of Surgery, Christian Medical College, Vellore, Tamilnadu - 632004, India

Correspondence Address:
B V John
Departments of Medicine, Christian Medical College, Vellore, Tamilnadu - 632004
India
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Source of Support: None, Conflict of Interest: None


PMID: 15048011

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How to cite this article:
John B V, Ganesh A, Aggarwal S, Clement E. Persistent hypotension and splenic rupture in a patient with Plasmodium vivax and falciparum co-infection. J Postgrad Med 2004;50:80-1

How to cite this URL:
John B V, Ganesh A, Aggarwal S, Clement E. Persistent hypotension and splenic rupture in a patient with Plasmodium vivax and falciparum co-infection. J Postgrad Med [serial online] 2004 [cited 2019 Jul 22];50:80-1. Available from: http://www.jpgmonline.com/text.asp?2004/50/1/80/6665


Sir,

A 28-year-old man was admitted with fever, abdominal pain, vomiting and loose stools of three days′ duration. He was from a region non-endemic for malaria. There was no history either of previous episodes of malarial infection or of travel to an endemic area. On examination, the pulse rate was 106/min and blood pressure was 100/70 mm of Hg. He was febrile (temperature 400C), and was pale and icteric. His abdominal examination revealed a soft abdomen, with hepatosplenomegaly and mild left hypochondrial tenderness.



Investigations revealed haemoglobin of 5.7 gm/dl, total leucocyte count of 4.9x109/L and a platelet count of 23x109/L. Thin blood smear revealed Plasmodium vivax rings, schizonts and gametocytes. Gametocyte and ring stages of Plasmodium falciparum were also seen. The parasitic index for Plasmodium falciparum and vivax (combined parasitaemia) was 4%. Total bilirubin was 5.1 mg/dl and direct bilirubin was 0.5 mg/dl. The aspartate aminotransferase, alanine aminotransferase and alkaline phosphatase were 130, 31 and 43 IU/L respectively. The serum creatinine was 1.2 mg/dl. He was started on intravenous infusion of quinine at a dose of 10 mg/kg/dose, every eight hours and transfused one unit of blood. Since the post- transfusion haemoglobin was only 6.1 gm/dl, a further unit was transfused, following which the haemoglobin increased to 7.1gm/dl.



He continued to have abdominal pain, vomiting and loose stools. In spite of transfusing six litres of intravenous fluids and two units of blood, the systolic blood pressure continued to be between 90 and 100 mm of Hg. An ultrasound examination of the abdomen revealed moderate splenomegaly (17 cm) with a large perisplenic haematoma, and moderate intraperitoneal haemorrhage. Computerised tomography revealed a mixed density lesion in the perisplenic region with left-sided pleural effusion, confirming the diagnosis of splenic rupture.



He underwent an emergency laparotomy, which revealed hemoperitoneum with over one litre of blood in the peritoneal cavity and friable spleen with capsular tear. Splenectomy was performed. Pathological examination revealed a laceration on the antero-superior surface. The post- operative period was uneventful and he was discharged after 7 days. The repeat thin blood smear done after one week of therapy revealed occassional rings and gametocytes of both Plasmodium vivax and falciparum, however, the parasitic index of plasmodium falciparum and vivax had decreased to 0.1%. He was discharged on oral quinine and primaquine.



Splenic rupture as a cause of death or morbidity has been well described, mostly in individuals residing in non-endemic areas,[1] as was the case in our patient. It is more common with plasmodium vivax infection and has been described in the acute phase of the illness. The majority of the patients described in the literature had classic features of splenic rupture, including signs of peritonitis and marked left hypochondrial pain, tenderness and guarding. Our patient had no prominent intra-abdominal signs. The clinical presentation was that of a patient with malaria with unexplained hypotension and severe anaemia unresponsive to transfusions. In countries where physicians encounter malaria frequently, it is important to remember that this life-threatening complication may present with subtle clinical features that may not help to readily localize the pathology to the spleen.



Our patient had a mixed Plasmodium vivax and falciparum infection. To the best of our knowledge, this is the first report of a Plasmodium vivax and falciparum mixed infection with splenic rupture. Since there is no data, it is difficult to comment on the relative prognosis of patients with mixed infection as compared to that of patients with isolated Plasmodium vivax or falciparum infection. The vast majority of cases of spontaneous splenic rupture have been described with plasmodium vivax and the presence of Plasmodium vivax as one of the infecting species, rather than the mixed infection, may have predisposed this patient to spontaneous splenic rupture.



Conservative, non-operative management of splenic rupture has received some attention, particularly because of the risk of future episodes of malaria in an asplenic patient.[2],[3] Trans-catheter embolisation of the splenic artery has been described.[4] However, conservative therapy requires rapid availability of unlimited quantities of blood, high quality of clinical monitoring, and sophisticated imaging techniques while splenectomy is a relatively rapid and effective way of handling a life-threatening complication. Hence, operative management of splenic rupture is likely to remain the treatment in many situations.[5] It is crucial for clinicians to remember the possibility of spontaneous splenic rupture because early diagnosis coupled with a relatively simple surgery can lead to dramatic recovery, and the failure to do so, to high mortality.

 
 :: References Top

1.Zingman BS, Viner BL. Splenic complications in malaria: Case report and review. Clin Infect Dis 1993;16:223-32.  Back to cited text no. 1  [PUBMED]  
2.Hamel CT, Blum J, Harder F, Kocher T. Nonoperative treatment of splenic rupture in malaria tropica: Review of literature and case report. Acta Trop 2002;82:1-5.   Back to cited text no. 2  [PUBMED]  [FULLTEXT]
3.Davies GR, Venkatesan P. Successful conservative management of splenic rupture in vivax malaria. Trans R Soc Trop Med Hyg 2002;96:149-50.   Back to cited text no. 3  [PUBMED]  
4.Ribordy V, Schaller MD, Martinet O, Doenz F, Liaudet L. Spontaneous rupture of the spleen during malaria treated with transcatheter coil embolization of the splenic artery. Intensive Care Med 2002;28:996.  Back to cited text no. 4  [PUBMED]  
5.Yagmur Y, Kara IH, Aldemir M, Buyukbayram H, Tacyildiz IH, Keles C. Spontaneous rupture of malarial spleen: two case reports and review of literature. Crit Care 2000;4:309-13.  Back to cited text no. 5  [PUBMED]  [FULLTEXT]



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Online since 12th February '04
2004 - Journal of Postgraduate Medicine
Official Publication of the Staff Society of the Seth GS Medical College and KEM Hospital, Mumbai, India
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