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Table of Contents   
CASE REPORT  
Year : 2013  |  Volume : 6  |  Issue : 5  |  Page : 578-580
Fatal complications of Plasmodium vivax malaria: A series of three case reports


Department of Internal Medicine, Post Graduate Institute of Medical Education and Research and Dr. Ram Manohar Lohia Hospital, New Delhi, India

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Date of Web Publication3-Jun-2014
 

   Abstract 

Plasmodium vivax malaria once thought to be benign, is now being seen increasingly as complicated disease in various manifestations. These complications include cerebral malaria, acute respiratory distress syndrome, acute pancreatitis, hepatic dysfunction, coagulopathy-associated hemorrhages, and others. Even if at the onset, disease appears benign, clinicians should be careful to watch for the complications and timely management.

Keywords: ARDS, pancreatitis, Plasmodium vivax, upper GI bleed

How to cite this article:
Sundriyal D, Kumar N, Chandrasekharan A, Sharma B, Patnaik I, Kamble U. Fatal complications of Plasmodium vivax malaria: A series of three case reports. Ann Trop Med Public Health 2013;6:578-80

How to cite this URL:
Sundriyal D, Kumar N, Chandrasekharan A, Sharma B, Patnaik I, Kamble U. Fatal complications of Plasmodium vivax malaria: A series of three case reports. Ann Trop Med Public Health [serial online] 2013 [cited 2019 Jun 26];6:578-80. Available from: http://www.atmph.org/text.asp?2013/6/5/578/133748

   Introduction Top


Malaria is one of the most important parasitic diseases of humans. It is a common cause of febrile illness in tropical countries. Malaria can present with wide range of complications like cerebral malaria, renal failure, hepatic dysfunction, pulmonary edema, bleeding disorders, hypotension, and shock. Sometimes, the diagnosis may remain unrecognized, which can prove fatal. Complicated malaria is usually associated with Plasmodium falciparum and less commonly with P. vivax. A total of three cases of unusual complications of P. vivax malaria are being reported here.


   Case Reports Top


Case 1

A 35-year-old male sedentary worker presented to medical emergency with complaints of moderate-high fever for 2 days associated with mild headache and lethargy. There was no history of cough, pain abdomen, vomiting, or burning micturition. There was no history of any addiction. Patient first consulted at a clinic and was prescribed paracetamol tablet. On examination, he was conscious, oriented, febrile with temperature of 104.5°F, blood pressure of 92/66 mm Hg, pulse rate of 132/min low in volume, no pallor, icterus, or clubbing. Examination of the chest, abdomen, and cardiovascular system was noncontributory. OptiMAL malaria antigen test was performed in the emergency which was positive for P. vivax. Subsequently, peripheral blood smear also revealed schizonts of P. vivax. Patient was started on injection artesunate and intravenous fluids. On 2 nd day of hospital stay, he developed acute onset pain in abdomen localized to epigastrium and umbilical region. On examination, abdomen was soft, tenderness was present in the epigastrium, no free fluid or organomegaly was noted. An erect skiagram of abdomen was done which was normal. Serum amylase was sent which was elevated (756 U/L). Serum lipase was also found to be elevated (414U/L). Kidney function tests and liver function tests were normal. Serum calcium and serum triglyceride level were also normal. Ultrasonography of the abdomen was done which revealed bulky head of the pancreas. Rest of the pancreas was obscured by bowel gases. Liver gall bladder and bile ducts were normal. Patient was again interviewed for any drug intake besides paracetamol prior to hospitalization but he denied. A diagnosis of P. vivax induced acute pancreatitis was made. Patient was managed conservatively with intravenous fluids, analgesics and clindamycin was added to artesunate to complete the artemesinin combination therapy. A contrast-enhanced computed tomography (CT) scan of the abdomen was done on 3 rd day which was suggestive of diffuse pancreatitis with CT severity index of 5. Patient was managed conservatively, recovered completely, and was discharged.

Case 2

An 18-year-old girl was admitted to the medical emergency with complaints of high grade fever for past 5 days and yellowness of eyes for past 3 days. There was no history of cough, breathlessness, pain abdomen, burning micturition, or bleeding from any site. On examination, she was febrile with a temperature of 103.6°F, blood pressure of 102/68 mm Hg, pulse rate of 120/min. Icterus was present. There was no clubbing or pedal edema. Systemic examination was normal. OptiMAL malaria antigen test was positive for P. vivax. Hemogram revealed hemoglobin of 11.2 g/dL, total leucocyte count of 5400/cumm, platelet count of 2.1 lac/cumm. Peripheral smear examination revealed schizonts of P. vivax. Liver function test showed total bilirubin of 3.8 mg/dL with indirect fraction of 1.4mg/dL, AST of 126 U/L, ALT of 187 U/L, ALP of 102 U/L. NS1 Ag test for dengue virus turned out to be negative. Blood urea and serum creatinine were within normal range. Patient was started on antimalarial therapy. After 12 h of hospital stay, she reported difficulty in breathing which was progressively increasing. On examination, she was tachypnoeic, respiratory rate of 32/min, oxygen saturation of 94 percent on room air, blood pressure of 106/66 mm Hg, pulse rate of 108/min, temperature of 99.4°F. On chest examination, there were crackles in bilateral lower zones. An urgent chest skiagram was done which was normal. Arterial blood gas was ordered which revealed hypoxemia with a pO2/FiO2 ratio of 250. Patient was given oxygen inhalation through mask. However, her condition continued to deteriorate and on repeat chest examination crackles were present in bilateral infrascapular, axillary, infraaxillary, and inframammary regions. A chest skiagram was repeated after 12 h which was suggestive of bilateral fluffy shadows in all lung fields. There was no evidence of cardiomegaly. Arterial blood gas was suggestive of hypoxemia with a pO2/FiO2 ratio of 110. A bedside two-dimensional echocardiography was done which was suggestive of normal study. A diagnosis of malaria induced acute respiratory distress syndrome (ARDS) was made and the patient was provided with BiPAP support. Her condition improved considerably. Ventilatory support was withdrawn after 48 h. She was discharge after completion of treatment.

Case 3

A young girl of 22-year age reported to our emergency with complaints of high grade fever for 3 days, jaundice for 2 days, and hematemesis and melena for last 1 day. There was no history of any drug intake, addiction, or similar episodes in past. On examination, she was febrile with a temperature of 104°F, blood pressure of 84/56 mm Hg, pulse rate of 134/min, low volume. She was pale and icterus was present. Chest, abdomen, and cardiovascular examination were normal. A nasogastric tube was put and there was evidence of fresh blood in it. She was immediately resuscitated with intravenous fluids. Investigations revealed a hemoglobin of 6.8 g/dL, total leukocyte count of 12000/cumm, platelet count of 1.7 lac/cumm. Peripheral smear revealed schizonts of P. vivax. Optimal test was positive for P. vivax. Liver function test showed total bilirubin of 5.7 mg/dL with indirect fraction of 2.7mg/dL. Serum AST value was 321 U/L and serum ALT was 433 U/L. Prothrombin time (test) was 58 s against a control of 13 s. INR was 5.2. HBsAg, anti-HAV immunoglobulin M (IgM), anti-HEV IgM, and anti-HCV antibody test were negative. NS1 antigen test for dengue virus was negative. Kidney function test revealed blood urea of 49 mg/dL and serum creatinine of 1.2 mg/dL. Patient was transfused with packed red blood cells and fresh frozen plasma. Injection artesunate and clindamycin was started. Her blood pressure and pulse rate normalized in due course of time. Ultrasonography of abdomen was done which was suggestive of mild hepatomegaly. There was no evidence of portal hypertension. An upper gastrointestinal endoscopy was done subsequently which was suggestive of hemorrhagic gastritis. No actively bleeding lesions were noted. Her melena subsided after 4 th day of hospital stay, icterus subsided, and LFT improved. She was discharged after completion of treatment.


   Discussion Top


Malaria is a major public health problem in India, accounting for sizeable morbidity and mortality. P. falciparum is usually responsible for complicated malaria. However, increasingly case reports of complicated malaria due to P. vivax have been reported in literature. [1],[2],[3],[4],[5],[6],[7],[8] Studies have shown that 21%-27% of severe malaria are because of P. vivax monoinfection. [9]

There are a few reports of pancreatitis due to complicated malaria and these are all associated with P. falciparum species. [2] Pancreatitis as a complication of P. vivax infection is extremely rare. [3] The likely mechanism of pancreatitis in malaria is the microvascular occlusion leading to ischemia, activation of pancreatic enzymes, and injury to the pancreatic tissue. There was no evidence of alcoholism, gall stones, drugs, trauma, or any metabolic abnormality leading to pancreatitis in our patient and hence diagnosis of malaria induced pancreatitis was justified.

ARDS is the severe form of lung injury in malaria. The pathogenesis of ARDS in malaria involves multiple causes which include sequestration of parasite containing erythrocytes, host immunologic reaction, coexistent sepsis, and pulmonary infections which finally cause increased alveolar permeability induced by cytokines. ARDS is also known to occur in P. vivax infection, but in a very few cases and which shows much less microvascular sequestration than P. falciparum. Sequestration of parasites in the lungs accompanied by posttreatment inflammatory response is the probable explanation of lung injury in P. vivax malaria. As compared with complicated falciparum malaria with ARDS, the prognosis is relatively better in ARDS in patients with complicated vivax malaria. [4],[5],[6],[7]

Gastrointestinal hemorrhage as a complication of P. vivax malaria again is extremely rare. [8] In our patient, it was due to malaria induced hepatic dysfunction and coagulopathy. Hemorrhage stopped after correction of coagulopathy and administration of antimalarial therapy and thus indicated malaria as its cause.


   Conclusion Top


Do increasing number of reports of severe malaria because of P. vivax means that parasite is evolving or there had been an earlier bias in reporting which used to devote more space to more lethal P. falciparum? Research is needed to answer this question and understand the mechanism underlying severe P. vivax malaria. But this is clear that vivax malaria which hitherto has gone by the name of benign malaria is actually not so benign. A high index of suspicion should be kept for the diagnosis of malaria and its complications so that morbidity and mortality can be minimized.

 
   References Top

1.Song JY, Park CW, Jo MY, Kim JY, Kim JH, Yoon HJ, et al. Two cases of Plasmodium vivax Malaria with the clinical picture resembling septic shock. Am J Trop Med Hyg 2007;77:609-11.  Back to cited text no. 1
    
2.Mohapatra MK, Gupta MP. Falciparum malaria complicated with acute pancreatitis: A report of case series. J Vector Borne Dis 2011;48:177-9.  Back to cited text no. 2
    
3.Sharma V, Sharma A, Aggarwal A, Bhardwaj G, Aggarwal S. Acute pancreatitis in a patient with Vivax malaria. JOP 2012;13:215-6.  Back to cited text no. 3
    
4.Mohan A, Sharma SK, Bollineni S. Acute lung injury and acute respiratory distress syndrome in malaria. J Vector Borne Dis 2008;45:179-93.  Back to cited text no. 4
    
5.Price L, Planche T, Rayner C, Krishna S. Acute respiratory distress syndrome in Plasmodium vivax malaria: Case report and review of literature. Trans R Soc Trop Med Hyg 2007;101:655-9.  Back to cited text no. 5
    
6.Sarkar S, Saha K, Das CS. Three cases of ARDS: An emerging complication of Plasmodium vivax malaria. Lung India 2010;27:154-7.  Back to cited text no. 6
[PUBMED]  Medknow Journal  
7.Agarwal R, Nath A, Gupta D. Non-invasive ventilation in Plasmodium vivax related ALI/ARDS. Intern Med 2007;46:2007-11.  Back to cited text no. 7
    
8.Kochhar R, Goenka MK, Mehta S, Mehta SK. Gastrointestinal bleeding in malaria. Indian J Gastroenterol 1990;9:295-6.  Back to cited text no. 8
    
9.Price RN, Douglas NM, Anstey NM. New developments in Plasmodium vivax malaria: Severe disease and the rise of chloroquine resistance. Curr Opin Infect Dis 2009;22:430-5.  Back to cited text no. 9
    

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Correspondence Address:
Deepak Sundriyal
79, Pocket 5, Sector 12, Dwarka, New Delhi - 110 078
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1755-6783.133748

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