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LETTERS TO THE EDITOR
Year : 2022  |  Volume : 25  |  Issue : 3  |  Page : 549-551
 

Cerebral venous thrombosis as a complication of plasmodium vivax Malaria: A report of 2 cases


1 Department of Neurology, All India Institute of Medical Sciences, New Delhi, India
2 Department of Neuroradiology, All India Institute of Medical Sciences, New Delhi, India

Date of Submission20-Nov-2021
Date of Acceptance07-Dec-2021
Date of Web Publication09-Feb-2022

Correspondence Address:
M V Padma Srivastava
Department of Neurology, Cardioneurosciences Centre, AIIMS, Room No 701, New Delhi
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/aian.aian_996_21

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How to cite this article:
Agarwal A, Murali S, Warrier A, Thomas A, Antil Y, Chadha A, Vishnu VY, Garg A, Padma Srivastava M V. Cerebral venous thrombosis as a complication of plasmodium vivax Malaria: A report of 2 cases. Ann Indian Acad Neurol 2022;25:549-51

How to cite this URL:
Agarwal A, Murali S, Warrier A, Thomas A, Antil Y, Chadha A, Vishnu VY, Garg A, Padma Srivastava M V. Cerebral venous thrombosis as a complication of plasmodium vivax Malaria: A report of 2 cases. Ann Indian Acad Neurol [serial online] 2022 [cited 2022 Aug 9];25:549-51. Available from: https://www.annalsofian.org/text.asp?2022/25/3/549/337445




Sir,

Cerebral malaria is the most severe complication associated with Plasmodium falciparum infection.[1] This clinical syndrome is defined by coma (at least 1 h after seizure termination or hypoglycemia correction) along with the presence of asexual parasite forms on peripheral blood smear, with no plausible alternative cause for to account for coma.[2] Patients develop fever, body ache, and/or headache with progressive deterioration in sensorium.[1] This results from sequestration of the parasitized red blood cells in the cerebral microcirculation, and potentiated by concomitant metabolic abnormalities and proinflammatory milieu.[3] Similar sequestration elsewhere in the body leads to anemia, thrombocytopenia, hepatic and renal impairment, and pulmonary edema.[1] Neuroimaging in cerebral malaria reveals cerebral edema with or without small hemorrhagic cortical infarcts and white matter changes.[4],[5] Rarely, cerebral venous thrombosis (CVT) can result.[6],[7] It has been described with Plasmodium falciparum infection alone or with mixed falciparum and vivax infections, and is rarely reported with Plasmodium vivax infection. We report 2 cases of CVT from isolated infection with the same.

Case 1: A 21-year-old gentleman presented with moderate grade, intermittent fever with holocranial headache of 3 days duration followed by 2 episodes of seizures (unknown onset to bilateral tonic-clonic; regained awareness after the first episode) and altered sensorium. He was started on intravenous anti-seizure drugs and electroencephalogram showed diffuse slowing, without features suggestive of nonconvulsive status epilepticus. His routine blood investigations were normal but the peripheral smear revealed the presence of trophozoites of Plasmodium vivax. Non-contrast computed tomography (NCCT) head revealed a hemorrhagic infarct in the right temporo-occipital region with perilesional edema and midline shift [Figure 1]a. Magnetic resonance imaging (MRI) brain revealed similar findings with magnetic resonance venography (MRV) suggestive of thrombosis of right transverse and sigmoid sinus [Figure 1]b,[Figure 1]c,[Figure 1]d,[Figure 1]e,[Figure 1]f. He was thereafter started on parenteral artesunate with oral doxycycline and subcutaneous low molecular weight heparin. He started improving from day 2 and was fully conscious and oriented by day 6 of therapy. Artesunate was given for 7 days followed by 2-week treatment with oral primaquine. Work up for all other causes (vasculitic profile, chronic infections like HIV, hepatitis B and C, leptospira, and pro-coagulant status) was negative and the patient denied any addictions. Oral anticoagulation was continued for 3 months and then stopped, and the patient continues to be asymptomatic.
Figure 1: (a) NCCT head revealing right temporo-occipital intraparenchymal hemorrhage with perilesional edema and midline shift. (b-e) MRI brain revealing a hemorrhagic infarct on FLAIR (d) with Diffusion weighted imaging (DWI) imaging (b) and Apparent diffusion coefficient (ADC) maps (c) showing diffusion restriction. Susceptibility weighted imaging (SWI) images (e) show evidence of hemorrhages. (f) MRV shows right transverse and sigmoid sinus thrombosis (arrow)

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Case 2: A 20-year-old gentleman presented with high grade, intermittent fever and left hemi-cranial throbbing headache of moderate intensity for 7 days followed by acute onset horizontal binocular diplopia with reduced alertness and responsiveness. On examination, his Glasgow Coma Scale score was 13/15 with bilateral papilloedma and left lateral rectus palsy and mild splenomegaly. His routine investigations were normal apart from thrombocytopenia (platelet count 59,000/mm3) and peripheral smear revealed Plasmodium vivax trophozoites. NCCT head revealed a hemorrhagic infarct in the left frontal region with perilesional edema [Figure 2]a. MRI brain with MRV revealed similar parenchymal changes with cortical vein thrombosis in the left frontal lobe [Figure 2]b,[Figure 2]c,[Figure 2]d,[Figure 2]e,[Figure 2]f. He was managed with parenteral artersunate and doxycycline for 7 days along with subcutaneous low molecular weight heparin with complete recovery. Work up for other potential causes (listed in case 1) were all normal. He was also treated with oral anticoagulants for 3 months and was asymptomatic at last follow-up visit.
Figure 2: (a) NCCT head revealing left frontal intraparenchymal hemorrhage with perilesional edema and midline shift. (b-e) MRI brain revealing a hemorrhagic infarct on FLAIR (d) with DWI imaging (b) and ADC maps (c) showing diffusion restriction. SWI images (e) show evidence of hemorrhages. (f) MRV shows thrombosis left frontal cortical veins

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Atypical manifestations of malaria are rising in endemic regions probably due to the large patient number, development of immunity, anti-malarial drug resistance, and its indiscriminate use.[7] CVT is one such manifestation and may result from hypercoagulability secondary to alteration in phospholipids in infected cells which leads to increased levels of von Willebrand factor[8] and release of tissue factor from damaged endothelial cells.[9] Treatment with artesunate may lead to good response unlike the past where parenteral quinine was the drug of choice in severe malarial infections. Both our patients improved when compared with mortality in 2 out of the 3 cases reported by Krishnan et al.[6] (treated with quinine). It is imperative to investigate and treat concomitant malarial infection in CVT, since early diagnosis improves outcome and prevents sequelae.

We seek to emphasize a low threshold for malarial testing in patients presenting with fever and neurological deficits, especially in endemic regions, where atypical presentations may commonly occur. Early diagnosis and treatment lead to good patient outcomes.

Key points

  1. Rule out malarial infection in all patients presenting with fever and CVT, especially in endemic regions.
  2. Plasmodium vivax infections can also lead to vascular and microvascular complications like Plasmodium falciparum.
  3. Early treatment with parenteral artesunate usually leads to good functional outcomes.


Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
   References Top

1.
Idro R, Marsh K, John CC, Newton CRJ. Cerebral malaria: Mechanisms of brain injury and strategies for improved neurocognitive outcome. Pediatr Res 2010;68:267-74.  Back to cited text no. 1
    
2.
World Health Organization. Severe falciparum malaria. World Health Organization, communicable diseases cluster. Trans R Soc Trop Med Hyg2000;94:S1-90.  Back to cited text no. 2
    
3.
Clark IA, Alleva LM. Is human malarial coma caused, or merely deepened, by sequestration? Trends Parasitol2009;25:314-8.  Back to cited text no. 3
    
4.
Cordoliani YS, SarrazinJL, Felten D, Caumes E, Leveque C, Fisch A. MR of cerebral malaria. Am J Neuroradiol 1998;19:871-4.  Back to cited text no. 4
    
5.
Patankar T, Karnad DR, Shetty PG, Desai AP, Prasad SR. Adult cerebral malaria: Prognostic importance of radiologic find- ings and correlation with post mortem findings. Radiology 2002;224:811-6.  Back to cited text no. 5
    
6.
Krishnan A, Karnad DR, Limaye U, Siddharth W. Cerebral venous and dural sinus thrombosis in severe falciparum malaria. J Infect 2004;48:86-90.  Back to cited text no. 6
    
7.
Singla N, Gupta M, Singh R, Kumar A. Atypical neurological manifestations of malaria. BMJ Case Rep 2014;2014:bcr2014204807. doi: 10.1136/bcr-2014-204807.  Back to cited text no. 7
    
8.
Ghosh K, Shetty S. Blood coagulation in falciparum malaria–A review. Parasitol Res 2008;102:571-6.  Back to cited text no. 8
    
9.
Francischetti IM, Seydel KB, Monteiro RQ, Whitten RO, Erexson CR, Noronha ALL, et al. Plasmodium falciparum-infected erythrocytes induce tissue factor expression in endothelial cells and support the assembly of multi-molecular coagulation complexes. J Thromb Haemost 2007;5:155-65.  Back to cited text no. 9
    


    Figures

  [Figure 1], [Figure 2]



 

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