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VOLUME 10 , ISSUE 3 ( September-December, 2021 ) > List of Articles

CASE REPORT

Patient with Severe Traumatic Brain Injury and Malaria in a Middle Eastern Country

Amani NH Alansari, Suresh Arumugam

Citation Information : Alansari AN, Arumugam S. Patient with Severe Traumatic Brain Injury and Malaria in a Middle Eastern Country. Panam J Trauma Crit Care Emerg Surg 2021; 10 (3):134-138.

DOI: 10.5005/jp-journals-10030-1363

License: CC BY-NC 4.0

Published Online: 18-01-2022

Copyright Statement:  Copyright © 2021; The Author(s).


Abstract

Aim and objective: This manuscript reports a case of severe traumatic brain injury in a patient complicated by Falciparum malaria with review of the literature and discussion of possible underlying mechanism aggravating the secondary brain injury. Background: Plasmodium falciparum (P. falciparum) malaria accounts for more than 90% of deaths caused by malaria in the world. Parasitized red blood cells sequester and cause capillary occlusion, endothelial damage, cytokine activation, and dysregulation of coagulation leading to exacerbation of secondary injury after traumatic brain injury. Case description: The case reports highlight a rare case of 38-year-old patient admitted after traumatic brain injury with rapid deterioration. Patient was found to have P. falciparum malaria with 3.9% parasitised RBC. CT head revealed a large right sided subdural haemato-hygroma, midline shift and ischemia in the right posterior cerebral artery territory. Despite timely intervention and evacuation of subdural haematoma, patient had a poor outcome with multiple infarcts, hemorrhagic transformation, and early hydrocephalus. Patient remains in a vegetative state in a long-term unit. Conclusion: Combined effect of endothelial, microcirculatory, inflammatory, and clotting dysfunction caused by traumatic brain injury and parasitaemia leading to aggravation of secondary brain injury. Clinical significance: This case report highlights the intricate relationship between endothelial, inflammatory, and coagulation cascade triggered after brain injury. The nature of coagulopathy in such patients is complex with state of hypo-coagulation early followed by a hyper-coagulatory state in the late phase.

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