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-oldpatient admitted after traumatic brain injury with rapid deterioration. Patient was found to haveP. falciparummalaria 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, haemorrhagic 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-coagulationearly followed by a hyper-coagulatorystate in the late phase.
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