Marathon related death due to brainstem herniation in rehydration-related hyponatraemia: a case report

Abstract

Introduction: Identifying marathon runners at risk of neurological deterioration at the end of the race (within a large cohort complaining of exhaustion, dehydration, nausea, headache, dizziness, etc.) is challenging. Here we report a case of rehydration-related hyponatraemia with ensuing brain herniation.

Case presentation: We report the death of runner in his 30's who collapsed in the recovery area following a marathon. Following rehydration he developed a respiratory arrest in the emergency room. He was found to be hyponatraemic (130 mM). A CT brain scan showed severe hydrocephalus and brain stem herniation. Despite emergency insertion of an extraventricular drain, he was tested for brainstem death the following morning. Funduscopy demonstrated an acute-on-chronic papilledema; CSF spectrophotometry did not reveal any trace of oxyhemoglobin or bilirubin, but ferritin levels were considerably raised (530 ng/mL, upper reference value 12 ng/mL), consistent with a previous bleed. Retrospectively it emerged that the patient had suffered from a thunderclap headache some months earlier. Subsequently he developed morning headaches and nausea. This suggests that he may have suffered from a subarachnoid haemorrhage complicated by secondary hydrocephalus. This would explain why in this case the relatively mild rehydration-related hyponatremia may have caused brain swelling sufficient for herniation.

Conclusion: Given the frequency of hyponatraemia in marathon runners (serum Na <135 mM in about 13%), and the non-specific symptoms, we discuss how a simple screening test such as funduscopy may help to identify those who require urgent neuroimaging.

Figure 1

CT brain scan signs of hydrocephalus, high intracranial pressure and brain stem herniation. Brain CT (axial slices) in a male patient in his 30's who died of brain stem herniation after completing a marathon. The CT shows (A) loss of the rostral cerebral sulci suggesting increase in ICP, (B) and (C) a large hydrocephalus with widening of both temporal horns. The grey matter can still be differentiated from the white matter, but all sulci are lost. This suggests that the brain oedema is of relative recent onset and massive tissue ischaemia has not yet occurred. (D) Compression of the fourth ventricle with dilatation of the third ventricle and the caudal aspect of both temporal horns. This is observed with considerable brain oedema and obstructive hydrocephalus. (E) Herniation of the medulla and pons into the foramen magnum. (F) The tonsils are located at the level of the dens which is a good indicator for foramen magnum herniation. (All images are from the case presented here).

Figure 2

Funduscopic signs of high intracranial pressure. (A) The disc shows florid hemorrhages with relatively little swelling, indicating a rapid, dramatic increase in CSF pressure. Progressive changes of optic disc oedema are seen in a patient with an intracranial tumour who declined treatment (B-D). (B) Early nerve fiber dilatation is seen particularly superiorly, inferiorly and nasally. (C) This increases and venous engorgement develops. (D) Temporal nerve fiber dilatation and swelling of the disc increases and hemorrhages appear. (E) In gross chronic disc oedema the normal retinal vasculature is masked and dilated superficial capillaries are observed. (F) In atrophic optic disc oedema nerve fibers are eventually destroyed and the optic disc without viable nerve fibers does not swell. This patient had longstanding benign intracranial hypertension. Retinochoroidal venous collaterals are present (black arrowhead). (All images are reprinted from reference 17, with permission).