Prolonged but reversible coma: an unusual complication of severe heatstroke

Abstract

Dear Editor, Heatstroke (HS) is usually defined as a core temperature over 40 C associated with central nervous system abnormalities. Neurological symptoms are usually transient and reversible after resolution of heat stress. Here we report the case of a patient who presented with prolonged but reversible coma after severe HS. This 48-year-old man was admitted to our ICU for coma, Glasgow coma scale (GCS) 3, associated with shock and fever. Proxies did not report any significant medical history. He was discovered outside (at an open-air car park) on a very sunny and hot day. The patient’s first measured temperature was 41.6 C. Soon after admission, he developed multiple organ failure (MOF) with shock needing large fluid infusion and administration of norepinephrine up to 0.7 lg/kg/min. Metabolic acidosis, acute renal failure, rhabdomyolysis, and signs of disseminated intravascular coagulation were also noted. There was no evidence of poisoning, meningitis, or sepsis. A non-injected brain CT scan was normal. HS was therefore retained as the cause of symptoms. The patient was immediately treated with external cooling, which allowed his core temperature to normalize in 6 h. Although MOF resolved in 2 days, the patient remained comatose despite metabolic control with dialysis and absence of pharmacological sedation. On day 10, he was still comatose (GCS 6). At that time, an electroencephalography did not record any seizures and brain magnetic resonance imaging (MRI) was therefore performed (Fig. 1). Axial fluid attenuated inversion recovery (FLAIR) images revealed symmetric hyperintensity of the pallidum. This hyperintensity became hypointense on T2* sequence, suggesting a recent bleeding. However, hypersignal on diffusion-weighted imaging was followed by a decrease of the apparent diffusion coefficient (ADC). These results suggested a mixed lesion (ischemic and hemorrhagic). This hypothesis was confirmed by T1 sequence with gadolinium injection revealing a hyperintense annular enhancement. Other cerebral structures (and particularly cerebellum) were considered normal. The patient remained comatose for 3 weeks. Then a gradual improvement of his neurological condition was observed. He was weaned from mechanical ventilation after 1 month and transferred to a rehabilitation center. Eight weeks after admission, the patient only presented moderate sequels like disorientation and cerebellar syndrome. A second MRI performed on day 45 showed similar findings (not shown). Neurological symptoms of HS are usually transient after resolution of heat stress. In most cases, cerebral imaging is normal or shows delayed isolated cerebellar atrophy. Definitive neurological damage (such as cerebellar syndrome) is rare but was previously reported [1]. In three cases, late cerebellar syndrome was associated with abnormalities of the