Unique Persistent Neurological Sequelae of Heat Stroke

Military Medicine, Jun 2007 by Rav-Acha, Moshe, Shuvy, Mony, Hagag, Shalom, Gomori, Moshe, Biran, Iftah

Heat stroke is a rare clinical phenomenon, characterized by systemic heat and cytokine-induced organ damage. Permanent neurological deficits rarely develop following heat strokes, and cerebellar dysfunction predominates among these rare cases. We report a case of severe heat stroke with recovery from severe multiorgan failure but with persistent neurological manifestations. These included a combination of resolving right-sided signs as well as persistent frontal subcortical dysfunction, with minimal, if any, cerebellar involvement. This combination and the absence of cerebellar involvement is an unusual neurological sequelae of heat stroke.

Case Report

A 30-year-old seminar student was admitted to our hospital unconscious and hyperthermic (40�C) 2 hours after he collapsed during a strenuous hike in the Judean desert, under warm conditions (temperature, 28�C; relative humidity, 30%). According to his colleagues, he complained of generalized weakness and fatigue 3 days before the occasion and suffered from diarrhea the previous day. No febrile illness was noticed. On the day of the outing, the patient was weak but had no specific complaints. During the hike, his colleagues observed increased fatigue and disorientation, for which multiple rest periods were used. Nevertheless, after 4 hours of hiking, the patient collapsed and, soon after, generalized convulsions were noticed. There was no history of snake or insect bite during the tour. His past medical history was unremarkable. There were no known chronic illnesses or drug and alcohol abuse.

Physical examination upon admission revealed a comatose patient (Glasgow Coma Scale 3). Pupils were equal and reacted slowly to light. Comeal reflex was elicited bilaterally. The limb tone was flaccid and the deep tendon reflexes were diminished. The patient was tachypneic but hemodynamically stable. Examination of his heart, lungs, and abdomen did not reveal any pathologic findings.

Initial laboratory tests revealed normal blood count, normal electrolytes (140 mM sodium, 5 mM potassium, 5 mM glucose), moderate renal function impairment (4.1 mM urea, 170 �M creatinine), elevated hepatocellular and muscle enzymes (140 U of alanine aminotransferase (ALT), 570 U of aspartate aminotransferase (AST), 60 U of alk-p, 40 U of guanosine 5'-triphosphate, 10 �M total bilirubin, O �M direct bilirubin, 1,420 U of lactate dehydrogenase, and 6,940 U of creatine kinase). An arterial blood gas test revealed metabolic acidosis with increased lactate (pH 7.32, 32 PCO^sub 2^, 16.5 HCO^sub 3^, 8.2 mM lactate). The urine toxic screen was negative. Brain computed tomography (with and without contrast) on his admission was normal and the patient was transferred to the intensive care unit. Upon arrival, the patient was intubated and extensive cooling efforts, including pouring large quantities of tap water, coverings with ice packs and intravenous fluids, were initiated. During his intensive care unit period, the patient developed clinical bleeding diathesis, with the laboratory results suggesting disseminated intravascular coagulation (DIC) (4.65 international normalized ratio, partial thromboplastin time 79 seconds, 105 mg% fibrinogen, 1,379 ng/mL D-Dimer), marked exacerbation of hepatocellular enzyme disturbance (3,830 U of alanine aminotransferase, 5,200 U of aspartate aminotransferase, 73 U of alk-p, 40 U of guanosine 5'-triphosphate, 156 �M total bilirubin, 21,290 U of lactate dehydrogenase) and severe rhabdomyolysis (50,000 U/L creatine kinase, 70,000 ng/mL myoglobin) accompanied by anuria and renal function deterioration (23 mM urea, 580 �M creatinine) which necessitated hemodialysis.

The patient remained unconscious for 7 days. Neurological examination upon regaining consciousness suggested right hemiparesis. Repeat brain computed tomography (without contrast) was normal with no evidence of brain hemorrhage, ischemia, or edema. During the following month, a gradual normalization of his renal function, hepatic, and muscle enzymes was noticed and hemodialysis was stopped due to normal urine output. Although there was marked improvement in his physical state, the patient exhibited persistent generalized slowness and incoherent speech. Neurological examination, 5 weeks following the heat stroke occasion, demonstrated the following: moderately slowed and effortful speech without any distinct pattern of dysarthria such as the cerebellar explosive and scanning speech. Cranial nerves were intact and there was no nystagmus. No significant motor deficit was noticed except for mild fanning of his right upper limb fingers with minimal writhing movements. Limb tone and muscle stretch reflexes were normal without any pyramidal signs. There were no sensory signs. His cerebellar examination was normal, without any evidence of dysmetria, rebound, or impairment in rapid alternating movements. Cognitive assessment documented minimal impairment in attention, with digit span of six forward and four backward. His orientation was intact. Immediate memory was slightly impaired (two of three words). Language functions were intact aside from impaired writing and slowed speech. Naming, repetition, and comprehension were all intact and there was no right-left disorientation. There was no apraxia. Visual functions were intact. There was slight disinhibition in a go-no-go task and motor programming was intact.