CLASSIC HEAT STROKE IN A CASE OF SIMPLE HYPOHYDROSIS WITH “BAD PROGNOSTIC INDICATORS” BUT A REMARKABLE RECOVERY

Abstract

Heat stroke occurs in the desert area of Saudi Arabia quite frequently and manifest in different patterns including coagulopathy . Frequently encountered complications include renal or hepatic failure, rhabdomyolysis, acute respiratory distress syndrome (ARDS), disseminated intravascular coagulation (DIC), and seizure . Not all of these complications usually occur in the same patient, in case it occurs the mortality reported is significantly high. We describe a case of heat stroke that had nearly all the known complications of heat stroke but recovered from all, except minor neurological deficit in the form of dysarthria and exaggerated deep reflexes.

• Heat stroke
• Rhabdomyolysis, Acute renal failure

CASE REPORT

A 30-year old male, sailor by profession for the last 5 years, was found in an unconscious state in the month of July in a very hot and humid cabin on board ship and was brought in about 30 min to Dammam Central Hospital, Dammam, Saudi Arabia. It was not known how long he was unconscious on the boat. There was no known history of alcoholism, drug intake, hypertension and diabetes mellitus. On arrival, he was unconscious with rectal temperature of 41°C and in a state of shock (no peripheral pulse and unrecordable blood pressure). The skin was dry. There was no alopecia, tooth or nail defect. Later, when the patient became conscious, he gave the history of diminished sweating since childhood but never had heat-related illness. He also told that this was his first visit to this area in the summer season. There was no family history of such illness or diminished sweating. There was no lower limb edema but had jaundice and peripheral cyanosis. Nervous system examination showed deeply comatose status with pupils equal and reacting to light. There was no neck rigidity but deep jerks were diminished with equivocal bilateral planter. The urgent work up on the day of admission showed Hb 14.3 Gm/dL, Hct 45%, platelet count 109,000/cumm, INR 16, PTT 1′24″, Serum Fibrinogen 52 mg/dL (150–360), fibrinogen degradation products 32,000 ng/mL (< 8 μg/mL), Random blood sugar 100/mg/dL, Blood urea 141 mg/dL, serum creatinine 6.4 mg/dL, Serum bilirubin (Total) 4.86 mg/dL, Serum Aspartate Aminotransferase 1645 IU/L, Serum Creatine phosphokinase 27910 IU/L, Serum Alanine Aminotransferase 1259 IU/L, Serum Lactic dehydrogenase- 4115 IU/L, Serum calcium 7.75 mg/dL, Serum Phosphate 5 mg/dL,Serum Sodium 1.38 mmol/L, Serum Potassium 6.5 mmol/L, Uric acid 20 mg/dL. Arterial Blood Gases (ABG) pH 7.313, PO2 60 mmHg, PCO2 17.3 mmHg, HCO3 8.8 mmol/L, Saturation 95.5%. Plain Computed tomography of brain did not show any evidence of focal or space occupying lesion. Blood and urine screening for toxicology was negative. The ultrasonogram of the abdomen was normal. The patient was managed in intensive care with rapid cooling and resuscitated with isotonic saline under central venous pressure guidance. In spite of it the patient remains anuric with further deterioration in renal function, hence he was started on continuous arterio-venous hemofilteration (CAVH) from the day of admission and then shifted on hemodialysis for 25 days before the urine output started to increase with the improvement of renal function and serum creatinine reaching the level of 1.4 mg/dL in about 6 weeks time. He also developed ARDS for which he was put on a ventilator. His neurological status was slow to improve and became fully conscious at the end of third week. The examination of cerebrospinal fluid was normal. He was extubated after 2 weeks of admission. The rhabdomyolysis and hepatic impairment also improved gradually. The DIC was managed by fresh frozen plasma and platelet transfusion. He developed upper GIT bleeding due to stress ulcer which was managed by H2 blocker and blood transfusion. He was discharged after 56 days of hospital stay with normal hepatic, renal function, coagulogram, muscle enzymes but had mild neurological deficit in the form of dysarthria and exaggerated deep tendon reflexes; the CT scan of brain with contrast revealed cortical atrophic changes. Thus, the final diagnosis was “CLASSIC HEAT STROKE IN A CASE OF SIMPLE HYPOHYDROSIS COMPLICATED BY RHABDOMYOLYSIS, ACUTE RENAL FAILURE, ARDS, HEPATITIS, DIC AND STRESS ULCER WITH RESIDUAL NEUROLOGICAL DEFICIT”

DISCUSSION

Heat stroke occurs when body thermal regulation is unable to dissipate adequate amount of heat with rise in body temperature [[3]]. It can be of two types i.e. classic and exertional forms. In our patient, the heat stroke seems to be of classic type because the patient was unconscious with dry skin, which is the known feature of this type. Though the classic heat stroke is seen in older individuals and those having preexisting chronic disease (congestive heart failure), diabetes mellitus, alcoholism [4-6] which was not associated in this case. Our patient's CVP was within normal range, which has been reported in 64.7% of heat stroke cases at the time of presentation [[7]]. The bad prognostic indicators of heat stroke are coma, hypotension, DIC and the necessity for intubation [[6]] which were all present in our patient. In spite of it our patient made remarkable recovery.

We conclude that multi organ failure and bad prognostic indicator complicated this case of classic type heat stroke in a professional sailor, without any predisposing factor, at the time of presentation leading to therapeutic challenge. The urgency of management in the intensive care unit with ventilator and dialysis support led to complete recovery with minimal neurological deficit indicating that the course of disease can be favorably changed even in the presence of all adverse parameters.