We report a 41-year-old man who developed rhabdomyolysis and severe hepatocellular damage following a run of 9km. He made a full clinical recovery with conservative management. The case highlights the clinical features of his presentation. It demonstrates that exertional heat stroke (EHS) can occur even in temperate climates, that clinical recovery is possible with conservative management, and it highlights the significance of early body cooling and serial monitoring of biochemical parameters.  

EHS is a medical emergency, requiring prompt recognition and treatment, as it is associated with life threatening complications.¹ Early recognition with immediate cooling can ameliorate the elevated core body temperature; and this may prevent organ failure and improve prognosis.¹

Case report

A previously healthy 41-year-old man collapsed at the 9km mark while partaking in a half marathon. Past history was significant for a similar episode of collapse but with no sequelae. On this occasion, he lost consciousness, but regained consciousness during transfer to the emergency department (ED) via a standby ambulance.

Examination revealed a clinically dehydrated, disorientated individual without focal neurological deficits. His tympanic temperature measured 38.5^oC. He was tachypnoeic at 34 breaths per minute and had a sinus tachycardia on electrocardiogram of 133 beats/minute. His Glasgow coma scale (GCS) was 13/15. Bed side capillary blood glucose was 9.8mmol/l and troponin I <0.05ng/ml.

A preliminary diagnosis of EHS was made. He was treated immediately with fluid resuscitation and body cooling with ice packs. Blood profiles were normal for blood counts, liver tests, urea, electrolytes and coagulation. Mild elevation of serum creatinine 154µmol/L. Arterial blood showed lactate 6.8mmol/L, pH 7.4 and bicarbonate 24.3mmol/L. He was discharged once his vital signs and GCS normalised.

He returned three days later with fatigue and vomiting. GCS, vital signs and tympanic temperature were normal. Scleral icterus was seen without organomegaly or hepatic encephalopathy.

Investigations revealed severe hepatocellular damage with elevated creatine kinase (CK) (see Figure 1).  Total bilirubin 115µmol/L, gamma-glutamyl transpeptidase 139 IU/L, lactate dehydrogenase 2945 IU/L (< 500 IU/L), and platelet count 115 x 109/L (150 to 400), international normalised ratio (INR) 1.69 and prothrombin time (PT) 19.4 seconds, lactate 0.9mmol/L, pH 7.4, bicarbonate 24.3mmol/L and normal renal function.

Investigations for hepatitis were negative and included: urine and serum toxicology, serology for viral hepatitis, leptospirosis, alpha1-antitrypsin, ceruloplasmin, immunoglobulin levels and autoantibody screening. Ultrasonography revealed a grossly normal liver with no large vessel thrombosis. Holter monitor showed sinus rhythm with heart rate varying from 33 to 129 beats/min and no malignant arrhythmia. Gradual improvements in laboratory parameters were seen. Clinical recovery was observed by the 12th day. CK had decreased to 167 IU/L on the 26th day, and liver blood tests were normal by day 30.

Figure 1: Line graph demonstrating differential improvement in hepatic enzymes and CK, creatine kinase. AST, aspartate aminotransferase (normal < 42 IU/L), ALT, alanine aminotransferase (normal < 40 IU/L)(click to enlarge)

Discussion

EHS can be fatal despite adequately lowering body temperature, and survivors may sustain permanent neurologic damage.^2,3 Both direct thermal injury and hypoxia appear to play a major role in the pathophysiology. 

Complications for heat stroke are multi-organ dysfunction, including rhabdomyolysis and hepatocellular injury.^2,4 CK levels (>1,000U/L), metabolic acidosis and liver enzymes more than twice normal are predictive for poor prognosis.⁵ CK measured on day five after collapse, confirms our patient had rhabdomyolysis.⁵ No renal dysfunction developed; likely due to appropriate and timely fluid resuscitation. 

Reports have suggested that systemic or intrahepatic coagulation disturbance, as seen in disseminated intravascular coagulation (DIC)⁶, and portal vein thrombosis⁷, can cause the liver insult. However, in our patient liver ultrasound with duplex study ruled out any portal venous anomalies. Whether the reduced platelet count and raised PT observed in our patient were manifestations of early DIC or the result of EHS induced hepatocellular damage remains controversial. 

In conclusion, this case demonstrates that a diagnosis of EHS should be considered in temperate climates. Serial monitoring of biochemical parameters should be undertaken, as initial liver tests can be normal, which usually peak on the third day after exposure to the heat insult.³

References

1. Heled Y, Rav-Acha M, Shani Y, Epstein Y, Moran DS. The ‘golden hour’ for heatstroke treatment. Mil Med 2004; 169(3):184-6
2. Knochel JP, Reed G. Disorders of heat regulation. In: Maxwell & Kleeman’s clinical disorders of fluid and electrolyte metabolism, Narins R, (5th ed). New York: McGraw-Hill; 1994. p. 1549-90
3. Dematte JE, O’Mara K, Buescher J, Whitney CG, Forsythe S, McNamee T, et al. Near-fatal heat stroke during the 1995 heat wave in Chicago.  Ann Intern Med. 1998; 129(3): 173-81.
4. Al-Mashhadani SA, Gader AG, Harthi SS, Kangav D, Shaheen FA, Bogus F. The coagulopathy of heatstroke: alterations in coagulation and fibrinolysis in heatstroke patients during the pilgrimage (Haj) to Makkah. Blood Coagul Fibrinolysis. 1994; 5: 731-6
5. Varghese GM, John G, Thomas K, Abraham OC, Mathai D. Predictors of multi-organ dysfunction in heatstroke. Emerg Med J. 2005; 22(3): 185-7
6. Irie H, Mori W. Fatal hepatic necrosis after shock. Acta Pathol Jpn. 1986; 36(3): 363-74
7. Scobie BA. Gastrointestinal emergencies with marathon-type running: omental infarction with pancreatitis and liver failure with portal vein thrombosis. N Z Med J 1998; 111(1067): 211-12