Life-threatening heat stroke presenting with ST elevations: a report of consecutive cases during the heat wave 11 3
Summary Heat stroke is a life-threatening condition due to an acute thermoregulatory failure during expo-sure to high environmental temperatures. We report a series of four cases (three exertional, one classic heat stroke) during the heat wave of July 2013 in Austria. All of them presented with a core temperature > 41 °C, central nervous dysfunction, acute respiratory and renal failure, disseminated intravascular coagulation, rhabdomyoly-sis, and severe electrocardiographic changes, two cases even mimicking ST-elevation myocardial infarction. The patients were cooled to normal temperature with the “Arctic sun” external cooling system within hours. Elec-trocardiographic changes resolved quickly. All patients primarily recovered from multiple organ dysfunction and could be discharged from intensive care unit. Unfor-tunately, the two elder patients died 1 week and 5 weeks later because of late complications.
Lebensbedrohlicher „Hitzschlag“ mit ST-Hebungen – ein Bericht von konsekutiven Fällen während der Hitzewelle in Österreich im Juli 2013
Zusammenfassung Der Hitzschlag ist ein lebendsbe-drohlicher Zustand als Folge eines Versagens der Ther-moregulationsmechanismen im Rahmen einer extremen Hitze-Exposition. Wir berichten eine Serie von 4 Fällen (3
belastungsinduzierte, 1 klassischer Hitzschlag) während der Hitzewelle im Juli 2013 in Österreich. Alle wiesen ein Körperkerntemperatur von > 41 °C, Bewusstseins-trübung, akute respiratorische und renale Insuffizienz, disseminierte intravaskuläre Coagulation (DIC), Rhab-domyolyse und ausgeprägte EKG-Veränderungen auf, in 2 Fällen das Bild eines ST-Hebungs-Infarktes (STEMI). Die Patienten wurden binnen Stunden mittels exter-nem Kühlsystem („Arctic Sun“) auf Normaltemperatur gekühlt, woraufhin sich die EKG Veränderungen rückbil-deten. Alle Patienten erholten sich vom Multiorganver-sagen und konnten stabil von der Intensivstation verlegt werden. Leider verstarben die beiden älteren Patienten 1 bzw. 5 Wochen später an Spätkomplikationen.
Heat stroke is defined as an elevated core body tem-perature exceeding 40 °C and associated central nervous dysfunction such as delirium or coma, as well as convul-sions. It may be complicated by respiratory, hepatic, and renal failure, disseminated intravascular coagulation (DIC), and rhabdomyolysis. It is caused by a thermoregu-latory failure due to exposure to extreme environmental heat [1]. In Austria, there was a period with extraordinary high temperatures in July 2013 after weeks of coldness below average.
We report a series of four cases of life-threatening heat stroke, all presenting within the first 3 days of the heat wave. Besides the frequent complications such as mul-tiple organic failure, all patients additionally showed severe changes in electrocardiogram—two of them even presenting with distinct ST elevations.
Dr. E. Lassnig () · P. Dinkhauser · E. Maurer · B. EberCardiology and Intensive Care Medicine, Department of Internal Medicine II, Klinikum Wels-Grieskirchen,Griekirchner Strasse 42, 4600 Wels, Austriae-mail: [email protected]
Life-threatening heat stroke presenting with ST elevations: a report of consecutive cases during the heat wave in Austria in July 2013
Elisabeth Lassnig · Patrick Dinkhauser · Edwin Maurer · Bernd Eber
case report
2 Life-threatening heat stroke presenting with ST elevations: a report of consecutive cases during the heat wave 1 3
Case reports
Patient 1
Patient 1 was a 57-year-old man with suspected myocar-dial infarction. He was a construction worker who col-lapsed at the building site on late afternoon after doing hard work all day long, exposed to an environmental temperature of 36 °C. The emergency doctor docu-mented a blood pressure of 70/50 mmHg, tachypnea, and tachycardia as well as inferior and V1–V3 ST-segment elevations on electrocardiogram (ECG). The patient was intubated on site; electrical cardioversion was tried out-of-hospital without any effect on tachycardia. The patient was admitted to our intensive care unit (ICU), where he presented hypotonia and tachycardia with ST elevations furthermore (Fig. 1a). A body temperature of 42.6 °C was measured (ear thermometer) and confirmed by measur-ing bladder temperature. Cooling with cold intravascular fluids and external cooling with “Arctic sun” was started
immediately. Echocardiography showed a hyperdynamic left ventricle. Adenosine had no effect on the tachycar-dia, and only intravenous metoprolol could slow it (Fig 1b); ST elevations showed a Brugada pattern. Acute coro-nary angiography was performed to rule out acute coro-nary syndrome. Within 3 h, body core temperature was in normal ranges, and tachycardia as well as ST-segment changes resolved (Fig 1c). Laboratory findings revealed renal failure, rhabdomyolysis, thrombopenia, and decreased prothrombin time. Nevertheless, the patient could be extubated the next day. After 1 day of mental confusion and agitation, he became normal again with retrograde amnesia. Laboratory parameters normalized and the patient was discharged from ICU.
Patient 2
Patient 2 came in the ambulance the day after patient 1, late afternoon again, and the environmental temperature was again 36 °C. He was a 56-year-old man with severe schizophrenia and chronic obstructive pulmonary dis-ease (COPD). He had been found in the park of the psy-chiatric institution where he lived. He was comatose, cyanotic, hypotonic, and tachypneic. He had to be intu-bated instantly. Body core temperature was 42.8 °C. ECG showed similar ST changes as in patient 1 (Fig. 2a). Echo-cardiography showed preserved left ventricular function. Cooling with cold fluids and external pads (“Arctic sun”) was started. ECG normalized after some hours (Fig. 2b). Like patient 1, rhabdomyolysis, renal impairment, and signs of DIC were found in laboratory examination,
Fig. 2 a ECG of patient 2 at admission. b ECG of the same patient 3 h later with normal body temperature: complete res-titution of ECG changes
Fig. 1 a Electrocardiogram (ECG) of patient 1 at admission with ST elevations and tachycardia. b ECG of patient 1 after 5-mg metoprolol administration. c ECG of patient 1 at a body core temperature of 36.5 °C
case report
Life-threatening heat stroke presenting with ST elevations: a report of consecutive cases during the heat wave 31 3
Course and discussion
There are two types of heat stroke. The “classic” (non-exertional) heat stroke is seen in people with underlying medical conditions that influence thermoregulation [2]. Patients are often elder with neurologic or psychiatric disorders and consuming drugs like diuretics or anticho-linergic substances. The “exertional” heat stroke often occurs in young, active individuals doing strong exercise without accommodation period while environmental temperatures are high [3].
All our patients presented with tachypnea and tachy-cardia, were hypotonic and comatose, and had a body core temperature of more than 41 °C. All showed respi-ratory insufficiency and required invasive mechanical ventilation (patient 1, 3, and 4 over 24 h, patient 2 over 14 days). All patients developed acute renal failure, rhabdo-myolysis, and DIC. Patient 4 also had repetitive seizures.
Heat stroke and the progression to multiorgan dys-function syndrome are the consequence of a complex interaction of the physiological changes of the organism in association with hyperthermia, the direct cytotoxic effect of heat on the cells, and the inflammatory and coagulation responses of the host [1]. This leads to altera-tion in blood flow in the microcirculation and results in injury to the endothelium and tissue, which is compa-rable with SIRS.
Cardiac manifestations associated with heat have already been reported [4]. Tachycardia and nonspecific ECG changes are common. However, ST elevations in hyperthermia are rare and were suggested to be due to myocardial ischemia. Echocardiographic findings with reversible hypokinesia have been published [5, 6]. In our two patients who presented with ST elevations, the changes were isolated electrically. Despite remarked ST elevation, both patients did not have any contrac-tion abnormality on echocardiographic investigation. In patient 1, even coronary angiography was performed, which showed coronary arteries without stenosis and with normal blood flow. Cardiac biomarker high sen-sitive troponine was only slightly elevated. The ECG changes immediately disappeared when normal body core temperatures were achieved. One could suspect a “Brugada-like” reaction due to a temperature-depen-dent conduction change of the myocardial ion channels, whereas the ECGs of our patients did not show the typical Brugada pattern. However, fever is known as a trigger for Brugada ECG. We performed an ajmalin test in patient 1 on day 3. Administration of 50 mg of ajmalin did not result in ST-segment elevations in V1–V3. Sympathicoto-nus and endogenous catecholamines during heat stress and heat stroke could also influence myocardium and lead to ECG changes, just like in stress cardiomyopathy (tako-tsubo cardiomyopathy) [7].
All patients were successfully cooled with an external cooling system (“Arctic sun®”). A body core temperature < 38 °C could be achieved within 2 h. Renal failure, DIC, and hemodynamic instability recovered in normother-mia and after fluid resuscitation. Except patient 2, all
which also normalized after 2 days. After normothermia was reached and the external cooling was stopped, body temperature started rising again up to 39–40 °C, refrac-tory to antipyretic substances. Neuroleptics were paused and benzodiazepines started to rule out malignant neu-roleptic syndrome, but there was no effect. Weaning from respirator was not possible initially because of central tachypnea. Cerebral computed tomography (CT) scan and magnetic resonance imaging revealed no additional information. He needed a tracheostoma. In 4 weeks of intensive care, he awoke slowly, and could be weaned from the respirator but had severe cognitive deficits. He died of pneumonia 2 weeks after transfer to the psychiat-ric institution.
Patient 3
Patient 3 also came with the ambulance and was admit-ted in the ICU the day after patient 2, late afternoon again, and the environmental temperature was again 36 °C. He was a 57-year-old construction worker who lost consciousness at the end of his working day at the building site. He presented with a temperature of 41.6 °C, respiratory rate of 45/min, and blood pressure of 80/60 mmHg. ECG showed tachycardia and ST depres-sion in the anterior leads. The patient was intubated and cooled to normothermia. Laboratory findings revealed renal impairment, rhabdomyolysis, and DIC similarly to the cases before. Extubation was carried out without problems the day after. Similarly to patient 1, disorien-tation, confusion and agitation occurred for 24 h. After-ward, transfer to normal station was possible.
Patient 4
Patient 4 was admitted 1 h after patient 3. Again, it was a construction worker who collapsed, 33 years old and otherwise healthy. His body temperature was 42.3 °C. Glasgow Coma Scale score was 3, and hypotension, tachycardia, and ST depressions were present. He was intubated and cooled as well. Despite analgosedation, he had repetitive seizures. Acute CT scan ruled out a structural cerebral source. Levetiracetam was given once. The patient stabilized the next day and was extu-bated. He also had a phase of mental confusion, and he additionally developed acute liver failure. All medica-tions were stopped on day 2. His serum transaminases and bilirubin levels increased (Aspartataminotransfer-ase (AST): 8512 U/l (normal < 35), alaninaminotranfer-ase (ALT): 6193 U/l (normal < 45), lactatdehydrogenase (LDH): 6284 U/l (normal < 250), bilirubin 6,5 mg/dl), prothrombin time decreased to 22 %, and AT III reduced to 47 %. He recovered without additional interventions after 1 week.
case report
4 Life-threatening heat stroke presenting with ST elevations: a report of consecutive cases during the heat wave 1 3
systemic inflammatory response syndrome (SIRS). It can cause remarked ECG changes, even mimicking myocar-dial infarction. The primary goal must be to lower core body temperature, whereas external cooling with “Arctic sun®” was very effective in our cases.
Conflict of interestThe authors declare no conflict of interest.
References
1. Bouchama A, Knochel JP. Heat stroke. N Engl J Med. 2002;346:1978–88.
2. Klenk J, Becker C, Rapp K. Heat-related mortality in resi-dents of nursing homes. Age Ageing. 2010;39:245.
3. Hirshey Dirksen SJ, Larach MG, Rosenberg H, et al. Future directions in malignant hyperthermia research and patient care. Anesth Analg. 2011;113:1108.
4. Kew MC, Tucker RB, Bersohn I, Seftel HC. The heart in heatstroke. Am Heart J. 1969;77:324–35.
5. Akhtar MJ, al-Nozha M, al-Harthi S, Noush MS. Elektro-cardiographic abnormalities in patients with heat stroke. Chest. 1993;104:411–4.
6. Wakino S, Hori S, Mimura T, et al. A case of severe heat stroke with abnormal cardiac findings. Int Heart J. 2005;46:543–50.
7. Al-Hadramy MS, Ali F. Catecholamines and heat stroke. Mil Med. 1989;154:263–4.
patients could be extubated after 24–48 h. All of them had organic psychosyndrome with confusion and hyperactiv-ity. Patient 4 was the only one suffering from hepatic fail-ure with coagulation malfunction and extensive increase of serum transaminases with a peak on day 3 and nor-malizing in 1 week.
Patient 2 was different. He was the only patient with classic heat stroke and severe comorbidities—schizo-phrenia and COPD. Neuroleptic medication might have influenced thermoregulation, and the mental disorder let him ignore heat exposition. His comorbidities may have influenced his prognosis. He had a long ICU stay and was discharged with severe cognitive deficits—due as well to heat injury as to hypoxia.
The other patients were discharged from ICU on day 3–4. However, patient 3 died of cardiac arrest due to ful-minant pulmonary embolism 10 days later, just 1 day before he planned leaving the hospital, despite being on low-molecular-weight heparin and full mobilization. Thrombus formation might have been the result of com-plex reactions in coagulation system during systemic inflammatory response in heat stroke.
Conclusion
Heat stroke is a life-threatening condition that requires immediate therapy. It may affect all organs and lead to
