Authors: Pertsas E1a, Flioni EN2a, Aslanidis Th 3ab*
1 MD, Cardiology-Critical care
2 MD, Anesthesiology-Critical care
3 MD, PhD, Anesthesiology–Critical Care-Prehospital emergency medicine.
a Intensive Care Unit, “Agios Pavlos” General Hospital, Thessaloniki, Greece
b Anesthesiology Department, “Agios Pavlos” General Hospital, Thessaloniki, Greece
*Correspondence: Doridos str 4, PC 54633, Thessaloniki, Greece. E-mail: , Tel.: +306972477166.
As climate changes accelerate, heatstroke becomes more and more often; both in its classical (non-exertional) form and in its exertional form. We hereby present a case of exertional heatstroke in a young man that was hospitalized in intensive care unit and discuss the relevant literature.
During the last decade, Europe became known as a major climatic hotspot1, due to the world’s highest increase in average temperature; thus, associated with an increase in the frequency and intensity of heat waves and hot summers2. Furthermore, climate future projections reveal a tendency towards more increased average temperatures and intense weather conditions that will affect even more people3.
Heat poses a major contributing morbidity and mortality factor to high-risk populations in Europe and worldwide. Almost 71,500 additional deaths occurred in Europe during the summer 20034. A more recent study estimated that almost 62000 heat-related deaths in Europe between 30 May and 4 September 20225.
The most dangerous form of heat-related illness is heatstroke. Heat stroke is a life-threatening condition that occurs when thermorelatury fails. It is divided into exertional and non‐exertional (classical) heat stroke. While classical heat stroke victims are usually elderly and vulnerable persons, exertional heat stroke, emerges in previously healthy young people exercising, usually in hot and humid climates, probably without being acclimatized. In the present article we present the management of a patient with severe exercise-related heatstroke and we discuss the implication of critical care and anesthesia in similar cases.
A 39-year-old man (body weight: 72kg, height – 178 cm) was transported comatose to a regional hospital. The man was participating in a marathon (41km) race and lost consciousness 3km before the finish line. At the time, ambient temperature (to) was about 32oC, ambient moisture 49% with South-East light wind of about 2-3 BFT (Beaufort scale). Patient’s medical history was free.
At Emergency Department (ED), his vitals were: heart rate (HR) 110bpm, blood pressure (BP) 140/70 mmHg, to – 38.8oC, Glasgow Coma Scale (GCS)– E1/V1/M5, pupils -equal, reactive yet with mydriasis, and with increased muscle rigidity. Initially GCS improved to E4/V4/M5 with normalization of pupils’ size. Yet soon after, local epileptic activity emerged with concomital neck rigidity, and eyeballs’ left deviation. Initial management with fluid (Ringer’s lactate 2lt), Diazepam 10 mg iv, paracetamol 1gr, levetiracetam 1500mg iv, a loading dose of 1200mg of sodium valproate over 30 min, followed by continuous infusion of 1200 mg/24h seized epileptic activity, but CGS decreased to E3/V1/M5. Diagnostic spinal puncture and brain computer tomography did not reveal any abnormalities. Emergency cardiological evaluation did not found major abnormalities: electrocardiography (ECG)-sinus rhythm (SR) (105 bpm) with right-bundle branch block (RBBB), transthoracic echocardiography (TTE)–ejection fraction 50% with no regional wall abnormalities, no valvular diseases or pericardial effusion. However, 2 consecutive troponin (Tn) measurements were abnormally increased (612 and 516 ng/ml)
The patient was intubated and transferred to our intensive care unit. He was presented with metabolic acidosis (pH -7.22, BE -2.7, PaCO2 – 50.1 mmHg, Lactate – 3.05 mmol/lt, blood glucose 100 mg/dl) and good oxygenation status (PaO2/FiO2 ratio 410); but with leucocytosis, thrombocytopenia, acute kidney injury, acute liver injury, rhabdomyolysis, and elevated lactate dehydrogenase, troponin ,β-natriuretic peptid (BNP), procalcitonin (PCT); and a mean to of 37.8 (pick 39oC) for the first 24h (Table 1). There was minimal need for hemodynamic support (noradrenaline civ 0.1 μγ/kg/min). On admission, APACHE II score was 23.
|ED||ICU day 1||ICU day 2||ICU day 3||ICU day 4||ICU day 5|
WBC-white blooc cells (k/ml), PLT- platelets (k/μl), INR-international normal ratio, Fib-fibrinogen (mg/dl), Cr-creatinine (mg/dl), Ur-urea (mg/dl), SGOT-aspartate aminotransferase (U/l), SGPT-alanine aminotransferase (U/l), LDH-lactade dehydrogenase (U/l), CPK–creatine phosphokinase (U/l), Chol-cholerythrin total (mmol/l), PCT procalcitonin (μg/l), CRP-C reactive protein (mg/dl).
Table 1. Course of selected laboratory parameters during ICU stay
However, his clinical status improved relatively fast. Thus, he was transferred to ward after 5 days and was discharged from the hospital 7 days later without any sequelae.
Heat stroke (HS) is the most severe form of heat-related illness. The other two more mild and frequent forms are heat fatigue and heat exhaustion. To date, no universally accepted definition of heat stroke exists. The most popular definition is the Bouchama’s definition: core body temperature that rises above 40 C, accompanied by hot dry skin and central nervous system abnormalities, such as delirium, convulsions, or coma6. The same author proposed and a pathophysiology -based definition: heat stroke is a form of hyperthermia associated with a systemic inflammatory response that leads to a syndrome of multiorgan dysfunction, predominantly encephalopathy. Other authors, such as Pease et al or Misset et al , described different cut-off temperature limit (40.6oC and 40.5oC respectively) with including or omitting the “core” for the core body temperature.
The fullest definition comes from the work of Japanese Association for Acute Medicine (JAAM) and JAAM Heat Stroke Committee working group (HS-WS) in 2015-20167 (Table 2).
|Environment||Exposure to high environmental temperature||Exposure to high environmental temperature|
|Nervous system||Impaired consciousness JCS ≥ 2, cerebellar symptoms, convulsive seizures||GCS score ≤ 14|
|Coagulopathy||Diagnosed as DIC by JAAM||JAAM DIC score ≥ 4|
|Follow-up after admission to hospital, hepatic or renal impairments requiring inpatient hospital care||Creatinine or total bilirubin levels ≥ 1.2 mg/dL|
GCS Glasgow Coma Scale, JAAM Japanese Association of Acute Medicine, JAAM-HS-WG Japanese Association of Acute Medicine heat stroke committee working group, JCS Japan Coma Scale, DIC disseminated intravascular coagulation.
Table 2. JAAM Heat stroke definition criteria
The body temperature was not included in these diagnostic criteria because of several fatal cases of patients whose body temperatures were below 40°C that were observed in clinical practice. Examples of such cases are a report f Giersky et al. of a EHS with consequent liver failure in a 31-year-old male after running 5km at 21oC at Norway, and of fatal EHS due to DIC and intracerebral haemorrhage in a 20-year-old male after 3h mountain biking in 26oC heat in forest at Netherlands7.
In general, there are two forms of HS: classical (induced by heat exposure in the absence of physical) exertional (EHS). EHS s induced by vigorous physical activity performed normally, but not always, in hot or humid environments. EHS is the third leading cause of mortality in athletes during physical activity with epidemiological data showing a mortality rate of upto 27% with survivors display long term negative health consequences ranging from neurological to cardiovascular dysfunction8.
Several risk factors, such as dehydration, electrolyte imbalance, sex, body composition, age and previous clinical status are implicated in EHS; yet no definite indication exists that they increase EHS predisposition. Dehydration may lead to greater blood viscosity from decreased plasma volume which causes cardiac drift, leading to greater cardiac strain9. Obesity and even greater adipose tissue body probably contribute to an increased core temperature and decreased heat loss. They also cause chronic inflammation and metabolic disease, predisposing for higher EHS incidence9. In our case, we do not have information about the hydration status before the incidence, nor the pre-event physical activity status.
Differential diagnosis includes a plethora of conditions, such as meningitis, encephalitis, malaria, malignant neuroleptic syndrome, hyponatremia, septic shock, thyroid crisis, acute myocardial infarction, malignant hyperthermia, and drug use or reactions. There is no single laboratory test that can confirm or exclude the diagnosis of heatstroke. In our case, laboratory features that support the diagnosis of heatstroke include leucocytosis, increased urea and creatinine, increased serum transaminases, increased creatinine kinase, coagulopathy, metabolic acidosis and rhabdomyolysis10. High serum PCT levels can be observed in heatstroke without any concomitant documented bacterial infection. The PCT is not a valid mortality predictor in heatstroke but could be an indicator of the severity of illness11.
EHS consist of an emergency life-threatening condition with complex pathophysiology that may involve different organs and system. Rapid evaluation and early management are critical for successful outcomes. A high suspicion is also needed, event in the cases in which enviromental conditions look “safe”.
Additional materials: No
Acknowledgements: Not applicable
Authors’ contributions: TA, KM: primary case-management, TA, EP: literature review and manuscript preparation from input of all authors. All authors read and approved the final manuscript.
Funding: Not applicable.
Availability of supporting data: Not available
Ethical approval and consent to participate: No IRB approval required.
Consent for publication: Patient’s informed consent was obtained.
Competing interests: The authors declare that they have no competing interests.
Received: September 2023, Accepted: September 2023, Published: September 2023.
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|Citation: Pertsas E, Flioni EN, Aslanidis Th. Exercise-Related Heatstroke in the Intensive Care Unit: A Case Report. Greek e j Perioper Med. 2023;22(c): 40-45.|
|This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution – ShareAlike 4.0 International license (CC BY-SA 4.0) (https://creativecommons.org/licenses/by-sa/4.0/)|