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Case Studies

  • Additional Resources
  • Workers' Rights

The following heat-related case studies are the result of from OSHA enforcement investigations. Some identifying details have been changed to protect the privacy of workers and employers.

Case #1: Roofing worker

Roofing Worker - Photo Credit: iStock - 157191789 | Copyright: Steve Debenport

In July, a 42-year-old man started a new job as a roofer. His employer did not have a formal plan to protect new workers from heat-related illness although there was plentiful water, ice, and Gatorade available at the site. The worker felt fine during his first two days of work. His third day on the job was slightly warmer, with a high temperature of about 86°F and relative humidity of 57%, for a heat index of 90°F. In the afternoon, the worker told his co-workers he felt hot and sick. He climbed down from the roof and went to sit by himself in the sun. When his co-workers checked on him a few minutes later, he had symptoms of heat stroke. He was taken to a hospital where he died. Scattered clouds may have reduced the radiant temperature somewhat but reconstruction showed a wet-bulb globe temperature of 82°F based on data from a nearby airport.

Lessons to learn from this case:

  • Protect new workers during their first two weeks on the job. Make sure they take plenty of rest breaks and drink enough fluids.
  • Never leave workers alone when they complain of heat-related symptoms. Their condition can worsen quickly! Take them to a cool location and provide first aid. Even a brief delay in first aid can make the difference between life and death.
  • Temperatures do not have to be extremely hot to cause heat stroke in workers. Remember, total heat stress is a combination of environmental heat and workload. Air temperatures in the 80s (°F) are high enough to result in a Heat Index value of 90°F. They are also high enough to kill some workers.

Case #2: Delivery worker

Delivery worker - Photo Credit: iStock - 623273520 | Copyright: nullplus

A 50-year-old man had been working at a delivery company for six years. His job involved driving a vehicle and walking in residential neighborhoods to deliver mail and packages. In late May, the weather suddenly became hotter. On the second day of hot weather, this worker developed heat cramps and heat exhaustion. He was hospitalized for two days with acute kidney failure due to dehydration. His condition improved after intravenous fluid replacement.

  • Even experienced workers are vulnerable to heat-related illness when the weather becomes warmer. Throughout the first week of warmer conditions, treat all workers as if they need to adapt to working in the heat. Take extra precautions to protect them from heat-related illnesses.
  • Make sure workers drink enough fluids during warm or hot weather.

Case #3: Foundry worker

Foundry worker - Photo Credit: iStock - 492798423 | Copyright: HadelProductions

A 35-year-old employee had worked at a foundry for six years. The indoor workplace had high levels of environmental heat from ovens and molten metal. His normal job tasks were in a cooler area of the building. On the day of the incident, he was asked to perform a job in a hotter environment near an oven. He wore heavy protective clothing to prevent skin burns. After several hours of work, the man collapsed and died of heat stroke.

  • Heat-related illness can occur indoors. The risk is not limited to outdoor workers.
  • Some types of work clothing prevent the release of heat from the body. Environmental heat measurements underestimate the risk of heat-related illness in these situations.
  • Workers are at risk of heat-related illness when they are reassigned to warmer job tasks.

More OSHA Cases

Review a list of heat-related fatalities and catastrophes investigated by OSHA.

  • Case report
  • Open access
  • Published: 28 January 2021

Severe heat stroke complicated by multiple cerebral infarctions: a case report

  • Ryo Kamidani 1 ,
  • Hideshi Okada 1 ,
  • Yuichiro Kitagawa 1 ,
  • Keigo Kusuzawa 1 ,
  • Masahiro Ichihashi 1 ,
  • Yoshinori Kakino 1 ,
  • Hideaki Oiwa 1 ,
  • Ryu Yasuda 1 ,
  • Tetsuya Fukuta 1 ,
  • Naomasa Yoshiyama 1 ,
  • Takahito Miyake 1 ,
  • Haruka Okamoto 1 ,
  • Kodai Suzuki 1 ,
  • Noriaki Yamada 1 ,
  • Tomoaki Doi 1 ,
  • Takahiro Yoshida 1 ,
  • Hiroaki Ushikoshi 1 ,
  • Keisuke Kumada 1 ,
  • Shozo Yoshida 1 &
  • Shinji Ogura 1  

Journal of Medical Case Reports volume  15 , Article number:  24 ( 2021 ) Cite this article

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Heat-related illnesses include symptoms such as heat syncope/cramps, heat exhaustion, and life-threatening heat stroke. Usually, a heat stroke causes cerebellar ataxia, cognitive impairment, dysphagia, and aphasia. We report a very rare case of a patient who developed severe heat stroke complicated by multiple cerebral infarctions.

Case presentation

An 80-year-old Asian woman was found lying unconscious at her house, with no air conditioner and closed windows; the highest outside temperature was 36.1 °C. She was brought to our hospital unconscious with a high bladder temperature (42.5 °C) and disseminated intravascular coagulation (DIC score 4). She was diagnosed with severe heat stroke and managed with rapid cooling, intravenous fluids therapy, antibiotic therapy, and anti-coagulation therapy for DIC. Anti-coagulation therapy consisted of treatment with recombinant thrombomodulin for 4 days (days 1–4) and recombinant antithrombin for 1 day (day 1). A head computed tomography (CT) and magnetic resonance imaging (MRI) examination were performed on day 3, because she was still unconscious. Diffuse-weighted imaging showed high-signal intensities, indicating multiple lesions. An intracranial magnetic resonance angiography showed normal results. Imaging indicated new multiple cerebellar infarctions complicated with DIC. A tracheotomy was performed on day 9 because her conscious condition had not improved. She was transferred to another hospital for subacute care on day 23.

Conclusions

Early management of heat stroke using anti-DIC, anti-bacterial, and fluid resuscitation therapy can help prevent complications such as intracranial hemorrhaging.

Peer Review reports

Heat-related illnesses include diverse symptoms such as heat syncope/cramps, heat exhaustion, and life-threatening heat stroke [ 1 ]. Acute severe heat stroke may be associated with rhabdomyolysis, disseminated intravascular coagulation (DIC), acute renal failure, liver damage, acute respiratory distress disease syndrome, electrolyte imbalance, and neurologic complications [ 2 , 3 , 4 , 5 , 6 ]. The typical neurologic complications are cerebellar ataxia, cognitive impairment, dysphagia, and aphasia. We report a very rare case of a patient who developed severe heat stroke complicated by multiple cerebral infarctions.

An 80-year-old Asian woman with Alzheimer dementia was found lying unconscious at her house, which had no air conditioner and the windows were kept closed; the highest outside temperature was 36.1 °C. There was no history of seizure, previous use of medication, diabetes mellitus, hypertension, alcohol abuse, smoking, or cardiac disease. During transportation, a physician began to assist her ventilation, and she was intubated because her SpO 2 level was 78% under room air. She was brought by the ambulance with a physician onboard to our hospital unconscious. Her Glasgow Coma Scale score was 6 (eye, 1; verbal, 1; motor, 4), with a high bladder temperature (42.5 °C). On arrival, her blood pressure was 104/79 mmHg and pulse rate was abnormal at 110 beats/min. She was vomiting but had no traumatic scars. Results of an arterial blood gas examination are shown in Table 1 . Laboratory data revealed renal dysfunction and an elevated white blood cell count at 13,890/μL (normal range 3000–9000/μL) (Table 1 ). Her DIC score was 5 points as per the DIC diagnostic criteria established by the Japanese Association for Acute Medicine (JAAM) on admission. On day 2, she met the criteria (5 points) of a different diagnostic system established by the International Society on Thrombosis and Hemostasis (ISTH) [ 7 ]. Her blood culture was sterile. An electrocardiogram, chest X-ray, and two-dimensional transthoracic echocardiography showed normal results. Serology laboratory tests for venereal disease, human immunodeficiency virus, and viral hepatitis markers (hepatitis A virus (HAV), hepatitis B virus (HBV), and hepatitis C virus (HCV)) were negative. No abnormal lesion was found on the head computed tomography (CT) examination performed on arrival (Fig. 2 upper panels).

The patient was diagnosed with severe heat stroke, placed under intensive care, and managed with rapid cooling, intravenous fluid therapy, antibiotic therapy, and anti-coagulation therapy for DIC (Fig. 1 ). Anti-coagulation therapy consisted of treatment with recombinant thrombomodulin for 4 days (days 1–4) and recombinant antithrombin for 1 day (day 1). We transfused 10 U of platelet concentrate because her platelet count had decreased to 1.7×10 4 /μL due to exhaustion on day 2.

figure 1

Summary of the clinical course. rAT: recombinant anti-thrombin, rTM: recombinant thrombomodulin, BT body temperature, FDP fibrin/fibrinogen degradation products, PT-INR prothrombin international normalized ratio

Head CT (Fig. 2 lower panels ) and magnetic resonance imaging (MRI) (Fig. 3 ) examinations were performed on day 3 because she was still unconscious. Diffuse-weighted imaging showed high-signal intensities in the bilateral cerebellar hemisphere, bilateral occipital lobe, and basal ganglia. Intracranial magnetic resonance angiography showed normal results. Imaging indicated new multiple cerebellar infarctions (Fig. 3 ). As described above, she had no arrhythmia or organic cardiac disease, and the location of the infarcts included the cerebellum. It was thought that heat stroke with DIC complicated the acute infarctions. A tracheotomy was performed on day 9 because her unconscious condition had not improved. She was transferred to another hospital for subacute care on day 23.

figure 2

Head computed tomography on days 1 and 3. Head computed tomography (CT) examination on day 1 (upper panels) and day 3 (lower panels). No abnormal lesion is found on day 1. On day 3, low-intensity areas are detected in the cerebellum and left occipital lobe (yellow arrows).

figure 3

Brain magnetic resonance imaging on day 3. Diffuse-weighted imaging showing high-signal areas on the bilateral cerebellar hemisphere, occipital lobe, semioval center, actinic crown, and basal ganglia. The apparent diffusion coefficient (ADC) map shows a partial decline of the ADC value. An intracranial magnetic resonance angiography shows normal results. Yellow arrows indicated new multiple cerebellar infarctions.

Discussion and conclusions

Heat stroke is a serious and life-threatening emergency, with a high mortality rate (20%) [ 1 , 8 ]. This is thought to be because heat stroke has several complications, especially neurological ones such as cerebellar ataxia, cognitive impairment, dysphagia, aphasia, other minor symptoms (irritability, irrational behavior, hallucinations, downbeat nystagmus, and opsoclonus), and severe features such as cranial nerve abnormalities, seizures, and coma [ 9 ]. It was previously reported that the incidence of after-effects from heat stroke on the central nervous system (CNS) is 1.5 % (22/1,441 cases) [ 10 ].

It is presumed that two factors caused the neurologic complications. One reason is that the CNS is highly sensitive to hyperthermia, especially the cerebellum, basal ganglia, anterior horn cells, and peripheral nerves. Bazille et al. and Malamud et al reported that Purkinje cells were highly sensitive to hyperthermia [ 3 , 11 ]. A second reason is vasogenic edema and cytotoxic edema due to vascular hyperpermeability, which can be induced by hypercytokinemia. Hypercytokinemia may also cause destruction of the blood–brain barrier. Its radiological characteristic is posterior reversible encephalopathy syndrome-like because of restricted diffusion caused by edema.

Leakage of endotoxin due to bacterial translocation and cytokine release from muscles can activate white blood cells and the vascular endothelium, causing inflammation. This results in the release of inflammatory cytokines (for example, tumor necrosis factor α, interleukin-1β, and interferon-γ) and anti-inflammatory cytokines for example, interleukin-6 and interleukin-10), activation of coagulation (with reduced levels of proteins C and S, and antithrombin), and the inhibition of fibrinolysis [ 12 ].

Previous reports indicated that the dual effects of elevated PAI-1 activity and decreased t-PA activity in the fibrinolytic balance may be a major contributor to the pro-thrombotic shift of heat stroke, rather than the platelet-related pro-thrombotic activity, in human umbilical vein endothelium cells [ 13 , 14 ]. Although these reports are in vitro studies, they indicate that endothelium cells exposed to hyperthermia are involved in fibrinolytic balance, as seen in clinical practice.

As described above, the inflammatory and coagulation response to heat stroke results in vascular endothelium disorder, microthrombosis, and DIC via strong inhibition of fibrinolysis, with subsequent improvement of hyperthermia. Clinical and laboratory diagnostic criteria and a scoring system for DIC have been established by the ISTH and JAAM (Tables 2 and 3 ). In Japan, we often use the JAAM diagnostic criteria (new Japanese criteria) for early diagnosis of DIC in the field of emergency and critical care medicine. Although the ISTH established two sets of criteria for overt and non-overt DIC, the non-overt DIC criteria are more appropriate for early diagnosis. A recent study showed that the diagnostic sensitivity of the new Japanese criteria was as high as that of the non-overt DIC criteria [ 15 ]. Furthermore, the new Japanese criteria allowed for the earliest diagnosis and the most accurate outcome prediction among all DIC criteria. In this case, the patient met the new Japanese criteria (5 points), but not the overt DIC criteria (3 points) on admission. However, she ultimately progressed to meeting the overt DIC criteria (5 points) on day 2. That is, we were able to institute early management of her DIC, but could not prevent the complications associated with DIC and hypercytokinemia.

In addition, increased intracranial pressure and autonomic dysfunction, caused by vasogenic and cytotoxic edema due to hypercytokinemia, leads to cerebral hypoperfusion and ischemia. In the present case, the patient had multiple infarctions in the bilateral cerebellar hemisphere, bilateral occipital lobe, and basal ganglia. DIC and hypercytokinemia induced by heat stroke cause microthrombosis, which results in small vessel ischemic damage and cerebral infarction. We hypothesized that these mechanisms were initiated by the infarctions because she had no history of cardiac disease or risk factors for vascular diseases.

There are few reports about CNS complications due to heat stroke, and acute infarction is especially rare. Our patient may be the first reported case of multiple cerebral infarctions due to heat stroke that had persistent neurologic features in the form of a coma.

In conclusion, early management of heat stroke using DIC therapy, anti-bacterial therapy, and fluid resuscitation therapy is required. Even if there is no DIC, anti-coagulant therapy is desirable considering the possible risk of an intracranial hemorrhage.

Availability of data and materials

The datasets obtained and analyzed in the current study are available from the corresponding author on reasonable request.

Abbreviations

Apparent diffusion coefficient

Central nervous system

Disseminated intravascular coagulation

International Society on Thrombosis and Hemostasis

Japanese Association for Acute Medicine

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Acknowledgements

The authors would like to thank the paramedical crews for the use of their data. We would like to thank Editage ( www.editage.com ) for English language editing.

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Advanced Critical Care Center, Gifu University Hospital, 1-1 Yanagido, Gifu, 501-1194, Japan

Ryo Kamidani, Hideshi Okada, Yuichiro Kitagawa, Keigo Kusuzawa, Masahiro Ichihashi, Yoshinori Kakino, Hideaki Oiwa, Ryu Yasuda, Tetsuya Fukuta, Naomasa Yoshiyama, Takahito Miyake, Haruka Okamoto, Kodai Suzuki, Noriaki Yamada, Tomoaki Doi, Takahiro Yoshida, Hiroaki Ushikoshi, Keisuke Kumada, Shozo Yoshida & Shinji Ogura

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Contributions

RK, YK, KK, MI, YK, H Oiwa, RY, TF, NY, TM and SY treated the patient. RK wrote the manuscript. H Okada revised and edited the manuscript. SO supervised this report. All authors read and approved the final manuscript.

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Correspondence to Hideshi Okada .

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Kamidani, R., Okada, H., Kitagawa, Y. et al. Severe heat stroke complicated by multiple cerebral infarctions: a case report. J Med Case Reports 15 , 24 (2021). https://doi.org/10.1186/s13256-020-02596-2

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Published : 28 January 2021

DOI : https://doi.org/10.1186/s13256-020-02596-2

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  • Heat stroke
  • Intracranial hemorrhaging
  • Magnetic resonance angiography
  • Multiple cerebral infarctions

Journal of Medical Case Reports

ISSN: 1752-1947

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case study for heat stroke

Risk Factors for the 90-Day Prognosis Of Severe Heat Stroke: a Case-Control Study

Affiliations.

  • 1 Department of Critical Care Medicine, The First Affiliated Hospital, Guizhou University of Chinese Medicine, Guiyang, China.
  • 2 Department of Critical Care Medicine and Infection Prevention and Control, The Second People's Hospital of Shenzhen and First Affiliated Hospital of Shenzhen University, Health Science Center, Shenzhen, China.
  • 3 Department of Critical Care Medicine, The Affiliated General Hospital of Southern Theatre Command of PLA, Southern Medical University, Guangzhou, China.
  • 4 Department of Critical Care Medicine, The Affiliated General Hospital of Southern Theatre Command of PLA, Guangzhou, China.
  • 5 Department of Pediatrics, General Hospital of Southern Theatre Command of PLA, Guangzhou, China.
  • 6 Key Laboratory of Hot Zone Trauma Care and Tissue Repair of PLA, General Hospital of Southern Theatre Command of PLA, Guangzhou, China.
  • PMID: 32590693
  • DOI: 10.1097/SHK.0000000000001589

Background: Severe heat stroke is a clinical syndrome caused by host stress dysfunction due to heat stress and subsequent life-threatening organ dysfunction. We aimed to explore the early risk factors affecting the 90-day prognosis of severe heat stroke patients.

Methods: A case-control study was used to retrospectively analyze the clinical data of 117 severe heat stroke patients admitted to the intensive care unit of the General Hospital of Southern Theater Command from April 2014 to May 2019. The risk factors affecting the 90-day mortality of the patients were analyzed, and subgroup analysis was performed comparing the complete recovery and the sequelae subgroups of survivors.

Results: Thirteen patients (11.1%) died within 90 days. The multivariate Cox risk regression model showed that cooling time (HR 4.87; 95% CI: 1.94-12.18; P = 0.001), heart rate (HR 1.04; 95% CI: 1.01-1.09; P = 0.027), and Sequential Organ Failure (SOFA) score (HR 1.41; 95% CI: 1.21-1.65; P < 0.001) were independent risk factors affecting the survival of patients. The area under the Receiver Operating Characteristic (ROC) curve of the combination of cooling time, heart rate, and SOFA score for the prediction of mortality due to severe heat stroke was 98.1% (95% CI 0.957-1.000, P < 0.001), the sensitivity was 96.2%, and the specificity was 92.3%.

Conclusions: The longer the cooling duration, the faster the heart rate at admission, and the higher the SOFA score, the lower the 90-day survival rate was. These three indicators can be used in combination to predict 90-day mortality and poor prognosis in patients with severe heat stroke.

Copyright © 2020 by the Shock Society.

Publication types

  • Research Support, Non-U.S. Gov't
  • Case-Control Studies
  • Heat Stroke / complications
  • Heat Stroke / mortality*
  • Heat Stroke / therapy
  • Middle Aged
  • Organ Dysfunction Scores
  • Proportional Hazards Models
  • Risk Factors
  • Sensitivity and Specificity
  • Young Adult
  • Open access
  • Published: 22 May 2018
  • Heat stroke
  • Toru Hifumi 1 , 5 ,
  • Yutaka Kondo 2 ,
  • Keiki Shimizu 3 &
  • Yasufumi Miyake 4  

Journal of Intensive Care volume  6 , Article number:  30 ( 2018 ) Cite this article

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Heat stroke is a life-threatening injury requiring neurocritical care; however, heat stroke has not been completely examined due to several possible reasons, such as no universally accepted definition or classification, and the occurrence of heat wave victims every few years. Thus, in this review, we elucidate the definition/classification, pathophysiology, and prognostic factors related to heat stroke and also summarize the results of current studies regarding the management of heat stroke, including the use of intravascular balloon catheter system, blood purification therapy, continuous electroencephalogram monitoring, and anticoagulation therapy.

Two systems for the definition/classification of heat stroke are available, namely Bouchama’s definition and the Japanese Association for Acute Medicine criteria. According to the detailed analysis of risk factors, prevention strategies for heat stroke, such as air conditioner use, are important. Moreover, hematological, cardiovascular, neurological, and renal dysfunctions on admission are associated with high mortality, which thus represent the potential targets for intensive and specific therapies for patients with heat stroke. No prospective, comparable study has confirmed the efficacy of intravascular cooling devices, anticoagulation, or blood purification in heat stroke.

The effectiveness of cooling devices, drugs, and therapies in heat stroke remains inconclusive. Further large studies are required to continue to evaluate these treatment strategies.

Heat stroke is a life-threatening injury requiring neurocritical care, and there have been at least 3332 deaths attributed to heat stroke from 2006 to 2010 in the USA [ 1 ]. Regarding heat stroke, 28-day and 2-year mortality rates have been reported to be 58 and 71%, respectively [ 2 ]. In addition, the number of deaths from heat stroke has been reported to increase due to climate change [ 1 ]. By the 2050s, heat stroke-related deaths are expected to rise by nearly 2.5 times the current annual baseline of approximately 2000 deaths [ 2 ].

Unfortunately, heat stroke has not been comprehensively examined due to several possible reasons. First, while sepsis, acute respiratory distress syndrome (ARDS), and acute kidney injury (AKI) include simple and commonly used definitions, no universally accepted definition of heat stroke exist in the clinical settings. Second, because a large number of heat stroke victims are uncommon in the USA or European countries (ex. 1995, and 1999 in Chicago, 2003 in Paris) [ 2 , 3 , 4 , 5 ], clinical research has not been continuously conducted in these regions.

Several review articles regarding heat stroke focusing on critical care have been published in the early 2000s [ 6 , 7 ]; moreover, additional new devise for cooling, blood purification therapy for renal/hepatic failure, continuous electroencephalogram (cEEG) monitoring, and the use of drugs, such as anticoagulants, for treating heat stroke have become readily available, and substantive clinical research regarding such devises/drugs has been published in the 2010s [ 8 , 9 , 10 , 11 , 12 , 13 ].

Thus, in the current review, we elucidate the definition/classification, pathophysiology, and prognostic factors associated with heat stroke and also summarize the results of current studies regarding the management of heat stroke, including the use of intravascular balloon catheter systems, blood purification therapy, cEEG monitoring, and anticoagulants.

Definition and classification of heat stroke

Historically, heat stroke has been classified into two groups according to the presence or absence of exertion. Exertional heat stroke develops in able-bodied individuals, such as athletes, soldiers, or laborers, and performing rigorous physical activities [ 1 ]. In contrast, nonexertional heat stroke can develop during low-level physical activities among elderly, ambulatory individuals with comorbidities including obesity, diabetes, hypertension, heart disease, renal disease, dementia, and alcoholism [ 1 ].

To date, no universally accepted definition of heat stroke exists. The most commonly used definition of heat stroke worldwide is the Bouchama’s definition [ 6 ]. Bouchama has defined heat stroke as a core body temperature that rises above 40 °C, accompanied by hot dry skin and central nervous system abnormalities, such as delirium, convulsions, or coma. Heat stroke results from exposure to a high environmental temperature or from strenuous exercise [ 6 ]. Bouchama has also proposed an alternative definition of heat stroke on the basis of its pathophysiology, stating that heat stroke is a form of hyperthermia associated with a systemic inflammatory response that leads to a syndrome of multiorgan dysfunction, predominantly encephalopathy [ 6 ].

Pease et al. have reported an unusual heat wave that lasted 9 days in France in 2003 [ 14 ] and referred to the following criteria according to the Bouchama’s definition: the alteration of mental status (coma, delirium, disorientation, or seizures); a body core temperature of > 40.6 °C or a documented evidence of cooling before the first record temperature; a reliable history of compatible environmental exposure; and the presence of hot, dry, or flushed skin. In another study, Misset et al. defined heat stroke as “the presence of hyperthermia of >40.5°C” [ 15 ], but the phrase “core body temperature” was not included in their definition. Consequently, specific body temperature and the use of phrase “core body temperature” vary across studies.

In Japan, the Japanese Association for Acute Medicine (JAAM) has collected data through a nationwide heat-related illness registry of patients diagnosed as having heat-related illnesses (including heat stroke) regardless of the core body temperature since 2006 [ 16 , 17 ]. The JAAM has established and published the criteria for heat-related illnesses, including heat stroke, in 2014 [ 18 ] (Fig.  1 ).

figure 1

Japanese Association of Acute Medicine Heat-Related Illness criteria. DIC, disseminated intravascular coagulation; JCS, Japan Coma Scale

Heat stroke was defined as patients exposed to high environmental temperature who met one or more of the following criteria:

Central nervous system manifestation (impaired consciousness with a Japan Coma Scale score of ≥ 2 [ 19 ], cerebellar symptoms, convulsions, or seizures);

Hepatic/renal dysfunction (follow-up following admission to hospital, hepatic or renal impairment requiring inpatient hospital care);

Coagulation disorder [diagnosed as disseminated intravascular coagulation (DIC) by the JAAM] [ 20 , 21 ].

Apparently, 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 [ 22 ].

In 2016, the JAAM Heat Stroke (JAAM-HS) Committee launched a working group (JAAM-HS-WG) to analyze the collected megadata regarding heat-related illnesses. The JAAM-HS-WG further simplified the heat stroke classification [ 22 ]. The modified JAAM heat stroke definition included patients exposed to high environmental temperature and meeting at least one of the following criteria:

Glasgow Coma Scale (GCS) score of ≤ 14,

Creatinine or total bilirubin levels of ≥ 1.2 mg/dL,

JAAM DIC score of ≥ 4.

The difference between the definitions/classifications of heat stroke among Bouchama’s definition and the JAAM and JAAM-HS-WG criteria is summarized in Table  1 .

Pathogenesis

Thermoregulation.

A normal body temperature is maintained at approximately 37 °C by the anterior hypothalamus through the process of thermoregulation [ 23 , 24 ]. Several mechanisms related to sweating, such as vaporization, radiation, convection, and conduction, function to cool the body surface [ 25 ]. As the body temperature increases, active sympathetic cutaneous vasodilation increases blood flow in the skin and initiates thermal sweating [ 26 , 27 ]. Cutaneous vasodilation causes a relative reduction in intravascular volume, leading to heat syncope [ 28 ]. The loss of salts and water through sweat induces dehydration and salt depletion, which are associated with heat exhaustion and cramps unless appropriate supplementations of water and salt are initiated [ 28 ]. Further loss of salt and water impairs thermoregulation followed by the reduction of visceral perfusion due to shunt from the central circulation to the skin and muscles, resulting in organ failure [ 6 , 28 , 29 ]. Therefore, heat stroke is a condition of multiple organ failure caused by hot environment.

Heat shock response

Heat shock proteins (HSP) are a family of proteins produced by nearly all cells in response to stressful conditions, including heat shock as well as other stresses, such as exposure to cold and ultraviolet light [ 6 , 30 ]. Increased levels of HSPs, such as HSP70, are necessary for acquired heat tolerance. Moreover, the overexpression of HSP70 in response to heat stress can protect against organ dysfunction and reduces mortality in rats [ 30 ].

Pathophysiology

Hyperthermia due to passive heat exposure facilitates the leakage of endotoxin from the intestinal mucosa to the systemic circulation as well as the movement of interleukin (IL)-1 or IL-6 proteins from the muscles to the systemic circulation [ 31 ]. This causes an excess activation of leukocytes and endothelial cells manifested by the release of various cytokines and high-mobility group box 1 protein (HMGB1), which is a prototypic alarmin (endogenous molecules that signal tissue and cellular damage). Together, these processes cause the systemic inflammatory response syndrome [ 6 , 32 , 33 ].

The inflammatory and coagulation responses to heat stroke, together with direct cytotoxic effects of heat, injure the vascular endothelium, causing microthromboses [ 6 ]. Platelet counts decrease because of microthrombosis, the secondary consumption of platelets, and hyperthermia-induced platelet aggregation. Heat stroke also suppresses platelet release from bone marrow due to megakaryocyte susceptibility to high temperature exposures. Heat stroke-induced coagulation activation and fibrin formation clinically manifest DIC.

Prognostic factors

As mentioned above, because the definition of heat stroke varies across studies, detailed examinations, rather than mere results, are required to understand these study findings (Table  2 ).

Patients exposed to the August 2003 heat wave in Paris were examined to identify the prognostic factors, and several studies examining different populations have been published. Hausfater et al. have examined all patients who developed the core temperatures of > 38.5 °C, who were admitted to one of the emergency departments during the August 2003 heat wave in Paris. Previous treatment with diuretics, living in an institution, age > 80 years, the presence of cardiac disease or cancer, core temperature > 40 °C, systolic arterial pressure < 100 mmHg, GSC scale < 12, and transportation to hospital in ambulance were identified as prognostic factors associated with death for nonexertional heatstroke [ 34 ]. Argaud et al. examined long-term outcome in 83 patients with nonexertional heatstroke resulting from the August 2003 heat wave in Paris and having core temperatures > 40 °C. Multivariate cox proportional hazard model analysis revealed an independent contribution to 2-year mortality if patients were staying at an institution (hazard ratio (HR), 1.98; 95% confidence interval (CI), 1.05–3.71), if they used long-term antihypertensive medications (HR, 2.17; 95% CI, 1.17–4.05), or if they presented with anuria (HR, 5.24; 95% CI, 2.29–12.03), coma (HR, 2.95; 95% CI, 1.26–6.91), or cardiovascular failure (HR, 2.43; 95%CI, 1.14–5.17) at admission [ 2 ]. Misset et al. have conducted a questionnaire survey and a multivariate analysis, wherein the occurrence of heatstroke at home or in a healthcare facility (vs. in a public area), high Simplified Acute Physiology Score (SAPS) II score [ 35 ], initial high body temperature, prolonged prothrombin time, the use of vasoactive drugs within the first day in intensive care unit (ICU), and patient management in an ICU without air conditioning were independently associated with an increased risk of hospital death [ 15 ].

Tsuruta et al. have examined 77 mechanically ventilated patients with heat-related illnesses who met the JAAM-HS criteria. Their systolic blood pressure (SBP) and SpO2 at scene and arterial base excess were identified as independent risk factors for poor outcomes (death and with sequelae).

Hifumi et al. have examined 705 patients who met the JAAM-HS-WG criteria for heat stroke and observed that the hospital mortality was 7.1% (50 patients) [ 22 ]. Multiple regression analysis revealed that hospital mortality was significantly associated with SBP (odds ratio (OR), 0.99; 95% CI, 0.98–0.99; p  = 0.026), GCS score (OR, 0.77; 95% CI, 0.69–0.86; p  < 0.01), serum creatinine levels (OR, 1.28; 95% CI, 1.02–1.61; p  = 0.032), and the presence of DIC on admission (OR, 2.16; 95% CI, 1.09–4.27; p  = 0.028) [ 22 ].

According to the detailed analysis of risk factors, careful attention should be paid for the prevention of heat stroke in patients living in a healthcare facility, aged > 80 years, and previously treated with diuretics. Moreover, because hematological, cardiovascular, neurological, and renal dysfunctions on admission are associated with high mortality, these dysfunctions represent potential targets for intensive and specific therapies for patients with heat stroke.

Heat stroke progresses to multiorgan dysfunction syndrome; therefore, rapid, effective cooling followed by close monitoring and specific treatment for injured organs are fundamental to treatment success.

Initial cooling

Target temperature of initial cooling.

There is no evidence to support a specific temperature end point; however, a rectal temperature of 39.4 °C has been used in large series and has been proven to be safe [ 6 ].

Initial cooling method

To date, several cooling methods are available in the clinical settings, including immersion [ 36 ], evaporation [ 37 ], and the use of cold water bladders, gastric and rectal lavage [ 38 ], and noninvasive cooling systems [ 39 ]. However, there is no evidence supporting the superiority of any one cooling method for patients with heat stroke [ 6 ]. An intravascular balloon catheter system has been approved in the USA for therapeutic core cooling and rewarming in humans during or following cardiac or neurological surgery and following stroke [ 40 ]. However, a few cases have reported the use of intravascular cooling for heat stroke [ 41 , 42 ]. Hamaya et al. have reported for the first time a good recovery in a case of severe heat stroke, followed by multiple organ dysfunction, which was successfully treated through initial intravascular cooling [ 12 ]. In this case, at an average rate of 0.1 °C/min, the core temperature of the patient’s body reached 38.8 °C after just 17 min. Yokobori et al. have conducted a prospective study examining the feasibility and safety of a convection-based intravascular cooling device (IVC) in patients with severe heat stroke. Comparison between IVC plus conventional cooling (CC) and CC was made in patients with severe heat stroke. The IVC group showed a significant decrease in the Sequential Organ Failure Assessment score during the first 24 h (from 5.0 to 2.0, P  = 0.02). Moreover, all patients in the IVC group ( N  = 9) experienced favorable outcomes defined as modified Rankin scale score of 0–2 at discharge and at 30 days after the admission. Their findings indicate that accurate temperature management may prevent organ failure and produce better neurological outcomes. The Fukuoka University Hospital group has used extracorporeal circulation with hemodiafiltration circuits for cooling patients with severe heat stroke and has reported improved cooling efficiency [ 43 ]. To date, there have been no prospective, comparative studies confirming the superiority of the initial cooling method. Intravascular balloon catheter system does not result in cutaneous vasoconstriction as external cooling does, but it requires the placement of cooling balloon.

Management for organ dysfunctions in ICU

Central nervous system dysfunction.

Nakamura et al. have examined central nervous system sequelae of heat-related illnesses and have observed that 22 of 1441 cases (1.5%) exhibited the central nervous system sequelae of heat-related illnesses. Heatstroke patients presenting with lower GCS scores and higher body temperatures at admission were more likely to experience central nervous system sequelae and required longer cooling times to achieve the target body temperature. Therefore, rapid cooling followed by neuromonitoring might be associated with the neurological sequelae of heat stroke.

Recently, Hachiya et al. have reported the usefulness of cEEG in patients with severe heat stroke complicated with multiorgan failure [ 13 ]. The patients developed a persistent disturbance of consciousness; therefore, cEEG monitoring was applied. cEEG monitoring confirmed triphasic waves, which indicated hepatic failure as the cause of the persistent disturbance of consciousness. The patient’s condition improved following an artificial liver support therapy [ 13 ]. Thus, no prospective, comparable study has revealed the adequate neuromonitoring and the effect of temperature control on central nervous system.

Coagulation disorder

Anticoagulation therapy.

Antithrombin: Pachlaner et al. have reported good recovery in a patient with near-fatal heat stroke treated with type III antithrombin (AT-III) [ 44 ]. On admission, although the patient’s AT-III activity was 98%, a treatment with AT-III concentrate was initiated within 24 h due to DIC, which was aimed toward achieving supranormal plasma concentrations. Plasma AT concentrations were maintained at > 120% by continuous intravenous supplementation [ 44 ]. Additionally, in a rat model of heat stroke, AT-III treatment decreased serum cytokines (IL-1 β, tumor necrosis factor-α, and IL-6), and HMGB1 [ 45 ]. Thus, prospective studies will be needed to confirm the efficacy of AT-III supplementation in improving the clinical outcome of heat stroke.

Thrombomodulin (TM): Recombinant soluble thrombomodulin α (rTM), which is currently under phase III clinical trials for use in patients with severe sepsis, could also be a candidate for the treatment of heat stroke-induced DIC [ 46 ] because it serves as a negative feedback regulator of blood coagulation [ 47 ]. In basic research, rTM prevents heat stroke by inhibiting HMGB1 [ 48 ]. Sakurai et al. have reported (in Japanese) two cases of good recovery from heatstroke-induced DIC, which were successfully treated with TM administration [ 49 ]. Prospective studies will be needed to confirm the efficacy of rTM.

Hepatic/renal dysfunction

  • Blood purification therapy

Blood purification therapy has not been discussed in the two previously reported review articles; however, good recovery cases have been reported in Japan [ 6 , 7 ].

Ikeda et al. have reported three cases of survival following multiorgan failure secondary to heat stroke that was treated with blood purification therapy, including continuous venovenous hemofiltration and plasma exchange (PE) [ 8 ]. Blood purification therapy removes proinflammatory cytokines related to heat stroke [ 8 ]. Chen et al. have conducted a retrospective study including 33 patients with severe exertional heat stroke and have compared clinical effects of continuous renal replacement therapy (CRRT) and routine therapy in these patients. They reported significantly lower 30-day mortality in the CRRT group than in the control group (15.2% vs.45.5%, p  = 0.029) although initial APACHE II scores in both groups were similar [ 10 ].

Recently, Inoue et al. have reported a case of severe exertional heat stroke with multiple organ failure that was successfully treated with continuous plasma diafiltration (PDF) [ 11 ]. PDF is a blood purification therapy in which PE is performed using a selective membrane plasma separator while the dialysate flows outside the hollow fibers. This separator has a small pore size (0.01 mm) and a sieving coefficient of 0.3 for albumin, which can selectively remove low- or intermediate-molecular weight albumin-bound substances [ 50 , 51 , 52 ].

In the clinical practice, decisions to continue blood purification therapy are difficult because this therapy is time-consuming and costly. Yonemitsu et al. have published a case report and literature review of cases of heat stroke treated with blood purification therapy [ 53 ]. The review includes several survival cases treated more than three times with PE; therefore, withdraw therapy following only a few trials. No prospective, comparable study has confirmed the efficacy of blood purification in heat stroke.

Cardiovascular dysfunction

Hart et al. have observed that supplementary vasoactive agents necessary to elevate blood pressure were associated with both high mortality rates and neurologic disability in patients with heat stroke [ 54 ]. Misset et al. have demonstrated that the use of vasoactive drugs within the first 24 h of admission to ICU was an independent factor associated with mortality. These findings suggest a close association between hypotension and poor outcomes. To date, no prospective, comparable study has confirmed the efficacy of targeted fluid administration or specific vasoactive drugs in heat stroke.

It would be acceptable to consider prevention, rather than the treatment of organ dysfunctions, because therapeutic options for organ dysfunction are rather limited even in the late 2010s, as described above. Nonetheless, heat-related deaths and illnesses are preventable [ 6 , 55 ]. Heat stroke prevention strategies, such as using air conditioner; limiting outdoor activities during the daytime; consuming ample fluids; wearing loose-fitting light-colored clothing, being aware of medication side effects that may cause fluid losses, decrease sweating, or decreased heart rate; and never leaving impaired adults or children in a car unattended, are important [ 55 ]. Centers for Disease Control and Prevention has uploaded a video titled “ How to Stay Cool in Extreme Heat” to YouTube [ 56 ].

Conclusions

In the present review, we elucidated the clinical diagnosis of heat stroke. Regarding the definition/classification of heat stroke, the Bouchama’s definition and the JAAM criteria are the two available systems. Intravascular cooling devises provided rapid cooling in the small number of heat stroke patients. Although few case reports and retrospective case-series for the use of anticoagulation and blood purification therapies have been reported, particularly in Japan, no prospective, comparative study has been conducted to date. Further large studies are warranted to evaluate these treatment strategies among patients with heat stroke.

Abbreviations

Acute Kidney Injury

Acute Respiratory Distress Syndrome

Conventional cooling

Continuous Electroencephalogram

Continuous Renal Replacement Therapy

Disseminated Intravascular Coagulation

Glasgow Coma Scale

High-mobility group box 1

Heat shock proteins

Intensive care unit

Convection-based intravascular cooling device

Japanese Association for Acute Medicine

Japanese Association of Acute Medicine heat stroke committee working group

Japan Coma Scale

Plasma diafiltration

Plasma exchange

Simplified Acute Physiology Score II score

Systolic blood pressure

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How to Stay Cool in Extreme Heat [ https://www.cdc.gov/disasters/extremeheat/how_to_stay_cool_video.html ].

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Emergency Medical Center, Kagawa University Hospital, 1750-1 Ikenobe, Miki, Kita, Kagawa, 761-0793, Japan

Toru Hifumi

Department of Emergency and Critical Care Medicine, Juntendo University, Urayasu Hospital, 2-1-1 Tomioka,Urayasu-shi, Chiba, 279-0021, Japan

Yutaka Kondo

Emergency and Critical Care Center, Tokyo Metropolitan Tama Medical Centre, 2-8-29 Musashidai, Fuchu-shi, Tokyo, 183-8524, Japan

Keiki Shimizu

Department of Emergency Medicine, Teikyo University School of Medicine, 2-11-1 Kaga, Itabashi-Ku, Tokyo, 173-8606, Japan

Yasufumi Miyake

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Hifumi, T., Kondo, Y., Shimizu, K. et al. Heat stroke. j intensive care 6 , 30 (2018). https://doi.org/10.1186/s40560-018-0298-4

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case study for heat stroke

Hyperthermia & heat stroke

June 20, 2021 by Josh Farkas

  • Rapid Reference 🚀
  • Definition & diagnosis of hyperthermia
  • Differential diagnosis
  • Sedation & Shivering tx
  • Intubation if necessary
  • (1) Internal cooling: IV fluid
  • (2) Surface cooling
  • (3) Respiratory cooling
  • Management of complications
  • Questions & discussion

(back to contents)

what is hyperthermia?

  • Fever is temperature elevation due to activity of the hypothalamus, in response to cytokines. Such cytokines may be triggered by infection or sterile inflammation.
  • Unlike fever, hyperthermia involves complete loss of thermal control.

heat stroke

  • Disease caused by an imbalance of heat generation versus heat clearance from the body (without another primary underlying cause).
  • (a) Temperature >40C (104F).
  • (b) Neurologic manifestations (e.g. altered mental status, ataxia, seizure).
  • (c) Caused primarily by exertion or exposure.

exertional heat stroke

  • Caused by exertion in hot weather (e.g. marathoners, military recruits).
  • Diagnosis is generally reasonably obvious based on history.
  • Patients can be sweaty.

non-exertional heat stroke

  • Results from lack of adequate hydration and air conditioning during a heat wave.
  • Usually affects elderly with medical comorbidities.
  • Presentation may be less obvious than exertional heat stroke (should have high index of suspicion during a heat wave).
  • Examination may show dry skin, delirium, and abnormal vital signs (e.g. hyperthermia, tachycardia, hypotension).

heat stroke (see above)

Toxicologic.

  • Malignant hyperthermia.
  • Neuroleptic malignant syndrome.
  • Serotonin syndrome.
  • Sympathomimetic overdose.
  • Salicylate intoxication.
  • Anticholinergic intoxication.

CNS disease

  • Meningitis or encephalitis.
  • Hypothalamic disease (e.g. CVA or hemorrhage).

endocrinopathy

  • Thyroid storm.
  • Pheochromocytoma.
  • Adrenal crisis.
  • (a) CNS infection (meningitis/encephalitis).
  • (b) Sepsis + other factors limiting heat loss (e.g. anticholinergics, phenothiazines).

evaluation for organ damage

  • Immediate fingerstick glucose if mental status alteration.
  • Chemistries, including Ca/Mg/Phos.
  • Complete blood count with differential.
  • Liver function tests (hyperthermia can cause hepatic failure).
  • Coags, fibrinogen, D-dimer (hyperthermia can cause DIC).
  • Creatinine kinase (hyperthermia commonly causes rhabdomyolysis).

investigations to determine the etiology (if this is unclear)

  • Review medications, changes in medications, and drug interactions (focusing on serotonergic medications).
  • Cultures, lumbar puncture.
  • Thyroid stimulating hormone, cortisol.
  • Neuroimaging (CT scan +/- MRI).
  • Acetaminophen and salicylate levels.
  • Urine toxicologic screen may be considered.

Some patients with hyperthermia have a causative problem that requires specific management (e.g. brainstem stroke, meningitis, septic shock). However, the most important aspect of care overall is usually meticulous and aggressive supportive care.

role of sedation

  • May be important, regardless of whether the patient is intubated.
  • Muscular exertion may increase risk of rhabdomyolysis.
  • Activity increases heat generation, impairing the ability to control hyperthermia.
  • Never use physical restraints to control agitation (struggling against restraints will further increase heat generation).

potential options

  • Especially useful in hyperthermia that is due to intoxication (e.g. sympathomimetics).
  • Beneficial properties include muscle relaxation and anti-seizure effects.
  • May be useful for immediate control of profound agitation.
  • Useful among intubated patients.
  • Advantages include anti-seizure activity and the ability to lift sedation to re-evaluate mental status.
  • Sources of pain should be treated appropriately (especially if these are drivers of agitation).
  • If serotonin syndrome is possible, then fentanyl should be avoided.
  • Possible consideration for non-intubated patients, since it is titratable and doesn't suppress respiration.
  • Sympatholytic properties may assist with control of shivering.
  • Logistically challenging to initiate rapidly (loading bolus should be avoided given potential for bradycardia).

suppression of shivering

  • Shivering will impair temperature management and should be controlled during the acute cooling phase.
  • For the intubated patient, paralysis with a non-depolarizing muscle relaxant may be used to control shivering (see below).
  • IV benzodiazepines and/or IV dexmedetomidine (depending on patient's mental status reserve).
  • Fentanyl (if there is no suspicion of serotonin syndrome).
  • Pain-dose ketamine infusion has some anti-shivering properties (e.g. 0.15-0.3 mg/kg/hr).
  • IV magnesium.
  • Buspirone 30 mg enterally.
  • IV ondansetron has some anti-shivering effects.

indications to consider intubation

  • When in doubt, an alternative approach is to cool the patient and determine if mental status normalizes. If temperature control normalizes mental status, this argues against meningitis or CVA.
  • (2) Severe rigidity interferes with mechanical ventilation or temperature control (e.g. in extreme serotonin syndrome).
  • Seizure can rapidly initiate a vicious cycle of worsening hyperthermia and intractable seizure leading to death.
  • In any patient with hyperthermia and repeated or ongoing seizure, there should be a very strong consideration to immediately treat with propofol and ketamine (to control seizure) and subsequently intubate.
  • Worsening respiratory failure
  • Refractory agitation

intubation procedure itself

  • May confuse matters later regarding the possibility of malignant hyperthermia.
  • May worsen hyperkalemia (which can occur in these patients).
  • Obviously, ensure that the patient is adequately sedated during this period.
  • Paralysis will eliminate all heat generation by skeletal muscles, accelerating achievement of target temperature.
  • Core temperature should ideally be monitored in real time, to prevent overshoot hypothermia.
  • The best ways to achieve this are usually an esophageal probe (intubated patients) or a bladder probe (non-intubated patients).
  • Rectal temperature may be monitored if nothing else is available, but this may tend to lag behind other modes of temperature measurement.

temperature goals

  • (#1) Initially, drop the core temperature to 38C (100.4F) as rapidly as possible.
  • (#2) Stop active cooling when the temperature reaches 38-39C (100.4-102F ) to prevent overshoot.
  • (#3) Continue monitoring for ongoing thermal instability (ideally at least for 6 hours).

multi-modal cooling

  • Each technique removes thermal energy from the body. These techniques function in an additive fashion.
  • The most important technique is surface cooling (#2 below) which is absolutely essential. Agressive surface cooling will work fine on its own. However, internal and respiratory cooling are useful adjunctive techniques which are easy and may help achieve target temperature faster.

refrigerated crystalloid

  • Ideally there should be a supply of pre-chilled IV fluid (e.g. bags of Lactated Ringers stored in a refrigerator).
  • Each liter of chilled crystalloid will cool the patient by roughly ~1 degree Centigrade.

pharmacokinetics of thermal energy: cooled IV fluid directly affects the core temperature

  • A core temperature exists in the large blood vessels and organs receiving high levels of perfusion (e.g. heart, brain). This is more important with regards to target organ damage (especially brain injury).
  • A peripheral temperature exists in tissues contacting the environment (e.g. skin and soft tissues).
  • Surface cooling techniques involve removal of thermal energy from the skin, with the aim that cooler temperatures will eventually be transmitted to the core. This is generally very effective, but it may be delayed in shocked patients with peripheral vasoconstriction (which delays temperature exchange between the core and periphery).
  • In shocked patients, cooled fluid might even have a disproportionate effect on the core body tissues (which would be desirable).

why external fluid is effective for cooling , but not for warming

  • Infusion of warmed fluid is poorly effective for warming patients with hypothermia .
  • Infusion of cooled fluid is moderately effective for cooling patients with hyperthermia
  • Hypothermia: The body is ~32C, warmed fluid is perhaps ~40 C, so the temperature gradient is ~8 C .
  • Hyperthermia: The body is ~44C, cooled fluid is perhaps ~4 C, so the temperature gradient is ~40 C .
  • Physiology works in our favor here: the hotter the patient is, the more effective the cooled fluid will be. Evidence regarding the efficacy of cooled fluids was mostly obtained in patients starting at a normal temperature, so cooled fluids might be a bit more effective in hyperthermia.

evidentiary basis for cooled fluids

  • Cooled fluids haven't been studied in hyperthermia. However, the physiology and efficacy of cooled crystalloid is well established in a variety of contexts (pre-hospital medicine, anesthesiology, and neurocritical care).
  • Numerous studies support the ability of chilled crystalloid (at 0-4 C) to reduce core body temperature by roughly ~1 C per liter (i.e. ~2 C drop following receipt of 30-40 cc/kg). ( 22371279 , 10969294 , 18312676 , 23809038 , 25348858 , 15733765 , 25563645 , 12505732 , 16352954 ) This is extremely well established at this point, for example it's been validated in large prospective RCTs. ( 24240712 )

Choice of physical cooling method depends on available resources and the cause of hyperthermia. The best options here are evaporative cooling or an ice bath.

remove all clothing

  • Clothing impedes heat egress from the body.
  • Regardless of which technique you're using for cooling, clothing will work against you.
  • Don't cover patients with sheets – this will likewise impair cooling ( especially with evaporative cooling).

preferred technique for severe heat stroke: immersive ice bath

case study for heat stroke

  • The gold standard for rapid cooling is filling a bath of water with ice and allowing water in the bath to reach zero degrees centigrade prior to patient immersion (true ice water immersion ). This is often set up near marathons in anticipation of exertional heat stroke and it's insanely effective.
  • Water plays an important role here by maximizing the amount of area of the patient's skin that comes into contact with cold material. Simply placing ice cubes on the patient's body will not achieve this.
  • Rare hospitals may have a dedicated immersive ice bath.
  • (1) Putting the patient in a body bag and filling the body bag with ice and water (figure above). ( 33000014 ) This has the advantage that ice and body bags are widely available in any hospital.
  • (2) Placing the patient on a plastic sheet, covering the patient in ice, and then wrapping the sheets closed (“tarp taco” technique). ( 31221601 )

Epic video on Bellevue's Immersive Water Bath by Adaira Landry:

if an immersive ice bath isn't available: evaporative cooling

  • Note that the water shouldn't be cold (this will decrease the amount of evaporation).
  • Evaporation is very effective at cooling the body (roughly ~0.1 C per minute, roughly half as fast as immersive cooling).
  • (1) Add a cooling blanket underneath the patient to maximize heat loss through the posterior body surface.
  • (2) Ice packs may also be placed (e.g. on the groin, axillae, and neck).
  • Conductive heat loss is faster than evaporative heat loss. These add-ons will therefore increase the rate of cooling. As more and more ice packs are added and the patient is covered in ice this approach will eventually start to resemble an immersive ice bath (below).
  • Evaporation won't work if the ambient humidity is high (e.g. >70%); this may fail in areas which aren't dehumidified.

external pads with adaptive water-based cooling system (e.g., Arctic Sun)

  • This will eventually work, but it is very sluggish to get set up and running (it may take the machine a while to cool down).
  • 🛑 This is not a preferred technique here, because the goal is decreasing the patient to target temperature in <30-60 minutes. The delay to set up external pads will make it impossible to meet this goal.

caveats to this section

  • (1) There isn't much evidence supporting these interventions.
  • (2) These techniques are intended only for short-term use (e.g. 1-3 hours) to help bring the patient's temperature down from an immediately threatening level.
  • (3) These techniques are solely adjunctive techniques ( not intended as the primary technique for cooling).

physiology of cooling via the respiratory tract

  • Dry air is provided to the respiratory tract (either nasal passages or lungs). ( 27635468 )
  • Water vapor evaporates from the respiratory tract. This process of evaporation transfers thermal energy out of the body (exactly the same way evaporative cooling works with regards to surface cooling).
  • Evaporative cooling via the respiratory tract can be continued only for a short period of time due to nasal dryness (if using a nasal cannula) or tenacious secretions (if using a ventilator).

(a) high-flow dry air via nasal prongs

  • Don't use oxygen, because that would provide an excessive amount of oxygen, potentially leading to hyperoxia.
  • (i) Patients must be able to saturate adequately on air (they must not have hypoxemic respiratory failure). For patients requiring some oxygen, air and oxygen could conceivably be blended together by merging inputs from an oxygen flowmeter and air flowmeter, but this may be tricky.
  • (ii) Since the air isn't heated or humidified, this will be less comfortable than a standard high-flow nasal cannula setup. The flow rate may need to be down-titrated to achieve patient comfort.
  • Ideally, this could be done using a high-capacity flowmeter attached to a medical air supply (figure above). Try to titrate to ~40 liters/minute flow (may down-titrate if not tolerated).
  • If a high-capacity flowmeter isn't available, this can also be done using a standard flowmeter. A flow rate of 20-40 liters/minute may be achieved by turning the flow rate up to 15 liters/minute and then increasing the flow a bit further beyond that.

(b) high-flow dry air using nasal CPAP

  • Another way to deliver dry gas at high flows is the use of nasal CPAP. ( 30919302 , 30359664 )
  • This has the advantage of allowing the FiO2 to be titrated (for patients with respiratory failure and some supplemental oxygen requirement).
  • Disable humidification of the gas.
  • Titrate up the CPAP pressure to achieve a flow rate of ~20-40 liters/minute (keeping the pressure under 20 cm).

(c) intubated patient

  • (a) Most ventilators have a heat-moisture exchanger (HME) which tends to trap warmth in the ventilator circuit. This may be removed during active cooling.
  • (b) Most ventilators have some sort of warming device which increases gas to ~36C. This should be disabled.
  • Nasal application of dry air works by causing evaporative cooling from the nasal turbinates (not the lungs).
  • This has been shown to work even in intubated patients. ( 30359664 ) The techniques used are exactly the same as above (in the non-intubated patient).

potential complications include:

  • Rhabdomyolysis.
  • Acute hepatic failure (rarely leading to fulminant failure requiring transplantation).
  • Aspiration pneumonia; ARDS.
  • Stress-induced cardiomyopathy, arrhythmia.
  • Disseminated intravascular coagulation (DIC).
  • Hypoglycemia.
  • Hyponatremia.

These complications should be treated using standard supportive measures. Consider monitoring laboratory studies (especially creatinine kinase and liver function tests) over the first 24 hours to watch for the emergence of these problems.

case study for heat stroke

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  • Failure to promptly cool hyperthermic patients, resulting in thermal organ damage.
  • Use of non-core temperature measurements.
  • If you're going to use a respiratory cooling technique (e.g. removal of the ventilator heat and moisture exchanger), make sure to discontinue this after a few hours, once the patient has reached a safe temperature.
  • There's no role for acetaminophen or other antipyretic medications (hyperthermia isn't mediated by the thalamus, so these medications will have no efficacy).
  • Avoid the use of vasopressors if possible, as this may cause cutaneous vasoconstriction which impairs heat release.

Guide to emoji hyperlinks

  • 📄 = Link to open-access journal article.
  • 31216400 Epstein Y, Yanovich R. Heatstroke. N Engl J Med. 2019 Jun 20;380(25):2449-2459. doi: 10.1056/NEJMra1810762 [ PubMed ]
  • 31221601 Lipman GS, Gaudio FG, Eifling KP, Ellis MA, Otten EM, Grissom CK. Wilderness Medical Society Clinical Practice Guidelines for the Prevention and Treatment of Heat Illness: 2019 Update. Wilderness Environ Med. 2019 Dec;30(4S):S33-S46. doi: 10.1016/j.wem.2018.10.004 [ PubMed ]
  • 33000014 Kim DA, Lindquist BD, Shen SH, Wagner AM, Lipman GS. A body bag can save your life: a novel method of cold water immersion for heat stroke treatment. J Am Coll Emerg Physicians Open. 2020 Jan 8;1(1):49-52. doi: 10.1002/emp2.12007 [ PubMed ]
  • 33856299 Rublee C, Dresser C, Giudice C, Lemery J, Sorensen C. Evidence-Based Heatstroke Management in the Emergency Department. West J Emerg Med. 2021 Feb 26;22(2):186-195. doi: 10.5811/westjem.2020.11.49007 [ PubMed ]

The Internet Book of Critical Care is an online textbook written by Josh Farkas ( @PulmCrit ), an associate professor of Pulmonary and Critical Care Medicine at the University of Vermont.

We are the EMCrit Project , a team of independent medical bloggers and podcasters joined together by our common love of cutting-edge care, iconoclastic ramblings, and FOAM.

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case study for heat stroke

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Hyperthermia

Case Presentation

It was July 20 in Houston and the fourth straight day that would have a high temperature above 100°F. Janice was running some errands and decided to stop by her mother's house. Janice's mother, Marian, was eighty-four and in pretty good health. She was able to keep up with her housekeeping and still tended a small garden in her backyard. Just that morning, Janice had told her mother not to spend too much time working in the garden today. Janice knew that the heat could be dangerous, especially to the elderly, and her mother's place didn't have an air conditioner, but Janice felt that her mother was alert enough to know her own limits.

When Janice reached her mother's house, she found her mother unconscious on the couch in the living room. All of the windows in the house were closed. Janice immediately tried to rouse her mother and was able to get her to say a few words, but Marian seemed delirious. Janice grabbed the telephone and called for help. The emergency services operator instructed Janice to apply cold wash cloths to her mother's forehead and face and if possible to position her mother in front of a fan while using a spray bottle to spray tepid water on her skin.

When the paramedics arrived Marian was conscious but confused and feeling nauseous. At the hospital the doctor told Janice just how lucky she was to have visited Marian at that moment. He informed Janice that Marian had suffered heat stroke, a form of hyperthermia and that Janice's quick action at the house had saved her mother's life. Marian was making rapid progress to recovery but was being given fluids and electrolytes intravenously and was going to stay in the hospital overnight for observation.

Case Background

Hyperthermia occurs when the body temperature increases without an increase in the set point of the thermoregulatory center in the hypothalamus. Heat exhaustion and heatstroke are two common forms of hyperthermia. Symptoms of heat exhaustion include thirst, fatigue, profuse sweat, and giddiness or delirium. Individuals with heat exhaustion generally have a normal or only slightly elevated body temperature and the symptoms are the result of the loss of water and electrolytes. Symptoms of heatstroke include a temperature of 104°F, absence of sweating, and loss of consciousness. If untreated, heat exhaustion precedes heatstroke, and heat stroke is often fatal. Treatment for hyperthermia consists of reducing the body temperature to normal. Special attention is placed on reducing the temperature of the brain as tissue damage can result if the body temperature rises above 109°F.

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Case Study: When Heat Stress Hits an Entire Group

By Tod Schimelpfenig

Jul 23, 2019

Backpackers hiking through grasslands

The Setting

You’re the supervisor for several crews doing volunteer trail maintenance in a local national forest.

Since your crew leaders are new, you decide to head out to their work sites to check on their work. (Plus, it’s a good reason to get out of the office, away from email, and enjoy a hike in the hills.)

The weather has been unusually hot and humid, with daytime temperatures in the 90s °F (30s °C).

You find one of your crews around lunchtime resting under a few trees. They look lethargic and tired.

One crew member is lying on his back with his feet elevated and a wet bandanna on his forehead. Your crew leader gives you a SOAP report on the patient.

SOAP Report

The patient is a 19-year-old male who complains of weakness, dizziness, heat stress, and a headache.

The patient is supine with feet elevated. He denies any injuries and head to toe exam does not find any sign of injury.

Vital Signs

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What is your assessment and plan? Take a few minutes to figure out your own assessment and make a plan. Don’t cheat—no reading on without answering this first!

Group working on a trail crew mending fence

  • Possible heat exhaustion and/or dehydration.
  • Heat stroke is unlikely as patient is A+OX4 and has a measured oral temperature of 99°F (37.2°C).
  • Move patient to shade and onto a pad to insulate him from the warm ground. Use cool, wet compresses to lessen heat stress.
  • Hydrate and feed patient.
  • Once he has time to recover, take patient back to camp to rest for the remainder of the day.

Anticipated problems

  • Heat stroke, heat cramps or hyponatremia

The Story Continues...

After listening to the SOAP report and approving the assessment and plan, you check in on the other members of this trail crew. They are all tired and stressed by the heat.

You learn the crew members have been drinking water, but only about 3 liters on average rather than the minimum of 4 liters recommended by staff (the water has a brackish taste that no one likes). This is on the low end of their fluid needs.

The work days are long and run from 8:00 a.m. until 6:00 p.m. It’s been warm in the evenings, the camp is noisy, and most of the crew members are sleeping poorly.

You notice several of the crew members have bandannas on their heads, none are wearing long sleeved shirts or wide brimmed hats, and all are red and bronzed from sun exposure.

Matching Systems to the Needs of the Group 

You decide to meet with your crew leaders and make changes to manage this heat stress.

  • First, you give everyone the afternoon off and take them to a lake where they can swim and cool off.
  • You can’t improve the water source, so you offer some drink mixes to entice the crew members to drink more fluid.
  • You encourage diligent monitoring of fluid intake by the crew leaders
  • You change the work schedule to early morning and evening shifts so that people rest in the shade in the heat of the day.
  • You require everyone to wear loose, long sleeved cotton shirts and hats to keep the sun at bay.
  • Finally, you review strategies for preventing heat illness , predisposing factors, and the subtle signs and symptoms of heat stress.

Notes from NOLS: Injury/Illness Prevention is a Leadership Skill

The supervisor in this case study recognizes that preventing heat illness is a leadership task, and steps in to manage it before it becomes a broader medical problem.

When the weather heads up, leaders need to be alert for signs of developing heat illness in their groups. Environmental risk factors of high heat and humidity, coupled with dehydration, exertion, and overdressing, should raise caution flags. The vague symptoms of fatigue, headache, weakness, irritability, and malaise should be recognized as indicators of dehydration and heat illness.

Flagging and Preventing Heat Illness

Sources of heat stress.

  • Environmental heat is an obvious source of stress that is increased when humidity lessens the efficiency of heat loss through sweat.
  • Other factors include dehydration, age, general health, use of medications or alcohol, and fatigue.
  • Heat illness can happen quickly if people have to work hard in very hot and humid conditions, or are not acclimatized to heat. It can also be cumulative and reveal itself after several days of heat stress have worn you down.

Higher-Risk Individuals & Conditions

  • Patients with underlying health problems (illness or injury)
  • Children, who have underdeveloped physical mechanisms that contribute to the incidence of heat illness.
  • Individuals with compromised heart function are less able to adjust when stressed by heat.
  • There is a correlation between lack of sleep, or fatigue, and the development of heat illness.
  • Antihistamines, antipsychotic agents, thyroid hormone medications, amphetamines, and alcohol are among the drugs that have been implicated in the development of heat illness. Some interfere with thermoregulation; others increase metabolic activity or interfere with sweating.

Preventing Heat Illnesses

Acclimatizing to heat.

We can acclimatize to heat. When acclimatized, sweating happens faster and sooner and with the loss of fewer electrolytes in the sweat, and with improved physical and mental tolerance to heat.

Acclimating to heat requires one to two hours of exercise in the heat daily for approximately 10 to 14 days.

General Tips

  • Stay hydrated, but avoid overhydration . Monitor urine output for color and quantity.
  • Individual fluid needs can vary depending on the person, activity, and environment. 3-4 liters of fluid a day is a good reference point for many people in general outdoor activities in moderate environments.
  • Exercise early or late in the day in hot environments. Rest often.
  • Give yourself 10–14 days to acclimatize to hot environments before you begin heavy exercise.
  • Wear well-ventilated, open weave clothing. Cover your head and wear sunglasses.
  • The very young and older adults are less efficient at heat loss, as are people who are very muscular or overweight.
  • Drugs that have been known to contribute to heat illnesses include: alcohol, antidepressants, antihistamines, some anesthetics, cocaine and amphetamines.

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case study for heat stroke

Tod Schimelpfenig

As a NOLS Instructor since 1973 and a WEMT, volunteer EMT on ambulance and search and rescue squads since the 70s, Tod Schimelpfenig has extensive experience with wilderness risk management. He has used this valuable experience to conduct safety reviews as well as serve as the NOLS Risk Management Director for eight years, the NOLS Rocky Mountain Director for six years, and three years on the board of directors of the Wilderness Medical Society, where he received the WMS Warren Bowman Award for lifetime contribution to the field of wilderness medicine. Tod is the founder of the Wilderness Risk Manager’s Committee, has spoken at numerous conferences on pre-hospital and wilderness medicine, including the Australian National Conference on Risk Management in Outdoor Recreation, and has taught wilderness medicine around the world. He has written numerous articles on educational program, risk management and wilderness medicine topics, and currently reviews articles for the Journal of Wilderness and Environmental Medicine. Additionally, he is the author of NOLS Wilderness Medicine and co-author of Risk Management for Outdoor Leaders, as well as multiple articles regarding wilderness medicine. Tod is the retired curriculum director for NOLS Wilderness Medicine and is an active wilderness medicine instructor

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It’s day 5 of a planned 12 day wilderness trip for teenagers in a western U.S. wilderness area. The closest road is 12 miles away, and the weather has been warm and dry for the whole trip—perfect for enjoying the mountains. You’re one of the trip leaders with current WFR training.

FOX News

Largest-ever COVID vaccine study links shot to small increase in heart and brain conditions

The largest COVID vaccine study to date has identified some risks associated with the shot.

Researchers from the Global Vaccine Data Network (GVDN) in New Zealand analyzed 99 million people who received COVID vaccinations across eight countries.

They monitored for increases in 13 different medical conditions in the period after people received a COVID vaccine .

The study, which was published in the journal Vaccine last week, found that the vaccine was linked to a slight increase in neurological, blood and heart-related medical conditions, according to a press release from GVDN.

LONG COVID IS HIGHEST IN THESE STATES, SAYS NEW CDC REPORT

People who received certain types of mRNA vaccines were found to have a higher risk of myocarditis, which is inflammation of the heart muscle.

READ ON THE FOX NEWS APP

Some viral-vector vaccines were linked to a higher risk of blood clots in the brain, as well as an increased likelihood of Guillain-Barre syndrome, a neurological disorder in which the immune system attacks the nerves.

Other potential risks included inflammation of part of the spinal cord after viral vector vaccines, and inflammation and swelling in the brain and spinal cord after viral vector and mRNA vaccines, the press release stated.

SHOULD THE CDC DROP ITS 5-DAY COVID ISOLATION GUIDELINES? DOCTORS WEIGH IN

"The size of the population in this study increased the possibility of identifying rare potential vaccine safety signals," lead author Kristýna Faksová of the Department of Epidemiology Research, Statens Serum Institut, Copenhagen, Denmark, said in the release.

"Single sites or regions are unlikely to have a large enough population to detect very rare signals."

Dr. Marc Siegel, clinical professor of medicine at NYU Langone Medical Center and a Fox News medical contributor, was not involved in the research but commented on the findings.

"The massive study and review of the data reveals some rare association of the MRNA vaccines and myocarditis, especially after the second shot, as well as an association between the Oxford Astra Zeneca adenovirus vector vaccines and Guillain Barre syndrome," he told Fox News Digital.

"But these risks are rare," he added, "and other studies show that the vaccine decreases the risk of myocarditis from COVID itself dramatically."

COVID VARIANT JN.1 NO MORE SEVERE THAN PREVIOUS STRAINS, CDC DATA SHOWS

Siegel noted that all vaccines have side effects.

"It always comes down to a risk/benefit analysis of what you are more afraid of — the vaccine's side effects or the virus itself, which can have long-term side effects in terms of brain fog, fatigue, cough and also heart issues ," he said.

"Denying or exaggerating a vaccine's side effects is not good science — nor is underestimating the risks of the virus, especially in high-risk groups," Siegel added.

The key is for doctors and their patients to carefully weigh the risks and benefits, the doctor emphasized.

"This study does not really change anything; it just provides much further evidence of what we already know," he said.

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Dr. Jacob Glanville, CEO of Centivax, a San Francisco biotechnology company, also reacted to the study’s findings. 

"This study is confirming in a much larger cohort what has been previously identified in the original studies during the pandemic — myocarditis and pericarditis as a rare side effect of mRNA vaccines and clots as a rare side effect of the viral vectored vaccines," he told Fox News Digital.

"The odds of all of these adverse events are still much, much higher when infected with SARS-CoV-2 (COVID-19) , so getting vaccinated is still by far the safer choice."

This study was part of a more widespread research initiative, the Global COVID Vaccine Safety (GCoVS) Project.

The project is supported by Centers for Disease Control and Prevention (CDC), a component of the U.S. Department of Health and Human Services (HHS).

More than 80% of the U.S. population has received at least one dose of the COVID vaccine, per the CDC.

Fox News Digital reached out to Pfizer and Moderna, makers of mRNA COVID vaccines, for comment.

For more Health articles, visit www.foxnews.com/health .

Original article source: Largest-ever COVID vaccine study links shot to small increase in heart and brain conditions

More than 80% of the U.S. population has received at least one dose of the COVID vaccine, per the CDC. iStock

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Heat stroke with bimodal rhabdomyolysis: a case report and review of the literature

Toshihiko yoshizawa.

1 Department of Acute Critical Care Medicine, Shizuoka Hospital, Juntendo University, Tokyo, Japan

Kazuhiko Omori

Ikuto takeuchi, yuto miyoshi, hiroshi kido.

3 Tokushima University, Tokyo, Japan

Etsuhisa Takahashi

Kei jitsuiki, kouhei ishikawa, hiromichi ohsaka, manabu sugita.

4 Juntendo University, Tokyo, Japan

Youichi Yanagawa

2 1129 Nagaoka, Izunokuni City, Shizuoka 410-2295 Japan

Severe heat stroke tends to be complicated with rhabdomyolysis, especially in patients with exertional heat stroke. Rhabdomyolysis usually occurs in the acute phase of heat stroke. We herein report a case of heat stroke in a patient who experienced bimodal rhabdomyolysis in the acute and recovery phases.

Case presentation

A 34-year-old male patient was found lying unconscious on the road after participating in a half marathon in the spring. It was a sunny day with a maximum temperature of 24.2 °C. His medical and family history was unremarkable. Upon arrival, his Glasgow Coma Scale score was 10. However, the patient’s marked restlessness and confusion returned. A sedative was administered and tracheal intubation was performed. On the second day of hospitalization, a blood analysis was compatible with a diagnosis of acute hepatic failure; thus, he received fresh frozen plasma and a platelet transfusion was performed, following plasma exchange and continuous hemodiafiltration. The patient’s creatinine phosphokinesis (CPK) level increased to 8832 IU/L on the fifth day of hospitalization and then showed a tendency to transiently decrease. The patient was extubated on the eighth day of hospitalization after the improvement of his laboratory data. From the ninth day of hospitalization, gradual rehabilitation was initiated. However, he felt pain in both legs and his CPK level increased again. Despite the cessation of all drugs and rehabilitation, his CPK level increased to 105,945 IU/L on the 15th day of hospitalization. Fortunately, his CPK level decreased with a fluid infusion. The patient’s rehabilitation was restarted after his CPK level fell to <10,000 IU/L. On the 31st day of hospitalization, his CK level decreased to 623 IU/L and he was discharged on foot. Later, a genetic analysis revealed that he had a thermolabile genetic phenotype of carnitine palmitoyltransferase II (CPT II).

Conclusions

Physicians should pay special attention to the stress of rehabilitation exercises, which may cause collapsed muscles that are injured by severe heat stroke to repeatedly flare up.

Severe heat stroke tends to be complicated with rhabdomyolysis, especially in patients with exertional heat stroke [ 1 – 4 ]. Rhabdomyolysis may lead to systemic effects, including the local occurrence of compartment syndrome, hyperkalemic cardiac arrest, and/or lethal disseminated intravascular coagulopathy [ 5 – 7 ]. Rhabdomyolysis usually occurs in the acute phase of heat stroke. We herein report a case of heat stroke in a patient who experienced bimodal rhabdomyolysis in the acute and recovery phases.

A 34-year-old male patient was found lying unconscious with a head injury on the road after participating in a half marathon in the spring. It was a sunny day with a maximum temperature of 24.2 °C and a humidity of 54%. A physician who was transported by helicopter to check on the patient reported that his Glasgow Coma Scale score was 6 and that he presented marked restlessness. His blood pressure was 110/80 mmHg, his heart rate was 140 beats per minute (BPM), his respiratory rate was 40 breaths per minute (BPM), and his axillary temperature was 40.8 °C. He was transported to our hospital by a ground ambulance after the infusion of a sedative agent and the rapid infusion of cooled lactated Ringer. His medical and family history was unremarkable. He did not have sign of flu in a few days. Upon arrival, his Glasgow Coma Scale score was 10. His blood pressure was 116/86 mmHg, his heart rate was 164 BPM, his respiratory rate was 36 BPM, his SpO 2 level was 95% with oxygen (8 l/min by mask), and his bladder temperature was 40.2 °C. The physiological findings included hyperhidrosis with restless confusion. After the rapid infusion of 3500 ml of cooled lactated Ringer and gastric lavage with iced water, his bladder temperature decreased to 38.8 °C within 30 min of his arrival and the patient became calm. A chest roentgen revealed no abnormal findings, while an electrocardiogram showed sinus tachycardia without a change in the ST segments. Head CT, which was performed to determine the cause of the patient’s unconsciousness, revealed no brain abnormalities; however, the patient’s marked restlessness and confusion returned. To secure the patient’s safety, a sedative was administered and tracheal intubation was performed. The main results of a blood analysis are shown in Table  1 . On the second day of hospitalization, a blood analysis revealed the following findings: aspartate aminotransferase (AST), 144 IU/L; alanine aminotransferase (ALT), 86 IU/L; prothrombin activation ratio, 22%; platelet count, 5 × 10 4 /mm 3 ; and ammonia level, 108 μg/dl. These values were compatible with a diagnosis of acute hepatic failure (according to the Japanese guidelines) [ 8 ]; thus, he received fresh frozen plasma and a platelet transfusion was performed. On the third day of hospitalization, a blood analysis revealed the following findings: AST level, 14,894 IU/L; ALT level, 14,355 IU/L, prothrombin activation ratio, 43.8%; and platelet count, 3.8 × 10 4 /mm 3 ; thus, plasma exchange was performed for 2 days, followed by continuous hemodiafiltration for 3 days. The time course of the changes in the patient’s creatinine phosphokinesis (CPK) levels is shown in Fig.  1 . The patient’s CPK level increased to 8832 IU/L on the fifth day of hospitalization and then showed a tendency to transiently decrease. The patient was extubated on the eighth day of hospitalization, after showing the ability to respond to commands and the improvement of his laboratory data. From the ninth day of hospitalization, gradual rehabilitation was initiated; this included transferring to a wheelchair or standing at his bedside. However, he felt pain in both legs and his CPK level increased again. Despite the cessation of all drugs and rehabilitation, his CPK level increased to 105,945 IU/L on the 15th day of hospitalization. During this period, he had a low-grade fever ranging from 37.2 to 37.8 °C. Fortunately, his CPK level decreased with a fluid infusion, which was administered to prevent renal failure. The patient’s rehabilitation was restarted after his CPK level fell to <10,000 IU/L. On the 31st day of hospitalization, his CPK level decreased to 623 IU/L and he was discharged on foot. Later, a genetic analysis revealed that he had a thermolabile genetic phenotype of carnitine palmitoyltransferase II (CPT II).

The laboratory analysis results

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The time course of the changes in the patient’s creatinine phosphokinesis (CPK) data. The patient’s CPK level increased to 8832 IU/L on the fifth day of hospitalization and then showed a transient tendency to decrease. From the ninth day of hospitalization and following the start of rehabilitation, the patient’s CPK level increased again to reach 105,945 IU/L on the 15th day of hospitalization. PE plasma exchange, CHDF continuous hemodiafiltration

We herein report a case of heat stroke in a patient with bimodal rhabdomyolysis in the acute and recovery phases. We performed a PubMed search to identify any related articles using the key words “heat stroke” and “rhabdomyolysis”. As a result, we found 110 articles about heat stroke with rhabdomyolysis. Among these cases, we found 17 cases involving individuals with heat stroke complicated with rhabdomyolysis in which the time course of the CPK level was described [ 1 , 9 – 24 ]. We summarized these cases, including the present case, in Table  2 . Among them, only two reports from Japan showed bimodal rhabdomyolysis [ 15 , 22 ]. In one of these two reports, Takahashi et al. described a 16-year-old male patient who experienced convulsions 3 days after living donor liver transplantation [ 22 ]. After the convulsions on postoperative day 5, the patient’s CPK level, which had been showing a tendency to decrease, increased from 715 to 24,985 IU/L. Convulsions can cause rhabdomyolysis; thus, this case report was excluded from the studies that described the natural course of bimodal rhabdomyolysis induced by heat stroke [ 25 ]. Two reports by Miura et al. described the case of 38-year-old man who experienced a life-threatening flare-up of rhabdomyolysis (CPK level of 84,612 IU/L on the third hospital day) and who was treated by plasma exchange, hemodiafiltration, steroid pulse therapy, and anticoagulant treatment [ 15 ]. His general condition was initially thought to be improving; however, his smoldering rhabdomyolysis suddenly flared up with a marked increase in his CPK level (105,231 IU/L on the 18th day of hospitalization) when the steroid dosage was reduced and rehabilitation was initiated. Thereafter, his condition rapidly deteriorated and he eventually died, despite the provision of aggressive treatment. In addition, Fink et al. reported the case of a 16-year-old male athlete with heat stroke and rhabdomyolysis [ 19 ]. The patient survived and was discharged on day 14, but his CPK level was more than 1000 IU/L for several weeks after his discharge. Their report did not indicate whether the patient’s rhabdomyolysis was bimodal. Similarly to our case, in the four Japanese reports of six patients who suffered bimodal rhabdomyolysis in the acute and recovery phases (more than 2 weeks after severe heat stroke), all of the patients could survive and start rehabilitation (Table  3 ) [ 26 – 29 ]. Accordingly, the authors’ hypothesized that during the recovery phase, the stress of rehabilitation exercises can cause collapsed muscles that are injured by heat stroke to repeatedly flared up. Drugs that are administered during intensive treatment in the acute phase may be involved in the occurrence of bimodal rhabdomyolysis. However, this possibility was considered to be unlikely in the present case because drug-induced rhabdomyolysis usually subsides when the drugs are stopped [ 30 ]. In our search of the literature, heat stroke-induced bimodal rhabdomyolysis was only described in Japanese case reports; thus, genetic differences may affect this phenomenon.

A summary of the reports on heat stroke in which the time course of rhabdomyolysis was described

? means not described, D day, Reha rehabilitation, wks weeks, CPK creatinine phosphokinesis, HD hemodialysis, max maximum

The Japanese reports of bimodal rhabdomyolysis after heat stroke

D day, CPK creatinine phosphokinesis, HD hemodialysis, max maximum

CPT II is a pivotal enzyme in mitochondrial fatty acid oxidation, which is essential for energy production during simultaneous glucose sparing and a requirement for major energy supply, such as during prolonged fasting or exercise [ 31 ]. Cases with the thermolabile genetic phenotype of CPT II have been described mainly in Japan and China. Recent studies have suggested the association of this phenotype with influenza-associated encephalopathy, encephalopathy during a high-grade fever caused by human herpesvirus-6, enterovirus 71, Echo virus, Coxsackievirus, rotavirus, respiratory syncytial virus, adenovirus infection, or sudden unexpected death in infancy [ 31 – 40 ]. Generally, CPT II deficiency has three clinical presentations: a lethal neonatal form, a severe infantile hepatocardiomuscular form, and a myopathic form (which is usually mild and can manifest from infancy to adulthood) [ 41 ]. While the former two are severe multisystemic diseases characterized by liver failure with hypoketotic hypoglycemia, cardiomyopathy, seizures, and early death, the latter is characterized by recurrent exercise-induced muscle pain and weakness, sometimes associated with myoglobinuria, resembling our case [ 41 ]. The myopathic form of CPT II deficiency is the most common disorder of lipid metabolism affecting the skeletal muscle and is the most frequent cause of hereditary myoglobinuria, and males are more likely to be affected than females [ 41 ]. Accordingly, the thermolabile genetic phenotype of CPT II in the present case might have affected the occurrence of bimodal rhabdomyolysis, even during mild exercise like rehabilitation after depletion of energy in the muscle due to an initial attack of heat stroke [ 42 ]. Oda et al. also suggested that the thermolabile genetic phenotype of CPT II was a risk factor for severe heat stroke [ 43 ]. Like Reye syndrome, heat stoke induced by thermolabile genetic phenotype of CPT II might be classified as a fatty acid oxidation disorder in the future [ 44 ].

Acknowledgements

This manuscript obtains financial support from the Ministry of Education, Culture, Sports, Science and Technology (MEXT)-Supported Program for the Strategic Research Foundation at Private Universities, 2015–2019 concerning [The constitution of total researching system for comprehensive disaster, medical management, corresponding to wide-scale disaster].

Authors’ contributions

KO, IT, YM, KJ, KI, HO, and MS provided medicine for the patient and edited the draft of the manuscript. HK and ET provided genetic analysis. TK and YY provided medicine for the patient and wrote the manuscript as a corresponding author. All authors read and approved the final manuscript.

Competing interests

The authors declare that they have no competing interests.

Consent for publication

Written informed consent was obtained from the patient for publication of this case report and any accompanying images.

Ethics approval and consent to participate

The study was approved by our institutional ethics committee (Juntendo Igakugufuzoku Shizuoka Byouin Rinrishinnsa Iinkai). There was no reference number.

Abbreviations

IMAGES

  1. case study for heat stroke

    case study for heat stroke

  2. case study for heat stroke

    case study for heat stroke

  3. case study for heat stroke

    case study for heat stroke

  4. Heatstroke First Aid

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  5. What are the two types of heat stroke?

    case study for heat stroke

  6. Premium Vector

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COMMENTS

  1. Heat

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  4. Risk Factors for the 90-Day Prognosis Of Severe Heat Stroke: a Case

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  5. Case report: severe heat stroke with multiple organ dysfunction

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  6. ACSM Expert Consensus Statement on Exertional Heat Illness ...

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  11. Hyperthermia & heat stroke

    (a) Temperature >40C (104F). (b) Neurologic manifestations (e.g. altered mental status, ataxia, seizure). (c) Caused primarily by exertion or exposure. exertional heat stroke Caused by exertion in hot weather (e.g. marathoners, military recruits).

  12. A Tale of Two Heat Strokes: A Comparative Case Study

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  13. Evidence-Based Heatstroke Management in the Emergency Department

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  14. Case Study: Hyperthermia

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  15. Web‐Based Data to Quantify Meteorological and Geographical Effects on

    After the comparison of real heat stroke cases and HSSI (Table S3 in Supporting Information S1), we selected the 75th and 90th percentile values of HSSI to indicate different levels of heat stroke risk, where the 75th percentile means that heat stroke cases may appear (case number ≥ 2) and the 90th percentile means that a large number of heat ...

  16. PDF Treatment of Heat Stroke in the Field

    In one US military study, cold saline administered in the "eld was shown to signi"cantly reduce heat stroke complications when compared to room temperature saline. 5 EMS providers therefore have the ability achieve target temperature prior to hospital arrival by rapidly administering 1-2 liters of saline in the "eld, as described in the case above.

  17. It's Getting Hot in Here: A Rare Case of Heat Stroke in a ...

    Heat stroke is a severe acute illness characterized by a core temperature greater than 40°C (104°F) and central nervous system manifestations, such as delirium, convulsions, or coma, resulting from exposure to environmental heat or strenuous physical activity.

  18. Heat stroke

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  19. Case Study: A Hot Day Becomes a First Aid Situation

    Objective The patient is lying on their back, crying out in pain with obvious spasms in their legs. The patient says these spasms began a few minutes before, as they were kneeling in the canoe. The patient is A+Ox4 (alert and oriented to person, place, time, and situation) and denies losing responsiveness or being submerged in the river.

  20. Case Study: When Heat Stress Hits an Entire Group

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  21. New study raises questions about niacin and heart health

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  22. Heat Stroke

    Introduction Heat-related illness is a spectrum of conditions progressing from heat exhaustion, heat injury, to life-threatening heat stroke. Heat stroke is a clinical constellation of symptoms that include a severe elevation in body temperature which typically, but not always, is greater than 40°C.

  23. MSN

    MSN

  24. Heat stroke with bimodal rhabdomyolysis: a case report and review of

    Background Severe heat stroke tends to be complicated with rhabdomyolysis, especially in patients with exertional heat stroke. Rhabdomyolysis usually occurs in the acute phase of heat stroke. We herein report a case of heat stroke in a patient who experienced bimodal rhabdomyolysis in the acute and recovery phases. Case presentation