Electronic ISSN 2287-0237

VOLUME

HYPOTHERMIA AFTER COOLING THERAPY IN EXERTIONAL HEAT STROKE: A CASE STUDY

SEPTEMBER 2018 - VOL.14 | CASE REPORT

Since the beginning of the 21st century, global temperatures have risenand are predicted to rise even higher.1 Heat reduces worker’sproductivity and affects body thermoregulation and homeostasis. Thehypothalamic thermoregulatory center and peripheral heat receptors areactivated when body temperature reaches 37ºC.2,3 Inadequate body responsecauses inflammation in heat-related illness which occurs as a spectrum fromheat edema, heat cramp, heat syncope, heat exhaustion to heat stroke.4-7Clinical outcome depends on environmental conditions, physical activitiesand individual biological factors. The environmental component includesclimate, geographic and socio-economic factors. Individuals who aremotivated and perhaps fear losing their job might do strenuous physicalactivities beyond their heat tolerance.3,8 Physical exertion produces moreheat while protective clothing and equipment may worsen the condition.9Moreover, medical or mental conditions, youth, aging, pregnancy, takingdrugs or some medications, history of previous heat illness and heatacclimatization may influence the variation of heat response.7,10,11

Heat illness usually starts with a mild outcome such as heat edema orheat cramp. If left untreated, it may in turn become more critical such asheat stroke and heat exhaustion. Hyperthermia directly damages cells andreduces oxidative phosphorylation in cellular production of energy.2,3 Patientsmay present with multi-organ failure, disseminated intravascular coagulationor even death. Heat stroke is diagnosed when a patient presents with a coretemperature higher than 40ºC and significant neurological deficit such ascoma, delirium or convulsion.3,12 Exposure to high temperatures in theenvironment may cause classic heat stroke (CHE) while strenuous exercisewith pathologic hyperthermia may cause exertional heat stroke (EHS).13Absence of central nervous involvement and lower core temperature makeheat exhaustion differ from heat stroke.14 To reduce body temperature, removing the patient out of the heat and rapid cooling shouldbe managed.10 A target temperature near 38ºC for evaporativecooling and 39ºC for immersion cooling were seen in themajority of studies.15 Hypothermia from overcooling maylead to life-threatening cardiac arrhythmia.15 When rewarminga patient with high-grade hypothermia, core temperatureafterdrop can be one of its complications.16 It is described asfurther drop of core body temperature after removing thepatient from a cold environment.17 This case demonstrated anEHS patient with iatrogenic hypothermia, which should be ofconcern in both emergency and delivery medical care.Furthermore, core temperature afterdrop was also observedduring management of his hypothermia.

A 33-year-old male ranger was admitted to a 90-bed districthospital with unconsciousness and general tonic-clonic seizure.He had been fatigued and nauseated during his first few daysof an advanced military training course. He felt too unwell totake food or drink during the strenuous training. At the districthospital, his medical record showed axillary temperature of42ºC, blood pressure of 60/40 mmHg, and pulse rate at 160beats per minute. Endotracheal intubation, volume resuscitationwith 2 liters of room temperature normal saline, Foley’scatheter and continuous inotrope (epinephrine) were provided.The seizure was controlled with medications (diazepam andphenytoin). Intravenous glucose was also given due tohypoglycemia of 59 mg/dL. He was then referred to a tertiaryhospital. Documentation showed that his axillary temperaturewas 34.2ºC when leaving the district hospital. During 1-hourtransportation, he was laid down on a plastic sheet, surroundedwith ice cubes and water without core temperature monitoring.

At an emergency room of a tertiary hospital, his bloodpressure was 110/60 mmHg. Glasgow Coma Score wasE1VTM1. Ten minutes later, he was transferred to an intensivecare unit (ICU) where his esophageal temperature measurementwas 29ºC. Heat stroke with iatrogenic hypothermia andhypovolemic shock was diagnosed. Medical electric blanketwas applied to keep temperature above 36ºC. His lowesttemperature during rewarming was 28ºC. Figure 1 shows hisbody temperature. During the first two days, his coretemperature and central blood pressure were measured. Initialelectrocardiogram (EKG) showed junctional rhythm with Jwave between QRS complex and ST segment (Osborn wave).Continuous monitoring of cardiac wave showed no adverseevent and the wave became regular sinus rhythm after rewarming.No evidence of intracranial hemorrhage, recent infarction orherniation in brain tomography. Table 1 demonstrates hislaboratory findings during treatment. On the first day, theinvestigations showed metabolic acidosis with respiratoryalkalosis, hypokalemia, hypophosphatemia, rhabdomyolysis,pre-renal azotemia, and elevated liver transaminases.Intravenous fluid was administered and electrolyte imbalancewas corrected. He gained consciousness with stable vital signson the second day of admission. The inotrope was discontinuedand extubation was performed.

Hyperthermia, thrombocytopenia with normal fibrinogenlevel developed on day 2. Empirical antibiotic (ceftriaxone)was given. Septic workup showed a positive hemoculture forEnterococcus faecalis. Neurological deficit was assessed onday 6. Only weakness of right nasolabial fold remainedwithout swallowing difficulty. Cerebellar signs were intact.Thai Mental State Examination (MSE) was normal (score25/30). He was sent to a community hospital in his hometownto complete the treatment for infection.

Figure 1: Fluctuation of temperature in this case.

 

Table 1: Laboratory data of the patient

This young and healthy man with hyperthermia and lossof consciousness after extreme outdoor training is a typicalpresentation of EHS.3 He was experiencing severe dehydrationthat led to hypovolemic shock and hyponatremia. Environmentaland physical predisposing factors in the case were advancedmilitary training, tropical ambient environment, thick greyoutfits and inadequate rehydration. One to two liters of sweatper hour or 15 liters per day could be lost during strenuoustraining.2,3 Dehydration burdens the heart, increases work ofsodium-potassium adenosine pump in cellular metabolism andlowers the heat transport.3,18 Heat distribution to capillarynetwork of skin is served by splanchnic vasoconstriction andcutaneous vasodilatation.2,3 Heat destroys megakaryocyte anddecreases platelet levels. Splanchnic hypoperfusion andischemia from heat injury usually present with nausea andvomiting.18 Permeability of intestinal mucosa increases afterheat damage.2 Translocation of gastrointestinal bacteria andendotoxin to systemic circulation led to E. faecalis septicemiaand systemic inflammatory response syndrome (SIR).3 Elevationof hepatic aminotransferases demonstrates typical hepaticinjury in heatstroke.18 This impairs gluconeogenesis andinduces hypoglycemia.18 Abnormal CPK and creatinine fromrhabdomyolysis and acute renal failure are mainly found inEHS rather than CHS.18 Amphetamine did not involve therhabdomyolysis in this case. Rhabdomyolysis usually presentswith hyperkalemia and hyperphosphatemia. However, a reportshowed 8 out of 24 military heat injury cases with rhabdomyolysishad hypokalemia.19 Hypophosphatemia can be associated withsevere heat exhaustion.20 Metabolic acidosis and respiratoryalkalosis were found in heat injury.19 Alkalinisation mayincrease activity of pH-sensitive phosphofructokinase whichenhances cellular uptake of phosphorous.21

Temperature was not measured on arrival at the emergencydepartment of the tertiary hospital because oral temperature isnot accurately correlated to core temperature.22 Instead,esophageal temperature probe was placed in the ICU. Thispatient encountered both hyperthermia and hypothermia.Most studies successfully used temperature below 39ºCfor termination of ice immersion in heat injury to avoidhypothermia.13,15,23 The patient’s axillary temperature beforeleaving the first hospital was already under the usual targettemperature. Cooling with 2ºC water cooling can reduce corebody temperature by 0.35ºC per minute.24 Using this methodduring long distance transportation caused hypothermia.

Hypothermia in this patient was moderately severe (mild =32.2-35.1ºC , moderate = 28.1-32.1ºC, severe = less than 28.1ºC ).16Osborn wave in the EKG is a diagnostic pattern when bodytemperature reaches below 32ºC.25 Risk of atrial fibrillation andcardiac arrest is increased.16,25 Rewarming is indicated in thiscase.25 His temperature shows core temperature afterdrop from 29 ºC to 28ºC in the first hour of rewarming. This phenomenonoccurs from convection and conduction heat loss from increasedblood flow form core to peripheral region during rewarming.17It disappears after the balancing of core and peripheraltemperature.25 A case has been reported with no complicationafter termination of cooling.26

Neurological deficit after treatment was mild in this case.Recently, successful therapeutic hypothermia of 33ºC innon-response heat stroke patients has been reported.27,28Neurological benefit after therapeutic hypothermia has alsobeen shown in cardiac arrest patients.29 No exact mechanismmay describe the weakness of right nasolabial area. A studyshowed that incidence of Bell’s palsy in the American armywas significantly higher in waterless regions.30

Concern with risk factors, early detection, cooling methods,management pitfalls and return to duty program are essentialin primary, secondary and tertiary prevention of exertionalheat injury (EHI).24,31 This patient should have 2 weeks ofwork restriction, at least 1 month of physical training and atleast 1 month of gradual acclimatization.31 However, return tothe military training is not possible in this case. His work planwas uncertain. Brief advice was given for return to work plan.Evaluation tests on heat tolerance would be recommended ifhe continued his military service.8,31,32

Occupational EHS is preventable. Workplaces with heatsources should measure and assess occupational heat stress.Health and safety controls can reduce modifiable risk factorsin metabolic heat production and heat exchange.32 Airventilation, insulation and air conditioning equipment can beused in engineering control.32 Administrative control mayinclude work/rest schedules and acclimatization.32 Medicalmonitoring programs before and during employment shouldbe established.32 Health and safety training for workers shouldaim to teach effective self-preparedness such as properrehydration and early recognition of symptoms.32 Supervisorsshould be able to monitor weather warnings.32 Workplaceheat alert programs are recommended for emergencypreparedness.32

This case report demonstrates the EHS patient withmultiple organ dysfunction and overcorrection of core bodytemperature. Continuous application ice cubes and water whiletransfer for prolonged period of more than 1 hour has put thepatient at risk of hypothermia. The typical Osborn wave in theEKG was also reported. To prevent the sequelae of hypothermia,we recommended that the patient’ core temperature duringcooling method should be monitored closely not only in thehospital but also in the transfer vehicle. It is of note that thetransfer of EHS patients from one medical facility to anothershould become a national issue for emergency medical service,especially in the vicinity of military camps.

In conclusion, preparedness and training for emergencyresponse, safety during transfer are necessary for both highrisk workplaces and the medical settings in charge in order toprevent and control of heat stroke and its fatal consequences.