Hypothermia and hyperthermia
How cold and hot patients are recognised and treated in emergency care, from J waves and rewarming rules to heat stroke cooling and drug-induced hyperthermia.
- Hypothermia is a core temperature below 35°C. Heat stroke is a core temperature above 40°C (more specifically 40.5°C in exertional heat stroke) together with central nervous system dysfunction. Heat exhaustion is the milder, self-limited form. [1]
- In hypothermia, severity is classified by core temperature: mild 35 to 32°C, moderate 32 to 28°C, severe below 28°C. Mortality is driven by arrhythmia, not by the number on the thermometer. [2]
- ECGs in hypothermia show slow conduction: prolonged RR, PR and QRS intervals, QTc prolongation and, in many patients, Osborn (J) waves. These are best seen in leads V2 to V5 and are most marked below 32°C. [2]
- Cardiac arrest in hypothermia is treated as "not dead until warm and dead": continue resuscitation during rewarming, because the cold brain is protected. Do not stop because of a low end-tidal CO2 below 10 mmHg. [2]
- Heat stroke is a cooling emergency: immerse in cold water at 5 to 15°C and continue until the rectal temperature is below 39°C. Cool first, transport second. [3]
- Fever is a raised hypothalamic set point (pyrogens); hyperthermia is failure of heat dissipation (or excess heat production) with a normal set point. Antipyretics help fever, not hyperthermia.
- Four drug syndromes cause dangerous hyperthermia: malignant hyperthermia (anaesthetics), neuroleptic malignant syndrome (antipsychotics), serotonin syndrome (serotonergic drugs) and anticholinergic toxicity. Each has a different trigger, onset and antidote.
By the end of this page you should be able to:
- Define hypothermia and heat stroke, and stage hypothermia by core temperature.
- Describe the causes and risk factors of both, including why secondary hypothermia is common in hospital.
- Recognise the ECG signature of hypothermia and the cardiac arrest rules.
- Plan rewarming by severity, and treat cold injuries.
- Recognise and treat heat exhaustion and heat stroke, including ice-water immersion.
- Tell the four hyperthermic drug syndromes apart by trigger, onset, features and treatment.
- Distinguish fever from hyperthermia and explain why antipyretics differ between them.
DefinitionHypothermia
Accidental hypothermia is an unintentional fall in core body temperature below 35°C from environmental exposure, impaired thermoregulation or secondary medical conditions, rather than clinically induced therapeutic hypothermia.[1] It is primary when cold exposure is the cause and secondary when acute illness, endocrine or metabolic disease, neurological impairment or drugs disrupt temperature control.[1]
DefinitionHeat-related illness
Exertional heat stroke is an emergency defined by exercise-induced hyperthermia, generally a core body temperature of 40.5°C or above, with central nervous system dysfunction such as confusion, aggressiveness, delirium or altered consciousness.[3] Heat exhaustion is the milder form: the inability to continue exertion from cardiovascular insufficiency, hypotension, energy depletion and central fatigue; its prognosis is benign.[3]
Core temperature cut-offs are the backbone of classification, because signs and treatment follow them.
| Severity | Core temperature | Typical clinical picture |
|---|---|---|
| Mild | 32 to 35°C | Shivering, confusion, tachycardia |
| Moderate | 28 to 32°C | Lethargy, bradycardia or other arrhythmia, decreased or absent pupillary reflexes, decreased or absent shivering |
| Severe | below 28°C | Coma, hypotension, arrhythmia, pulmonary oedema, rigidity |
United States
In the United States, in 2022 the age-adjusted death rate for hypothermia was 0.92 per 100,000, roughly double the 0.44 per 100,000 reported in 1999; in 2021 the comparable figure for heat-related deaths was 0.4 per 100,000.[2]
Primary hypothermia from exposure can occur in any climate and in any season; fatal heat stroke is rare but feared. The global figures that matter are the mortality ranges in hospitalised patients. Across the five studies in one recent systematic review of accidental hypothermia in hospitalised adults, in-hospital mortality ranged from 13% to 26%, with trauma patients at particularly high risk, with an odds ratio of about 5.18 compared with normothermic trauma patients.[1] In a multicentre Japanese registry of 1,194 adults with core temperatures of 35°C or less, 30-day mortality was 24.5%.[1] In 241 adults in northern Finland, 30-day survival was 85%.[1] In 358 adults with core temperatures of 32°C or below, in-hospital mortality was 26.3%.[1]
Hypothermia in hospital is usually secondary rather than primary, and usually preventable. Secondary causes include acute medical illness (especially sepsis), endocrine or metabolic disease (hypothyroidism, adrenal insufficiency), neurological impairment, and drugs that blunt thermoregulation such as sedatives and alcohol.[1] The groups at highest risk are older adults (65 to 75 years and above), men, people with alcohol misuse, reduced independence in the activities of daily living, and people with neurological or endocrine comorbidity.[1] Iatrogenic factors matter: cool procedure rooms, unwarmed intravenous fluids and inadequate thermal insulation all strip heat from a patient.[1]
Heat stroke occurs when the body cannot dissipate metabolic and environmental heat. Exertional heat stroke classically arises in fit athletes during intense effort in heat and humidity, but it also affects unacclimatised workers and older adults. Heat exhaustion, defined above, is more common and benign.[3] Risk rises with dehydration, excess motivation, high ambient temperature, humidity, solar radiation and lack of wind.[3]
Temperature-dependent enzymes slow first. Then myocardial conduction becomes unstable: the impulse travels slowly through cardiac tissue, producing prolonged RR, PR and QRS intervals and QTc prolongation, with Osborn (J) waves in many patients.[2] Coagulation, immunity and drug metabolism are all impaired. Even modest cooling raises arrhythmic risk, and severe hypothermia brings hemodynamic instability, metabolic acidosis, hyperkalaemia from cell lysis and neurological compromise.[1][2]
Wet clothing and handling matter beyond the numbers. Hypothermic hearts are irritable: rough movement during extrication can trigger fatal arrhythmia, a phenomenon called rescue collapse.[2] Removing wet clothing gently is therefore not optional.
When the heart arrests in the cold there is time, because hypothermia has neuroprotective effects; complete neurological recovery has been reported despite prolonged resuscitation lasting hours.[2]
In exertional heat stroke, hyperthermia of generally 40.5°C or above is accompanied by central nervous system dysfunction, and can be lethal if rapid on-site cooling is not provided before hospital transport.[3] The mechanism is not a reset thermostat but a heat load that overwhelms dissipation; muscle breakdown, rhabdomyolysis, acute kidney injury and multi-organ dysfunction follow.
Fever is a raised hypothalamic set point driven by pyrogens; antipyretics lower it and it serves a defensive role. Hyperthermia is an uncontrolled rise in body temperature with a normal set point, caused by failure of heat dissipation or excess heat production, as in heat stroke, malignant hyperthermia, neuroleptic malignant syndrome and serotonin syndrome. Antipyretics act on the hypothalamic set point and do not control hyperthermia that arises from muscular heat production; this is why antipyretics are ineffective in these syndromes.[4]
The symptoms scale with severity, and it is worth learning the table above alongside the physical signs.
- Mild (35 to 32°C): shivering, confusion, tachycardia.[2]
- Moderate (32 to 28°C): lethargy, bradycardia or other arrhythmia, decreased or absent pupillary reflexes, decreased or absent shivering.[2]
- Severe (below 28°C): coma, hypotension, arrhythmia, pulmonary oedema, rigidity.[2]
A well-described trap is that outcomes have not correlated with the initial core temperature. Instead, prognosis is driven by the development of a life-threatening arrhythmia or bradycardia.[2]
Cold injuries deserve a mention: frostbite, chilblains and trench foot. Rewarming of frostbitten tissue is most effective by immersing the area in water heated to 37 to 39°C, with appropriate analgesia; tissue plasminogen activator with heparin has been used when there are no contraindications and presentation is within 24 hours of injury, because of vascular thrombosis in frostbitten areas.[2] Prophylactic antibiotics are controversial; treat proven infection.[2]
Heat exhaustion presents with the inability to continue exertion: cardiovascular insufficiency, hypotension, energy depletion and central fatigue.[3] Body temperature may be raised but is not the defining feature, and the condition responds to rest, cooling and rehydration.[3]
Heat stroke is defined by hyperthermia with central nervous system dysfunction: disorientation, confusion, aggressiveness, hysteria, delirium, altered consciousness or irrational behaviour.[3] Common presentations include collapse, irritability, seizures, dehydration, vomiting, dizziness, fatigue and weakness.[3] Exertional heat stroke is defined by exercise-induced hyperthermia, generally a core body temperature of 40.5°C or above.[3] While a rectal temperature above 40°C has previously been used as diagnostic criteria, several authors have identified that 40.5°C may be more specific for the diagnosis.[3]
In hypothermia, obtain an accurate core (rectal) temperature and an ECG early, and handle the patient gently.[2] In heat stroke, rectal temperature is the only valid and practical measure of core temperature in the prehospital setting, and the probe should be inserted at least 10 cm.[3]
Hypothermia produces recognisable and specific ECG patterns.[2]
- Intervals: slow conduction prolongs RR, PR, QRS and QTc.[2]
- Osborn (J) waves: J-point elevation from disturbances in membrane repolarisation. Best seen in the precordial leads V2 to V5, they are more marked as temperature falls and are typically appreciated in patients with core temperatures below 32°C.[2]
- Mechanism quoted in sources: increased outward potassium current, or transmural voltage-gradient differences between epicardium and endocardium; sources disagree on both the typical leads and on whether Osborn waves predict mortality.[2]
- QTc prolongation is commonly seen, sometimes with otherwise normal sinus rhythm.[2]
Arrhythmias range from sinus bradycardia through atrial fibrillation to ventricular fibrillation. Cardiac irritability rises as temperature falls, so all procedures are done gently; nevertheless, lifesaving interventions must not be withheld.[2]
- Core temperature: rectal, for both hypo- and hyperthermia; tympanic or axillary measurements are not reliable enough for decisions.[2][3]
- ECG in hypothermia: look for the interval and J-wave changes above.[2]
- Bloods in hypothermia: urea and electrolytes (hyperkalaemia), creatinine, creatine kinase, arterial blood gas, coagulation (fibrinogen), full blood count, glucose, and toxicology as indicated. Creatine kinase may be high from rhabdomyolysis.[2]
- In heat stroke: blood glucose and sodium (exclude exercise-associated hyponatraemia and hypoglycaemia), renal and liver function, creatine kinase, clotting.[3]
- Drug syndromes: see the diagnostic criteria for NMS in the table below and the Hunter criteria for serotonin syndrome (sensitivity 84%, specificity 97%).[4] Helpful investigations include creatine kinase (usually above 1000 international units/L in NMS), electrolytes, creatinine, blood cultures, brain imaging and lumbar puncture when infection or structure is possible.[4]
These rules are worth knowing verbatim.
- Do not stop resuscitation because of low end-tidal CO2 below 10 mmHg; this may reflect the diminished metabolic rate rather than poor perfusion.[2]
- Hyperkalaemia: cell lysis produces profound hyperkalaemia. Survival with serum potassium of 12 mEq/L or more has not been reported; some reports use 8 mEq/L as a cut-off to discontinue resuscitation.[2]
- Other poor prognostic markers: fibrinogen below 50 mg/dL, ammonia above 420 mcg/dL, elevated lactate, sodium or creatinine.[2]
- "Not dead until warm and dead": hypothermic cardiac arrest can have complete neurological recovery after prolonged resuscitation, so continue Advanced Cardiac Life Support during rewarming. Extracorporeal life support may be needed in severe hypothermia.[2][1]
- Rescue collapse: warn the team that movement of a severely hypothermic patient can precipitate arrest.[2]
The method of rewarming follows the severity of hypothermia.
| Technique | When to use | How and goal |
|---|---|---|
| Passive external rewarming | Mild hypothermia | Blankets or other insulation, warm environment around 28°C; goal 0.5 to 2°C per hour [2] |
| Active external rewarming | Moderate to severe, or mild not responding | Warm blankets, heating pads, warm baths, forced warm air; goal at least 2°C per hour [2] |
| Active internal rewarming | Core temperature below 28°C, or moderate not responding | Warm intravenous fluids, endovascular temperature-control catheters, peritoneal or thoracic lavage; goal 2 to 3°C per hour; venous rewarming raises temperature by 3 to 4°C per hour; cardiopulmonary bypass by up to 9.5°C per hour; ECMO in severe [2] |
Practical points:
- Start by removing the patient from the cold and from wet clothing, gently.[2]
- Rewarming shock is a real hazard: surface rewarming can cause peripheral vasodilatation and hypotension. If blood pressure falls, remove the active surface warmer, keep warmth on the torso and give warmed intravenous fluids.[2]
- Wet blankets over trunk only is safer than warming the whole body surface in moderate disease; follow local practice.[2]
- Active internal rewarming, including extracorporeal membrane oxygenation, can raise temperature much faster but needs the right team and equipment.[2][1]
- Slower rewarming with extracorporeal life support has been associated with better survival and neurological outcomes in historical guidance.[2]
- Cardiac arrest with hypothermia: continue CPR during rewarming and consider direct transport to a centre with extracorporeal rewarming.[2]
Rest, remove from heat, cool (shade, fans, cool cloths), replace fluid and salt, and observe. Most patients recover without hospital stay.[3]
This is a cooling emergency, not a transfer emergency.
| Step | Detail |
|---|---|
| Recognise | Collapse or CNS dysfunction in the heat; rectal temperature above 40°C, more specifically 40.5°C |
| Cool first | Whole-body cold water immersion at 5 to 15°C until rectal temperature is below 39°C |
| Monitor | Rectal temperature continuously during immersion; do not estimate the cooling rate from the starting temperature |
| Observe | Maintain below 39°C for at least 15 minutes after cooling [3] |
| Adjuncts | Rule out exercise-associated hyponatraemia and hypoglycaemia if it does not interrupt cooling |
| Transport | Only after cooling; hospital evaluation for muscle, kidney and liver damage |
Important details:
- Whole-body cold water immersion is the treatment of choice when available and has been associated with survival when delivered rapidly.[3]
- Water temperature should be 5 to 15°C with enough volume to submerge as much body surface area as possible, prioritising the torso.[3]
- Ice-water towels exchanged every 1 to 2 minutes can be used when a tub is not available.[3]
- "Cool first, transport second": every athlete diagnosed with exertional heat stroke must be cooled before transfer.[3]
- A feared complication is rebound hyperthermia: if the core temperature starts to rise again after removal, return to cooling.[3]
- If the core temperature drops rapidly towards 36°C after removal, dry the patient, remove wet clothing and insulate until transfer.[3]
- Antipyretics are not used, because heat stroke is not fever.[4]
The four main syndromes differ by trigger, time course and treatment. The table compares them on the features that decide management at the bedside.
| Syndrome | Trigger | Onset | Key features | First-line treatment |
|---|---|---|---|---|
| Malignant hyperthermia | Inhalational anaesthetics (for example sevoflurane, isoflurane) or succinylcholine in a susceptible person | During operation or in the first hour after anaesthesia ends | Hypermetabolic crisis, marked hyperthermia, muscle rigidity, tachycardia, raised end-tidal carbon dioxide | Dantrolene (2.5 mg/kg intravenously initially, then 1 to 2.5 mg/kg every 5 minutes; maintain with 1 mg/kg every 4 to 6 hours), plus cooling [4] |
| Neuroleptic malignant syndrome | Antipsychotics (high-potency agents such as haloperidol most often) | Most often within the first month of treatment | Hyperthermia (often above 40°C), lead-pipe rigidity, delirium, autonomic instability (tachycardia, labile blood pressure, sweating) | Stop the antipsychotic; supportive care; benzodiazepines; dantrolene 1 to 2.5 mg/kg intravenously every 6 to 8 hours (maximum 10 mg/kg/day); bromocriptine 2.5 mg orally every 8 hours, titrating to 5 to 10 mg every 6 to 8 hours [4] |
| Serotonin syndrome | Serotonergic drugs and their interactions | Within 24 hours of exposure or dose change | Triad: mental status change, autonomic instability (tachycardia, fever, sweating, mydriasis), neuromuscular hyperactivity (hyperreflexia, clonus, tremor) | Stop serotonergic agents; benzodiazepines; cyproheptadine 12 mg loading, then 4 to 8 mg every 6 hours (maximum 32 mg in 24 hours) [4] |
| Anticholinergic toxicity | Drugs with anticholinergic activity | Usually hours after exposure | Hot, dry flushed skin, dry mouth, mydriasis, tachycardia, urinary retention, ileus, delirium and hallucinations | Stop the offending drug; supportive care; benzodiazepines for agitation; physostigmine 0.5 to 2 mg intravenously slowly over 5 minutes in severe cases [4] |
Additional points from the literature:
- Malignant hyperthermia affects 1 in 100,000 anaesthetics, is more common in males by 2 to 1 and occurs in children in about half of reported cases; central core myopathy also carries susceptibility.[4]
- Neuroleptic malignant syndrome has an incidence between 0.2% and 3% among antipsychotic users. It more often occurs within the first month of therapy, with risk from rapid dose escalation, parenteral administration, dehydration, restraint and elevated ambient temperature.[4] Creatine kinase is usually above 1000 international units/L and reflects severity. Mortality is 3% to 38% if not recognised early.[4]
- Antipyretics are ineffective in neuroleptic malignant syndrome, malignant hyperthermia and serotonin syndrome because the hyperthermia comes from muscular or metabolic activity rather than a raised hypothalamic set point, and the heat is not lowered by agents that target the set point.[4]
- Serotonin syndrome usually resolves within 24 hours of stopping the drug, while neuroleptic malignant syndrome usually resolves in 1 to 2 weeks, and longer after long-acting depot injections.[4]
- Hyperthermia above 41.1°C in serotonin syndrome warrants immediate sedation, non-depolarising neuromuscular paralysis, intubation and active cooling.[4]
- Benzodiazepines are the sedative backbone in all four: lorazepam 1 to 2 mg intravenously or diazepam 5 to 10 mg intravenously in the source review's table of hyperthermic-rigid syndromes.[4]
- In neuroleptic malignant syndrome, dantrolene acts on muscle calcium release and may be combined with bromocriptine, a dopamine agonist; amantadine is an alternative dopaminergic agent.[4] Whether these improve outcome is contested and based on case series.[4]
- In serotonin syndrome, cyproheptadine is the specific serotonin antagonist, and antipsychotics and bromocriptine are not recommended because they may worsen the picture.[4]
- In anticholinergic toxicity, physostigmine (0.5 to 2 mg intravenously over 5 minutes) reverses central anticholinergic effects where indicated; benzodiazepines cover agitation and seizures.[4]
The flow below is a teaching approach, not a substitute for local guidance and senior support.
The patient with a high temperature
- High temperature recordedConfirm core temperature: rectal for heat stroke or collapse; treat the patient, not only the number
- Immediate safetyAirway, breathing, circulation; remove from heat; remove wet clothing; start cooling if hypothermic or hyperthermic
- Question: Is the temperature 40°C or above with confusion, collapse or seizure?
Yes
- Heat stroke until proven otherwiseCool first, transport second: cold water immersion 5 to 15°C until rectal temperature below 39°C
- Continue monitoringKeep below 39°C for at least 15 minutes; reassess for rebound
No
- Question: Evidence of drug exposure or recent anaesthesia?
Yes
- Consider malignant hyperthermia, neuroleptic malignant syndrome, serotonin syndrome or anticholinergic toxicityStop the offending agent; give the specific antidote from the table; supportive care and active cooling
No
- Question: Exertion in heat with heavy sweating and fatigue but no confusion?
Yes
- Heat exhaustionRest, oral or intravenous rehydration, cooling, observation
No
- Fever or other causeSearch for infection, inflammation or malignancy; antipyretics may help fever; investigate as for pyrexia
- Hypothermia: arrhythmias, coagulopathy, rhabdomyolysis, acute kidney injury, infection and prolonged stay; the lethal triad of hypothermia, acidosis and coagulopathy in trauma.[1][2]
- Heat stroke: rhabdomyolysis, acute kidney and liver injury, disseminated intravascular coagulation and neurological damage, especially if cooling is delayed.[3][4]
- Drug syndromes: seizures, rhabdomyolysis, renal and respiratory failure, disseminated intravascular coagulation, arrhythmias.[4]
Prognosis in hypothermia is driven by arrhythmia and comorbidity, not by the initial temperature.[2] Hospital mortality is 13% to 26% in reported series, higher after trauma.[1] Heat stroke still carries significant morbidity but survival is excellent when rapid whole-body cooling is applied within minutes of collapse.[3] Neuroleptic malignant syndrome carries mortality of 3% to 38% if not recognised; serotonin syndrome and malignant hyperthermia are life threatening but usually reversible if treated promptly.[4]
- Keep vulnerable inpatients warm: avoid unnecessary exposure, warm intravenous and irrigation fluids, use forced-air or warmed blankets perioperatively.[1]
- Plan for heat at mass-participation events: heat deck, ice water, rectal thermometers, and four trained providers per patient.[3]
- Prescribe antipsychotics cautiously: start low, titrate slowly, avoid dehydration and restraints, and screen for prior neuroleptic malignant syndrome.[4]
- Remember serotonergic interactions when adding new drugs to a patient on antidepressants.[4]
- Older adults are the commonest group to develop secondary hypothermia in hospital and to fare badly; they need the slow, careful rewarming described above.[1][2]
- Children account for about half of reported malignant hyperthermia events, and central core myopathy carries added risk.[4]
- Athletes are the population in whom exertional heat stroke is best studied; the cooling protocols come from sport.[3]
- A rectal thermometer and a cold water bath with ice are the two tools that change survival in heat stroke. Interrupting cooling to achieve intravenous access is not worth it.[3]
- In hypothermia, passive and active external rewarming, pulse oximetry, an ECG and warmed intravenous fluids are realistic anywhere; extracorporeal rewarming needs transfer.
- Antipyretics remain useful for fever but should not be relied on for heat stroke or drug-induced hyperthermia.[4]
- Hypothermia is a core temperature below 35°C; mild 35 to 32°C, moderate 32 to 28°C, severe below 28°C.[1][2]
- Secondary hypothermia from acute illness, endocrine disease, neurological impairment or drugs is common in hospital and often preventable.[1]
- The ECG in hypothermia shows slowed conduction and Osborn (J) waves, best in V2 to V5, usually below 32°C.[2]
- Cardiac arrest from cold: continue resuscitation during rewarming, do not stop for low end-tidal CO2 below 10 mmHg, and treat potassium of 12 mEq/L or more with caution.[2]
- Rewarm with passive external (0.5 to 2°C per hour), active external (at least 2°C per hour) or active internal (2 to 3°C per hour, faster with bypass) therapy matched to severity.[2]
- Frostbite is best rewarmed in water at 37 to 39°C.[2]
- Heat stroke is core temperature above 40°C with altered mental status and needs cold water immersion at 5 to 15°C until rectal temperature is below 39°C, then 15 minutes of observation.[3]
- Heat exhaustion has benign prognosis and responds to rest, cooling and rehydration.[3]
- Fever (raised hypothalamic set point, responds to antipyretics) differs from hyperthermia (normal set point, does not respond to antipyretics).[4]
- Malignant hyperthermia, neuroleptic malignant syndrome, serotonin syndrome and anticholinergic toxicity all raise temperature by different mechanisms; their treatments differ: dantrolene (malignant hyperthermia, neuroleptic malignant syndrome), bromocriptine (neuroleptic malignant syndrome), cyproheptadine (serotonin syndrome) and benzodiazepines for all.[4]
- Cool first, transport second applies to heat stroke.[3]
Answer each one in your head first, then open the answer.
A 78-year-old man is found confused on the floor of a cold ward. Core temperature is 33°C. What does his temperature stage mean, and what is the preferred first rewarming strategy?
Show answerHide answer
A 24-year-old collapse runner is unresponsive after a half-marathon in 34°C heat. Rectal temperature is 41.2°C. What is the diagnosis and the immediate action?
An unconscious 43-year-old woman has a temperature of 28.3°C. Her arterial blood gas shows potassium 11.0 mEq/L. Should resuscitation be stopped?
Show answerHide answer
No. Survival with potassium of 12 mEq/L or more has not been reported, but 11 mEq/L does not meet that reported cut-off; continue Advanced Cardiac Life Support during rewarming and treat severe hyperkalaemia per local protocols. Low end-tidal CO2 below 10 mmHg alone would also not justify stopping.[2]
A 50-year-old man on haloperidol develops fever of 40.5°C, lead-pipe rigidity and tachycardia three weeks after starting treatment. Which syndrome is this, and what antidote is used if benzodiazepines are not enough?
Show answerHide answer
Neuroleptic malignant syndrome, most often in the first month of antipsychotic therapy.[4] Dantrolene (1 to 2.5 mg/kg every 6 to 8 hours, maximum 10 mg/kg/day) and bromocriptine (starting 2.5 mg every 8 hours, titrating to 5 to 10 mg every 6 to 8 hours) are the specific agents discussed, alongside supportive care and stopping the drug.[4]
A 30-year-old with severe depression starts a selective serotonin reuptake inhibitor and later takes dextromethorphan for a cough. She becomes agitated with fever, hyperreflexia and bilateral ankle clonus. Her temperature is 40.0°C. Which antidote is specific to this condition, and which agents should be avoided?
Why are antipyretics ineffective in neuroleptic malignant syndrome and heat stroke?
Show answerHide answer
Because the fever in these conditions arises from muscular or metabolic heat production, not from a raised hypothalamic temperature set point.[4] Antipyretics act on the set point and do not reduce that peripheral heat production.
A 22-year-old develops a cardiac arrest after induction of anaesthesia with sevoflurane and succinylcholine. What syndrome does this fit, and what is the specific antidote?
- Cardiac arrest and cardiopulmonary resuscitation in the emergency department
- ECG interpretation and arrhythmias
- Rhabdomyolysis and acute kidney injury
- Fever of unknown origin
- Frostbite and cold injuries
- Shock (distributive and hypovolaemic)
- Anaesthesia: malignant hyperthermia
- Waqas R, Kalsoom I, Qaiser Aziz Khan M, Shetty S, Suliman MGH, Kaur A, Khan SB, Ahmad B. Accidental Hypothermia in Hospitalized Adults: Risk Factors, Management Strategies, and Clinical Outcomes: A Systematic Review. Cureus 2026;18(2):e103205. doi:10.7759/cureus.103205. Accessed .
- Cullin S, Shah S. Hypothermia Complications and Associated Electrocardiogram (EKG) Findings. Cureus 2026;18(5):e108742. doi:10.7759/cureus.108742. Accessed .
- Hosokawa Y, Racinais S, Akama T, et al. Prehospital management of exertional heat stroke at sports competitions: International Olympic Committee Adverse Weather Impact Expert Working Group for the Olympic Games Tokyo 2020. Br J Sports Med 2021;55(24):1405–1410. doi:10.1136/bjsports-2020-103854. Accessed .
- Kelly DM, Kelleher EM. Acute Febrile Encephalopathy with Rigidity. J Intensive Care Med 2026;41(11):1053–1069. doi:10.1177/08850666251345448. Accessed .
Educational content for medical students and doctors. It is not a substitute for clinical judgement or local guidelines.