Temperature Monitoring & Regulation

Module 01 of 09 · Core

Thermoregulatory Physiology

The human body is a furnace with a sophisticated thermostat. Understanding the balance of heat production and loss is the foundation of perioperative temperature management.

Core Concept Humans are homeotherms — we maintain a nearly constant core temperature (~37°C) despite wide fluctuations in environmental temperature. This is achieved by a balance between heat production and heat loss, controlled by the hypothalamic thermostat.

Normal Body Temperature

Core Temperature

36.5–37.5

°C (97.7–99.5°F)

Oral

36.3–37.3

°C

Rectal

36.6–37.7

°C (0.3–0.5 higher than oral)

Axillary

35.8–36.8

°C (0.3–0.5 lower than oral)

Tympanic

36.5–37.5

°C (reflects core)

Oesophageal

36.5–37.5

°C (gold standard for core)

Pulmonary Artery

36.5–37.5

°C (true core)

Skin (mean)

33–35

°C (varies widely)

The Hypothalamic Thermostat

The preoptic area of the anterior hypothalamus is the primary thermoregulatory centre. It receives input from peripheral thermoreceptors (skin, deep tissues) and central thermoreceptors (spinal cord, viscera, hypothalamus itself), and orchestrates the response.

Anterior hypothalamus: Heat loss centre — activates when core temperature rises
Posterior hypothalamus: Heat conservation centre — activates when core temperature falls
Set point: The reference temperature (~37°C) around which the system defends
Interthreshold range: The range of temperatures between the thresholds for heat production and heat loss — normally ~0.4°C. Within this range, no thermoregulatory response occurs.
Gain: The intensity of the response per degree deviation from the threshold

Thermoregulatory Effector Responses

Response	Stimulus	Mechanism	Effect
Cutaneous vasoconstriction	Cold	Sympathetic α₁-adrenergic	Reduces convective heat loss from skin
Non-shivering thermogenesis	Cold (neonates, some adults)	Brown adipose tissue; uncoupling protein 1 (UCP1)	Increases heat production without shivering
Shivering	Cold	Skeletal muscle contraction; increased metabolic rate 2–5×	Increases heat production
Behavioural	Cold or heat	Voluntary actions — clothing, shelter, posture	Most important in daily life; abolished under anaesthesia
Cutaneous vasodilation	Heat	Sympathetic withdrawal; active vasodilation	Increases convective heat loss
Sweating	Heat	Sympathetic cholinergic	Evaporative heat loss (up to 1.5 L/h)
Panting / tachypnoea	Heat (animals)	Increased respiratory evaporative loss	Limited in humans

Heat Production

Basal metabolic rate (BMR): ~70 kcal/h in a 70 kg adult — the minimum heat production at rest
Muscular activity: Can increase heat production 10–20× during exercise
Shivering: Increases heat production 2–5×; can raise metabolic rate to 200–300% of BMR
Non-shivering thermogenesis: Brown adipose tissue; important in neonates and hibernating mammals
Specific dynamic action (SDA): Heat produced by digestion and metabolism of food
Fever: Cytokine-mediated increase in the hypothalamic set point → heat production and conservation
Thyroid hormones, catecholamines: Increase metabolic rate and heat production

Heat Loss

Heat is lost from the body via four mechanisms. Under normal conditions, the skin is the primary site (90%), with the respiratory tract accounting for ~10%.

Mechanism	Description	Percentage (rest)	Modifiers
Radiation	Transfer of heat via infrared radiation to cooler objects	~60%	Large surface area; cold environment; vasodilation
Convection	Heat transfer to air or water moving over the skin	~15%	Air currents; fans; water immersion (25× faster)
Conduction	Direct transfer to cooler surfaces in contact with skin	~3%	Cold operating table; ice packs; conductive mats
Evaporation	Insensible loss from skin and lungs; sweating	~22%	Sweating; dry air; tachypnoea; open wounds

✦ Clinical Pearl — The Cold OR The operating room is a hostile thermal environment: cold ambient temperature (18–21°C), high airflow, cold IV fluids, cold skin prep, and large exposed surface area. Under general anaesthesia, behavioural responses are abolished and thermoregulatory vasoconstriction is impaired — leading to rapid heat loss.

The Interthreshold Range

Normal: ~0.4°C — the range of core temperature within which no thermoregulatory effector response is activated
Under general anaesthesia: The interthreshold range widens dramatically (up to 4°C) — thermoregulation is impaired
Under regional anaesthesia: Interthreshold range widens to ~1–2°C; below the block, vasoconstriction and shivering are impaired
Neonates: Narrower interthreshold range; larger surface area to volume ratio; limited shivering ability
Elderly: Impaired thermoregulation; reduced shivering; delayed vasoconstriction
Drugs: Opioids, volatile anaesthetics, propofol, and muscle relaxants all widen the interthreshold range

Why Perioperative Thermoregulation Fails 1. Anaesthetic-induced impairment: Volatile agents, propofol, and opioids widen the interthreshold range and inhibit vasoconstriction and shivering. 2. Redistribution hypothermia: Core-to-periphery heat redistribution after induction. 3. Heat loss: Exposure, cold IV fluids, dry gases. 4. Reduced heat production: Muscle relaxation, decreased metabolic rate.

Fever — A Regulated Rise in Set Point

Fever is not the same as hyperthermia. Fever is a regulated rise in the hypothalamic set point, mediated by endogenous pyrogens (IL-1, IL-6, TNF-α) and prostaglandin E₂ (PGE₂) in the hypothalamus. The body actively defends the new, higher temperature.

Feature	Fever	Hyperthermia
Set point	Elevated	Normal
Body's defence	Actively defends higher temperature (shivering, vasoconstriction)	Attempts to dissipate heat (sweating, vasodilation)
Response to antipyretics	Effective	Ineffective
Examples	Infection, inflammation, malignancy	Heat stroke, malignant hyperthermia, NMS
Skin	Cool, vasoconstricted (early)	Hot, vasodilated, dry (late)

Key Point Antipyretics work in fever by lowering the elevated set point (inhibiting COX-2 → PGE₂). They are ineffective in hyperthermia where the set point is normal — cooling and treating the cause are required.

Fever vs Hyperthermia — The Critical Distinction

Fever: The body is actively heating — the patient may feel cold and shiver. Core temperature is defended at the new, higher set point. Skin may be cool and mottled.
Hyperthermia: The body is overheating — the patient feels hot, sweats profusely (early), and vasodilates. The set point is normal; the body is failing to dissipate heat.
Malignant hyperthermia: A pharmacogenetic hypermetabolic crisis triggered by volatile anaesthetics and succinylcholine. Core temperature rises rapidly (1–2°C every 5 min). It is a form of hyperthermia, not fever. Dantrolene is the specific antidote.
Neuroleptic malignant syndrome (NMS): A hyperthermic syndrome triggered by dopamine antagonists. It is a form of hyperthermia, not fever. Dantrolene may be used but is less effective; bromocriptine and supportive care are key.

Module 02 of 09 · Core

Temperature Measurement

Core, peripheral, and surrogate sites — the devices, the accuracy, and the pitfalls. What to use, when, and why it matters.

Core vs Peripheral Temperature

Core temperature: The temperature of the deep tissues — brain, heart, abdominal organs. It is the temperature that the hypothalamus defends and the one that matters for metabolic function.
Peripheral temperature: The temperature of the skin, subcutaneous tissue, and limbs. It is lower than core, varies with ambient temperature, and is subject to vasoconstriction.
Gradient: Normally 2–4°C between core and skin. The gradient widens with vasoconstriction (cold) and narrows with vasodilation (heat).
Clinical relevance: In shock and hypothermia, peripheral temperature falls before core — a widened core-peripheral gradient is a marker of poor perfusion.

Measurement Sites — Accuracy and Applicability

Site	Type	Accuracy	Lag	Clinical Use	Limitations
Pulmonary artery (PA)	Core	Gold standard	None	ICU, cardiac surgery; true core	Requires PAC; invasive; not for routine
Oesophageal	Core	Excellent	Minimal	Anaesthesia, cardiac surgery; reflects core if tip in lower third	Position-dependent; risk of malposition; contraindicated in oesophageal disease
Tympanic	Core (surrogate)	Good	Small	Routine clinical; reflects hypothalamic temperature	Operator-dependent; cerumen; otitis; perforation risk; infrared devices less accurate
Nasopharyngeal	Core (surrogate)	Good	Small	Anaesthesia; reflects brain temperature	Position-dependent; epistaxis; discomfort
Rectal	Core (surrogate)	Acceptable	Significant	Historical; paediatrics	Lag behind core; risk of perforation; contraindicated in neutropenia, rectal surgery
Bladder (urinary catheter)	Core (surrogate)	Good	Moderate	ICU, post-operative; convenient if catheter in situ	Requires adequate urine output; lag if low flow
Oral	Peripheral	Acceptable	Moderate	Ward; screening	Affected by hot/cold drinks, mouth breathing, tachypnoea
Axillary	Peripheral	Poor	Large	Neonates, children; screening	Underestimates core; affected by ambient; poor sensitivity
Skin (surface probe)	Peripheral	Poor	Large	Trending; gradient calculation	Not a measure of core; affected by ambient and vasoconstriction
Temporal artery (TA)	Surrogate	Variable	Minimal	Non-invasive screening	Affected by sweating, ambient, technique

Devices and Principles

Device	Principle	Sites	Notes
Thermistor	Resistance changes with temperature	PA, oesophageal, bladder, rectal	Most accurate; requires probe; reusable or disposable
Thermocouple	Voltage generated at junction of two dissimilar metals	Surface probes, needle probes	Fast response; less accurate than thermistor; reference junction needed
Infrared (IR) tympanic	Infrared emission from tympanic membrane	Tympanic	Quick, non-invasive; accuracy variable; operator-dependent
Infrared temporal artery	Infrared emission from temporal artery	Forehead	Non-invasive; affected by sweating, ambient; variable accuracy
Liquid crystal	Colour change with temperature	Skin	Continuous visual; poor accuracy; screening only
Chemical dot	Colour change	Oral, axillary	Single-use; screening only; poor accuracy
Zero-heat-flux	Insulated probe; heat flux zeroed	Forehead	Non-invasive; correlates well with core; useful for continuous monitoring

⚠ Accuracy Matters Not all thermometers are equal. Axillary and oral measurements can differ from core by 0.5–1.0°C. For clinical decisions — especially in perioperative and critical care — use a core site (PA, oesophageal, tympanic, nasopharyngeal, or bladder).

Choosing a Site — Practical Guidance

Setting	Preferred Site	Alternative
General anaesthesia (routine)	Oesophageal or nasopharyngeal	Tympanic, bladder
Cardiac surgery / CPB	PA, oesophageal, nasopharyngeal	Bladder, rectal
ICU (general)	Bladder (if catheter), PA (if PAC)	Oesophageal, rectal, tympanic
ICU (shock / hypothermia)	PA or oesophageal	Bladder (with caution if low urine output)
Ward (routine)	Tympanic	Oral
Neonates / children	Axillary (screening), oesophageal (intubated)	Rectal (historical), tympanic
Outpatient / screening	Oral, tympanic, temporal artery	Axillary

Monitoring During Anaesthesia — Standards

When to monitor: Any procedure with expected duration >30 minutes, any major surgery, any patient at risk of hypothermia or hyperthermia, all paediatric cases, all cardiac surgery, all patients receiving large fluid volumes or blood products.
Minimum frequency: Continuous or at least every 15 minutes. The AAGBI recommends continuous monitoring during anaesthesia.
Core site preferred: Oesophageal, nasopharyngeal, tympanic, or bladder — not axillary or skin alone.
Documentation: Record temperature at regular intervals, along with all warming interventions.
Alarms: Set upper and lower limits (e.g., 35.5–37.8°C) to alert the team.
Reference: AAGBI, ASA, and NICE guidelines all recommend temperature monitoring and active warming for procedures >30 minutes.

Special Considerations

Cardiac surgery with CPB: Multiple sites (PA, oesophageal, nasopharyngeal, bladder) to monitor core and gradient; temperature is manipulated (hypothermia and rewarming).
Neurosurgery: Core temperature directly affects cerebral metabolic rate and ICP; maintain normothermia (or mild hypothermia if indicated).
Paediatrics: High surface area to volume ratio; rapid heat loss; monitor closely; use forced-air warming and fluid warmers.
Burns: Loss of skin barrier; evaporative losses can be massive; monitor core temperature and warm aggressively.
Trauma: The "trauma triad" (hypothermia, acidosis, coagulopathy) — hypothermia is an independent predictor of mortality; warm all fluids, use external warming, and monitor core temperature.

✦ The Takeaway For accurate core temperature measurement, use a core site — oesophageal, nasopharyngeal, tympanic, bladder, or PA. Peripheral sites (oral, axillary) are acceptable for screening but not for clinical decisions. The choice of site depends on the setting, the patient, and the required accuracy.

Module 03 of 09 · Applied

Perioperative Temperature Changes

Why every surgical patient becomes hypothermic — and the consequences that follow. The three phases of perioperative hypothermia and the physiological insult.

The Three Phases of Perioperative Hypothermia

1 · Redistribution
Core → periphery

→

2 · Heat loss
Exceeds heat production

→

3 · Plateau
Vasoconstriction

Perioperative hypothermia develops in three distinct phases, each with different mechanisms and management implications.

Phase 1 — Redistribution (First 30–60 Minutes)

Mechanism: Anaesthetic-induced vasodilation and inhibition of tonic thermoregulatory vasoconstriction → core heat redistributes to the periphery
Result: Rapid fall in core temperature (0.5–1.5°C in the first hour)
Note: This is not heat loss to the environment — it is internal redistribution of heat
Prevention: Pre-warming (before induction) — increases peripheral tissue temperature, reducing the core-to-periphery gradient
Drugs: Propofol, volatile agents, opioids, and muscle relaxants all contribute
Magnitude: The larger the core-to-periphery gradient, the greater the redistribution

Phase 2 — Heat Loss (Hours 1–3)

Mechanism: Heat loss to the environment exceeds metabolic heat production
Contributors: Radiation (60%), convection (15%), conduction (3%), evaporation (22%)
Magnitude: Core temperature falls more slowly than Phase 1 (0.5–1.0°C per hour)
Result: Continued cooling until thermoregulatory vasoconstriction is triggered (at ~36.5°C in the anaesthetised patient)
Prevention: Forced-air warming, warm IV fluids, humidified gases, increased ambient temperature, insulation

Phase 3 — Plateau (After 2–4 Hours)

Mechanism: Core temperature reaches the vasoconstriction threshold → active vasoconstriction in the periphery reduces further heat loss
Result: Core temperature stabilises at a lower-than-normal level (typically 34.5–36.0°C) — the plateau
Note: The plateau is not normothermia — it is a new, lower steady state
Risk: Patients remain hypothermic; shivering is inhibited by anaesthesia
Management: Continue active warming throughout surgery; monitor core temperature; aim for normothermia by the end of surgery

⚠ The Redistribution Problem Redistribution hypothermia is the most important cause of early perioperative hypothermia. Pre-warming for 15–30 minutes before induction can significantly reduce the core-to-periphery gradient and prevent the initial rapid fall in core temperature.

Consequences of Perioperative Hypothermia

System	Effect	Mechanism	Clinical Impact
Cardiovascular	Arrhythmias, myocardial ischaemia, increased SVR	Sympathetic activation, shivering, coronary vasoconstriction	Increased cardiac morbidity (MI, arrhythmias)
Coagulation	Impaired platelet function, reduced clotting factor activity	Enzymatic slowing, platelet dysfunction	Increased bleeding, transfusion requirements, re-operation
Immune	Impaired neutrophil function, reduced oxidative killing	Impaired phagocytosis, cytokine production	Increased surgical site infection
Wound healing	Delayed collagen deposition, reduced tensile strength	Impaired oxygen delivery, fibroblast function	Dehiscence, poor cosmetic outcome
Metabolic	Increased oxygen consumption (shivering), acidosis	Shivering increases VO₂ by 200–500%	Myocardial strain, hypoxaemia
Drug metabolism	Prolonged action of anaesthetics and muscle relaxants	Reduced hepatic metabolism, renal excretion	Delayed recovery, prolonged ventilation
Thermoregulation	Shivering, discomfort, delayed recovery	Post-anaesthetic shivering	Increased oxygen consumption, patient distress
Coagulopathy	Impaired clot formation	Reduced platelet function and enzyme activity	Bleeding, haematoma, transfusion
Length of stay	Increased hospital stay	All of the above	Increased cost, morbidity

Post-Anaesthetic Shivering (PAS)

Definition: Involuntary shivering during recovery from anaesthesia, typically within 30 minutes of emergence
Incidence: 5–65% depending on anaesthetic technique (higher with volatile agents, lower with propofol/TIVA)
Mechanism: Multifactorial — thermoregulatory (hypothermia), non-thermoregulatory (pain, sympathetic activation, opioid reversal, volatile agents)
Consequences: Increased oxygen consumption (200–500%), increased cardiac output, myocardial strain, wound pain, patient distress
Treatment: Active warming (forced-air), opioids (meperidine/pethidine is most effective — 12.5–25 mg IV), clonidine, nefopam, magnesium, ondansetron, dexmedetomidine
Prevention: Maintain normothermia intraoperatively; use TIVA instead of volatile; pre-warming; opioid-sparing techniques

Risk Factors for Perioperative Hypothermia

Patient Factors	Surgical Factors	Anaesthetic Factors
Extremes of age (neonates, elderly)	Prolonged surgery (>2 hours)	General anaesthesia (vs regional)
Low BMI / cachexia	Large exposed surface area	Volatile agents (dose-dependent)
Pre-existing hypothermia	Cold skin prep (alcohol, chlorhexidine)	Propofol (vasodilation, redistribution)
Endocrine disease (hypothyroidism, adrenal insufficiency)	Open body cavities (evaporative loss)	Muscle relaxants (abolish shivering)
Burns / skin loss	Cold IV fluids / blood products	Opioids (widen interthreshold range)
Trauma	Cold irrigating solutions	Regional anaesthesia (blocks thermoregulation)
Spinal cord injury	Low ambient OR temperature	Prolonged anaesthesia
Malnutrition	Tourniquet use	Neuraxial anaesthesia

Prevention and Management

Intervention	Mechanism	Evidence	Notes
Pre-warming (forced-air, 15–30 min before induction)	Increases peripheral temperature; reduces core-to-periphery gradient	Strong — reduces redistribution hypothermia	Most effective for Phase 1; apply to whole body or lower body
Forced-air warming (intraoperative)	Convective warming; most effective method	Strong — reduces hypothermia and its complications	Apply to upper body or whole body; avoid direct contact with skin
Warm IV fluids (37°C)	Prevents conductive heat loss from cold fluids	Strong — especially for large volumes	Use fluid warmer for >500 mL/h
Humidified, warmed gases	Reduces respiratory heat loss	Moderate — small contribution	Use HME or heated humidifier
Increased ambient temperature	Reduces radiative and convective loss	Moderate — raises OR temperature to 24–26°C	Uncomfortable for staff; use selectively
Insulation (blankets, hats, socks)	Reduces radiative and convective loss	Weak — alone insufficient	Use as adjunct; cover head and extremities
Conductive warming (water-circulating mattress)	Direct conduction	Moderate — can cause burns if >40°C	Monitor skin; avoid pressure points
Forced-air warming gowns	Pre-operative and intraoperative warming	Strong — improves patient comfort and reduces hypothermia	Can be used pre-operatively on the ward
Pharmacological (opioids, clonidine)	Reduce shivering threshold; do not actively warm	Weak — for shivering prevention, not warming	Meperidine 12.5–25 mg IV for PAS

✦ The Bottom Line Every surgical patient is at risk of hypothermia. Pre-warm before induction, warm actively during surgery, and continue warming in recovery. Maintain core temperature ≥36.0°C. This reduces surgical site infections, bleeding, cardiac events, and length of stay.

Module 04 of 09 · Applied

Hypothermia — Accidental & Therapeutic

From the cold operating room to the cold water immersion — the stages, consequences, and management of hypothermia.

Classification of Hypothermia

Stage	Core Temperature	Clinical Features	Management
Mild	32–35°C	Shivering, vasoconstriction, tachypnoea, tachycardia, confusion, dysarthria, cold diuresis	Passive warming, active external warming (forced-air), warm fluids
Moderate	28–32°C	Shivering stops, bradycardia, hypotension, reduced consciousness, hyporeflexia, dilated pupils, J waves on ECG, atrial fibrillation	Active core warming: warm IV fluids, humidified gases, bladder irrigation, peritoneal/pleural lavage, extracorporeal rewarming
Severe	24–28°C	Coma, areflexia, fixed dilated pupils, bradycardia, ventricular arrhythmias, asystole, pulmonary oedema, oliguria	Extracorporeal rewarming (CPB, ECMO), active core warming, ACLS with prolonged resuscitation
Profound	<24°C	Asystole, areflexia, flat EEG, "apparent death"	Extracorporeal rewarming — "not dead until warm and dead"

The Swiss Staging System for Hypothermia Stage I: Conscious, shivering — mild. Stage II: Impaired consciousness, no shivering — moderate. Stage III: Unconscious, vital signs present — severe. Stage IV: Vital signs absent — profound. Stage V: Death from irreversible hypothermia.

Clinical Features by System

System	Mild (32–35°C)	Moderate (28–32°C)	Severe (<28°C)
CNS	Confusion, dysarthria, amnesia, apathy	Stupor, hyporeflexia, dilated pupils	Coma, areflexia, flat EEG
Cardiovascular	Tachycardia, hypertension, shivering	Bradycardia, hypotension, AF, J waves	Ventricular arrhythmias, asystole
Respiratory	Tachypnoea, bronchorrhoea	Bradypnoea, hypoventilation	Apnoea, pulmonary oedema
Renal	Cold diuresis	Oliguria	Anuria
Metabolic	Increased metabolic rate (shivering)	Decreased metabolic rate	Severe acidosis, hyperkalaemia
Coagulation	Mild impairment	Coagulopathy	DIC-like picture

ECG Changes in Hypothermia

J waves (Osborn waves): Positive deflection at the QRS–ST junction — characteristic of moderate hypothermia (often at <32°C)
Prolonged PR, QRS, QT intervals: Slowed conduction
Atrial fibrillation: Common at <32°C
Ventricular arrhythmias: Ventricular fibrillation, asystole — risk increases below 28°C
Bradycardia: Progressive, often unresponsive to atropine

Management of Hypothermia

General Principles

Remove from cold environment — move to warm, dry area; remove wet clothing
Handle gently — rough handling can precipitate ventricular arrhythmias in severe hypothermia
ABC assessment — airway, breathing, circulation; assess for associated trauma, drowning, or medical cause
Monitor core temperature — use a low-reading thermometer (not standard clinical thermometer, which stops at 34°C)
Monitor ECG continuously — for arrhythmias
Bloods: ABG (corrected for temperature), glucose, electrolytes, coagulation, lactate, toxicology

Rewarming Techniques

Technique	Rewarming Rate	Indications	Notes
Passive external	0.5–1.0°C/h	Mild hypothermia (conscious, shivering)	Warm environment, blankets, remove wet clothes; shivering generates heat
Active external	1.0–2.5°C/h	Mild–moderate; not shivering	Forced-air warming, warm water immersion, heating pads
Active core	0.5–2.0°C/h	Moderate–severe	Warm IV fluids (40–42°C), humidified gases, bladder irrigation, peritoneal/pleural lavage
Extracorporeal	2–5°C/h	Severe, profound, cardiac arrest	CPB, ECMO, haemodialysis, arteriovenous rewarming
Airway rewarming	—	Adjuvant	Humidified oxygen (40–45°C) — limited effect

⚠ The "Not Dead Until Warm and Dead" Principle In severe hypothermia with apparent death (asystole, areflexia, fixed pupils), resuscitation should continue until the patient is rewarmed to at least 32–35°C. Survival with full neurological recovery has been reported after prolonged hypothermic cardiac arrest. Extracorporeal rewarming (CPB or ECMO) is the gold standard for severe hypothermia with cardiac arrest.

Complications of Rewarming

Rewarming shock: Peripheral vasodilation → hypotension; may need fluid and vasopressors
Afterdrop: Continued fall in core temperature after rewarming begins — due to return of cold peripheral blood to the core. Prevent by active core warming.
Arrhythmias: Ventricular fibrillation may occur during rewarming — be prepared for defibrillation (often refractory until >30°C)
Coagulopathy: Rewarming can unmask or worsen coagulopathy
Hyperkalaemia: Can develop during rewarming — monitor and treat
Rhabdomyolysis: From prolonged hypothermia and shivering — monitor CK, renal function

Therapeutic Hypothermia

Deliberate cooling of the body to 32–36°C for neuroprotection. It is used in specific clinical situations where it has proven benefit.

Indication	Target Temperature	Duration	Evidence
Post-cardiac arrest (witnessed, shockable rhythm)	32–36°C	12–24 h	Strong — improves neurological outcome and survival
Neonatal hypoxic-ischaemic encephalopathy	33.5–34.5°C	72 h	Strong — reduces mortality and neurodevelopmental disability
Traumatic brain injury (refractory ICP)	32–35°C	Variable	Moderate — can reduce ICP; no clear mortality benefit
Cardiac surgery (CPB)	28–32°C (or deep 18–20°C)	Duration of CPB	Standard — reduces metabolic demand and ischaemic injury
Acute liver failure (selected)	32–35°C	Variable	Weak — may reduce ICP; limited evidence

Module 05 of 09 · Applied

Hyperthermia — Fever & Hyperthermic Syndromes

When the body gets too hot — the distinction between fever and hyperthermia, the hyperthermic syndromes, and the management of heat stroke.

Fever vs Hyperthermia — A Revisit

Feature	Fever	Hyperthermia
Set point	Elevated (hypothalamus)	Normal
Body's response	Actively raises temperature (shivering, vasoconstriction)	Attempts to dissipate heat (sweating, vasodilation)
Response to antipyretics	Effective	Ineffective
Response to cooling	Body defends the new set point	Cooling is effective
Skin	Cool, vasoconstricted (early)	Hot, vasodilated, dry (late)
Examples	Infection, inflammation, malignancy	Heat stroke, MH, NMS, serotonin syndrome, thyroid storm

Hyperthermic Syndromes

Syndrome	Trigger	Mechanism	Core Features	Treatment
Malignant hyperthermia (MH)	Volatile anaesthetics, succinylcholine	Ryanodine receptor (RYR1) mutation → uncontrolled Ca²⁺ release	Masseter spasm, hypercarbia, tachycardia, rigidity, hyperthermia, rhabdomyolysis	Dantrolene 2.5 mg/kg IV, stop trigger, cool, supportive
Neuroleptic malignant syndrome (NMS)	Dopamine antagonists (haloperidol, metoclopramide, antipsychotics)	Central dopamine blockade → rigidity, hyperthermia	Rigidity ("lead-pipe"), hyperthermia, autonomic instability, altered mental status	Stop drug, dantrolene, bromocriptine, cooling, supportive
Serotonin syndrome	Serotonergic drugs (SSRIs, SNRIs, MAOIs, tramadol, triptans)	Excess serotonin → hyperthermia, rigidity, clonus	Clonus, hyperreflexia, agitation, hyperthermia, diarrhoea	Stop drug, cyproheptadine, benzodiazepines, cooling
Thyroid storm	Untreated hyperthyroidism + stress/surgery	Excess thyroid hormone → hypermetabolism	Hyperthermia, tachycardia, agitation, heart failure	Beta-blockers, propylthiouracil, iodine, steroids, cooling
Phaeochromocytoma	Catecholamine-secreting tumour + stress	Excess catecholamines → vasoconstriction, hypermetabolism	Hyperthermia, hypertension, sweating, tachycardia	Alpha-blockade (phenoxybenzamine), beta-blockade, surgery
Heat stroke	Environmental heat + exertion	Failure of thermoregulation → core >40°C	Hyperthermia, hot dry skin, CNS dysfunction (coma, seizures)	Rapid cooling (ice, cold water), supportive; no antipyretics

Heat Stroke

Definition: Core temperature >40°C with CNS dysfunction (delirium, coma, seizures) in the setting of environmental heat exposure or exertion
Classic (non-exertional): Elderly, infants, chronic illness, medications (anticholinergics, diuretics, beta-blockers) — passive exposure to heat
Exertional: Young, healthy individuals during strenuous activity in heat (athletes, military, labourers)
Pathophysiology: Thermoregulatory failure → uncontrolled heat gain → protein denaturation, cellular damage, multi-organ failure, DIC
Clinical features: Hyperthermia (>40°C), hot dry skin (classic), CNS dysfunction, tachycardia, hypotension, coagulopathy, rhabdomyolysis, AKI, ARDS
Treatment: Rapid cooling — ice water immersion (most effective), evaporative cooling, cold IV fluids, ice packs to groin/axilla/neck; supportive care; avoid antipyretics (ineffective and may worsen hepatic injury)
Mortality: Up to 50% in severe cases; rapid cooling improves outcome

⚠ Heat Stroke is an Emergency Every minute of hyperthermia increases organ damage and mortality. Cool aggressively — "cool first, transport second." Target core temperature <39°C within 30 minutes. Do not use antipyretics (they do not work and may worsen liver injury).

Malignant Hyperthermia — A Focused Review

Malignant hyperthermia (MH) is a pharmacogenetic disorder of skeletal muscle triggered by volatile anaesthetics and succinylcholine. It is the most important hyperthermic crisis in anaesthesia.

Pathophysiology

Genetic basis: Mutation in the RYR1 gene (ryanodine receptor) on chromosome 19 — accounts for ~70% of cases; CACNA1S mutations in others
Mechanism: Uncontrolled calcium release from the sarcoplasmic reticulum → sustained muscle contraction → hypermetabolism → heat production, oxygen consumption, CO₂ production, and rhabdomyolysis
Trigger agents: All volatile anaesthetics (sevoflurane, desflurane, isoflurane, enflurane, halothane) and succinylcholine
Safe agents: Propofol, opioids, nitrous oxide, non-depolarising muscle relaxants, local anaesthetics (except high-dose bupivacaine — but this is not a trigger)
Inheritance: Autosomal dominant with variable penetrance
Incidence: 1 in 10,000–50,000 anaesthetics; higher in children

Clinical Features

Feature	Mechanism	Notes
Masseter spasm	Succinylcholine-induced	May be the first sign; may be isolated or progress to MH
Hypercarbia (ETCO₂ rise)	Increased CO₂ production	Most sensitive early sign; unexplained rise despite increased ventilation
Tachycardia	Sympathetic activation	Often the first cardiovascular sign
Hyperthermia	Uncontrolled heat production	Late sign — temperature rises rapidly (1–2°C every 5 min); may exceed 42°C
Muscle rigidity	Sustained contraction	Generalised rigidity; may be masked by muscle relaxants
Rhabdomyolysis	Muscle breakdown	Myoglobinuria, elevated CK, risk of AKI
Hyperkalaemia	Muscle breakdown	Can cause arrhythmias
Metabolic acidosis	Anaerobic metabolism	Elevated lactate; mixed respiratory and metabolic acidosis
Arrhythmias	Electrolyte disturbance, acidosis	Ventricular tachycardia, fibrillation

Management of Malignant Hyperthermia

1. Stop triggers
Discontinue volatile + succinylcholine

→

2. Call for help
MH kit / dantrolene

→

3. Hyperventilate
100% O₂, high flow

→

4. Dantrolene
2.5 mg/kg IV bolus

→

5. Cool
Active cooling

→

6. Treat complications
Arrhythmias, hyperkalaemia, acidosis

Intervention	Dose / Detail	Notes
Dantrolene	2.5 mg/kg IV bolus; repeat every 5–10 min until stable; up to 10 mg/kg	Specific antidote; inhibits Ca²⁺ release from sarcoplasmic reticulum; prepare 20 mg in 60 mL sterile water (difficult to dissolve)
Hyperventilation	100% O₂, 2–3× minute ventilation	Wash out CO₂; treat respiratory acidosis
Cooling	Cold IV fluids, ice packs, surface cooling, bladder lavage	Target core <38.5°C; stop cooling at 38°C to avoid overshoot
Sodium bicarbonate	1–2 mEq/kg IV	For metabolic acidosis; guided by ABG
Arrhythmia management	Standard ACLS; avoid calcium channel blockers (interact with dantrolene)	Treat hyperkalaemia (calcium, insulin/dextrose, bicarbonate)
Urine output	Target >1–2 mL/kg/h	Prevent myoglobinuric AKI; consider mannitol, furosemide
ICU admission	All patients	Monitor for recrudescence (can occur up to 24–48 h after initial episode)

⚠ Dantrolene — The Life-Saving Drug Dantrolene is the specific antidote for MH. Every anaesthetising location must have a MH kit with at least 36 vials of dantrolene (20 mg each) immediately available. The traditional formulation is difficult to reconstitute (requires sterile water and vigorous shaking) — new formulations (Ryanodex) are easier. Mortality from MH has fallen from >70% to <5% with early dantrolene.

Prevention in Susceptible Patients

Pre-operative assessment: Personal or family history of MH, unexplained hyperthermia during anaesthesia, masseter spasm, elevated CK
Trigger-free anaesthesia: Use propofol, opioids, nitrous oxide, non-depolarising muscle relaxants (avoid succinylcholine)
Avoid volatile agents: Use TIVA (propofol + remifentanil)
Machine preparation: Flush anaesthetic machine with 100% O₂ at high flow for 10–15 minutes; remove vaporisers; change CO₂ absorbent; use new breathing circuit
Monitoring: Continuous temperature, ETCO₂, ECG, SpO₂; avoid triggers throughout
Dantrolene prophylaxis: Not routinely recommended; reserve for therapeutic use
Genetic testing: Refer to MH centre for caffeine-halothane contracture test or genetic testing (RYR1)

Neuroleptic Malignant Syndrome (NMS)

Trigger: Dopamine antagonists (haloperidol, chlorpromazine, metoclopramide, prochlorperazine) or withdrawal of dopamine agonists
Mechanism: Central dopamine blockade → rigidity, hyperthermia, autonomic instability
Clinical features: "Lead-pipe" rigidity, hyperthermia, altered mental status, autonomic instability (labile BP, tachycardia, diaphoresis), elevated CK
Onset: Hours to days after starting or increasing the offending drug
Treatment: Stop the offending drug; dantrolene (for rigidity and hyperthermia); bromocriptine (dopamine agonist); supportive care; cooling
Difference from MH: NMS is not triggered by anaesthetics; it is triggered by dopamine antagonists. Dantrolene is less effective than in MH; bromocriptine is more important.

Serotonin Syndrome

Trigger: Serotonergic drugs — SSRIs, SNRIs, MAOIs, tramadol, triptans, lithium, St John's wort
Mechanism: Excess serotonin → hyperthermia, rigidity, clonus, autonomic instability
Clinical features: Clonus (especially lower limbs), hyperreflexia, agitation, confusion, hyperthermia, diarrhoea, dilated pupils
Onset: Within 24 hours of starting or increasing a serotonergic drug
Treatment: Stop the offending drug; cyproheptadine (serotonin antagonist); benzodiazepines; cooling; supportive care
Difference from NMS: Serotonin syndrome has rapid onset (hours), clonus and hyperreflexia prominent, and responds to cyproheptadine; NMS has slower onset (days), rigidity more prominent, and responds to dantrolene/bromocriptine.

Module 06 of 09 · Crisis

Malignant Hyperthermia — In Depth

The most important inherited disorder in anaesthesia. Pathophysiology, recognition, dantrolene, and the MH kit.

⚠ Time-Critical Emergency Malignant hyperthermia is a life-threatening hypermetabolic crisis. Early recognition and immediate dantrolene administration are the keys to survival. Mortality has fallen from >70% to <5% with modern management.

Genetics & Pathophysiology

Inheritance: Autosomal dominant with variable penetrance
Genes: RYR1 (ryanodine receptor 1) on chromosome 19q13.1 — ~70% of cases; CACNA1S (dihydropyridine receptor) — ~1% of cases
Mechanism: Mutated ryanodine receptor → uncontrolled calcium release from sarcoplasmic reticulum in response to triggers → sustained muscle contraction → ATP hydrolysis → heat, CO₂, and lactate production
Triggers: All volatile anaesthetics (halothane, isoflurane, sevoflurane, desflurane, enflurane) and succinylcholine
Safe agents: Propofol, opioids, nitrous oxide, non-depolarising muscle relaxants, local anaesthetics, ketamine, benzodiazepines
Exertional heat illness / rhabdomyolysis: Some RYR1 mutations also predispose to exertional heat stroke and rhabdomyolysis

Clinical Presentation — The MH Score

The Clinical Grading Scale (CGS) or MH Score helps estimate the likelihood of MH. It includes:

Category	Feature	Points
Rigidity	Generalised rigidity; masseter spasm	15 (generalised), 5 (masseter)
Muscle breakdown	CK >20,000; myoglobinuria; cola-coloured urine	15, 10, 5
Respiratory	ETCO₂ >55 mmHg; unexplained tachypnoea	15, 10
Cardiac	Unexplained tachycardia; ventricular arrhythmias	10, 15
Temperature	Rapid rise >2°C/h; >38.8°C	15, 10
Family history	MH in first-degree relative	10
Other	Acidosis, hyperkalaemia	5 each

Interpretation: Score >50 = almost certainly MH; 35–49 = probably MH; 20–34 = some likelihood; <20 = unlikely.

Early vs Late Signs

Early Signs	Late Signs
Unexplained rise in ETCO₂ (most sensitive)	Hyperthermia (may be late; rapid rise)
Tachycardia (often first cardiovascular sign)	Generalised muscle rigidity
Masseter spasm (after succinylcholine)	Rhabdomyolysis (myoglobinuria, high CK)
Tachypnoea (spontaneous ventilation)	Hyperkalaemia
Metabolic acidosis (lactate)	Ventricular arrhythmias
Skin mottling	DIC
Unexplained tachycardia	Cardiac arrest

⚠ The Classic Presentation The classic MH crisis: unexplained rise in ETCO₂ despite increased ventilation → tachycardia → masseter spasm (if succinylcholine used) → generalised rigidity → hyperthermia (late) → rhabdomyolysis → arrhythmias. Do not wait for hyperthermia to start treatment. The earliest sign is usually hypercarbia, not hyperthermia.

Dantrolene — The Specific Antidote

Mechanism: Inhibits calcium release from the sarcoplasmic reticulum by binding to the ryanodine receptor (RYR1)
Dose: 2.5 mg/kg IV bolus, repeated every 5–10 minutes until stable (max 10 mg/kg)
Preparation: Each 20 mg vial must be reconstituted with 60 mL sterile water — difficult and time-consuming; new formulations (Ryanodex) are easier
Side effects: Muscle weakness, phlebitis, nausea, diarrhoea, dizziness; rare hepatotoxicity
Monitoring: Continue dantrolene for at least 24–48 hours after stabilisation to prevent recrudescence; monitor CK, urine output, electrolytes
Availability: Every anaesthetising location must have an MH kit with at least 36 vials (720 mg) of dantrolene immediately available

The MH Kit — Essential Contents Dantrolene: ≥36 vials (20 mg each) · Sterile water: 60 mL per vial (for reconstitution) · Large syringes: 60 mL · IV tubing: For dantrolene infusion · Cooling equipment: Ice packs, cold IV fluids, cooling blankets · Sodium bicarbonate: 1–2 mEq/kg · Antiarrhythmics: Amiodarone, lidocaine (avoid calcium channel blockers) · Insulin/dextrose: For hyperkalaemia · Mannitol/furosemide: For urine output · ABG/electrolyte kits: For monitoring · Checklist: MH management protocol

Management Algorithm — Step by Step

Prevention in Susceptible Patients

Pre-operative assessment: Personal or family history of MH, unexplained hyperthermia during anaesthesia, masseter spasm, elevated CK
Trigger-free anaesthesia: TIVA (propofol + remifentanil) + nitrous oxide + non-depolarising muscle relaxants (avoid succinylcholine)
Machine preparation: Remove vaporisers; flush with 100% O₂ at 10 L/min for 10–15 minutes; change CO₂ absorbent and breathing circuit
Monitoring: Continuous temperature, ETCO₂, ECG, SpO₂; avoid triggers throughout
Dantrolene prophylaxis: Not routinely recommended; reserve for therapeutic use
Genetic testing: Refer to MH centre for caffeine-halothane contracture test (CHCT) or genetic testing (RYR1)
Patient education: Advise patient to inform all future anaesthetists; provide MH information card; consider MedicAlert bracelet

Exertional Heat Illness & Rhabdomyolysis

Some RYR1 mutations also predispose to exertional heat stroke and exertional rhabdomyolysis
Patients may present with hyperthermia, muscle pain, weakness, and dark urine after strenuous exercise
Management is similar to MH — cooling, dantrolene if severe, supportive care
Consider MH susceptibility in any patient with unexplained exertional heat illness or rhabdomyolysis
Genetic counselling and testing may be indicated

Module 07 of 09 · Advanced

Therapeutic Temperature Management

Deliberate cooling and warming — the evidence, the methods, and the clinical applications from cardiac arrest to cardiac surgery.

Targeted Temperature Management (TTM)

The term TTM replaced "therapeutic hypothermia" to reflect the fact that different patients may benefit from different target temperatures — not all need to be cooled to 33°C.

Condition	Target Temperature	Duration	Evidence
Post-cardiac arrest (shockable rhythm, witnessed)	32–36°C	12–24 h	Strong — improves neurological outcome and survival
Post-cardiac arrest (non-shockable rhythm)	32–36°C	12–24 h	Moderate — may benefit; individualise
Neonatal hypoxic-ischaemic encephalopathy	33.5–34.5°C	72 h	Strong — reduces mortality and neurodevelopmental disability
Traumatic brain injury (refractory ICP)	32–35°C	Variable	Moderate — reduces ICP; no clear mortality benefit
Cardiac surgery with CPB	28–32°C (or 18–20°C for circulatory arrest)	Duration of CPB	Standard — reduces metabolic demand and ischaemic injury
Acute liver failure (selected)	32–35°C	Variable	Weak — may reduce ICP; limited evidence
Fever control in ICU (e.g., sepsis, stroke)	36.5–37.5°C	Until source controlled	Moderate — may improve outcomes; avoid fever

Methods of Cooling

Method	Rate	Advantages	Disadvantages
Ice packs (groin, axilla, neck)	Slow	Available everywhere; cheap	Labour-intensive; uneven cooling; skin injury; shivering
Cold IV fluids (4°C, 30 mL/kg)	Moderate	Rapid; easy; also resuscitative	Risk of volume overload; not effective for maintenance
Surface cooling (water-circulating blankets, pads)	Moderate	Effective; widely used; controlled	Skin injury; shivering; slow to initiate
Forced-air warming (can also cool)	Moderate	Same device for warming and cooling	Less effective for cooling than dedicated devices
Intravascular cooling (endovascular catheter)	Fast	Precise; rapid; less shivering	Invasive; requires CVC; expensive; thrombosis risk
Extracorporeal cooling (CPB, ECMO)	Very fast	Fastest; used for severe hypothermia and cardiac arrest	Requires specialised equipment and team; invasive
Nasopharyngeal cooling	Moderate	Rapid brain cooling	Limited evidence; special device required
Selective brain cooling (helmet, nasal)	Variable	Targets brain	Not widely used; limited evidence

Shivering Management During TTM

Why treat shivering: Increases metabolic rate and oxygen consumption (200–500%), counteracts cooling, increases ICP, and causes patient distress
Non-pharmacological: Warm blankets over extremities, forced-air warming of face and hands, skin counterwarming
Pharmacological: Opioids (fentanyl, meperidine/pethidine), dexmedetomidine, clonidine, magnesium, buspirone, ondansetron
Surface counterwarming: Apply forced-air warming to face and hands — reduces shivering threshold without affecting core cooling
Neuromuscular blockade: For refractory shivering — use only in intubated patients; monitor with TOF
Monitoring: Continuous core temperature, ECG, SpO₂, ETCO₂; watch for arrhythmias and coagulopathy

Complications of Therapeutic Hypothermia

System	Complication	Management
Cardiovascular	Bradycardia, hypotension, arrhythmias	Usually tolerated; treat if symptomatic; avoid rewarming too fast
Coagulation	Coagulopathy, bleeding	Monitor coagulation; transfuse if needed; be aware of impaired platelet function
Metabolic	Hyperglycaemia, electrolyte disturbance (K⁺, Mg²⁺, Ca²⁺)	Monitor and correct; insulin for hyperglycaemia
Immune	Increased infection risk	Surveillance cultures; treat infections promptly
Renal	Cold diuresis, hypovolaemia	Monitor urine output; replace fluids as needed
Drug metabolism	Prolonged drug action	Reduce doses; monitor effect; avoid drugs with narrow therapeutic index
Skin	Pressure ulcers, cold injury	Regular skin checks; avoid direct ice contact; use protective barriers
Rewarming	Afterdrop, rewarming shock, hyperkalaemia	Rewarm slowly (0.25–0.5°C/h); monitor electrolytes and haemodynamics

Rewarming — The Critical Phase

Rate: 0.25–0.5°C/h — slow rewarming to avoid complications
Afterdrop: Continued fall in core temperature after rewarming begins — due to return of cold peripheral blood to the core. Prevent by active core warming.
Rewarming shock: Peripheral vasodilation → hypotension; may need fluid and vasopressors
Hyperkalaemia: Can develop during rewarming — monitor and treat
Arrhythmias: Ventricular fibrillation may occur during rewarming — be prepared for defibrillation (often refractory until >30°C)
Coagulopathy: Rewarming can unmask or worsen coagulopathy
Target: Rewarm to 36.5–37.5°C — avoid hyperthermia

The Evidence — Key Trials

Trial	Population	Intervention	Finding
HACA (2002)	Post-cardiac arrest (shockable rhythm)	33°C vs normothermia	Improved neurological outcome and survival
Bernard (2002)	Post-cardiac arrest (shockable rhythm)	33°C vs normothermia	Improved neurological outcome
TTM (2013)	Post-cardiac arrest (all rhythms)	33°C vs 36°C	No difference — both are acceptable
HYPERION (2019)	Post-cardiac arrest (non-shockable rhythm)	33°C vs normothermia	Improved neurological outcome with 33°C
CoolCap (2005)	Neonatal HIE	33.5°C vs normothermia	Reduced mortality and disability
TOBY (2009)	Neonatal HIE	33.5°C vs normothermia	Reduced mortality and disability
NICHD (2005)	Neonatal HIE	33.5°C vs normothermia	Reduced mortality and disability

Practical Protocol — Post-Cardiac Arrest TTM

1. Assess
Inclusion/exclusion

→

2. Initiate cooling
Target 32–36°C

→

3. Maintain
12–24 h

→

4. Rewarm
0.25–0.5°C/h

→

5. Maintain normothermia
36.5–37.5°C

Inclusion: ROSC after cardiac arrest, comatose, haemodynamically stable (or stabilisable)
Exclusion: Pre-existing coma, terminal illness, severe coagulopathy, pregnancy (relative), cardiogenic shock with severe instability (relative)
Cooling: Start as soon as possible; cold IV fluids + surface cooling; target 32–36°C (institutional protocol)
Maintenance: 12–24 hours; monitor core temperature continuously
Rewarming: 0.25–0.5°C/h; avoid hyperthermia
Post-rewarming: Maintain normothermia (36.5–37.5°C) for at least 72 hours — fever is associated with worse outcomes
Prognostication: Delay until ≥72 hours after rewarming; use multimodal assessment (clinical examination, EEG, biomarkers, imaging)

Module 08 of 09 · Applied

Special Populations

Neonates, children, the elderly, pregnant patients, burns, trauma, and spinal cord injury — where thermoregulation is different.

Neonates and Infants

High surface area to volume ratio: ~3× that of adults — rapid heat loss
Limited shivering ability: Rely on non-shivering thermogenesis (brown adipose tissue) — cannot mount a sustained shivering response
Thin skin, poor insulation: Subcutaneous fat is limited, especially in preterm infants
High metabolic rate: Oxygen consumption is 6 mL/kg/min (vs 3–4 in adults)
Narrow interthreshold range: Thermoregulation is less precise
Consequences: Hypothermia → increased oxygen consumption, hypoglycaemia, acidosis, pulmonary vasoconstriction, apnoea, bradycardia, poor weight gain
Management: Warm delivery room (26°C), skin-to-skin contact, radiant warmers, incubators, warmed humidified gases, warm IV fluids, hat, plastic wrap for preterm
Target: Core temperature 36.5–37.5°C

Children

Higher surface area to volume ratio than adults: Greater heat loss
Shivering ability: Present but less efficient than adults; may not shiver until core temperature is significantly reduced
Higher metabolic rate: More heat production but also more heat loss
Consequences of hypothermia: Similar to neonates — increased oxygen consumption, acidosis, delayed recovery, increased infection risk
Management: Forced-air warming, warm IV fluids, humidified gases, increased ambient temperature, hats, pre-warming
Target: Core temperature 36.5–37.5°C

The Elderly

Impaired thermoregulation: Reduced ability to detect temperature changes and mount a response
Reduced shivering: Decreased muscle mass and efficiency
Delayed vasoconstriction: Reduced sympathetic response
Comorbidities: Diabetes, hypothyroidism, malnutrition, medications (beta-blockers, antipsychotics, diuretics)
Consequences: Greater risk of perioperative hypothermia and its complications
Management: Pre-warming, active warming throughout, monitoring core temperature, avoiding cold fluids, warm environment
Target: Core temperature ≥36.0°C

Pregnancy

Physiological changes: Increased metabolic rate (~20%), increased oxygen consumption, reduced FRC, increased minute ventilation
Thermoregulation: Generally intact, but the fetus is dependent on maternal temperature — maternal hyperthermia can cause fetal distress
Perioperative: Pregnant patients lose heat rapidly under anaesthesia; fetal monitoring important
Management: Active warming, warm IV fluids, left lateral tilt, monitoring maternal core temperature (target 36.5–37.5°C), fetal heart rate monitoring
Avoid: Hyperthermia (>38°C) — associated with fetal malformations (neural tube defects) in the first trimester and fetal distress later
Note: Maternal fever during labour is common (epidural-related or inflammatory) — distinguish from infection

Burns

Loss of skin barrier: Massive evaporative heat loss — can be >5000 kcal/day in major burns
Thermoregulatory failure: Loss of sweat glands and vasomotor control in burned areas
Increased metabolic rate: Hypermetabolic response — up to 2× normal
Risk of hypothermia: During resuscitation, transport, and surgery — especially during dressing changes and debridement
Management: Warm environment (28–32°C), warmed IV fluids, heated humidified gases, forced-air warming, occlusive dressings, early excision and grafting
Target: Core temperature 36.5–37.5°C; avoid both hypothermia and hyperthermia

Trauma

The trauma triad: Hypothermia, acidosis, coagulopathy — each worsens the others
Hypothermia in trauma: Common (up to 66% of major trauma patients); caused by exposure, cold fluids, impaired thermoregulation from shock, and alcohol/drugs
Consequences: Increased mortality, coagulopathy, arrhythmias, delayed recovery
Management: Warm environment, warm IV fluids, forced-air warming, humidified gases, warm blankets, remove wet clothes
Damage control resuscitation: Includes active warming — warm all fluids and blood products
Target: Core temperature ≥36.0°C — active warming is a priority in major trauma

Spinal Cord Injury

Thermoregulatory failure: Interruption of descending sympathetic pathways → impaired vasoconstriction, shivering, and sweating below the level of injury
Poikilothermia: Body temperature tends to follow environmental temperature — patients become hypothermic in cold environments and hyperthermic in hot environments
Risk during surgery: High risk of hypothermia; impaired ability to mount a thermoregulatory response
Management: Warm environment, active warming, monitoring core temperature, avoid cold fluids, careful monitoring for hyperthermia in warm environments
Autonomic dysreflexia: Can cause severe hypertension and hyperthermia — a separate emergency
Target: Core temperature 36.5–37.5°C

Other Populations

Obese patients: Increased insulation (adipose tissue) but also increased heat loss from large surface area; risk of hypothermia is similar to non-obese; warming is important
Malnourished patients: Reduced metabolic rate and subcutaneous fat → increased risk of hypothermia
Hypothyroid patients: Reduced metabolic rate → increased risk of hypothermia; may need higher ambient temperature and active warming
Patients on beta-blockers: Impaired thermoregulatory response (reduced shivering, vasoconstriction); increased risk of hypothermia
Patients on antipsychotics: Impaired thermoregulation; risk of NMS and hyperthermia
Patients on alcohol or drugs: Impaired thermoregulation, vasodilation, increased heat loss; common in trauma and emergency settings

Assessment

Self-Assessment

Thirty questions across all modules — from thermoregulatory physiology to malignant hyperthermia and therapeutic temperature management. Click an option to reveal the explanation.

▸ Questions — click to answer