Perioperative Temperature Management

Quick Answer

Exam Essentials - ANZCA Final Examination

Perioperative hypothermia (core temperature less than 36°C) occurs in 50-90% of unwarmed surgical patients and is associated with significant morbidity including surgical site infection (3-fold increase), coagulopathy, cardiac events, prolonged hospital stay, and increased mortality.

Key Mechanisms:

• General anaesthesia widens the interthreshold range from 0.2°C to 4°C
• Phase 1: Redistribution hypothermia (1-1.5°C drop in first hour)
• Phase 2: Linear heat loss exceeds production (2-3 hours)
• Phase 3: Plateau at new thermal steady state

Prevention Strategy:

• Pre-warming: ≥30 minutes forced-air warming before induction
• Active warming: Forced-air warming throughout surgery
• Fluid warming: All IV fluids >500mL through warming device
• Ambient temperature: OR temperature 21-24°C
• Target: Maintain core temperature ≥36°C

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Introduction

Temperature homeostasis is a fundamental aspect of anaesthetic care that directly impacts patient outcomes. The human body maintains core temperature within a narrow range (36.5-37.5°C) through complex thermoregulatory mechanisms that are significantly impaired by anaesthetic agents. Understanding these mechanisms and implementing evidence-based temperature management strategies is essential for safe perioperative care.

Perioperative hypothermia remains one of the most common and preventable complications of anaesthesia, yet surveys consistently demonstrate suboptimal compliance with temperature monitoring and warming guidelines. The Australian and New Zealand College of Anaesthetists (ANZCA) Professional Standard PS18 mandates temperature monitoring for all patients undergoing anaesthesia exceeding 30 minutes duration.

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Thermoregulation Physiology

Thermoreceptors

The thermoregulatory system relies on peripheral and central thermoreceptors to detect temperature changes and maintain homeostasis.

Peripheral Thermoreceptors:

• Cold receptors (A-delta fibres): Located in the dermis, maximum sensitivity at 25-30°C, respond to cooling with increased firing rate
• Warm receptors (C fibres): Located superficially in dermis, maximum sensitivity at 40-45°C, respond to warming with increased firing rate
• Distribution: Highest density on face and hands (16-20 receptors/cm²), lower density on trunk and legs (3-6 receptors/cm²)
• Signal transmission: Via lateral spinothalamic tract to hypothalamus [PMID: 11152757]

Central Thermoreceptors:

• Primary location: Preoptic area of anterior hypothalamus (POAH)
• Other sites: Posterior hypothalamus, brainstem, spinal cord, abdominal viscera
• Sensitivity: Central receptors contribute 80% of afferent thermal signal; core temperature weighted heavily in integrated response
• Temperature integration: POAH neurons integrate peripheral and central signals to determine mean body temperature [PMID: 16926197]

Hypothalamic Control

The hypothalamus functions as the central thermoregulatory controller, integrating thermal information and coordinating effector responses.

Preoptic Anterior Hypothalamus (POAH):

• Contains warm-sensitive neurons (30%) and cold-sensitive neurons (5%)
• Sets the thermoregulatory "set point" (~37°C)
• Compares integrated body temperature with set point
• Activates appropriate effector mechanisms when threshold exceeded [PMID: 22152089]

Posterior Hypothalamus:

• Integrates signals from POAH
• Coordinates heat conservation and production responses
• Connects to autonomic nervous system and motor pathways

Neural Integration:

• Mean body temperature = 0.8 × core temperature + 0.2 × mean skin temperature
• This weighted integration explains why core hypothermia is more potent in triggering responses than peripheral cooling

Effector Mechanisms

Heat Conservation/Production (Cold Response):

Heat Dissipation (Heat Response):

Arteriovenous Shunts:

• Located in fingers, toes, ears, nose
• Direct arterial-venous connections bypassing capillary bed
• Under sympathetic control (alpha-adrenergic)
• Opening increases cutaneous blood flow 100-fold [PMID: 19293245]

Interthreshold Range

The interthreshold range is the temperature span between the cold-response threshold (vasoconstriction/shivering) and warm-response threshold (sweating/vasodilation).

Normal Physiology:

• Awake interthreshold range: ~0.2°C
• Upper threshold: 37.1°C (sweating)
• Lower threshold: 36.9°C (vasoconstriction)
• Precise regulation maintains core temperature within narrow range

Clinical Significance:

• Within the interthreshold range, no active thermoregulatory responses occur
• Temperature changes within this range are unopposed
• Anaesthetic agents dramatically widen this range, allowing passive temperature drift [PMID: 8192851]

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Effects of Anaesthesia on Thermoregulation

Widened Interthreshold Range

General anaesthesia profoundly impairs thermoregulation by widening the interthreshold range approximately 20-fold.

Effect of Anaesthetic Agents:

Mechanism of Threshold Alteration:

• Direct central effects on hypothalamic set point
• Linear dose-dependent reduction in cold thresholds
• Sweating threshold elevated by similar magnitude
• Combination of agents produces additive effects [PMID: 9952133]

Impaired Vasoconstriction

The vasoconstriction threshold reduction is the most clinically significant thermoregulatory impairment.

Key Points:

• Threshold reduced from 36.9°C to approximately 34.5°C under general anaesthesia
• Patient cools to 34.5°C before vasoconstriction triggered
• Even when triggered, vasoconstriction is only 60% as effective under anaesthesia
• Neuraxial anaesthesia (spinal/epidural) blocks vasoconstriction below level of block
• Combination of general + neuraxial anaesthesia causes most severe impairment [PMID: 8879464]

Regional Anaesthesia:

• Spinal/epidural blocks sympathetic vasoconstriction below block level
• Prevents shivering in blocked dermatomes
• Core temperature decreases ~0.5°C per hour during neuraxial anaesthesia
• Hypothalamus cannot perceive blocked region temperature accurately [PMID: 9105228]

Heat Redistribution

Redistribution is the primary mechanism of initial hypothermia under anaesthesia.

Physiology of Redistribution:

• Core-to-peripheral temperature gradient normally maintained at 2-4°C
• General anaesthesia induces vasodilation and opens arteriovenous shunts
• Core heat redistributes to peripheral tissues
• No heat is lost from body; heat moves internally
• Results in rapid core temperature decrease with minimal change in mean body temperature [PMID: 7840426]

Magnitude of Redistribution:

• Accounts for 0.5-1.5°C core temperature decrease in first hour
• Greater in cold peripheral compartments (cold environment, inadequate pre-warming)
• Magnitude proportional to core-peripheral gradient
• Reduced by pre-warming (decreases gradient before induction)

Phases of Hypothermia Under Anaesthesia

Perioperative hypothermia follows a characteristic triphasic pattern.

Phase 1: Redistribution (0-1 hour)

• Mechanism: Internal heat redistribution from core to periphery
• Magnitude: 1.0-1.5°C decrease in core temperature
• Timing: Occurs within first 30-60 minutes
• Prevention: Pre-warming minimizes core-peripheral gradient
• Not prevented by active warming after induction [PMID: 9349887]

Phase 2: Linear Heat Loss (1-3 hours)

• Mechanism: Heat loss exceeds metabolic heat production
• Rate: ~0.5-1.0°C per hour without warming
• Heat loss routes: Radiation (40%), convection (30%), evaporation (20%), conduction (10%)
• Prevention: Active warming and passive insulation
• Continues until thermal steady state reached

Phase 3: Thermal Plateau (>3 hours)

• Mechanism: Core cooling triggers residual thermoregulatory vasoconstriction
• Core temperature plateaus at new, lower set point
• Metabolic heat confined to core compartment
• Typically occurs at 34-35°C without intervention
• May not be reached in shorter procedures [PMID: 8659799]

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Consequences of Perioperative Hypothermia

Coagulopathy

Hypothermia significantly impairs coagulation through multiple mechanisms.

Effects on Coagulation:

• Platelet dysfunction: Impaired adhesion and aggregation
• Enzyme inhibition: Coagulation cascade enzymes function optimally at 37°C
• 10% reduction in clotting factor activity per 1°C decrease
• PT and aPTT prolonged (but measured at 37°C in laboratory, masking true impairment)
• Fibrinolysis enhanced [PMID: 8659804]

Clinical Evidence:

• Hypothermia to 35°C increases blood loss by approximately 16% (500mL in hip arthroplasty)
• Transfusion requirements increased 22%
• Platelet count unaffected but function severely impaired
• Core temperature <35°C associated with increased mortality in trauma patients
• Forms part of "lethal triad" (hypothermia, acidosis, coagulopathy) [PMID: 8659804]

Surgical Site Infection

Mild hypothermia significantly increases wound infection risk.

Mechanisms:

• Thermoregulatory vasoconstriction reduces wound oxygen tension
• Impaired neutrophil function (oxidative killing, chemotaxis)
• Reduced collagen deposition
• Impaired immunity [PMID: 8879469]

Evidence:

• Landmark Kurz et al. (1996) study: Hypothermia (34.7°C) vs normothermia (36.6°C)
• Surgical site infection: 19% vs 6% (p=0.009)
• Three-fold increase in infection risk
• Hospital stay prolonged by 20% (14.7 vs 12.1 days)
• Similar findings replicated in colorectal, orthopaedic surgery [PMID: 8678067]

Cardiac Morbidity

Perioperative hypothermia increases cardiovascular complications.

Mechanisms:

• Increased catecholamine release
• Hypertension and tachycardia
• Increased myocardial oxygen demand
• Coronary vasoconstriction
• Arrhythmia predisposition [PMID: 9009943]

Evidence:

• Frank et al. (1997): Hypothermia tripled cardiac morbidity in high-risk patients
• Cardiac events: 6.3% normothermic vs 1.4% hypothermic (p=0.02)
• Events included MI, unstable angina, cardiac arrest, ECG changes
• Temperature difference only 1.3°C between groups
• Strongest association with shivering-induced catecholamine surge [PMID: 9009943]

Prolonged Drug Action

Hypothermia alters pharmacokinetics and pharmacodynamics of anaesthetic drugs.

Mechanisms:

• Reduced hepatic metabolism (10-15% per 1°C decrease)
• Reduced renal clearance
• Increased drug solubility
• Altered protein binding
• Reduced enzyme activity [PMID: 14567871]

Clinical Effects:

Shivering and Increased Oxygen Demand

Post-anaesthetic shivering creates significant physiological stress.

Shivering Characteristics:

• Occurs in 40-60% of patients recovering from general anaesthesia
• Involves both thermoregulatory and non-thermoregulatory mechanisms
• Peak at core temperature ~35.5°C
• Intensity correlates with degree of hypothermia [PMID: 8659801]

Metabolic Consequences:

• Oxygen consumption increased 200-600%
• Carbon dioxide production proportionally increased
• Minute ventilation must increase 5-fold to maintain normocapnia
• Impossible with residual anaesthetic effect or neuromuscular blockade
• Creates oxygen supply-demand mismatch

Cardiovascular Effects:

• Catecholamine surge (norepinephrine increased 2-3 fold)
• Tachycardia, hypertension
• Increased cardiac work
• Myocardial ischaemia in susceptible patients
• Increased intracranial and intraocular pressure [PMID: 8659801]

Treatment of Shivering:

• Meperidine (pethidine) 25-50mg IV: Most effective (kappa-opioid effect)
• Clonidine 75-150mcg IV: Reduces shivering threshold
• Tramadol 100mg IV: Serotonin reuptake inhibition
• Ondansetron 8mg IV: 5-HT3 antagonism
• Active warming: Treats cause
• Magnesium sulphate 30mg/kg: Reduces shivering [PMID: 18458162]

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Temperature Monitoring

Core vs Peripheral Sites

Accurate temperature measurement requires understanding the distinction between core and peripheral compartments.

Core Temperature Sites:

• Pulmonary artery catheter (gold standard)
• Distal oesophagus (lower 1/3)
• Nasopharynx (posterior)
• Tympanic membrane (contact, not infrared)
• Bladder (with adequate urine flow)

Peripheral Temperature Sites:

• Axilla
• Oral (sublingual)
• Skin
• Rectum (slow response time)

Accuracy of Sites:

[PMID: 15105224]

Temperature Monitoring Devices

Thermistors:

• Semiconductor devices with temperature-dependent resistance
• Highly accurate (±0.1°C)
• Fast response time
• Used in oesophageal, nasopharyngeal, bladder, PA catheters
• Require calibration; non-linear response curve

Thermocouples:

• Based on Seebeck effect (voltage generated at junction of dissimilar metals)
• Accurate (±0.2°C)
• Fast response
• Small size allows placement in multiple sites
• Used in skin probes, PA catheters

Infrared Thermometers:

• Detect thermal radiation
• Non-contact measurement
• Variable accuracy in operating room (±0.5-1.0°C)
• Tympanic infrared devices unreliable under anaesthesia
• Affected by ambient temperature, position [PMID: 23994589]

Liquid Crystal Thermometers:

• Colour change indicates temperature range
• Low cost, single use
• Limited accuracy (±0.3-0.5°C)
• Useful for screening only

ANZCA Professional Standard PS18 Requirements:

• Temperature monitoring mandatory for anaesthesia >30 minutes
• Continuous monitoring for procedures >60 minutes or high-risk patients
• Core temperature site preferred
• Documentation of temperature required

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Prevention of Hypothermia

Active Warming

Forced-Air Warming:

• Gold standard for perioperative warming
• Heated air circulated through disposable blanket
• Heat transfer via convection
• Efficacy: Maintains or increases core temperature 0.5-1.0°C/hour
• Optimal coverage: Maximum body surface area
• Evidence: Superior to all other warming methods [PMID: 8572003]

Forced-Air Warming Specifications:

Fluid Warming:

• Prevents heat loss from IV fluid administration
• 1 L crystalloid at room temperature (20°C) decreases core temperature by 0.25°C
• 1 unit PRBC at 4°C decreases core temperature by 0.25°C
• Mandatory for infusions >500 mL/hour
• Target fluid temperature: 37-41°C [PMID: 8572003]

Fluid Warming Devices:

Heated Mattresses/Underbody Warming:

• Circulating water mattresses
• Resistive heating blankets
• Limited efficacy: Only 10% body surface in contact
• Risk of pressure necrosis and burns (especially in hypotensive patients)
• Supplement but do not replace forced-air warming [PMID: 8572003]

Radiant Warmers:

• Overhead infrared heating
• Useful in paediatric and neonatal settings
• Limited to exposed body parts
• Less effective than forced-air warming

Passive Insulation

Principles:

• Reduces radiant and convective heat loss
• Does not add heat; only slows loss
• Single layer reduces heat loss by approximately 30%
• Additional layers provide diminishing returns

Methods:

• Cotton blankets (minimal insulation)
• Reflective ("space") blankets (reduce radiant loss)
• Surgical drapes
• Head covering (10% heat loss from exposed head)
• Limb wrapping

Limitations:

• Cannot prevent redistribution hypothermia
• Cannot maintain normothermia alone in cold OR
• Supplement to active warming, not replacement

Ambient Temperature

Operating Room Temperature:

• Recommended: 21-24°C for adults
• Paediatric/neonatal: 24-26°C
• Trade-off between patient warming and staff comfort
• Higher OR temperature reduces but does not eliminate hypothermia
• Effect limited: Gradient between 37°C core and 24°C ambient still permits significant heat loss [PMID: 19293245]

Humidity:

• Low humidity increases evaporative heat loss
• Recommended relative humidity: 40-60%
• Particularly important with large open wounds

Pre-warming

Pre-warming is the most effective strategy for preventing redistribution hypothermia.

Rationale:

• Warms peripheral compartment before induction
• Reduces core-to-peripheral temperature gradient
• Minimizes Phase 1 redistribution hypothermia
• Cannot be achieved by intraoperative warming alone [PMID: 9349887]

Protocol:

• Duration: Minimum 30 minutes, optimally 60 minutes
• Method: Forced-air warming blanket
• Setting: High temperature (43°C)
• Timing: Immediately before induction
• Evidence: Reduces Phase 1 hypothermia by 50-80%

Evidence for Pre-warming:

[PMID: 9349887]

Practical Implementation:

• Patient arrives in holding bay
• Apply forced-air warming blanket
• Continue until transfer to OR
• Particularly important for elderly, paediatric, cachectic patients

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Therapeutic Hypothermia

Post-Cardiac Arrest Targeted Temperature Management

Therapeutic hypothermia after cardiac arrest has undergone significant evolution based on landmark trials.

Historical Context:

• 2002 landmark studies (Bernard et al., HACA group) demonstrated benefit of cooling to 32-34°C
• Initial guidelines recommended therapeutic hypothermia for all VF/VT arrest survivors
• TTM trial (2013) questioned optimal target temperature
• Current guidelines recommend targeted temperature management 32-36°C [PMID: 12393823]

Mechanisms of Benefit:

• Reduced cerebral metabolic rate (6-7% per 1°C decrease)
• Attenuated reperfusion injury
• Reduced excitotoxicity and calcium influx
• Decreased free radical production
• Reduced blood-brain barrier permeability
• Anti-inflammatory effects

Current Recommendations (ANZCOR Guidelines):

TTM2 Trial (2021):

• Compared hypothermia (33°C) vs normothermia (37.5°C) with fever prevention
• No significant difference in 6-month mortality
• No difference in functional outcomes
• Fever prevention may be key factor
• Current emphasis on avoiding hyperthermia (≤37.5°C) [PMID: 34133859]

Cooling Methods:

• Surface cooling (ice packs, cooling blankets)
• Intravascular cooling devices
• Cold IV saline (30 mL/kg 4°C crystalloid)
• Combination approach most effective

Complications of Therapeutic Hypothermia:

• Shivering (manage with sedation, neuromuscular blockade)
• Bradycardia (usually well-tolerated)
• Electrolyte disturbances (hypokalaemia, hypomagnesaemia)
• Coagulopathy
• Increased infection risk
• Hyperglycaemia
• Drug metabolism changes [PMID: 12393823]

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Malignant Hyperthermia

Cross-Reference

For comprehensive malignant hyperthermia coverage, see: Malignant Hyperthermia

Brief Overview

Malignant hyperthermia (MH) is a pharmacogenetic disorder triggered by volatile anaesthetics and succinylcholine.

Key Points:

• Incidence: 1:10,000-15,000 anaesthetics (Australia)
• Inheritance: Autosomal dominant (RYR1 gene mutations most common)
• Triggers: All volatile agents, succinylcholine
• Safe agents: Propofol, opioids, nitrous oxide, all non-depolarising muscle relaxants

Clinical Features:

• Early: Masseter muscle rigidity, tachycardia, increased ETCO2
• Classic: Hyperthermia (late sign), muscle rigidity, rhabdomyolysis, arrhythmias
• Temperature rise: May be rapid (2°C every 5 minutes)

Management:

1. Cease trigger agents immediately
2. Hyperventilate with 100% O2 (high flows)
3. Dantrolene 2.5 mg/kg IV bolus, repeat to 10 mg/kg
4. Active cooling
5. Treat hyperkalaemia, arrhythmias
6. Supportive ICU care

MHAUS Hotline (Australia): 1800 000 XXX

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Hyperthermia: Causes and Management

Causes of Perioperative Hyperthermia

Anaesthesia-Related:

• Malignant hyperthermia
• Serotonin syndrome
• Neuroleptic malignant syndrome
• Drug reactions
• Over-aggressive warming
• Excessive draping

Surgical/Medical:

• Sepsis/infection
• Blood transfusion reaction
• Thyroid storm
• Phaeochromocytoma
• Drug fever
• Central nervous system injury

Environmental:

• Excessive ambient temperature
• Overwrapping (paediatric patients)
• Malfunction of warming devices

Differential Diagnosis of Rapid Temperature Rise

Management of Hyperthermia

General Principles:

1. Identify and treat underlying cause
2. Cease potential triggers
3. Active cooling if temperature >39°C
4. Supportive care

Cooling Methods:

• Remove drapes and warming devices
• Cold IV fluids (not for volume-replete patients)
• Surface cooling (ice packs to groin, axillae, neck)
• Cooling blankets
• Evaporative cooling (wet patient, fan)
• Peritoneal lavage (severe cases)
• Intravascular cooling devices

Monitoring:

• Continuous core temperature
• Cardiac monitoring (arrhythmias with rapid temperature changes)
• Electrolytes (particularly potassium)
• Acid-base status

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Indigenous Health Considerations

Cultural Safety in Temperature Management

Aboriginal and Torres Strait Islander peoples, as well as Māori, may have specific considerations affecting perioperative temperature management that require culturally informed care.

Australian Indigenous Populations

Aboriginal and Torres Strait Islander peoples experience higher rates of chronic diseases including diabetes mellitus, cardiovascular disease, and chronic kidney disease, which increase susceptibility to perioperative hypothermia and its complications. Impaired peripheral circulation from diabetes increases redistribution hypothermia risk, while cardiac disease elevates the consequences of shivering-induced myocardial stress.

Key Considerations:

• Higher prevalence of peripheral vascular disease affecting passive heat distribution
• Chronic kidney disease may alter drug clearance of anti-shivering medications
• Remote community surgery may have limited warming equipment availability
• Longer transfer times from remote areas increase pre-existing hypothermia risk
• Cultural protocols may affect willingness to be undressed for warming devices

Aboriginal Health Workers and Aboriginal Liaison Officers should be engaged to ensure culturally safe communication regarding temperature monitoring procedures and warming strategies. Family involvement in perioperative care, consistent with many Indigenous cultural practices, can support patient comfort and compliance with warming protocols.

Māori Health Considerations

Māori patients similarly experience health disparities affecting perioperative thermal management. Higher rates of diabetes and cardiovascular disease (2-3 times non-Māori rates) increase hypothermia-related cardiac morbidity risk.

Tikanga Considerations:

• Physical contact required for temperature probes may require cultural explanation
• Tūpāpaku (deceased) protocols if fatal outcomes occur
• Whānau involvement in care decisions
• Māori Health Workers should be consulted for cultural guidance

Equitable access to warming equipment in rural New Zealand facilities serving Māori communities should be ensured. Pre-warming protocols may require adaptation for patients travelling long distances to surgical centres. [PMID: 29024541]

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SAQ Practice Question

Question

ANZCA Final Examination SAQ - 15 marks

A 72-year-old man is scheduled for open abdominal aortic aneurysm repair. His past medical history includes ischaemic heart disease (previous NSTEMI, drug-eluting stent 2 years ago) and type 2 diabetes mellitus. The anticipated surgical time is 4 hours. The ambient operating room temperature is 20°C.

(a) Describe the mechanisms and phases of hypothermia that occur under general anaesthesia. (6 marks)

(b) Outline the specific risks of perioperative hypothermia for this patient. (4 marks)

(c) Detail your perioperative temperature management strategy for this patient. (5 marks)

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Model Answer

(a) Mechanisms and phases of hypothermia (6 marks)

Anaesthetic Effects on Thermoregulation:

• General anaesthesia widens the interthreshold range from 0.2°C to approximately 4°C
• Vasoconstriction threshold reduced from 36.9°C to ~34.5°C
• Sweating threshold elevated to ~38°C
• Core temperature can drift without triggering compensatory responses

Three Phases of Hypothermia:

Phase 1 - Redistribution (0-1 hour):

• Primary mechanism of initial hypothermia (1.0-1.5°C decrease)
• Anaesthesia-induced vasodilation allows core heat to redistribute to periphery
• Internal heat redistribution, not external heat loss
• Magnitude proportional to pre-existing core-peripheral temperature gradient
• Cannot be prevented by intraoperative warming; requires pre-warming

Phase 2 - Linear Heat Loss (1-3 hours):

• Heat loss exceeds metabolic heat production
• Rate approximately 0.5-1.0°C/hour without active warming
• Heat loss via: radiation (40%), convection (30%), evaporation (20%), conduction (10%)
• Large surgical incision increases evaporative and radiant losses
• Continues until compensatory mechanisms activated

Phase 3 - Thermal Plateau (>3 hours):

• Core temperature decrease eventually triggers residual vasoconstriction
• Core heat conserved; plateau at new lower temperature (~34-35°C)
• Metabolic heat production equals heat loss
• May not be reached in procedures <3 hours

(b) Specific risks for this patient (4 marks)

Cardiac Morbidity:

• History of ischaemic heart disease with previous NSTEMI places him at highest risk
• Hypothermia increases catecholamine release (2-3 fold increase in noradrenaline)
• Shivering increases myocardial oxygen demand 200-600%
• Evidence shows hypothermia triples perioperative cardiac events in high-risk patients

Coagulopathy:

• Major vascular surgery with significant blood loss expected
• Hypothermia impairs coagulation enzyme function
• Platelet dysfunction (adhesion and aggregation impaired)
• 10% reduction in clotting factor activity per 1°C decrease
• Contributes to "lethal triad" with acidosis and coagulopathy

Wound Infection:

• Abdominal surgery infection risk increased 3-fold with hypothermia
• Diabetic patients already at elevated infection risk
• Vasoconstriction reduces wound oxygen tension
• Impaired neutrophil function

Prolonged Drug Action:

• Reduced hepatic metabolism prolongs muscle relaxant duration
• May result in delayed extubation
• 4-hour procedure increases risk of significant hypothermia

(c) Temperature management strategy (5 marks)

Pre-operative:

• Pre-warming with forced-air warming blanket for minimum 30 minutes before induction
• Target skin temperature >36°C before transfer to operating room
• Reduces core-peripheral gradient, minimizing redistribution hypothermia

Intraoperative Monitoring:

• Continuous core temperature monitoring (oesophageal or nasopharyngeal)
• Target core temperature ≥36°C
• Document temperature regularly per ANZCA PS18

Active Warming:

• Forced-air warming blanket over upper body and lower limbs (areas not in surgical field)
• Maximum coverage within surgical constraints
• Set to high temperature (43°C) from induction

Fluid Warming:

• All intravenous fluids through in-line fluid warmer
• Mandatory for this case given expected large volume crystalloid and blood products
• Target fluid temperature 37-41°C
• Use Level 1 or similar device for rapid transfusion

Ambient Environment:

• Increase operating room temperature to 22-24°C (balance with surgical team comfort)
• Minimize exposure of non-surgical areas

Post-operative:

• Continue active warming in recovery
• Treat shivering promptly (meperidine 25-50mg IV first-line)
• Avoid extubation if temperature <35°C
• Given cardiac history, ensure full recovery from hypothermia before emergence

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Viva Scenario

Opening Stem

Examiner: You are the anaesthetist for a 65-year-old woman undergoing total hip replacement under general anaesthesia. The procedure is expected to take 2 hours. Forty-five minutes into the case, the surgeon comments that there seems to be more oozing than expected. You note the core temperature is 34.8°C.

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Expected Dialogue

Examiner: What are your initial thoughts about the bleeding and hypothermia?

Candidate: The temperature of 34.8°C represents significant hypothermia (>1°C below normal) and is likely contributing to the increased surgical bleeding. Hypothermia impairs coagulation through several mechanisms:

• Platelet dysfunction with impaired adhesion and aggregation
• Reduced activity of temperature-dependent coagulation enzyme cascades
• Approximately 10% reduction in clotting factor activity per 1°C decrease
• Enhanced fibrinolysis

At 34.8°C, I would expect clinically significant coagulation impairment that could account for the increased oozing, though I would also consider other causes of bleeding.

Examiner: How would you address this situation?

Candidate: My approach would be:

Immediate Actions:

1. Confirm temperature measurement is accurate (check probe position)
2. Implement aggressive warming:
   • Increase forced-air warmer to high setting
   • Maximize blanket coverage
   • Confirm fluid warmer functioning; warm all IV fluids
   • Increase ambient OR temperature if possible
3. Assess blood loss and consider transfusion if indicated

Surgical Communication:

• Inform surgeon of hypothermia as likely contributor to bleeding
• Request additional haemostasis measures while warming continues
• Discuss potential for extended procedure time for rewarming

Laboratory Assessment:

• Check point-of-care coagulation (TEG/ROTEM if available) or send formal coagulation studies
• Check blood gas for pH and lactate (acidosis worsens coagulopathy)
• Note: Standard PT/aPTT measured at 37°C may underestimate in vivo impairment

Examiner: The procedure finishes. Core temperature is now 35.2°C. The patient begins shivering vigorously in recovery. What are your concerns?

Candidate: Post-anaesthetic shivering in this patient is concerning for several reasons:

Physiological Concerns:

• Oxygen consumption increased 200-600% during vigorous shivering
• Proportional increase in CO2 production
• Creates significant oxygen supply-demand mismatch
• Catecholamine surge with 2-3 fold increase in noradrenaline

Patient-Specific Risks:

• 65-year-old: Higher likelihood of underlying coronary disease
• Post-major surgery: Already stressed cardiovascular system
• Recent hypothermia-related coagulopathy: Risk of wound haematoma

Clinical Consequences:

• Tachycardia and hypertension increasing cardiac work
• Myocardial ischaemia risk in susceptible patients
• Delayed recovery and patient discomfort
• Increased ICP and IOP

Examiner: How would you manage the shivering?

Candidate: My management approach:

Active Warming:

• Continue forced-air warming as primary treatment
• Target normothermia (≥36°C)

Pharmacological Treatment:

• First-line: Meperidine (pethidine) 25-50mg IV
  • Most effective anti-shivering agent
  • Kappa-opioid receptor mediated effect
  • Reduces shivering threshold
• Alternatives:
  • Clonidine 75-150mcg IV (reduces shivering threshold)
  • Tramadol 100mg IV
  • Ondansetron 8mg IV
  • Magnesium sulphate 30mg/kg IV

Supportive Care:

• Supplemental oxygen to meet increased demand
• Monitor for myocardial ischaemia (ECG, symptoms)
• Ensure adequate analgesia (pain worsens shivering)

Examiner: How could you have prevented this scenario?

Candidate: Prevention is always preferable to treatment:

Pre-operative:

• Pre-warming for minimum 30 minutes with forced-air warming before induction
• This is the single most effective intervention to prevent redistribution hypothermia
• Reduces core-peripheral temperature gradient

Intraoperative:

• Start forced-air warming immediately upon induction, not waiting for surgical positioning
• Warm all IV fluids from start of case
• Maximize surface coverage with warming blankets
• Appropriate ambient OR temperature (21-24°C)
• Minimize exposure of non-surgical areas

Monitoring:

• Continuous core temperature monitoring per ANZCA PS18
• Target ≥36°C; intervene early if temperature trending down
• Document temperature regularly

In this case, a 2-hour procedure with a core temperature of 34.8°C at 45 minutes suggests inadequate warming measures and likely no pre-warming. Following evidence-based warming protocols would have maintained normothermia and avoided the coagulopathy and shivering complications.

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Key Points Summary

ANZCA Final Examination Key Points

1. Interthreshold range: General anaesthesia widens from 0.2°C to ~4°C, allowing passive temperature drift

2. Three phases: Redistribution (first hour, 1-1.5°C drop), linear heat loss (1-3 hours), thermal plateau (>3 hours)

3. Pre-warming: Only effective method to prevent redistribution hypothermia; minimum 30 minutes

4. Consequences: Coagulopathy (3-fold SSI increase, 22% more transfusion), cardiac morbidity (3-fold increase), prolonged drug action

5. Monitoring sites: Core sites (oesophageal, nasopharyngeal, PA catheter) vs peripheral (unreliable under anaesthesia)

6. Active warming: Forced-air warming is gold standard; fluid warming mandatory >500mL

7. Shivering: Increases O2 consumption 200-600%; treat with meperidine 25-50mg IV

8. TTM post-cardiac arrest: Target 32-36°C for ≥24 hours; avoid fever; slow rewarming 0.25-0.5°C/hour

9. MH: Rapid temperature rise >2°C/hour is concerning; temperature rise is late sign; treat with dantrolene

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References

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Last updated: February 2025 | Next review: February 2026 ANZCA Professional Standard PS18: Recommendations on Monitoring During Anaesthesia