Inadvertent Hypothermia

DEFINITIONS
- Hypothermia: temperature <= 36°C
- Interthreshold range over which no thermoregulation occurs is extremely narrow - 0.4°C; under anaesthesia this increases to >= 3°C

THERMOREGULATION

(a) HEAT GAIN

Shivering
- high energy cost;
- increases VO2;
- 4-6 fold increase in heat production, 80% retained;
Chemical thermogenesis
- NST in neonates;
- thyroid hormone influence in adult on BMR;
Vasoconstriction
- enhances insulation;
Piloerection
- trivial in humans;
Behavioural adaptation.

(b) HEAT LOSS

Physical
- convection, conduction, radiation -> 75% heat loss;
- evaporation, insensible water losses -> remaining 25%.
Physiological mechanisms
- vasodilatation,
- sweating,
- panting (trivial in humans).

CONTROL MECHANISMS

(a) AFFERENT - thermoreceptors:
Peripheral - skin, viscera, skeletal muscle;
Central - spinal cord, midbrain lower pons (~ 20% contribution);

(b) CENTRAL CONTROLLER - hypothalamus;

(c) EFFECTORS - somatic and autonomic nervous systems -> peripheral effector systems.

PAEDIATRIC CONSIDERATIONS

(a) Increased heat loss:
- increased SA: body weight ratio;
- head relatively larger;
- increased transdermal water loss (preterm infants);
- thinner layer of skin and subcutaneous fat;
- smaller body mass \ body heat sink less;
- no shivering in the neonate during first few days unless TA <= 15°C.
(b) Zone of thermoneutrality:
- critical TA = 33°C at birth (below which heat production increases);
- 32°C by PGA = 2 weeks;
- 1 kg premature infant = 35.5°C;
- clothing decreases critical temperature by 6-8°.
(c) Heat loss mechanisms - neonate:
- 6x sweat gland density -> 1/3 response;
- cold stress -> NST, increased VO2 unless ill;
- conduction, convection, radiation, insensible losses.
(d) Heat gain mechanisms - neonate:
- NST - NA -> beta1-receptors brown fat;
- vasoconstriction.
(e) Consequences of hypothermia
- delayed recovery, CVS depression, lethargy, increased aspiration risk, cardiac arrhythmias, persistent foetal circulation. Changes reversible on rewarming.

MEASUREMENT OF BODY TEMPERATURE

SITE	COMMENT
Tympanic membrane	Close to ICA; good reflection of core temp; minimal lag time; trauma; heparinised patients
Nasopharyngeal	Also close to ICA; epistaxis; respiratory gases
Oesophageal	24 cm below larynx -> between aorta and LA
Rectal	Prolonged lag time; stool; affected by peritoneal lavage, cystoscopy etc
Bladder	Better reflection of core temp. but accuracy varies with urine flow rate
PA catheter	Mixed venous blood temperature; accurate Tc
Skin	Neonates - core-periph. gradient; affected by peripheral perfusion, sweating, vasoconstriction etc

Axillary - 0.5 - 1°C < oral;
Oral - 0.5 - 1°C < rectal; diurnal fluctuation - oral - 36.1°C in a.m. -> 38°C in evening.

EFFECT OF ANAESTHESIA ON THERMOREGULATION

Widens interthreshold range from 0.4 - 3°C. patient rendered poikelothermic
Decreases BMR by up to 15% routinely;

(a) PREOPERATIVE FACTORS:
(i) Age of patient - neonate/child vs adult vs geriatric patient;
Elderly - over 60 average heat production: 30 kcal.m^-2.h^-1 vs
- 20-40 year age group : 40 kcal.m^-1.h^-1;
Neonates - low birth weight/prem., severe hypothermia - incVO2, intrapulmonary haemorrhage, acidosis, apnoea, PFC, VF;
(ii) Trauma, alcohol intoxication, resuscitation fluids, severe illness;

(b) INTRAOPERATIVE PERIOD
(i) Exposure
- cold OR (TA 21-24° -> temp. stable at 36°C; <= 18°C all pts lost heat);
- clothes shed, cold irrigant, cold table, cold skin prep;
(ii) Cold IV fluids
- 1 unit cold bank blood requires 127 kJ to warm it, and decreases TB by 0.25-0.5 °C ;
- Infusion of 6-8 litres crystalloid at 20°C -> 2° body temp. decline - 1 litre = thermal loss of 71kJ on warming to 37°;
(iii) Evaporative heat losses
- dry anaesthetic gases,
- body cavity exposure,
(iv) Anaesthetic drugs
1. Volatiles
- depress threshold for thermoregulation 2-3°C;
- promote vasodilatation;
- muscle relaxation -> impede shivering;
2. Opioids
- potent sympatholytics - depress threshold ~ = volatiles;
3. Muscle relaxants
- prevent shivering;
4. Phenothiazines, barbiturates, butyrophenones
-> vasodilatation decTB;
5. Vasodilators
- promote heat loss.
(v) Regional anaesthesia
- hypothalamic thermoregulation intact -> heat loss enhanced by vasodilatation and impaired shivering below the level of the block. NB cold IV fluids.
(vi) Long operations

(c) POSTOPERATIVE PERIOD
(i) Continued exposure in recovery room, ICU;
(ii)Further IV infusions, irrigation etc;
(iii) Residual effects of regional anaesthetic (spinal/ED);

(d) MEDICAL CONDITIONS PREDISPOSING TO HYPOTHERMIA
1. Skin loss - burns, severe exfoliating dermatoses;
2. Autonomic neuropathy - para/quadriplegia, diabetes, uraemia;
3. Acute alcohol intoxication;
4. Endocrinopathies - myxoedema, adrenal insufficiency;
5. General debilitation;
(6. Sickle cell diseases - hypothermia can precipitate a crisis).

STAGES OF INTRAOPERATIVE HEAT LOSS
1. Initial sudden fall as heat redistributes from core to periphery - 1-1.5° fall in TC - very difficult to prevent.
2. Slower decline of 0.3-1.0 °/hour as net heat loss to environment occurs; net heat loss ~ 42-67 kJ.h^-1.
3. Plateau at ~ 34.5° - vasoconstriction esp. hands and feet with 25% reduction in rate of heat loss.

PHYSIOLOGICAL CONSEQUENCES OF HYPOTHERMIA

(a) CNS

TEMPERATURE (°C)     PHYSIOLOGICAL CHANGE(S)                                      
      33                Decreasing LOC                                               
      30                61% decrease in CBF; unconscious; with pupillary dilatation  
      28                65% decrease in CBF (and CMR)                              
      20                Isoelectric EEG                                              
      15                50 minutes of total circulatory arrest tolerated             
 
 

(b) RESPIRATORY SYSTEM
(i) (L) Shift in HbO2 dissociation curve reflecting increased affinity of Hb for O2 ;
(ii) Increased dissolved O2, CO2, and inhalational agents (also more potent);
(iii) SaO2 remains constant in spite of change in solubility;
(iv) Increased solubility slows rise in agent tension -> slower induction (opposed by lowering of MAC 2° to hypothermia);
(v) If saturation is over 90% the decrease in PaO2 = 7.2%/1°C;
(vi) Decreased CO2 production -> respiratory alkalosis with "normal" IPPV;
(vii) Temp < 24-26°C respirations cease;
(viii) Must use corrected blood gas values for calculation of P(A-a)O2 gradient;
(ix) Impairment of HPV.

(c) CVS

Temperature (°C)         Physiological change(s)                                      
           34            Vasoconstriction -> increased afterload                      
           32            Decreased contractility and CO                               
           30            Arrhythmias and conduction disturbances start at ~31°C;
                             30-40% decrease in CO J waves on ECG                   
        26 - 28          Spontaneous VF                                               
         ~ 20            Asystole                                                     
 
 

ECG changes - (all intervals increase) - QRS widening, "J" waves (pathognomonic below 30°C), P-R prolongation, ST elevation and T inversion.

(d) METABOLISM
6-7% decrease in BMR per 1°C -> 50% reduction by 28°C;
Depression of liver and renal function;
Catecholamine release, insulin resistance -> hyperglycaemia below ~ 32°C;
Lactate, citrate, heparin metabolism inhibited.

(e) ACID-BASE BALANCE
Acidosis - increased dissolved CO2;
- respiratory insufficiency;
- decreased CO;
- depression of renal and hepatic acid disposal;
Measurement - correction factors apply to ABG values tested at 37°C.

(f) RENAL
Decreased RBF, GFR (50% at 30°C), tubular reabsorption (especially Na⁺);
< 30°C -> reduced concentrating ability;
Saline diuresis can continue after normothermia restored.

(g) HAEMATOLOGICAL
(i) Rheology - increased viscosity -> sludging and reduced flow;
(ii) Coagulation:
- thrombocytopathy due to decthromboxane synthesis;
- thrombocytopoenia - sequestration portal circulation in deep hypothermia.;
- coagulation abnormalities not seen in blood tested at 37°.
- increased O2 affinity of Hb, etc.

(h) PHARMACOLOGICAL - Alteration pharmacokinetics/dynamics:
Impaired renal and hepatic function, acid-base changes, Hoffman elimination slowed,
- MAC halothane decrease 5%/°C;
- increased solubility of volatile agents;
- NMBs - curare, pancuronium -> prolonged action by:
(a) initial increase in ACh release in response to fall in temperature,
(b) reduces ACh mobilisation into readily available stores -> depletion;
- vecuronium duration doubled at 34°C;
- atracurium prolonged - t1/2 doubled at 26°C;
- changes in ionisation fractions/protein binding etc.

(g) MISCELLANEOUS
Delays wakening
Postop shivering -> increases VO2 -> decreases SvO2 -> adverse cardiac sequelae.

CONTROL OF BODY TEMPERATURE UNDER ANAESTHESIA

(a) Ambient temperature
Maintain 21-24°C for adults, higher with children (30-32°C), and higher still during neonatal procedures, burns etc;
Humidity, airflow also important.
(b) Insulation - wrapping exposed skin - children especially;
(c) Humidification of inspired gases
Evaporative heat loss from respiratory tract using dry gas mixtures:
- (2.45kJ.ml^-1) x volume lost = 6.45 kJ.h^-1.litre MV^-1.
Provision of fully saturated gases at 37°C results in reduction of net heat losses of 44 - 67 kJ.h^-1.
(i) HME - provide gases at 27°C and 85% RH with NRB systems;
- 29°C and 99% RH with circle system;
- saves 3-4 kJ.h^-1.litre MV^-1.
(ii) Circle system alone - 25°C and 40% RH - no additional humidification;
- reduce heat loss by 1.26 kJ.h^-1.litre MV^-1.
(iii) Heater humidifiers -> 37°C, 100% RH, 44 gH2O.L^-1;
Problems - rainout
- contamination,
- water overload (neonates);
- "hot pot tracheitis" - thermal burns (rare).
(d) Warming mattresses
Conductive heat transfer; ineffective if used alone, affecting 1/3 BSA;
Used with humidification -> more effective than either alone
Unheated towelling insulation (of exposed parts) similarly effective in conjunction with humidification (children).
Metallised "space " blankets ineffective preventing intraoperative heat loss.
(e) Forced-air exchange blanket
"Bair Hugger" - very effective insulation & active warming intra/postop;
Modifications permit intraoperative use, covering all or part of exposed surfaces.
Should not be applied to areas of reduced perfusion eg. distal to arterial clamp -> O2 supply-demand imbalance.
(f) Radiant heaters
Increase cutaneous thermal input to HT thermoregulating centre -> effectively reduce shivering , providing sensation of comfort even when central hypothermia persists.
Caution thermal burns.

PHYSIOLOGICAL AND PHYSICAL DATA
(i) Latent heat of vaporisation: 2.45 kJ.ml^-1;
(ii) Respiratory heat (dry gases): 6.45 kJ.h^-1.litre MV^-1;
(iii) Heat derived from basal metabolism: 167 kJ.m^-2.hr^-1;
(iv) Max. rate of sweating: 2 l.h^-1 -> calc'd heat loss of 2.7 MJ.m^-2.h^-1;
(v) Maximal daily sweat volume ~ 5 litres.day^-1.