Preoperative		Additional steroid cover
Patients currently taking steroids
<10 mg/day	Assume normal HPA function	Additional steroid cover not required
>10 mg/day	Minor surgery	25 mg hydrocortisone on induction
	Moderate surgery	Usual preoperative steroids + 25 mg hydrocortisone on induction + 100 mg/day for 24 h
	Major surgery	Usual preoperative steroids + 25 mg hydrocortisone on induction + 100 mg/day for 48–72 h
Patients stopped taking steroids
<3 months		Treat as if on steroids
>3 months		No perioperative steroids necessary

Equivalent steroid doses

• Hydrocortisone 20 mg

• Prednisolone 5 mg

• Methylprednisolone 4 mg

• Betamethasone 0.75 mg

• Dexamethasone 0.75 mg.

Bibliography

Alberti K.G., Thomas D.J. The management of diabetes during surgery. Br J Anaesth. 1979;51:693-703.

Annane D., Bellissant E., Bollaert P.E., et al. Corticosteroids in the treatment of severe sepsis and septic shock in adults: a systematic review. JAMA. 2009;301:2362-2375.

Bacuzzi A., Dionigi G., Del Bosco A., et al. Anaesthesia for thyroid surgery: perioperative management. Int J Surg. 2008;6:S8.

British National Formulary 59. http://bnf.org.bnf/extra/current/450062.htm. The reader is reminded that the BNF is constantly revised; for the latest guidelines please consult the current edition at www.bnf.org

Holdcroft A. Hormones and the gut. Br J Anaesth. 2000;85:58-68.

Lipshutz A.K.M., Gropper M.A. Perioperative glycemic control – an evidence-based review. Anesthesiology. 2009;110:408-421.

Malhotra S., Sodhi V. Anaesthesia for thyroid and parathyroid surgery. Contin Edu Anaesth, Crit Care Pain. 2007;7:55-58.

Mihai R., Farndon J.R. Parathyroid disease and calcium metabolism. Br J Anaesth. 2000;85:29-43.

NICE. Intraoperative nerve monitoring during thyroid surgery, 2008. March National Institute for Health and Clinical Excellence www.nice.org.uk/IPG255distributionlist ©c

Nicholson G., Burrin J.M., Hall G.M. Peri-operative steroid supplementation. Anaesthesia. 1998;53:1091-1104.

Pace N., Buttigieg M. Phaeochromocytoma. BJA CEPD Rev. 2003;3:20-23.

Robertshaw H.J., Hall G.M. Diabetes mellitus: anaesthetic management. Anaesthesia. 2006;61:1187-1190.

Smith M., Hirsh N.P. Pituitary disease and anaesthesia. Br J Anaesth. 2000;85:3-14.

Vaughan D.J., Brunner M.D. Anesthesia for patients with carcinoid syndrome. Int Anesthesiol Clin. 1997;35:129-142.

Webster N.R., Galley H.F. Does strict glucose control improve outcome? Br J Anaesth. 2009;103:331-334.

Malignant hyperthermia

Malignant hyperthermia (MH) is defined as a fulminant hypermetabolic state of skeletal muscle. The UK incidence is 1:200 000 in adults and 1:15 000 in children. Inheritance is autosomal dominant. There is a mortality of about 10% (improved from 24% in the 1970s).

The first description was published in the Lancet by Denbrough (Australia) in 1960. Animal model in Landrace pigs.

Signs

Early. Tachypnoea, rise in end-tidal CO₂, tachycardia, hypoxaemia, fever (>2°C.h⁻¹), masseter spasm.

Late. Generalized muscle rigidity (>75% cases), metabolic and respiratory acidosis, hyperkalaemia, increased muscle enzymes (CPK, LDH, SGOT) and myoglobinaemia.

Disease associations

ENT and trauma surgery (?because triggering agents used more often). Possibly myopathies and periodic paralysis. Kyphoscoliosis, pes cavus, squint and inguinal hernia are not now thought to be associated.

Triggering factors

• Definite – suxamethonium (may accelerate the onset of MH when using volatiles), all volatile agents (including isoflurane, desflurane and sevoflurane).

• Possible – atropine (may make attack more fulminant); phenothiazines (?neuroleptic malignant syndrome mistaken for MH).

• Unsure – stress, exercise.

Safe drugs

Opioids, all local anaesthetics, nitrous oxide, non-depolarizing neuromuscular blockers, benzodiazepines, propofol, thiopentone (delays onset of MH in animals), etomidate, ketamine, droperidol and metoclopramide.

Pathophysiology

Muscle contraction results from flooding of the cytoplasm by Ca²⁺ entering across the plasma membrane through voltage-gated Ca²⁺ channels and released from the sarcoplasmic reticulum (SR) through ryanodine-sensitive Ca²⁺ channels (Fig. 5.1). These channels occur in pairs where folds in the SR meet the sarcolemma of the t-tubule. The ryanodine (Ry₁) receptor is a large protein molecule comprising four identical monomers that sits between the two Ca²⁺ channels. Depolarization results in charge movement in the voltage-operated Ca²⁺ channels which activates the Ry₁ receptor to open and Ca²⁺ is released into the myoplasm. Volatile anaesthetic agents may increase the leak of Ca²⁺ through the Ry₁ protein, which does not cause clinical symptoms. In myopathic muscle, this leak may be sufficient to trigger a final common pathway with activation of contractile elements, ATP hydrolysis, O₂ consumption, CO₂ production, lactate and heat generation, uncoupling of oxidative phosphorylation, and cell breakdown with loss of myoglobin, CPK and K⁺ to cause the clinical picture of MH.

Figure 5.1 Mechanism of excitation–contraction coupling and calcium release in skeletal muscle.

All Landrace pigs have a defective ryanodine receptor, resulting from an arginine to cysteine mutation. Similar mutations have been found in about 5% of human MH cases, and glycine to arginine mutations have also been documented. The defective gene for mutations of the ryanodine receptor is located on or near the long arm of chromosome 19 (19q13.1 region). However, a number of MH families are not linked to this chromosome. There is evidence that mutations in other cytoplasmic proteins that contribute to the functioning of the Ry protein may also cause defective Ca²⁺ homeostasis (e.g. calsequestrin). Mutation of the α₂δ subunit of voltage-gated Ca²⁺ channels has also been documented in some patients with MH. In many cases, no genetic defects have been identified.

Dantrolene may bind to multiple sites other than the Ry protein. There is evidence that it may actually increase Ca²⁺ release, explaining why patients with MH treated with dantrolene may undergo a recrudescence of hypermetabolism.

Guidelines for the Management of a Malignant Hyperthermia Crisis

Association of Anaesthetists of Great Britain and Ireland 2007

Diagnosis

Consider MH if the following are together:

1. Unexplained, unexpected increase in end-tidal CO₂

2. Unexplained, unexpected tachycardia

3. Unexplained, unexpected increase in oxygen consumption.

Take measures to halt the MH process

1. Remove trigger drugs, turn off vaporizers, use high fresh gas flows (oxygen), use a new, clean non-rebreathing circuit, hyperventilate. Maintain anaesthesia with intravenous agents such as propofol until surgery completed.

2. Dantrolene: give 2–3 mg.kg⁻¹ i.v. initially and then 1 mg.kg⁻¹ PRN.

3. Use active body cooling but avoid vasoconstriction. Convert active warming devices to active cooling, give cold intravenous infusions, cold peritoneal lavage, extracorporeal heat exchange.

Monitor

ECG, SpO2, end tidal CO₂, invasive arterial BP, CVP, core and peripheral temperature, urine output and pH, arterial blood gases, potassium, haematocrit, platelets, clotting indices, creatine kinase (peaks at 12–24 h).

Treat the effects of MH

1. Hypoxaemia and acidosis: 100% O₂, hyperventilate, sodium bicarbonate.

2. Hyperkalaemia: sodium bicarbonate, glucose and insulin, i.v. calcium chloride (if in extremis).

3. Myoglobinaemia: forced alkaline diuresis (aim for urine output >3 mL.kg⁻¹.h⁻¹, urine pH >7.0).

4. Disseminated intravascular coagulation: fresh frozen plasma, cryoprecipitate, platelets.

5. Cardiac arrhythmias: procainamide, magnesium, amiodarone (avoid calcium channel blockers which interact with dantrolene).

ICU management

1. Continue monitoring and symptomatic treatment.

2. Assess for renal failure and compartment syndrome.

3. Give further dantrolene as necessary (recrudescence can occur for up to 24 h).

4. Consider other diagnoses, e.g. sepsis, phaeochromocytoma, myopathy.

5. Continue monitoring and symptomatic treatment.

Late management

1. Counsel patient and/or family regarding implications of MH.

2. Refer patient to MH unit.

Treatment

Admit patient to ITU. Do not stop treatment until symptoms have completely resolved, otherwise MH may recur (morbidity ∝ duration of symptoms). Continue dantrolene 1 mg/kg i.v. q.d.s. for up to 48 h (same dose can be given p.o. after 24 h).

Dantrolene. Each vial contains 20 mg orange dantrolene crystals and 3 g mannitol to aid solubility. Made up with 60 mL water to pH 9.5. Side-effects include phlebitis, nausea and vomiting, muscle weakness, uterine atony, placental transfer with fetal weakness, potentiation of non-depolarizing neuromuscular blockers, hyperkalaemia and CVS collapse.

Differential diagnosis

Overheating (blankets, heating mattress etc.), infection, thyrotoxicosis, phaeochromocytoma, transfusion reaction, CNS trauma, neuroleptic malignant syndrome, MAOIs, cocaine, tricyclics, atropine, glycopyrrolate, droperidol, ketamine, alcohol withdrawal and ecstasy.

Perioperative management of patients with known MH

Elective surgery. Run O₂ at 8 L/min through machine for at least 12 h preoperatively. Fit with new breathing circuit. Avoid triggering agents. Regional/local blocks are safe. Only use dantrolene prophylaxis (2.5 mg/kg i.v. preoperatively) if there is a risk of stress-induced MH or hypermetabolic state (e.g. thyrotoxicosis) because of dantrolene side-effects.

Dental patient. Any major surgery must be performed in hospital.

Obstetric patient. Stress of labour and delivery may increase susceptibility but dantrolene prophylaxis causes both increased blood loss due to uterine atony and fetal weakness. Best managed with early epidural. Rapid sequence induction must avoid suxamethonium (e.g. vecuronium 0.25 mg/kg). Obstetric drugs (terbutaline, oxytocin etc.) not shown to trigger MH.

Masseter muscle rigidity

There are three groups of patients:

1. Normal jaw stiffness

2. Jaw tightness interfering with intubation – change to safe drugs, carefully monitor and continue

3. True masseter muscle rigidity – jaw not able to be opened; 50% of children and 25% of adults are subsequently found to be MH-susceptible. Therefore, stop anaesthetic immediately and monitor closely for 24 h. Postoperative CPK >20 000 is highly suggestive of MH.

Screening

MH is autosomal dominant, so all parents, siblings and children should be screened. Muscle biopsy taken for in vitro halothane and caffeine contracture tests. The latter has been shown to have 97% sensitivity (3% false negatives) and 78% specificity (22% false positives). Genetic testing is now available to identify the 15 associated mutations identified on the myoplasmic RYR1 (ryanodine receptor) domain of the RYR gene.

Bibliography

Adnet P., Lestavel P., Krivosic-Horber R. Neuroleptic malignant syndrome. Br J Anaesth. 2000;85:129-135.

Association of Anaesthetists of Great Britain and Ireland. Guidelines for the management of a malignant hyperthermia crisis, 2007. Reproduced with the kind permission of the Association of anaesthetists of Great Britain and Ireland

Hopkins P.M. Malignant hyperthermia. Advances in clinical management and diagnosis. Br J Anaesth. 2000;85:118-128.

Robinson R.L., Hopkins P.M. A breakthrough in the genetic diagnosis of malignant hyperthermia. Br J Anaesth. 2001;86:166-168.

Anaesthesia for the morbidly obese patient

Prevalence of obesity continues to rise in both developed and developing countries (UK 700 000 people; USA 100 million). It is associated with a wide spectrum of medical and surgical pathologies.

Definition

Body mass index (BMI) = weight (kg)/height (m)². Normal = 22–28 kg/m².

• Obesity = BMI >30. Affects ≈︀25% of the population.

• Morbid obesity (MO) = BMI >35, or weight >ideal body weight (IBW) + 45 kg. Affects 1% of the population.

Pathophysiology

CVS. Increased blood volume, increased cardiac output by increased stroke volume, left ventricular hypertrophy; hypertension; increased O₂ consumption; cardiac autonomic dysfunction increasing risk of sudden death; fatty infiltration causing conduction blocks and arrhythmias. Hypertension. Increased risk of ischaemic heart disease and stroke.

Airway. Large tongue, high and anterior larynx, multiple chin skin folds and large breasts limit neck and head flexion/extension; fatty pharyngeal tissue narrows the airway.

Respiratory. Increased work of breathing, decreased compliance, decreased FRC <CC causes V/ mismatch and hypoxia, obstructive sleep apnoea progressing to Pickwickian syndrome (cor pulmonale, hypoxia, hypercapnia, polycythaemia). Increased O₂ consumption and low FRC cause faster desaturation.

GI. Increased gastric acidity and volume (90% of MO patients have gastric pH <2.5 and volume >25 mL). Incompetent lower oesophageal sphincter and hiatus hernia are common. Impaired liver function is common.

Renal. Increased GFR, increased renal clearance of drugs, microalbuminuria.

Other. Glucose intolerance, hyperlipidaemia and malignancies, osteoarthritis of weight-bearing joints.

Pharmacokinetic and pharmacodynamic changes

• Water-soluble drugs have similar V_D, clearance and half-life.

• Fat-soluble drugs, e.g. thiopentone, benzodiazepines and lignocaine, have ↑ V_D, ↑ half-life but normal clearance. Prolonged recovery does not occur with fat-soluble anaesthetic agents.

• Plasma protein levels and plasma protein binding are not changed significantly by obesity.

• Impaired hepatic and renal function may alter drug metabolism and elimination. Increased GFR increases clearance of drugs not biotransformed before renal excretion.

Drug doses

Some drug dosages may need to be altered for morbidly obese patients (see Table 5.2).

• High plasma cholinesterase levels, so use suxamethonium 1.5 mg/kg lean weight.

• Vecuronium dose should be based on lean body weight for normal recovery times.

• Atracurium dose should be based on absolute weight for normal recovery times.

Table 5.2 Changes in drug doses for morbidly obese patients

Unchanged dose per total weight	Unchanged dose per lean weight	Larger absolute dose but smaller dose per total weight
Midazolam	Vecuronium	Thiopentone
Diazepam	Propofol
Suxamethonium	Remifentanil
Pancuronium
Atracurium
Fentanyl
Alfentanil
Lignocaine

Perioperative management

OR preparation

Equipment must be able to cope with weight. Positioning and padding of the patient should be done with care. Excessive extension of head and limbs as they hang off the obese trunk may cause nerve injury. Lumbar support reduces backache. Powerful ventilator may be needed.

Premedication

Avoid intramuscular route. Sedative premed may cause respiratory depression in morbidly obese. Give antacid, H₂ antagonists and metoclopramide. Give anticholinergic if awake intubation is planned.

Monitoring

Use arterial line in all but the shortest cases (blood pressure cuffs overestimate BP if undersized). Capnograph, pulse oximeter, temperature, peripheral nerve stimulator (may need percutaneous electrodes). Consider arterial line and pulmonary artery catheter if there is cardiorespiratory disease.

Airway management

Endotracheal intubation is necessary because maintaining an airway with a face mask is difficult. There is a need for IPPV due to hypoventilation and risk of aspiration; 13% of MO patients are difficult intubations because of the presence of a fat pad at the back of the neck, and/or because of deposition of fat into the soft tissues of the neck. Such patients may also be at greater risk of acid reflux, and appropriate antacid prophylaxis should be instituted. Consider topically anaesthetizing upper airway and larynx in an attempt to visualize cords prior to induction. Awake intubation is recommended if >1.75 of IBW.

General anaesthesia

Rapid sequence induction with cricoid pressure. Dose on ideal body mass. Keep well relaxed. Balanced anaesthesia is recommended, using volatiles (sevoflurane gives quicker recovery than desflurane), opioids (remifentanil), non-depolarizing neuromuscular blockers ± extradural anaesthesia. N₂O has low fat solubility and minimal metabolism, but its use limits F_io₂.

Lithotomy, head-down and subdiaphragmatic packs may further impair respiration. IPPV is usually necessary. Use large tidal volumes based on IBW at 8–10 breaths/min. P_aco₂ <4 kPa increases shunt fraction. PEEP may improve oxygenation but lowers cardiac output and may reduce O₂ delivery.

Reversal

Neuromuscular block must be fully reversed and patient awake with protective upper airway reflexes before extubation.

Postoperative

Consider elective admission to ITU because of high risk of cardiorespiratory complications. Postoperative hypoxaemia may last for 6 days after intra-abdominal surgery so consider supplemental O₂ therapy on ward. Nurse at 30° head-up to reduce pressure of gut on diaphragm. High incidence of DVT, so use thromboprophylactic measures. Increased dose of anaesthetic drugs increases risk of renal and hepatic side-effects. Consider thromboprophylaxis.

Postoperative analgesia. There is perhaps a lesser need for opioid analgesics. Intramuscular injections are likely to be intrafat. Most reliable route is i.v., e.g. PCA. Epidural local anaesthetic or epidural opioid is associated with fewer postoperative respiratory complications and faster discharge home compared with i.v. opioids. Obstructive sleep apnoea syndrome is worse with opioids.

Regional/local anaesthesia

Local blocks may be difficult because of hidden anatomical landmarks. Use nerve stimulator. Epidural and subarachnoid blocks may not be as difficult as anticipated because there is less fat in the midline over the spine. Doses reduced by 20–25%, except normal doses for obstetric epidurals. Blocks above T₅ may cause respiratory compromise. Give supplemental O₂.

Never perform regional/local block unless able and ready to convert to a GA.

Perioperative Management of the Morbidly Obese Patient

Association of Anaesthetists of Great Britain and Ireland 2007

Key recommendations

All trained anaesthetists should be competent in the management of morbidly obese patients and familiar with the equipment and protocols in the hospitals in which they work.

All patients should have their height and weight recorded. Where possible this should be measured rather than relying on the patient’s estimate. The body mass index (BMI) should be calculated and recorded.

Although BMI is not an ideal measure of risk, it is the most useful of the currently available markers and is a simple measure to apply.

Every hospital should have a named consultant anaesthetist and a named theatre team member who will ensure that appropriate equipment and processes are in place for the perioperative management of morbidly obese patients.

Protocols including details of the availability of equipment should be readily to hand in all locations where morbidly obese patients may be treated.

Mandatory manual handling courses should include the management of the morbidly obese.

Preoperative assessment is a key component in the assessment and management of risk.

Early communication between those who will be caring for the patient is essential and scheduling of surgery should include provision for sufficient additional time, resources and personnel.

The absolute level of the BMI should not be used as the sole indicator of suitability for surgery or its location.

Bibliography

Association of Anaesthetists of Great Britain and Ireland: Peri-Operative Management of the Morbidly Obese Patient. Reproduced with the kind permission of the Association of Anaesthetists of Great Britain and Ireland, 2007.

Cheah M.H., Kam P.C.A. Obesity: basic science and medical aspects relevant to anaesthetists. Anaesthesia. 2005;60:1009-1021.

Lotia S., Bellamy M.C. Anaesthesia and morbid obesity. Contin Edu Anaesth, Crit Care Pain. 2008;8:151-156.

NICE. Obesity – guidance on the prevention, identification, assessment and management of overweight and obesity in adults and children, 2006. December National Institute for Health and Clinical Excellence www.nice.org.uk/CG043

Ogunnaike B.O., Jones S.B., Jones D.B. Anesthetic considerations for bariatric surgery. Anesth Analg. 2002;95:1793-1805.

Pieracci F.M., Barie P.S., Pomp A. Critical care of the bariatric patient. Crit Care Med. 2006;34:1796-1804.

Saravanakumar K., Rao S.G., Cooper G.M. Obesity and obstetric anaesthesia. Anaesthesia. 2006;61:36-48.

Metabolic response to stress

The stress response is an evolutionary response that has evolved to protect the body from injury and enhance chances of survival. Comprises a cardiovascular, thermoregulatory and metabolic response. It was first described by Cuthbertson in 1929.

The metabolic response is initiated by:

• Afferent neuronal input (somatic and autonomic) from operative site triggering neuroendocrine response

• Release of interleukins and histamine from damaged tissue, triggering synthesis of acute-phase proteins (cytokines [IL-1β, IL-2, IL-6], tumour necrosis factor, C-reactive protein, fibrinogen, complement and interferons) involved in haemostasis, tissue repair and regeneration.

This neurohumoral response (Fig. 5.2) converges on the hypothalamus to trigger:

• sympathetic response (rapid) – release of adrenaline and noradrenaline

• hormonal response (slow)

– increased catabolic hormones: ACTH, prolactin, glucagon, catecholamines, GH

– decreased anabolic hormones: insulin, testosterone, T₃

• metabolic response – increased breakdown of carbohydrate, lipid and protein and reduced peripheral glucose utilization. Results in thermogenesis, hyperglycaemia, acute-phase protein synthesis, leucocytosis, salt and water retention, and mineral and electrolyte imbalance. Decreased skeletal muscle protein, plasma divalent cations and zinc.

Figure 5.2 Metabolic changes triggered by the stress response.

Effects of surgery

Rapid increase in cytokines (particularly interleukin IL-6), proportional to degree of tissue damage. Laparoscopy is associated with reduced IL-6 levels compared with open laparotomy, but adrenaline and noradrenaline release is the same in both groups, i.e. visceral afferent stimulus is the main factor triggering the neuroendocrine response and is only ablated by complete block of sensory fibres.

Effects of anaesthesia on the stress response

Opioids

Low dose fentanyl (<15 μg.kg⁻¹) does not modify cytokine response to surgery. High-dose fentanyl (>50 μg.kg⁻¹) inhibits cortisol and GH responses to pelvic surgery but >100 μg.kg⁻¹ is required for upper abdominal surgery. High-dose opioids suppress most hormonal responses to surgery but not those triggered by cardiopulmonary bypass.

Induction agents

Etomidate inhibits 11β-, 17α- and 18β-hydroxylase and increases mortality in critically ill patients sedated with the drug. A single induction dose is not associated with adverse effects. Midazolam reduces adrenocortical response to major upper abdominal surgery.

Volatiles

Less effective than narcotics in suppressing the stress response. May contribute to hyperglycaemia by inhibiting insulin release.

Regional anaesthesia

Only affects those aspects of the stress response that are mediated by afferent neuronal stimulation. There is no evidence that neuronal blockade can decrease the inflammatory response to surgery. Complete afferent blockade (somatic and autonomic) is required to prevent the neuroendocrine response. Complete neuronal block can only be achieved for limbs, pelvic organs and the eye. Extradural block for pelvic surgery does not affect IL-6 levels but prevents anterior pituitary hormone changes and blocks catecholamine-mediated metabolic changes. Less effective for upper abdominal and thoracic procedures, probably because of incomplete blockade of afferent fibres.

Benefits of modifying the stress response

It is generally agreed that it is beneficial to decrease stress response in patients with cardiovascular disease. Neonates undergoing cardiac surgery show a decreased stress response when anaesthesia is supplemented with sufentanil and may suffer fewer postoperative complications.

There is no evidence that limiting the endocrine and metabolic responses to surgery is of benefit in all patients. However, regional anaesthesia may reduce complications in elderly high-risk patients (decreased CVS and respiratory complications, reduced hospital stay) but further studies are needed.

Patients on steroid therapy require supplementary doses perioperatively. However, excess may cause side-effects, particularly:

• impaired wound healing

• increased risk of infection

• hyperglycaemia

• stress ulcers

• fluid retention causing hypertension

• psychiatric disturbance.

Bibliography

Burton D., Nicholson G., Hall G. Endocrine and metabolic response to surgery. Contin Edu Anaesth, Crit Care Pain. 2004;4:144-147.

Desborough J.P. The stress response to trauma and surgery. Br J Anaesth. 2000;85:109-117.

Thermoregulation

Physiology

Normal thermoregulation

• Closely controlled at 37 ± 0.2°C

• Small deviation causes large physiological impact.

Afferent input

Warm receptors

• Quiescent at normothermia and increase rate of firing as temperature increases

• Unmyelinated C fibres.

Cold receptors

• Fire continuously and increase rate of firing as temperature decreases

• Aδ nerve fibres.

Five main areas each supply approximately 20% of sensory thermal input (Fig. 5.3). Core structures comprise 80% of this input, whereas the periphery is only 20% of the total input.

Figure 5.3 Sensory thermal input to the hypothalamus.

Central control

• Integration of afferent input begins in the spinal cord

• Further integration in the pre-optic nuclei of the anterior hypothalamus

• Reflex spinal cord pathways may control some responses

• Impaired control in elderly, obese, malnourished and severely ill.

Measurement

Nasopharyngeal and tympanic membrane temperature are good indicators of brain temperature. Axillary temperature is a less accurate measure of core temperature. Changes in rectal temperature lag behind changes at other core sites. Also blood temperature (via pulmonary artery catheter), bladder temperature and oesophageal temperature. Skin temperature is dependent upon skin blood flow.

Perioperative hypothermia

Perioperative hypothermia develops in three phases (see Figs 5.4 and 5.5):

1. Change in temperature distribution. GA causes peripheral vasodilation with ↑ peripheral temperature and ↓ core temperature, redistributing heat from core to periphery. Temperature (heat) content remains constant.

2. Linear phase. Slow decrease for 2–3 h as heat loss exceeds production. Heat is lost by radiation (40%), convection (30%), evaporation (20%) and conduction (10%) (Fig. 5.6). Heat loss is accelerated by naked patient in cold environment, cold skin preparation, cold i.v. fluids and cold gases from ventilator. GA decreases basal metabolic rate (BMR) with 15% less heat production and impairment of compensatory mechanisms. The greatest influence on heat loss is the operating room temperature.

3. Plateau phase. Temperature becomes constant as thermoregulatory vasoconstriction limits heat loss to a rate equal to heat production.