8 Endocrine and metabolic disease

Acromegaly 162

Thyroid disease 164

Parathyroid disorders 168

Adrenocortical insufficiency 170

The patient on steroids 172

Cushing's syndrome 174

Conn's syndrome 176

Apudomas 178

Hypokalaemia 182

Hyperkalaemia 184

Hyponatraemia 186

Hypernatraemia 187

Obesity 188

See also:

 Hypercalcaemia 584

 Hypocalcaemia 583

Inhibitory (physiologically more important)—inhibits lipolysis, proteolysis, glycogenolysis, gluconeogenesis, and ketogenesis.

Type II diabetes (80%): a disease of adult onset, associated with insulin resistance. Patients produce some endogenous insulin and their metabolic state often improves with fasting. The treatment may be diet control, oral hypoglycaemics, and/or insulin.

Renal: 40% of diabetics develop microalbuminuria, which is associated with hypertension, ischaemic heart disease, and retinopathy. This may be reduced by treatment with ACE inhibitors.

Respiratory: diabetics are prone to perioperative chest infections, especially if they are obese and smokers.

Airway: thickening of soft tissues (glycosylation) occurs, especially in ligaments around joints leading to limited joint mobility syndrome. Intubation may be difficult if the neck is affected or there is insufficient mouth opening.

Gastrointestinal: 50% of patients have delayed gastric emptying and are prone to reflux.

Diabetics are prone to infections.

Test urine for ketones and glucose.

Measure glycosylated haemoglobin (HbA1_c), a measure of recent glycaemic control (normal 3.8–6.4%). If HbA1_c is 7.5–10%, highlight suboptimal control to GP. Surgery may proceed with caution. A value >10% suggests inadequate control. Refer to diabetic team and only proceed if surgery is urgent.

Stop long-acting oral hypoglycaemics, e.g. metformin and glibenclamide, 24hr before surgery. Chlorpropamide should ideally be stopped 3d before surgery because of its long action and substituted with a shorter-acting drug such as gliclazide. It is no longer recommended in the UK.

Individuals with type 1 diabetes should NEVER go without insulin as they are at risk of diabetic ketoacidosis.

Glucose/insulin infusions should be administered through the same cannula to prevent accidental administration of insulin without glucose. Both infusions should be regulated by volumetric pumps, with an antireflux valve on the IV glucose line.

Hartmann's solution is controversial as lactate converts rapidly to glucose in the fasted state. Saline may be a more appropriate choice.

Check blood glucose hourly.

Consider a rapid sequence induction if gastric stasis is suspected.

Regional techniques may be useful for extremity surgery and to reduce the risk of undetected hypoglycaemia. Document any existing nerve damage.

Autonomic dysfunction may exacerbate the hypotensive effect of spinals and epidurals.

Characteristic signs are tachycardia, light-headedness, sweating, and pallor. This may progress to confusion, restlessness, incomprehensible speech, double vision, convulsions, and coma. If untreated, permanent brain damage will occur, made worse by hypotension and hypoxia.

Anaesthetised patients may not show any of these signs. Monitor blood sugar regularly and suspect hypoglycaemia with unexplained changes in the patient's condition.

If hypoglycaemia occurs, give 50ml of 50% glucose IV (or any glucose solution available) and repeat blood sugar measurement. Alternatively give 1mg of glucagon (IM or IV); 10–20g (2–4 teaspoons) of sugar by mouth or nasogastric tube is an alternative.

If K⁺ <4.5mmol/l, add 10mmol KCl to each 500ml bag dextrose.

Start IV insulin infusion using a syringe pump. Adjust according to sliding scale below. Test blood glucose hourly initially. Patients on >50U of insulin/day will need higher doses of insulin by infusion.

Calculate total daily insulin requirement from the preceding 24hr or the usual daily amount. Divide by four and give each dose just before meals and at bedtime.

Adjust doses as necessary.

If on sliding scale, stop sliding scale an hour after subcutaneous insulin injection.

Add 10–15U soluble insulin, plus 10mmol potassium chloride per 500ml bag.

Infuse at 100ml/hr.

Provides insulin 2–3U/hr, potassium 2mmol/hr, and glucose 10g/hr.

Airway: difficult airway management/intubation may occur—check for large jaw, head, tongue, lips, and general hypertrophy of the larynx and trachea. Also vocal cord thickening or strictures and chondrocalcinosis of the larynx. Consider direct/indirect laryngoscopy preoperatively if vocal cord or laryngeal pathology is suspected. Snoring and daytime somnolence may indicate sleep apnoea. Look for enlargement of the thyroid (25%) which may compress the trachea.

Drugs: somatostatin analogues (octreotide, lanreotide) may cause vomiting and diarrhoea. Bromocriptine, a long-acting dopamine agonist, is often used to lower growth hormone levels. It can cause severe postural hypotension.

Neurological: symptoms and signs of raised intracranial pressure.

CXR if cardiorespiratory problems.

Blood glucose—25% of cases are diabetic.

Positioning may be difficult due to size. A long table may be required.

Nerve compression syndromes are common so take care to protect vulnerable areas (ulnar nerve at the elbow, median nerve at the wrist, and common peroneal nerve below the knee).

Experience shows more problems with extubation than intubation.

If evidence of sleep apnoea, extubate the patient awake and sitting up.

Cardiovascular complications include decreased blood volume, cardiac output, and heart rate with a predisposition to hypotension and ischaemic heart disease. Pericardial effusions also occur.

Also associated with anaemia, hypoglycaemia, hyponatraemia, and impaired hepatic drug metabolism.

If clinical evidence of hypothyroidism, delay elective surgery to obtain euthyroid state. Liaise with endocrinologist. Suggest levothyroxine (T₄) (starting dose 50 microgram increasing to 100–200 microgram PO over several weeks). The elderly are susceptible to angina and heart failure with increasing cardiac work caused by thyroxine, so start with 25µg and increase by 25 mg at 3–4-weekly intervals.

If surgery is urgent then liothyronine (T₃) (10–50µg slow IV with ECG monitoring or 5–20 microgram in patients with known or suspected cardiac disease, followed by 10–25 microgram 8-hourly) can be used, but this is more controversial.

β-blockade (propranolol 30–60mg tds) is also started if there are signs of tremor or palpitations. The non-cardioselective β-blockers such as propranolol are more effective than the selective ones. β₁ adrenergic blockade treats the symptoms of tachycardia, but β₂ adrenergic blockade prevents peripheral conversion of T₄ to T₃.

Airway: look for tracheal deviation—a large goitre can cause respiratory obstruction. This is a particular problem when the gland extends retrosternally. Ask the patient about positional dyspnoea and dysphagia. Look for evidence of tracheal compression with shortness of breath, dysphagia, and stridor (occurs with 50% compression). Infiltrating carcinoma may make any neck movement difficult and is an independent predictor of difficult intubation.

Superior vena caval obstruction can occur. Look for distended neck veins that do not change with respiration.

Check for other autoimmune disorders.

CXR and thoracic inlet views essential to assess tracheal compression.

If tracheal compression present, perform CT or MRI scan to reveal site and length of narrowing and also presence of any calcification.

Refer to ENT surgeon for indirect laryngoscopy to document any preoperative vocal cord dysfunction.

Low metabolic rate predisposes to hypothermia, so actively warm.

Drug metabolism can be slow. Monitor twitch response and reduce dose of relaxants and opioids.

Usually presents 6–24h post-surgery with fever (>40°C), sweating, sinus tachycardia (>140bpm), coma, nausea, vomiting, and diarrhoea.

Rehydrate with IV saline and glucose.

Treat hyperthermia with tepid sponging and paracetamol. Do not give NSAIDs or aspirin as these displace thyroid hormone from serum binding sites.

Give propranolol (1mg increments up to 10mg) with CVS monitoring to decrease pulse rate to <90bpm. Alternatively give esmolol (loading dose 250–500µg/kg followed by 50–100µg/kg/min).

Give hydrocortisone (200mg IV qds) to treat adrenal insufficiency and to decrease T₄ release and conversion to T₃ at very high levels.

Give propylthiouracil (1g loading dose via nasogastric tube followed by 200–300mg qds). This inhibits thyroid hormone release and also decreases peripheral conversion of T₄ to T₃.

After blockade by propylthiouracil, give sodium iodide (500mg tds IV), potassium iodide (5 drops qds via nasogastric tube), or Lugol's iodine (5–10 drops qds via nasogastric tube).¹

Characterised by coma, hypoventilation, bradycardia, hypotension, and a severe dilutional hyponatraemia.

Precipitated by infection, trauma, cold, and central nervous system depressants.

Rehydrate with IV glucose and saline.

Stabilise cardiac and respiratory systems as necessary. May require ventilation.

Sudden warming may lead to extreme peripheral vasodilatation, so use cautious passive external warming.

Give levothyroxine 200–400µg IV bolus, followed by 100µg the next day. Use smaller doses in patients with cardiovascular disease.

Patients should first receive stress dose steroids (e.g. hydrocortisone 100mg qds IV), in case they have concomitant primary or secondary adrenal insufficiency, a common result of hypothyroidism.

Consider a combination of intravenous T₃ and T₄, particularly if urgent surgery required.² The conversion of T₄ to T₃ is suppressed in hypothyroid coma and T₃ is more active than T₄. For doses of IV T₃ see p. 164.

Transfer to ICU.

Presentation—50% of cases are asymptomatic and presentation often subtle. May present with anorexia, dyspepsia, nausea, vomiting and constipation, hypertension, shortened QT interval, polydipsia, polyuria, renal calculi, depression, poor memory, and drowsiness.

Serum calcium >4.5mmol/l is life-threatening and can be rapidly but transiently lowered with phosphate (500ml of 0.1M neutral solution over 6–8hr).

Rehydrate (4–6 litres of fluid often required).

Pamidronate (60mg in 500ml saline over 4hr) is first-line treatment. Effect is rapid and long lasting.

Calcitonin (3–4U/kg IV then 4U/kg SC bd). Causes a rapid but temporary decrease in skeletal release of calcium and phosphate.

Second-line treatment, once volume repletion has been achieved, is with forced saline diuresis with furosemide (40mg IV every 4hr). Loop diuretics decrease the proximal tubular resorption of calcium. Consider central pressure monitoring in elderly at risk of left ventricular failure.

Hydrocortisone (200–400mg IV daily) in patients with malignancy.

Dialysis is reserved for patients with renal failure.

Parathyroid hyperplasia causes a high PTH, normal or low calcium level, and a high phosphate level.

Usually presents as excessive bone resorption (seen earliest in the radial aspect of the middle phalanx of the second digit) or soft tissue calcification of the vascular and soft tissues including kidneys, heart, lungs, and skin.

Treat medically with dietary phosphate restriction, calcium, and vitamin D supplements. Medical therapy fails in 5–10% of patients on long-term dialysis and surgery becomes necessary.

Risks of surgery are bleeding, recurrent hyperparathyroidism, hypoparathyroidism, and injury to the recurrent laryngeal nerves. Patients should undergo dialysis within 1d of surgery and then 48hr postoperatively or as required.

Watch for postoperative hypocalcaemia and hypomagnesaemia.

Careful monitoring of neuromuscular blockade should be undertaken if non-depolarising muscle relaxants are used.

Results in hypocalcaemia—ionised calcium <0.9mmol/l, total calcium (corrected for albumin) <2.2mmol/l. Trough level usually occurs at 20hr following parathyroidectomy and typically normalises by day 2–3.

The presenting features are due to low calcium levels and manifest as carpopedal spasm, tetany, dysrhythmia, hypotension, and prolonged PR interval on ECG.

Treat with calcium (calcium gluconate 10ml 10% IV over 10min, followed by 40ml in 1 litre saline over 8hr).

Low serum magnesium is also common and can be treated with magnesium sulphate (1–5mmol IV slowly).

Fludrocortisone (0.1mg PO) to replace aldosterone (primary deficiency only)

4-hourly blood glucose and daily electrolytes.

Joint care with an endocrinologist is advisable.

With respect to mineralocorticoid potency, 20mg hydrocortisone is equivalent to 0.05mg fludrocortisone, so with hydrocortisone doses of 50mg or more, mineralocorticoid replacement in primary adrenal insufficiency can be reduced.

IV fluids. Colloid to restore blood volume, saline to replace Na⁺ deficit initially at 1000ml/hr and glucose for hypoglycaemia.

Hydrocortisone 200mg stat followed by 100mg qds. Baseline cortisol and ACTH prior to administration of hydrocortisone. Dexamethasone (4mg IV) can be used if the diagnosis has not been confirmed, since this does not interfere with measurement of cortisol and ACTH stimulation testing.

Inotropes/vasopressors as required. May be resistant in the absence of cortisol replacement.

Ascertain and treat precipitating cause.

Abnormal response to a short Synacthen^® test is a poor prognostic indicator.

Prednisolone is a synthetic glucocorticoid with the general properties of the corticosteroids. Prednisolone exceeds hydrocortisone in glucocorticoid and anti-inflammatory activity, being ∼3–4 times more potent on a weight basis than the parent hormone, but is considerably less active than hydrocortisone in mineralocorticoid activity. Therefore it is often given for chronic conditions to limit water retention, and is found only as an oral preparation. In contrast, the relatively high mineralocorticoid activity of hydrocortisone and the resulting fluid retention make it unsuitable for disease suppression on a long-term basis; however, hydrocortisone can be given as an oral or IV preparation, which is why it is often used perioperatively instead of prednisolone.

Low-dose steroid treatment, <10mg prednisolone per day, usually carries little danger of HPA suppression. Treatment with >10mg prednisolone (or equivalent) risks HPA suppression. This may occur after treatment via the oral, topical, parenteral, nebulised, and inhaled routes. These patients must be assumed to be suffering from an inability to mount a normal endogenous steroid response to stress and be supplemented accordingly.

HPA suppression can be measured using various methods. In practice the short Synacthen^® test (corticotropin test) is reliable, cheap, and safe. Patients are given Synacthen^® (synthetic corticotrophin) (250µg IV) and serum cortisol is measured at 0, 30, and 60min. Normal peak cortisol levels range from 420–700nmol/l and indicate the ability of the patient to mount a stress response. If the result is equivocal, an insulin tolerance test can be performed under the supervision of an endocrinologist.

Easy bruising and fragile skin, impaired glucose tolerance, diabetes

Hypertension, LVH, sleep apnoea

High Na⁺, HCO^–₃, and glucose; low K⁺ and Ca²⁺

Gastrointestinal reflux.

Increased urinary 17-(OH)-steroids.

Loss of suppression with dexamethasone 2mg.

ACTH level:

85% of patients are hypertensive and are often poorly controlled.

Sleep apnoea and gastro-oesophageal reflux are common.

60% of patients have diabetes or impaired glucose tolerance and a sliding scale should be started before major surgery if glucose is >10mmol/l.

Patients are often obese with difficult veins!

Patients are at risk of peptic ulcer disease so give prophylactic antacid medication.

Spontaneous hypokalaemia (K⁺ <3.5mmol/l); moderately severe hypokalaemia (K⁺ <3.0mmol/l) during diuretic therapy despite oral K⁺.

Muscle weakness or paralysis especially in ethnic Chinese (secondary to hypokalaemia).

Nephrogenic diabetes insipidus secondary to renal tubular damage (polyuria).

Impaired glucose tolerance in ∼50% of patients.

The patient should have normal serum potassium and bicarbonate, but this may be difficult to achieve.

Hypertension is usually mild and well controlled on spironolactone, but features of end organ damage, e.g. LVH, should be excluded.

Calcium channel blockers such as nifedipine are effective antihypertensive agents with aldosterone-secreting adenomas. This is a specific action.

Secondary hyperaldosteronism has a raised serum aldosterone with a normal ratio.

Important to distinguish between adenoma and hyperplasia as adenoma is usually treated surgically and hyperplasia medically.

Adrenal vein sampling, radiolabelling tests, CT, and MRI are all used.

Check blood glucose perioperatively.

Chronic hypokalaemia has an antagonistic action upon insulin secretion/release and may result in abnormal glucose tolerance with the stress of surgery.

Hypertension may persist after removal of the adenoma, due presumably to permanent changes in vascular resistance.

Mediators are metabolised in the liver; therefore only tumours with hepatic metastases or a primary tumour with non-portal venous drainage lead to the carcinoid syndrome.

Vasoactive substances include serotonin, bradykinin, histamine, substance P, prostaglandins, and vasoactive intestinal peptide.

Patients with an asymptomatic carcinoid tumour have simple carcinoid disease and do not present particular anaesthetic difficulties. Patients with carcinoid syndrome can be extremely difficult to manage perioperatively.

Vasoactive peptides resulting in flushing (90%) especially of the head, neck, and torso, or diarrhoea (78%), which may lead to dehydration and electrolyte disturbances. Other symptoms include bronchospasm (20%), hypotension, hypertension, tachycardia, hyperglycaemia, and right heart failure secondary to endocardial fibrosis affecting the pulmonary and tricuspid valves (mediators are metabolised in the lung before reaching the left heart).

Prevent the release of mediators—octreotide (100µg SC tds) for 2wk prior to surgery and octreotide (100µg IV slowly diluted to 10µg/ml) at induction.

Avoid factors that may trigger carcinoid crises—catecholamines, anxiety, and drugs that release histamine, e.g. morphine.

ECG and echocardiography if cardiac involvement is suspected.

CXR and lung function tests if indicated.

Monitoring should include invasive blood pressure preinduction (both induction and surgical manipulation of the tumour can cause large swings), CVP, and regular blood glucose and blood gases. Pulmonary artery flotation catheter if indicated due to cardiac complications.

Induction: prevent pressor response to intubation (etomidate/propofol and alfentanil/fentanyl). Suxamethonium has been used safely for rapid sequence induction, although fasciculations may theoretically stimulate hormone release by increasing intra-abdominal pressure.

Maintenance: isoflurane with vecuronium or rocuronium (not atracurium), and fentanyl, remifentanil, or low-dose epidural (avoiding hypotension as this may elicit bradykinergic crisis).

Octreotide (10–20µg boluses IV) to treat severe hypotension.

Avoid all histamine-releasing drugs and catecholamines (release serotonin and kallikrein, which activates bradykinins).

Labetalol, esmolol, or ketanserin can be used for hypertension.

Patients may waken very slowly (thought to be due to serotonin).

Avoid morphine and use either patient-controlled analgesia with fentanyl or pethidine, or an epidural.

Hypotensive episodes may occur, requiring further IV boluses of octreotide (10–20µg).

Wean octreotide over 7–10d following tumour resection.

Check clotting screen and liver function tests, since alterations in fat absorption may influence clotting factors and hepatic function may be affected by liver metastases.

Antacid prophylaxis preoperatively and rapid sequence induction.

Invasive pressure monitoring for major surgery.

Continue omeprazole postoperatively as the gastric mucosa may have become hypertrophied, producing excess acid.

Replace fluids and electrolytes.

Treat medically with somatostatin analogues (octreotide). If this fails, try steroids (such as methylprednisolone) and indometacin (a prostaglandin inhibitor).

60% become malignant with liver metastases, so all warrant resection.

Use invasive pressure monitoring for major surgery.

Frequent measurement of arterial blood gases to check acid base status and electrolytes.

Diazoxide (a non-diuretic benzothiazide which inhibits the release of insulin) has been used where surgery has failed but has unpredictable efficacy.

Tumours usually non-malignant, but if malignant, hepatic resection may be required.

Start glucose and potassium infusion preoperatively and monitor blood glucose closely perioperatively, particularly at time of tumour manipulation.

Patients usually have liver metastases at presentation.

Treatment consists of surgical debulking and somatostatin analogues.

Increased incidence of venous thromboses so give prophylactic antithrombotic therapy.

Increased potassium loss—vomiting or nasogastric suctioning, diarrhoea, pyloric stenosis, diuretics, renal tubular acidosis, hyperaldosteronism, magnesium depletion, leukaemia.

Intercompartmental shift—insulin, alkalosis (0.1 increase in pH decreases K⁺ by 0.6mmol/l), β₂-agonists and steroids.

Dysrhythmias, decreased cardiac contractility.

Skeletal muscle weakness, tetany, ileus, polyuria, impaired renal concentrating ability, decreased insulin secretion, growth hormone secretion, aldosterone secretion, negative nitrogen balance.

Encephalopathy in patients with liver disease.

Exclude Cushing's and Conn's syndromes.

Oral replacement is safest, up to 200mmol/d, e.g. potassium chloride (Sando-K^®) two tablets 4 times a day = 96mmol K⁺.

IV replacement—essential for patients with cardiac manifestations, skeletal muscle weakness, or where oral replacement not appropriate.

Aim to increase K⁺ to 4.0mmol/l if treating cardiac manifestations.

Maximum concentration for peripheral administration is 40mmol/l (greater concentrations than this can lead to venous necrosis); 40mmol KCl can be given in 100ml 0.9% sodium chloride over 1hr but only via an infusion device, with ECG monitoring, in HDU/ICU/theatre environment, and via a central vein. Plasma K⁺ should be measured at least hourly during rapid replacement. K⁺ depletion sufficient to cause 0.3mmol/l drop in serum K⁺ requires a loss of ∼100mmol of K⁺ from total body store.

For emergency surgery, if possible replace K⁺ in the 24hr prior to surgery. Aim for levels of 3.5–4.0mmol/l. If this is not possible use an IV replacement regime as documented above intra-/perioperatively.

If bicarbonate is raised, then loss is probably longstanding with low intracellular potassium and will take days to replace.

May increase sensitivity to neuromuscular blockade; therefore need to monitor.

Increased risk of digoxin toxicity at low K⁺ levels. Aim for K⁺ of 4.0mmol/l in a digitalised patient.

Decreased urinary excretion—renal failure (acute or chronic), adrenocortical insufficiency, drugs (K⁺ sparing diuretics, ACE inhibitors, ciclosporin, etc.).

Intercompartmental shift of potassium—acidosis, rhabdomyolysis, trauma, malignant hyperthermia, suxamethonium (especially with burns or denervation injuries), familial periodic paralysis.

Muscle weakness at K⁺ >8.0mmol/l.

Nausea, vomiting, diarrhoea.

Calcium (5–10ml 10% calcium gluconate or 3–5ml 10% calcium chloride). Calcium stabilises the myocardium by increasing the threshold potential. Rapid onset, short lived.

If acidotic, give bicarbonate (50mmol IV).

β₂ agonist—salbutamol (5–10mg nebulised—beware tachycardia).

Ion exchange resin—calcium resonium^® (15g PO or 30g PR 8-hourly).

If initial management fails, consider dialysis or haemofiltration.

Control ventilation to prevent respiratory acidosis.

Monitor K⁺ regularly.

Na⁺ <125mmol/l—neuropsychiatric symptoms, nausea/vomiting, muscular weakness, headache, lethargy, psychosis, raised intracranial pressure, seizures, coma, and respiratory depression. Mortality high if untreated.

Chronic symptomatic hyponatraemia (present for more than 48hr or duration unknown). Aim to correct serum Na⁺ by 5–10mmol/d. Rapid correction (serum Na⁺ rise of >0.5mmol/l/hr) can lead to central pontine myelinolysis, subdural haemorrhage, and cardiac failure. Give furosemide and replace saline losses with 0.9% sodium chloride IV. Monitor electrolytes and urine output carefully. SIADH—fluid restrict and demeclocycline (300–600mg daily).

Consult with endocrinologist.

Watch for resolution of symptoms.

Treat the cause.

Treat the cause.

Emergency surgery: consider risk to benefits. Consult endocrinologist.

Euvolaemia (water depletion): estimate the total body water deficit, treat with 5% glucose.

Hypervolaemic (Na⁺ excess): diuretics, e.g. furosemide (20mg IV) and 5% dextrose, dialysis if required.

Diabetes insipidus—replace urinary losses and give desmopressin (1–4µg daily SC/IM/IV).

Urgent surgery—use central venous pressure monitoring if volume status is uncertain or may change rapidly intraoperatively, and be aware of dangers of rapid normalisation of electrolytes.

Obesity is defined by a BMI >30kg/m² and morbid obesity by BMI >40kg/m².

Increase in cardiac output and stroke volume in proportion to oxygen consumption and weight gain.

Systemic hypertension is 10 times more prevalent due to increased cardiac output and blood volume.

Obesity is a risk factor for ischaemic heart disease.

FRC is reduced in the awake obese patient and decreases significantly following induction, which may encroach upon the closing capacity. Pulmonary compliance is decreased by up to 35% (due to heavy chest wall and splinted diaphragm). Increased ventilation/perfusion mismatch.

Obesity hypoventilation syndrome (OHS) occurs due to loss of central drive. Hypoxaemia, pulmonary hypertension, and polycythaemia can develop.

Obstructive sleep apnoea (OSA) is also more common in the obese. It occurs due to lack of central drive and peripheral anatomical abnormalities (see p. 122).

As a result, oxygen desaturation occurs rapidly in the obese apnoeic patient.

Technical problems of IV access and nerve blockade.

Increased risk of skin infections.

Hydrophilic drugs (e.g. neuromuscular blockers) have similar absolute volumes of distribution, clearance, and elimination half-lives. Base dose on lean body mass. Atracurium recovery is similar to the non-obese.

Lipophilic drugs (e.g. thiopental and benzodiazepines) have increased volumes of distribution, normal clearance, and increased elimination half-lives.

Increased plasma cholinesterase activity. Give suxamethonium in dose of 1.5mg/kg.

Ask about snoring, somnolence, and periodic breathing.

Evaluate patient for signs of systemic and/or pulmonary hypertension, signs of right and/or left ventricular failure, and ischaemic heart disease.

Premedication with respiratory depressants should be avoided. An H₂ blocker or proton pump inhibitor plus metoclopramide should be administered on the ward (±30ml sodium citrate 0.3M in the anaesthetic room).

Patients with a BMI >30 have an increased venous thromboembolic risk and need to be carefully assessed.

ABGs to identify baseline hypoxaemic and hypercarbic patients.

Pay particular care to protecting pressure areas.

Use short-acting agents to ensure rapid recovery.

Aortocaval compression may occur in the supine position and table tilt may help. Avoid head-down positioning, especially in spontaneous ventilation.

Fluid balance may be difficult to assess clinically and increased blood loss is common due to difficult surgical conditions.

Local anaesthetic doses for spinals and epidurals should be 75–80% of normal because engorged extradural veins and fat constrict these spaces.

Thromboembolic events are twice as common and so thromboprophylaxis is important.

Mobilise as soon as practical—ensure enough staff are available.

Pulmonary atelectasis is common and lung capacities remain decreased for at least 5d after abdominal surgery. To optimise the FRC/closing capacity ratio the obese patient should be nursed at 30–45° head-up tilt for this period. Humidified oxygen and early, regular physiotherapy should be administered.

Nocturnal nasal CPAP and continual pulse oximetry may be considered in obstructive sleep apnoea.

PCA is more predictable than IM opioids because injections are frequently into subcutaneous fat.

HDU care should be available for higher-risk patients with pre-existing respiratory disease, especially those undergoing thoracic or abdominal surgery.