Adrenal steroids: chronic corticosteroid therapy with the equivalent of prednisolone 10 mg daily within the previous 3 months suppresses the hypothalamic-pituitary-adrenal system. Without steroid supplementation perioperatively the patient may fail to respond appropriately to the stress of surgery and become hypotensive (see Ch. 34). A single dose of etomidate depresses the hypothalamic-pituitary-adrenal axis for a few hours but this is not associated with an adverse outcome.
Antibiotics: aminoglycosides, e.g. neomycin, gen-tamicin, potentiate neuromuscular blocking drugs.
ANAESTHESIA IN THE DISEASED, AND IN PARTICULAR PATIENT GROUPS
Anticholinesterases: can potentiate suxamethonium.
Antiepilepsy drugs: continued medication is essential to avoid status epilepticus. Drugs must be given parenterally (e.g. phenytoin, sodium valproate) or by rectum (e.g. carbamazepine) until the patient can absorb enterally.
Antihypertensives of all kinds: hypotension may complicate anaesthesia, but it is best to continue therapy. Hypertensive patients are particularly liable to excessive rise in blood pressure and heart rate during intubation, which can be dangerous if there is ischaemic heart disease. Postoperatively, parenteral therapy may be needed for a time.
¡¡-adrenoceptor blocking drugs: can prevent the homeostatic sympathetic cardiac response to cardiac depressant anaesthetics and to blood loss.
Diuretics: hypokalaemia, if present, will potentiate neuromuscular blocking agents and perhaps general anaesthetics.
Oral contraceptives containing oestrogen and postmenopausal hormone replacement therapy: predispose to thromboembolism (see p. 724).
Psychotropic drugs: neuroleptics potentiate or synergise with opioids, hypnotics and general anaesthetics.
Antidepressants: monoamine oxidase inhibitors can cause hypertension when combined with certain amines, e.g. pethidine, or indirect-acting sympathomimetics, e.g. ephedrine. Tricyclics potentiate catecholamines and some other adrenergic drugs.
Anaesthesia in the diseased, and in particular patient groups
The normal response to anaesthesia may be greatly modified by disease. Some of the more important aspects include:
Respiratory disease and smoking predispose the patient to postoperative pulmonary complications, principally infective. The site of operation, e.g. upper abdomen, chest, and the severity of pain influence the impairment to ventilation and coughing.
Cardiac disease. The aim is to avoid the circulatory stress (with increased cardiac work which can compromise the myocardial oxygen supply) caused by hypertension and tachycardia. Intravenous drugs are normally given slowly to reduce the risk of overdosage and hypotension.
Patients with fixed cardiac output, e.g. with aortic stenosis or constrictive pericarditis, are at special risk from reduced cardiac output with drugs that depress the myocardium and vasomotor centre, for they cannot compensate. Induction with propofol or thiopental is particularly liable to cause hypotension in these patients. Hypoxia is obviously harmful. Skilled technique rather than choice of drugs on pharmacological grounds is the important factor.
Hepatic or renal disease is generally liable to increase drug effects and should be taken into account when selecting drugs and their doses.
Malignant hyperthermia (MH) is a rare pharma-cogenetic syndrome with an incidence of between 1:15 000 and 1:150 000 in North America, exhibiting autosomal dominant inheritance with variable penetrance. The condition occurs during or immediately after anaesthesia and may be precipitated by potent inhalation agents (enflurane, halothane, isoflurane), or suxamethonium. The patient may have experienced an uncomplicated general anaesthetic previously. The mechanism involves a sudden rise in release of bound (stored) calcium of the sar-coplasm, stimulating contraction, rhabdomyolysis, and a hypermetabolic state. Malignant hyperthermia is a life-threatening medical emergency. Oxygen consumption increases by up to three times normal, and body temperature may rise as fast as 1°C every 5 min, reaching as high as 43°C. Rigidity of voluntary muscles may not be evident at the outset or in mild cases.
Dantrolene 1 mg/kg i.v., is given immediately. Further doses are given at 10-min intervals until the patients responds, to a maximum dose of 10 mg/kg. Dantrolene probably acts by preventing the release of calcium from the sarcoplasm store that ordinarily follows depolarisation of the muscle membrane. The t\ is 9 h.
Nonspecific treatment is needed for the hyperthermia (cooling, oxygen), and insulin and dextrose are given for hyperkalemia due to potassium release from contracted muscle. Hyperkalemia and acidosis may trigger severe cardiac arrhythmias.
Once the immediate crisis has resolved, the patient and all immediate relatives should undergo investigation for MH. This involves a muscle biopsy, which is tested for sensitivity to initiating agents.
Anaesthesia in MH-susceptible patients is achieved safely with total intravenous anaesthesia using propofol and opioids. Dantrolene for intravenous use must be available in every surgical theatre. The relation of malignant hyperthermia syndrome with neuroleptic malignant syndrome (for which dantrolene may be used as adjunctive treatment, see p. 388) is uncertain.
Diabetes mellitus: see page 695.
Thyroid disease: see page 705.
Porphyria: see page 141.
Muscle diseases. Patients with myasthenia gravis are very sensitive to (intolerant of) competitive but not to depolarising neuromuscular blocking drugs. Those with myotonic dystrophy may recover less rapidly than normal from central respiratory depression and neuromuscular block; they may fail to relax with suxamethonium.
Sickle-cell disease. Hypoxia and dehydration can precipitate a crisis.
Atypical (deficient) pseudocholinesterase. There is a delay in the metabolism of suxamethonium and mivacurium. The duration of neuromuscular block depends on the type of pseudocholinesterase.
Raised intracranial pressure will be made worse by high expired concentration inhalation agents, e.g. > 1% isoflurane, by hypoxia or hypercapnia, and in response to intubation if anaesthesia is inadequate. Without support from a mechanical ventilator, excessive doses of opioids will cause hypercapnia and increase intracranial pressure.
The elderly (see p. 126) are liable to become confused by cerebral depressants, especially by hyoscine. Atropine also crosses the blood-brain barrier and can cause confusion in the elderly; glycopyrronium is preferable. In general, elderly patients require smaller doses of all drugs than the young. The elderly tolerate hypotension poorly; they are prone to cerebral and coronary ischaemia.
Children (see p. 125). The problems with children are more technical, physiological and psychological than pharmacological.
Sedation in critical care units is used to reduce patient anxiety and improve tolerance to tracheal tubes and mechanical ventilation. Whenever possible, patients are sedated only to a level that allows them to open their eyes to verbal command; over-sedation is harmful. Commonly used drugs include propofol and midazolam, and opioids such as fentanyl, alfentanil, or morphine.
Neuromuscular blockers are only rarely required to assist mechanical ventilation. If pain is treated properly and patient-triggered modes of ventilation are used, many patients in the critical care unit will not require sedation. Reassurance from sympathetic nursing staff is extremely important and far more effective than drugs.
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