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Chapter: Modern Medical Toxicology: Neurotoxic Poisons: Anaesthetics and Muscle Relaxants

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Other Inhalational Anaesthetics

Isoflurane and its isomer enflurane are non-flammable, butpossess high vapour pressure and hence necessitate the use of a precision vapouriser.

Other Inhalational Anaesthetics

Isoflurane and its isomer enflurane are non-flammable, butpossess high vapour pressure and hence necessitate the use of a precision vapouriser. Isoflurane is a clear, colourless, volatile liquid, and has a pungent odour. Enflurane is a volatile fluori-nated methyl ethyl ether, and is a clear, colourless, volatile and stable liquid with a mild sweet odour; it is non-flammable. Isoflurane has also been used as a solvent and dispersant for fluorinated compounds.

Isoflurane produces hypotension, coma, seizures, respira-tory depression, and apnoea in overdose, but has a wide safety margin. The minimum lethal human dose to this agent has not been delineated. At normal anaesthetic doses isoflurane has been associated with hypotension, arrhythmias, miosis, seizures, nephrotoxicity, hepatotoxicity, neuroleptic malignant syndrome, and respiratory depression. Rarely it may induce malignant hyperthermia. The diagnosis of malignant hyper-thermia can be confirmed by muscle biopsy.

Enflurane may cause CNS and respiratory depression, coughing, laryngospasm, hypotension, hepatotoxicity, renal toxicity, and seizures. Up to 80% of patients who experience seizures will have them within the first 24 hours following surgery. Fatalities have been reported following the inhalational abuse of one entire bottle of enflurane. Enflurane has been reported to induce cerebral hyperexcitability which appears as a burst-suppression pattern on an EEG and may progress to seizures. Tricyclic antidepressants taken concurrently with enflurane may result in a lowered seizure threshold with resultant seizures. Shivering may occur in the postoperative period. ECG changes, nausea and vomiting, and malignant hyperthermia have occurred with enflurane anaesthesia. Rhabdomyolysis with acute renal failure is a rare effect. Malignant hyperthermia has occurred in a few cases.

Cardiac rhythm during isoflurane anaesthesia is generally stable, and isoflurane does not sensitise the heart to the effect of exogenous adrenaline. The hypercapnia associated with spontaneous ventilation during isoflurane anaesthesia increases heart rate. Blurred or double vision may be a temporary effect of both isoflurane and enflurane. Both agents lower intraocular pressure. Coughing, nausea, and vomiting are common to both.

Serum fluoride concentrations should be monitored in overdose cases involving either isoflurane or enflurane. Monitor vital signs in all patients. Follow temperature and monitor for signs of fever possibly leading to malignant hyperthermia. Monitoring complete blood count, urinalysis, and liver and kidney function tests is suggested for patients with significant exposure. Continuous cardiac monitoring is recommended.

Because of rapid absorption and onset of CNS depression, induced emesis is not recommended. Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Gastric lavage may be useful in significant ingestions. Enflurane ingestions have rarely been reported, while isoflurane ingestions have occurred more commonly. Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary. Administer 100% humidified supple-mental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta adren-ergic agonists if bronchospasm develops. Exposed skin and eyes should be flushed with copious amounts of water. Dantrolene and ice may be of use in malignant hyperthermia. Seizures can be successfully treated with barbiturates, phenytoin, or diazepam. Decrease depth of anaesthesia if hypotension occurs. Infuse 10 to 20 ml/kg of isotonic fluid and place in Trendelenburg position. If hypotension persists, administer dopamine or noradrenaline. Consider central venous pressure monitoring to guide further fluid therapy.

Evaluate for hypoxia, acidosis, and electrolyte disorders (particularly hypokalaemia, hypocalcaemia, and hypomag-nesaemia). Lignocaine and amiodarone are generally first line agents for stable monomorphic ventricular tachycardia, particularly in patients with underlying impaired cardiac function. Sotalol is an alternative for stable monomorphic ventricular tachycardia. Unstable rhythms require cardiover-sion. Atropine may be used when severe bradycardia is present and PVCs are thought to represent an escape complex.

Isoflurane has been implicated in causing myocardial ischaemia, but this effect appears to be limited to patients with coronary artery disease.

Electromyographic studies suggest that patients with myas-thenia gravis are more sensitive to the neuromuscular depres-sant effects of isoflurane than are normal patients.

Although isolated reports of liver dysfunction with isoflurane have appeared, a causal relationship has not been established; it is felt that isoflurane is highly unlikely to be even rarely responsible for postoperative hepatotoxicity. Hepatotoxicity develops infrequently following enflurane anaesthesia, but may be severe. However, most patients recover in 3 to 4 weeks with malaise being the only persistent effect.

Self-limited production of carbon monoxide (CO) via the degradation of enflurane in the presence of desiccated soda lime has been demonstrated under some situations. It was found that total CO production was linearly dependant on the amount of desiccated soda lime, and that if very large absorber systems are used, there may be increased potential to produce particu-larly large amounts of CO. This could cause carbon monoxide poisoning, particularly in children, after mask induction, or initial wash-in with enflurane.

Isoflurane produces bronchodilation and may be useful in the management of refractory status asthmaticus. However, acute asthma has been reported with enflurane use.

Desflurane is produced by substitution of chlorine of isoflu-rane with fluorine. While cardiac output is well maintained with controlled ventilation, desflurane has a tendency to induce cardiovascular depression.

Servoflurane is a non-flammable, non-irritating agent thatmay be nephrotoxic when carbon dioxide absorbers are used, since it gets degraded to produce an olefin.


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