Sevoflurane Fahrenheit Special Precautions

Sevoflurane should be administered only by person trained in the administration of general anaesthesia. Facilities for maintenance of a patient airway, artificial ventilation, oxygen enrichment and circulatory resuscitation must be immediately available. Sevoflurane should be delivered via a vaporizer specifically calibrated for use with Sevoflurane so that the concentration delivered can be accurately controlled. Hypotension and respiratory depression increase as anaesthesia is deepened.
During the maintenance of anaesthesia, increasing the concentration of Sevoflurane produces dose-dependent decreases in blood pressure. Excessive decrease in blood pressure may be related to depth of Sevoflurane. The recovery from general anaesthesia should be assessed carefully before patients are discharged from the recovery room.
In susceptible individuals, potent inhalation anesthetic agents may trigger a skeletal muscle hypermetabolic state leading to high oxygen demand and the clinical syndrome known as malignant hyperthermia. The syndrome may include non-specific feature such as muscle rigidity, tachycardia, tachypnoea, cyanosis, arrhythmias and unstable blood pressure. Treatment includes discontinuation of triggering agents (e.g. Sevoflurance), administration of intravenous dantrolene sodium, and application of supportive therapy. Renal failure may appear later, and urine flow should be monitored and sustained if possible. Sevoflurane should be used with caution in patients with renal insufficiency (baseline serum creatinine greater than 133 micromol/litre).
Sevoflurane produces low levels of Compound A (pentafluoroisopropenyl fluoromethyl ether (PIFE)) and trace amounts of Compound B (pentafluoromethoxy isopropyl fluoromethyl ether (PMFE)), when in direct contact with CO₂ absorbents. Levels of Compound A increase with: increase in canister temperature; increase in anaesthesia concentration; decrease in gas flow rate and increase more with the use of Baralyme rather than Soda lime.
Nephrotoxicity was seen exposed to levels of Compound A in excess of those usually seen in routine clinical practice. The mechanism of this renal toxicity is unknown.
Experience with repeat exposure to Sevoflurane is very limited. However, there were no obvious differences in adverse events between first and subsequent exposures.
Replacement of Desiccated CO₂ Absorbents: The exothermic reaction that occurs with Sevoflurane and CO₂ absorbents is increase when the CO₂ absorbent becomes desiccated, such as after an extended period of dry gas flow through the CO₂ absorbent canisters. Rare cases of extreme heat, smoke and/or spontaneous fire in the anaesthesia machine have been reported during Sevoflurane use in conjunction with the use of desiccated CO₂ absorbent. An unusually delayed rise or unexpected decline of inspired Sevoflurane concentration compared to the vaporizer setting may be associated with excessive heating of the CO₂ absorbent canister.
When clinician suspects that CO₂ absorbent may be desiccated, it should be replaced before administration of Sevoflurane. The color indicator of most CO₂ absorbents does not necessarily change as a result of desiccation. Therefore, the lack of significant color change should not be taken as an assurance of adequate hydration. CO₂ absorbents should be replaced routinely regardless of the state of the color indicator.
Pharmaceutical Precautions: Sevoflurane is chemically stable. As with some halogenated anaesthetics, minor degradation occurs through direct contact with CO₂ absorbents. The extent of degradation in clinically insignificant and no dose adjustments or change in clinical practice is necessary when rebreathing circuits are used. Higher levels of Compound A are obtained when using Baralyme rather than Sode lime.
Further Information: The low solubility of Sevoflurane in blood should result in alveolar concentrations which rapidly increase upon induction and rapidly decrease upon cessation of the inhaled agents.
ln humans <5% of the absorbed Sevoflurane is metabolized. The rapid and extensive pulmonary elimination of Sevoflurane minimizes the amount of anaesthetic available for metabolism. Sevoflurane is defluorinated via cytochrome P450(CYP)2E1 resulting in the production of hexafluoroisopropanol (HFIP) with release of inorganic fluoride and carbon dioxide (or a one carbon fragment). HFIP is then rapidly conjugated with glucuronic acid and excreted in the urine. The metabolism of Sevoflurane may be increased by known inducers of CYP2E1 (e.g. isoniazid and alcohol), but it is not inducible by barbiturates.
Transient increases in serum inorganic fluoride levels may occurs during and after Sevoflurane anaesthesia.
Generally, concentrations of inorganic fluoride peak within 2 hours of the end of Sevoflurane anaesthesia and return within 48 hours to preoperative levels.
Effects on Driving Ability and Operation of Machinery: As with other anaesthetic agents, patients should be advised that performance of activities requiring mental alertness, such as operating hazardous machinery, may be impaired for some time after general anaesthesia. Patients should not be allowed to drive for a suitable period after Sevoflurane anaesthesia.