PCP

Pre-existing hypertension or cardiovascular disease substantially increases risk of hypertensive crisis, stroke, and intracranial haemorrhage. Tachycardia occurs in 30% of cases.

PCP produces seizures in a dose-dependent manner, documented in clinical toxicology series. Pre-existing seizure disorders dramatically increase risk. StatPearls reports seizures as a significant complication above 20 mg.

PCP administration to patients with schizophrenia or other psychotic disorders produces exacerbation of their characteristic symptoms. This has been demonstrated in controlled challenge studies. Any personal or family history of psychotic disorders substantially increases risk of prolonged psychotic reactions lasting days to weeks.

PCP's triple dopaminergic mechanism creates risk of manic exacerbation in individuals with bipolar disorder. The stimulant-like and psychotomimetic properties may destabilise mood regulation.

Hepatic metabolism accounts for over 90% of PCP elimination. Liver impairment will prolong half-life (already 17-21 hours in healthy individuals) and increase risk of accumulation. Elevated LFTs occur in 50% of intoxication cases, suggesting direct hepatotoxic potential.

PCP-induced rhabdomyolysis (CK elevation in 70% of cases) generates myoglobin that can precipitate acute kidney injury. Patients with pre-existing renal impairment have markedly reduced capacity to tolerate this insult.

PCP is highly lipophilic and crosses the placenta. Developmental toxicity and neonatal effects have been reported. Absolute contraindication during pregnancy.