PCP Intoxication

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Tareg Bey, MD and Anar Patel, MD

Over 50% of adult patients present with the classic toxidrome of PCP intoxication: violent behaviour, nystagmus, tachycardia, hypertension, anaesthesia, and analgesia.

The clinical picture may wax and wane between extreme agitation and sedation, because PCP can produce CNS stimulation and depression through its different clinical effects in the CNS. With increasing concentrations, the drug binds to NMDA receptors, acts as a monoamine reuptake inhibitor, stimulates σ-opioid receptors, as well as nicotinic, muscarinic and GABA receptors. Sedation and loss of inhibition tend to occur with ingestions of 1 to 5 mg, with the CNS findings of slurred speech, violent behaviour and blank staring, horizontal, vertical, or rotatory nystagmus, ataxia, hyperthermia, and seizures at these doses.

PCP’s most unusual feature is that doses of 5 to 10 mg orally may induce acute schizophrenia, including agitation, psychosis, audiovisual hallucinations, paranoid delusions, and catatonia. Doses greater than 10 mg usually result in coma. In animal experimental studies PCP is used to investigate the neurochemical basis of schizophrenia. Low doses of phencyclidine have produced patterns of metabolic and neurochemical changes in rodent brains that resemble those in brains of schizophrenic patients. A typical PCP-induced coma is manifested as an unresponsive patient whose eyes remain open.

The very characteristics that made PCP ideal for anaesthesia at moderate doses – absence of cardiorespiratory depression or muscle hypotonia – make it dangerous at higher recreational doses. It produces sympathomimetic signs such as hypertension, tachycardia, and diaphoresis similar to cocaine, and cholinergic signs like bronchospasm, salivation, urinary retention, flushing, and miosis, similar to opiates. The most common of these are tachycardia and hypertension.

PCP has also been shown to be a direct cardiac irritant, and may induce arrhythmias and vasospasm. In addition, muscle tone becomes exaggerated, and patients may exhibit hyperreflexia, and myoclonic, dystonic or choreoathetoid movements such as opisthotonos and torticollis. Complications of this hypertonic muscle activity include hyperthermia and rhabdomyolysis.

Respiratory depression requiring intubation is uncommon in PCP intoxication; however, patients may exhibit irregular breathing, with episodes of both apnea and tachypnea. Furthermore, pharyngeal and laryngeal reflexes become hyperactive, and sympathomimetic effects create bronchorrhea, which exacerbate the risk of airway obstruction in an already obtunded patient.

Non-traumatic causes of death include cardiopulmonary arrest, intracranial hemorrhage in hypertension, and hyperkalemia secondary to rhabdomyolysis. Most deaths in PCP-intoxicated patients, however, result from patients’ violent behaviour, rather than direct effects of the drug. The bizarre and violent behaviour generated by PCP, combined with its analgesic effects, may result in significant self-inflicted trauma. Patients have walked into traffic, jumped from buildings, and even enucleated their own eye.

Patients recovering from PCP exposure may undergo an emergence reaction as the drug is eliminated, consisting of psychosis, bizarre behaviour, or depression that may last from days to weeks. Prolonged psychosis is more commonly seen in chronic abusers, and is a poor prognostic sign, as the patient may go on to develop true schizophrenia. Depression, anxiety, irritability, restlessness, anergia, and disturbances of thought and sleep have been described in as little as a day of abstinence in chronic abusers. Oculomotor hyperactivity, tremor, diarrhea, and piloerection were reported within 8 hours of abstinence in monkeys chronically administered PCP.

 

Management

The management of PCP intoxication begins just as any other intoxication would. First, the patient’s airway, breathing, circulation, thermoregulation, and neurologic status must be stabilized. The patient should then be restrained and sedated if necessary to prevent self-inflicted injury, which is the most common cause of morbidity and mortality in these patients.

Chemical restraints are preferred over physical restraints, which may exacerbate the risk of rhabdomyolyis. Benzodiazepines are recommended in patients without psychosis, as antipsychotics can amplify PCP-induced hyperthermia, dystonic as well as anticholinergic reactions, and lower the seizure threshold. However, haloperidol has been described as a useful treatment for PCP-induced psychosis provided the patient is not hyperthermic. The risks of lengthening of the QT interval, torsade de pointes and adverse neurologic effects limit the use of haloperidol in PCP intoxicated patients. Due to their more favourable side effect profile, atypical antipsychotics like olanzipine or ziprazidone would be a better choice than haloperidol when treating PCP-induced agitation and psychosis. Diphenhydramine 50mg IV or 1mg/kg can be used to treat PCP-induced (or haloperidol-induced) dystonic symptoms, but should be administered after a urine sample is obtained for toxicologic screening, since it may cause the specimen to test falsely positive for PCP. Diphenhydramine may also cause tachycardia and problems with thermoregulation via its anticholinergic effects, so the benefits of its use should be weighed against its potential side effects. Patients should then be closely observed in a dark and quiet environment, with minimal auditory and tactile stimuli so as not to provoke violent outbursts.

As with all intoxications, a blood glucose measurement should be obtained, and 100 mg thiamine and dextrose 50% should be administered if the blood sugar is abnormally low. Naloxone, to treat potentially coingested opiates, is not necessary in patients with adequate respiration.

Gastric lavage is controversial, and should only be used after consultation with a toxicologist. Activated charcoal at standard dose of 1 g/kg is strongly recommended in suspected PCP ingestion to prevent further absorption of the drug during its entero-hepatic recirculation, and serial doses may be necessary to prevent later redistribution from lipid stores. An intoxicated patient should always be assessed first for deterioration of mental status, aspiration potential and possible airway complications before administering charcoal.

Patients must be on continuous cardiac monitoring because of the frequency and severity of cardiac symptoms. Diastolic hypertension >115 mmHg may be transient, or fall after sedation, eliminating the need for further treatment.

There are case reports of intracerebral hemorrhage secondary to hypertension. Additionally, Welch et al. describes several cases of intracerebral hemorrhage in infants that were not visualized on CT and have been diagnosed by lumbar puncture, suggesting that physicians should have a low threshold for performing this procedure in the face of hypertension and neurologic abnormalities, especially in children.

In the past, PCP elimination was thought to be enhanced by urinary acidification via ammonium chloride or ascorbic acid; however, this is no longer recommended because acidic urine increases the risk of acute tubular necrosis secondary to myoglobinuria in rhabdomyolysis. Furthermore, only 9% of PCP is excreted in the urine. Urinary acidification will not affect the 91% that is metabolized by the liver, and thus will not increase overall removal of the drug. Hemodialysis is also ineffective because it simply removes the drug from the serum, clearing the path for redistribution from lipid stores. Hemodialysis is, however, a treatment option for renal failure caused by rhabdomyolysis. Renal failure is considered to be far more dangerous than PCP intoxication; therefore patients with rhabdomyolysis should be aggressively treated with fluids, sodium bicarbonate, mannitol and furosemide.

Status epilepticus should be treated with airway protection and IV benzodiazepines or phenobarbital. The patient should not be paralyzed after rapid sequence intubation (RSI) because it is then virtually impossible to monitor whether seizures are still ongoing, short of continuous EEG monitoring. Hyperthermia greater than 40°C may be the combined result of PCP-induced myotonic activity, seizures, and rhabdomyolysis, and should be aggressively treated with mechanical cooling measures. Benzodiazepines are a useful adjunct to prevent shivering and provide sedation.


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