Week 46: Psych: Substance Abuse

Schizoid personality disorder is classified as a cluster A personality disorder. This cluster describes patients with odd and eccentric behavior and includes paranoid personality disorder and schizotypal personality disorder. Patients with schizoid personality disorder generally prefer to be left alone. They do not enjoy engaging in social or sexual relationships or interactions. They are markedly detached from society, introverted, and primarily choose solitary activities or hobbies. They may be indifferent to praise or criticism and appear withdrawn or aloof. Schizoid patients are rarely seen in clinical practice. Patients with cluster A disorders may be difficult to treat because of an intrinsic distrust or suspicion of others. They may express resistance in engaging, but it is important to be clear in explaining management intentions without becoming overly involved in their personal lives. It is also important to remain professional, direct, and empathetic toward them and not to react emotionally to their odd, inappropriate or dramatic behavior.

Antisocial personality disorder (A) is a cluster B disorder characterized by selfishness, impulsivity, promiscuity, callousness, disregard for rules or other people, pervasive deception and lying, lack of remorse, and difficulty learning from prior experiences. Patients are commonly in trouble with the law. Borderline personality disorder (B) is also a cluster B disorder and is characterized by a lack of self-control, violence, aggression, and having unstable relationships (e.g., frequent break ups). Drug abuse and suicide attempts are very common in borderline individuals. Schizoaffective disorder (C) is not a personality disorder, but rather a condition on the spectrum schizophrenia-like disorders. It is characterized by the presence of delusions, hallucinations, disorganized speech, catatonia or grossly disorganized behavior, along with mood disturbance such as mania or major depression.

IM haloperidol
This presentation is consistent with acute psychosis. The safety of the health care staff and patient are paramount. In an uncooperative patient unable to follow commands, rapid sedation is indicated. Once the patient is calm, a focused medical assessment can be safely performed.

A. CT head, basic blood work, urine toxicology screen
This presentation is consistent with acute psychosis. The safety of the health care staff and patient are paramount. In an uncooperative patient, verbal deescalation and, if necessary, rapid sedation with an antipsychotic may be necessary. Verbal deescalation has failed in this patient, and blood testing and imaging are unlikely to be successful at this time.

C. Sublingual olanzapine
This presentation is consistent with acute psychosis. The safety of the health care staff and patient are paramount. While sublingual olanzapine is a great option in a cooperative patient, this patient is not following commands. In an acutely agitated and unncooperative patient without IV access, intramuscular administration is the safest and most effective.

D. IV midazolam
This presentation is consistent with acute psychosis. The safety of the health care staff and patient are paramount. In this uncooperative patient where verbal deescalation has failed, rapid sedation is most appropriate. Benzodiazepines would be an option, but starting a peripheral IV would be difficult in this aggressive patient.

Diphenhydramine IM
The patient in the above question is demonstrating signs of an acute dystonic reaction. Acute dystonic reactions can occur at any point during long-term or short-term antipsychotic therapy. They are more common with typical antipsychotics such as haloperidol. Symptoms include involuntary contraction of muscle groups commonly seen in the neck (torticollis), tongue (buccolingual crisis), and eyes (oculogyric crisis). Treatment of acute dystonic reaction includes IM diphenhydramine or IM benztropine. After receiving one of these muscular agents, patient should receive the same medication in oral form for 48-72 hours to prevent recurrence. Source
Pringsheim T, Doja A, Belanger S, Patten S. Treatment recommendations for extrapyramidal side effects associated with second-generation antipsychotic use in children and youth. Paediatr Child Health. 2011;16(9):590-8.
PMC3223903

A. Benztropine PO (incorrect)
Benztropine can also be used to treat dystonic reactions; however, the appropriate route of administration is IM followed by subsequent PO dosing for 48-72 hours

B. Dantrolene IV (incorrect)
Dantrolene would be more appropriate for the treatment of malignant hyperthermia or neuroleptic malignant syndrome

D. Lorazepam IM (incorrect)
Ativan is an agent that can be effectively used to treat mild agitation or akithesia. It is not the appropriate therapy for dystonic reactions

Certain risk factors have been identified for trafficking. A tattoo that the patient is reluctant to discuss is a potential red flag. Some traffickers brand their victims.

Trafficking should be considered if the individual is traveling with an older companion (B) who is not a guardian. Those trafficked into commercial sex are overly familiar with sexual language and practices (D). Physicians should be suspicious when the accompanying person tries to answer all the questions and insists on being present at all times (C).

Lorazepam
The correct answer is benzodiazepines. For sympathomimetic toxidromes, the most efficacious medicines to reduce blood pressure/tachycardia/hyperthermia are benzos. Beta blockers are contraindicated as they lead to unopposed alpha activity. Phentolamine is a difficult medicine to titrate.

B. Clonidine
This patient likely has a sympathomimetic toxidrome. Treatment of choice is a benzodiazepine, not clonidine.

C. Labetolol
Beta blockers are contraindicated in cocaine toxicity

D. Phentolamine
Rarely used and difficult to titrate

Phencyclidine (PCP) was initially developed for use as a general anesthetic. However, frequent emergent reactions led to its discontinuation in the therapeutic setting. PCP is well absorbed from any mucous membrane and can also be smoked. The drug affects many receptors and therefore causes a broad spectrum of clinical findings. In most cases, the sympathomimetic effects predominate and patients are agitated, exhibiting both bizarre and violent behavior. Patients may, however, demonstrate catatonic features. Nystagmus is often present and may be horizontal, vertical or rotatory. The patient’s hemodynamic status is most often consistent with a sympathomimetic picture with hypertension, tachycardia and possibly hyperthermia.

Crystal methamphetamine (A) is an amphetamine causing release of presynaptic catecholamines. Most commonly amphetamines are ingested, but can be crushed and injected as well. Patients develop typical sympathomimetic effects. With crystal methamphetamine, patients may also become paranoid with delusions. Its use has also been associated with engaging in high-risk behavior, specifically sexual in the men who have sex with men community. Gamma hydroxybutyrate (GHB) (B) is a popular recreational drug classified as a sedative/hypnotic. When ingested it produces a euphoria that is popular at rave parties. Particularly when mixed with ethanol, GHB has a marked CNS depressive effect often leading to respiratory depression requiring transient intubation. It has also been implicated as a date rape drug due to its sedative and amnestic effects. Lysergic acid diethylamine (LSD) (C) is a potent psychoactive drug taken orally as a tablet, liquid, powder, gelatin square or on a sheet of blotter paper. The medication is a hallucinogen with serotonin-like characteristics. Patients go on a “trip” during which perception between the user and environment are distorted. Patients may have an acute panic reaction after taking LSD.

This patient has gamma-hydroxybutyric acid (GHB) intoxication. GHB is an analogue of the inhibitory neurotransmitter GABA. It has been commonly used and abused by bodybuilders because of its anabolic effects. GHB also has euphoric effects, which has caused it to gain popularity as a club drug. Its sedative and amnestic effects have caused GHB to be implicated in cases of drug-facilitated sexual assault (“date rape”). Clinically, GHB overdose can range from euphoria to depressed mental status with or without coma. Vital sign abnormalities such as hypothermia, bradycardia, and hypotension may be present. U waves can be seen on ECG. Pupils are small and minimally responsive to light. Respiratory depression may occur, but—despite a comatose appearance—most GHB intoxicated patients maintain adequate ventilation. Effects of GHB overdose generally resolve within six to eight hours. The classic presentation of GHB overdose is a comatose patient who requires intubation then has an abrupt awakening. Care for GHB intoxication is largely supportive and includes benzodiazepines for agitation, fluid resuscitation, and keeping the patient in a safe environment.

Midazolam (B) is a short-acting benzodiazepine. Benzodiazepines are generally not found in bodybuilding supplements and rarely cause hypotension or bradycardia when ingested alone. The patient in this scenario has slow respirations, coma, and small pupils but does not respond to naloxone, making opioid intoxication (C) less likely. Opioids are also generally not found in bodybuilding supplements. Phenobarbital (D) is a long-acting barbiturate. Barbiturates can cause significant cardiovascular and central nervous system depression; however, given its long duration of action, it is unlikely that the patient would abruptly regain consciousness after six hours.

The boy has signs and symptoms consistent with opioid ingestion. Methadone ingestion can manifest with the classic opioid toxidrome of respiratory depression, sedation, and miosis. Signs of more severe toxicity can include bradycardia, hypotension, and hypothermia. Methadone has been associated with a prolonged QTc interval and risk of torsades de pointes. Patients with significant respiratory or CNS depression should be treated with naloxone, which is a mu receptor antagonist. Because the half-life of methadone is longer than naloxone, patients can require multiple doses of naloxone. Also, serial ECGs are needed to monitor for the development of a prolonged QTc interval. If a patient does develop a prolonged QTc, management includes close cardiac monitoring, repletion of electrolytes, and having magnesium readily available should the patient develop torsades de pointes.

Clonidine (A) toxicity manifests as lethargy, miosis, and bradycardia. Although, findings may be similar to opioid overdose, QTc interval prolongation and torsades de pointes are typically only seen with opioid overdose. Propanolol (C) toxicity causes bradycardia and hypotension that typically develops within six hours of ingestion. Heart block and hypoglycemia may also be seen. Clinical manifestations of salicylate (D) toxicity include nausea, vomiting, diaphoresis, and tinnitus. Moderate cases can manifest as tachypnea, tachycardia, and altered mental status.

Serotonin syndrome occurs when there is an excess of systemic serotonin, usually due to a combination of medications, in this case fluoxetine and phenelzine. Fluoxetine is a selective serotonin reuptake inhibitor (SSRI) that has a long half-life and active metabolites. Phenelzine is a monamine oxidase inhibitor (MAOI) that inhibits serotonin breakdown. Because of fluoxetine’s long half-life and the consequent risk of serotonin syndrome, a 6-week washout period is recommended postdiscontinuation before starting an MAOI. Serotonin syndrome is characterized by altered mental status, hyperreflexia, clonus, rigidity, and autonomic instability. Treatment includes removing the offending drugs, cooling measures, benzodiazepines, fluid resuscitation, and cyproheptadine, a serotonin antagonist.

Acute dystonic reactions (A) result from administration of dopaminergic-blocking agents (especially antipsychotics and some antiemetics) and include torticollis, akathisia, and pseudoparkinsonism. Unlike serotonin syndrome, altered mental status and autonomic instability do not occur with acute dystonic reactions. Hypertensive crisis (B) can occur in patients taking MAOIs, usually in the context of eating foods that are high in tyramine; however, altered mental status, hyperthermia, and movement disorders are not as common in this setting. Neuroleptic malignant syndrome (NMS) (C) occurs in the setting of antipsychotic medication administration. The onset is often more insidious then serotonin syndrome but can be difficult to distinguish because both can present with autonomic instability, hyperthermia, altered consciousness, and movement disorders. NMS is more commonly associated with bradykinesia and lead pipe rigidity. Patients with serotonin syndrome tend to have more agitation and myoclonus/hyperreflexia. A careful medication history can also help to distinguish the etiology.

Tricyclic antidepressant (TCA) overdose initially manifests with anticholinergic symptoms such as sinus tachycardia and hypertension and can progress to seizures, coma and cardiovascular collapse. A dose greater than 10 mg/kg or 1000 mg in an adult should be considered life threatening. Severe lactic acidosis impairs myocardial sodium conduction leading to hypotension, dysrhythmias and ultimately cardiac arrest. Changes on ECG include QRS prolongation (greater than 100 msec), PR prolongation and rightward shift of the terminal 40-msec QRS vector. Treatment begins with assessment of airway and breathing. If intubated, hyperventilation will aid in reversing the acidosis. If the QRS is greater than 100 msec and the patient is symptomatic with hypotension or a dysrhythmia, or if the patient is acidemic, then intravenous sodium bicarbonate should be administered. Sodium bicarbonate produces an alkaline pH and provides a sodium load to aid conductance through the myocardial sodium fast channels that are blocked by the TCA. Sodium bicarbonate is administered by IV boluses of 1 to 2 mEq/kg until the QRS narrows or until the pH increases to 7.50-7.55. Once this is achieved, then a continuous infusion can be maintained by adding three ampules of 8.4% sodium bicarbonate (50 mEq/ampule) to one liter of 5% dextrose in water. The initial infusion rate mirrors that of the patient’s usual maintenance rate of intravenous fluids and should be maintained for 4 to 6 hours.

Hypertonic sodium chloride (A) is considered treatment of hypotension, acidemia and widened QRS interval that is refractory to treatment with sodium bicarbonate and fluid resuscitation. Intralipid (B) may be considered for refractory hypotension due lipophilic drug overdose, including TCA overdose, but is not first line. Vasopressors, such as norepinephrine (C) or dopamine, may be considered in persistently unstable patients after sodium bicarbonate therapy is maximized or no longer being tolerated.