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Diagnosing drug abuse emergencies can be difficult, especially when the patient is psychotic from intoxication or delirious from withdrawal. Precise diagnosis can also be hindered if the patient has abused several substances or has an underlying psychiatric illness. Concurrent medical illness or injury can complicate the clinical picture by augmenting the drug's effect or masking the usual symptoms. In addition, a patient in withdrawal may have been ingesting drugs, thus obscuring signs and symptoms.
The drug of abuse cannot be established without a laboratory analysis of a drug sample and, when possible, the patient's body fluids and stomach contents. Even if the patient can identify the drug taken, a laboratory analysis is necessary to confirm the drug's identity, determine its dosage and purity, and detect contaminants. Despite its inherent difficulties, a diagnostic approach that includes mental status, physical, and neurologic findings can help establish the drug of abuse (see Triage approach to drug abuse, pages 56 and 57). This chapter reviews intoxication and withdrawal syndromes of the major classes of abused drugs.
Stimulant abuse, which has reached epidemic proportions in the United States, can lead to intoxication, delirium, or an organic delusional syndrome. Commonly abused stimulants include amphetamine, benzphetamine (Didrex), caffeine (No-Doz), cocaine, dextroamphetamine (Dexedrine), methamphetamine (Desoxyn), methylphenidate (Ritalin), phenmetrazine (Preludin), and phenter-mine (lonamin).
Symptoms of acute stimulant abuse include a heightened sense of well-being, increased sense of alertness, decreased anxiety, reduced social inhibitions, increased talkativeness, and poor judgment manifested by loss of money, sexual indiscretion, and illegal activities (Gawin and Ellinwood, 1989). The patient's symptoms usually resolve within 48 hours. When stimulant intoxication progresses to delirium, the patient exhibits grandiosity, psychomotor agitation, paranoid ideation, formication (sensation of insects crawling on the skin), bizarre behavior (such as sorting objects into various groups), stereotypical movements of the mouth and tongue (such as teeth grinding, lip biting, and skin picking), tactile or visual hallucinations, and distorted perceptions, including command hallucinations to harm oneself or others (DSM-III-R, 1987). Delusional states can also develop. In such cases, patients have temporary but dramatic paranoid delusions while remaining alert and fully oriented.
Physical findings include tachycardia, hypertension, hyperthermia. dilated pupils, perspiration or chills, hyperreflexia, nausea, and vomiting. You must conduct a careful neurologic and physical examination of the patient and establish a flow sheet for vital signs Patients who abuse stimulants, especially I.V. stimulants, are at risk for numerous medical complications that can ultimately be more problematic than the intoxication, such as endocarditis, tetanus. hepatitis, abscesses, acquired immunodeficiency syndrome (AIDS), stroke, intracranial hemorrhage, heart attack, fibrillation, respiratory arrest, and aspiration (Schuckit, 1989).
No laboratory tests, other than a toxicology screen, are helpful in diagnosing stimulant intoxication. However, medical complications that can occur secondary to acute intoxication may warrant such tests, depending on the patient's signs and symptoms.
| TRIAGE APPROACH TO DRUG ABUSE | |||||||||
| STIMULANTS | PHENCYCLIDINE | OPIOID OVERDOSE | OPIOID WITHDRAWAL | SEDATIVE INTOXICATION | SEDATIVE WITHDRAWAL | HALLUCINOGENS | CANNABIS | INHALANTS | |
| While awaiting laboratory analysis of a drug sample, the clinician can use the chart below to help determine the drug of abuse. A darkened circle indicates that the sign of the symptom is part of the clinical syndrome of overdose, intoxication, or withdrawal. | |||||||||
| Autonomic Signs | |||||||||
| Hypertension |
· |
· | · | · | |||||
| Hypotension | · | · | |||||||
| Tachycardia | · | · | · | ||||||
| Hyperthermia | · | · | · | · | · | ||||
| Hypothermia | · | · | |||||||
| Nausea and vomiting | · | · | · | · | · | ||||
| Neurologic signs | |||||||||
| Dilated pupils | · | · | · | ||||||
| Pinpoint pupils | · | ||||||||
| Nystagmus | · | · | · | ||||||
| Hyperreflexia | · | · | · | ||||||
| Hyporeflexia | · | ||||||||
| Ataxia | · | · | · | ||||||
| Psychological symptoms | |||||||||
| Hallucinations | · | · | · | ||||||
| Delusions | · | · | · | · | |||||
The differential diagnosis of stimulant abuse must exclude mania, schizophrenia, and phencyclidine intoxication. A toxicology screen is the most effective way to differentiate stimulant intoxication from these other causes; 10 ml of blood and 50 ml of urine are sufficient to carry out appropriate laboratory tests. Recognize, however, that patients with schizophrenia and mania may also abuse stimulants and other drugs, necessitating a dual diagnosis.
Schuckit (1989) recommends placing the patient in a quiet room. away from the general traffic of the emergency department (ED). If the patient is paranoid, avoid a confined setting, which will make him feel threatened, and maintain a comfortable distance between you. Carefully explain all procedures to the patient in detail. Don't touch him without permission, and try to avoid any sudden movements that may disturb him. Reassure the patient that the effects of the stimulant will subside. Because the patient should not be left alone, try to involve family members or friends who can join the session to provide further reassurance.
If interpersonal interventions fail to relieve the patients agitation and anxiety, a benzodiazepine, such as diazepam (Valium) 10 mg P.O. or 5 mg I.V. or lorazepam (Ativan) 2 mg P.O. or 2 to 4 mg (0.05 mg/kg) I.M., can be administered. If the patient does not respond to the benzodiazepine or is delusional, extremely agitated, or combative, a high-potency neuroleptic, such as thiothixene (Navane) 10 mg I.M. or 20 mg concentrate or haloperidol (Haldol) 5 mg I.M. or 10 mg concentrate, can be given every 30 to 60 minutes. Low-potency neuroleptics, such as thioridazine (Mellaril) or chlorpromazine (Thorazine), may precipitate an anticholinergic crisis if the patient has ingested a contaminant or unreported anticholinergic substance (see Chapter 16, Psychotropic Drug Reactions). To facilitate excretion of the stimulant, administer ammonium chloride (500 mg P.O. every 3 to 4 hours) with the goal of acidifying the patient's urine below a pH of 6.6 (Schuckit, 1989).
Patient education for drug abuse should cover the following:
With appropriate intervention, stimulant intoxication can be attenuated in the emergency department. Don't discharge the patient, however, until you have completed a thorough drug history and discussed the benefits of a drug rehabilitation program. Schedule the patient for a follow-up appointment the next day with a psychiatrist or a member of a rehabilitation program. When possible. ask the patient's family and friends to encourage his participation in treatment and to help ensure that he does not resume drug use. Caution them that the patient may experience depression, insomnia. and an intense craving for the stimulant. Consider hospitalizing the patient if he:
Stimulant withdrawal produces an intense craving for the drug, along with depression that can create a suicide risk. Severity of symptoms depends on the potency of the stimulant; I.V. and free-based stimulants cause an especially intense "crash." No detoxification regimen is available for stimulants. Usually, after several nights of sleep, the dysphoria resolves and the suicidal ideation remits. Clinical management involves observing the patient to prevent self-harm and to provide an opportunity for sleep and mood recovery. The clinician should evaluate the patient after sleep to ensure that symptoms of depression and suicidal ideation have disappeared. Occasionally, the suicidal preoccupation may be severe enough to warrant hospitalization. A patient undergoing an acute post-stimulant depression is at high risk for relapse and should be considered a candidate for inpatient rehabilitation. Such a patient may come to the emergency department seeking a sedative-hypnotic to relieve the symptoms (see "Drug-Seeking Behavior" in Chapter 15, Difficult Situations).
Do not discharge a patient who is intoxicated or in acute withdrawal. Make every effort to stabilize him, including hospitalization. If a patient is released prematurely, the emergency service could be held liable for any subsequent harm he causes.
Phencyclidine (PCP) intoxication commonly presents a confusing clinical picture, with diverse psychological, physiologic, and behavioral effects. Persons can become extremely violent when intoxicated with this drug. Readily absorbed by mouth, smoking, or snorting, PCP is often sold as or is a frequent contaminant of marijuana, lysergic acid diethylamide, cocaine, and amphetamines (Walker, 1983). Its effects usually last 3 to 4 hours but can persist for several days. Consider PCP intoxication a medical emergency, at least until you determine whether the patient's serum drug levels are rising. falling, or stable. No withdrawal syndrome occurs.
Primary mental status findings include calmness (to the point of sleep), agitation, hostility, disorientation, emotional lability, a sense of slowing of time, "out of body" feelings, belligerence, assaultiveness, unpredictability, impaired judgment, hallucinations, and paranoid ideation.
The physical examination is important for differentiating PCP intoxication from other types. Medical complications—vomiting (with the risk of aspiration), seizures, and extreme hypertension-make the physical evaluation essential to treatment. Establish a flow sheet. record the patient's vital signs at regular intervals, and monitor the patient for laryngeal stridor or respiratory depression. Clinical signs and symptoms usually correlate with dose and blood level (see Signs and symptoms of phencyclidine intoxication, page 62).
Other than toxicology screens, no routine laboratory tests can aid in diagnosing PCP intoxication. However, based on the physical and neurologic examination and the patient's history, laboratory tests may be clinically indicated.
| Signs and Symptoms of Phencyclidine Intoxication | ||
| Signs and symptoms of phencyclidine intoxication depend on the amount of drug the patient has ingested and the serum levels produced. Be aware, however, that dosage calibration is nonexistent in drug activity that occurs "on the streets." Also keep in mind that you may need to begin treatment before serum levels are obtained. If ingestion occurred within a few hours of your contact with the patient, be alert to signs of increasing serum levels. An apparently mildly intoxicated patient, left unattended, can soon become gravely distressed and die. | ||
| AMOUNT INGESTED | SERUM LEVELS | SIGNS AND SYMPTOMS |
| 1to5mg | 10to70ng/ml | Vertical and horizontal nystagmus, dysarthria, ataxia, toss of pain response, drooling, nausea, mild pulse rate and blood pressure elevation, hyperacusis |
| 5to20mg | 70to200ng/ml | Catatonia; rigidity, myoclonus; nonresponsiveness to pain, touch, and proprioception; neck spasms; excessive secretions; fever; elevated pulse rate and blood pressure; hyperreftexia |
| 20 mg | >200ng/ml | Unresponsiveness to stimuli, pupils fixed and dilated, hypertension, convulsion, death secondary to cardiovascular causes |
| Source: Weiss, 1983. | ||
The differential diagnosis of PCP intoxication includes the effects of other psychoactive substances, such as amphetamines and hallucinogens, as well as head trauma, schizophrenia, delirium, mania, and cerebrovascular accident (Daghestani and Schnoll. 1989). Ataxia, nystagmus, and undilated pupils help rule out stimulant and hallucinogen toxicity. Hyperreflexia and hypertension suggest PCP abuse rather than sedatives or hypnotics. Schizophrenia and mania can usually be ruled out or established based on the patients history. Closely examine the patient for head trauma and cardiovascular illness.
Because of the poor judgment of the PCP-intoxicated patient, protective supervision in a non-stimulating environment is essential. In contrast to the approach used for other intoxications, staff members should avoid "talking down" a patient who has taken PCP because it may further agitate him. If possible, obtain a psychiatric and drug use history, including drugs taken, duration of use, time of last dose, and previous adverse reactions. Staff members should carefully search the patient's belongings for drugs or paraphernalia, which can be analyzed to assist in making the diagnosis. (If the patient is lucid, seek his consent first.) Avoid using restraints, if possible. because the patient is at risk for muscle tissue breakdown, which can lead to acute renal failure.
Pharmacologic treatment of PCP intoxication is complex and should be planned in collaboration with a knowledgeable internist or emergency medicine physician. Treatment for PCP agitation includes the following:
For mild agitation, tension, anxiety, and excitement, administer diazepam 10 to 30 mg P.O. Lorazepam 2 to 4 mg (0.05 mg/kg) I.M. may be used as an alternative in uncooperative patients.
For severe agitation and excitement, with hallucinations, delusions, and bizarre behavior, consider haloperidol 5 mg I.M. or 10 mg concentrate P.O., thiothixene 10 mg I.M. or 20 mg concentrate P.O., or loxapine (Loxitane) 10 mg I.M. or 25 mg concentrate P.O. given every 30 to 60 minutes.
PCP is retained by body fluids, and its metabolism and excretion are influenced by pH levels in urine and gastric acid. Thus, PCP psychosis or delirium can last up to a week, with a waxing and waning of symptoms that reflect excretion into and reabsorption from the stomach, and a principal goal of treatment is to enhance excretion.
If the patient is comatose, administer ammonium chloride 2.75 mEq/kg dissolved in 60 ml of saline solution every 6 hours through a nasogastric tube until the urine pH is less than 5.5. Continuous gastric suctioning is recommended to recover large amounts of PCP left in the stomach.
For a noncomatose patient, urine acidification is accomplished by an I.V. infusion of vitamin C (ascorbic acid) at a rate of 2 g in 500 ml of water every 6 hours (Daghestani and Schnoll, 1989). To ensure an accurate dosage, check the urine pH two to four times a day. When the pH is below 5.0, diuresis can be forced, using furosemide (Lasix) 20 to 40 mg I.V. (Daghescani and Schnoll. 1989). When a diuretic is used, monitor serum electrolytes and administer potassium supplements when necessary.
Urine acidification should continue for at least 1 week: recommended doses are ammonium chloride 500 mg P.O. four times daily and ascorbic acid 1 g P.O. three times daily (Daghestani and Schnoll, 1989). Acidification is contraindicated in patients with severe liver disease and those with renal insufficiency. (See Complications and treatment of phencyclidine overdose for additional information.)
Educational interventions for PCP abuse are similar to those for stimulant abuse (see page 59).
Because of the serious behavioral and medical complications of PCP intoxication, the patient should be admitted for close observation. During hospitalization, a comprehensive drug and psychiatric history should be taken and plans instituted to transfer the patient to a drug treatment program.
| Complications and Treatment of Phencyclidine Overdose | |
| Complication | Treatment |
| Seizure and status epilepticus | No medication for a single seizure. For repeated seizures or status epilepticus, give diazepam (Valium) 10 to 20 mg IV. |
| Hypertension | Use hydralazine (Apresoline) or phentolamine (Regitine) IV. infusion 2 to 5 mg over 5 to 10 minutes. |
| Hyperthermia | Use a cooling blanket |
| Opisthotonos and acute dystonia | Usually resolves as serum drug levels decrease. If the problem persists, diazepam 2 to 10 mg IV. is usually effective. |
| Cardiac arrhythmia | Cardiology consultation |
| Rhabdomyolysis, myoglobinuria, acute renal failure | Nephrology consultation |
| Source: Daghestani and Schnoll, 1989, pp. 1213-1214. Adapted with permission of the publisher. | |
Medicolegal considerations for PCP abuse are similar to those for stimulant abuse (see page 60).
Opioid overdose-from opiates, such as heroin and morphine, and synthetic opioids, such as meperidine (Demerol) and oxycodone (Roxicodone) — is a life-threatening emergency that requires treatment by an experienced internist or emergency medicine physician. Most patients are found in a semicomatose or comatose condition with recent evidence of I.V. injection, such as a needle in the arm or nearby, or oral ingestion, such as an empty prescription bottle (Schuckit, 1989).
Because most patients are comatose and need immediate treatment, a complete mental status examination is not indicated.
Characteristic physical findings include decreased respiration: blue lips; blue or pale skin; pinpoint pupils (if brain damage has occurred, usually secondary to anoxia, pupils may be dilated; meperidine can cause mydriasis); hyperemic nasal mucosa (if the drugs have been snorted); recent needle marks on the arm or elsewhere: gasping, rattling respirations and rales secondary to pulmonary edema; and cardiac arrhythmias or seizures, especially when the overdose is caused by codeine, propoxyphene (Darvon), or meperidine (Schuckit, 1989). Death can occur secondary to pulmonary or cerebral edema.
The laboratory evaluation should include electrolyte and serum glucose levels, complete blood count (CBC), hepatic and renal profiles, electrocardiogram, arterial blood gas analysis, drug and alcohol screen, and a computed tomography scan. Occasionally, an electroencephalogram may be necessary to establish the level of brain impairment.
Symptoms of opioid overdose warrant immediate treatment with I.V. naloxone (Narcan). If the patient remains comatose, life-support measures should be instituted while other possible causes of the coma are investigated.
Because the patient is unconscious, interpersonal interventions are not warranted.
If the patient does not respond to an opioid antagonist challenge, further treatment is determined by medical complications, such as cardiac arrhythmia or pneumonia (see Treatment of opioid overdose, page 68, for guidelines).
Educational interventions for opioid overdose are similar to those for stimulant abuse (see page 59).
Because of the life-threatening risk of opioid overdose and its potential medical complications, the patient should be hospitalized for further evaluation and treatment.
Medicolegal considerations for opioid overdose are similar to those for stimulant abuse (see page 60).
Opioid withdrawal is precipitated by the abrupt cessation of opioid administration after 1 to 2 weeks of continuous use. Administration of a narcotic antagonist, such as naloxone, can also cause opioid withdrawal (DSM-III-R, 1987). When heroin or morphine use is discontinued, withdrawal symptoms appear within 6 to 8 hours, peak on the second or third day, and disappear by the 10th day. Meperidine withdrawal begins more quickly, with symptoms appearing within 3 to 4 hours, peaking within 8 to 12 hours, and disappearing after 4 to 5 days. Methadone (Dolophine) withdrawal may not begin until 1 to 3 days after the last dose, with symptoms usually dissipating in 10 to 14 days. Withdrawal symptoms for semisynthetic and synthetic opioids are similar to those for heroin. Usually, substances with a short duration of action (such as meperidine) produce intense withdrawal symptoms, whereas substances that are more slowly eliminated (such as codeine) produce milder symptoms.
| Treatment of Opioid Overdose | ||
| 1. | Establish airway. | |
| 2. | Check pulse rate and initiate advanced cardiac life support, if necessary. | |
| 3. | Prevent aspiration by positioning the patient on his side or using a tracheal tube with an inflatable cuff. | |
| 4. | Begin an IV infusion with a large-gauge needle. | |
| 5. | Evaluate for pulmonary edema, blood loss, and cardiac arrhythmias. | |
| 6. | Administer a narcotic antagonist. Naloxone (Narcan) is the preferred drug, given in doses of 0.4 mg (1 ml) or 0.01 mg/kg I.V. and repeated in 3 to 10 minutes if no reaction occurs. This drug loses its effect in 2 to 3 hours, so the patient in a heroin overdose should be monitored for at least 24 hours and receive methadone (Dolophine) for at least 72 hours. | |
| 7. | General guidelines for other medical complications include: | |
| (a) | blood loss or hypotension- plasma expanders or pressor drugs | |
| (b) | pulmonary edema-positive-pressure oxygen, but avoid over oxygenating and decreasing respiratory drive | |
| (c) | cardiac arrhythmias-appropriate antiarrhythmic drugs | |
| (d) | hypoglycemia-50 ml of 50% glucose | |
| (e) | infection-monitor for infection because pneumonia develops in more than 50% of patients with pulmonary edema. | |
| Source: Schuckit, 1989. Adapted with permission of the publisher. | ||
The amount of opioid that has been ingested can be difficult to determine; for example, about 95% of a "bag" of heroin may consist of adulterants, such as quinine, mannitol, or lactose (Tomb. 1988). Therefore, treatment for opioid withdrawal must be based on objective physical findings rather than on the patient’s subjective complaints or statements about opioid habits.
Most patients are irritable and have a craving for an opioid. Otherwise, no significant mental status findings are associated with opioid withdrawal.
Physical findings - the diagnostic key to recognizing opioid withdrawal - include nausea and vomiting, diarrhea, dilated pupils, muscle aches and pains, insomnia, lacrimation (tearing eyes), flulike weakness, rhinorrhea (running nose), piloerection (goose flesh), sweating, flushing, abdominal pain, increased temperature, yawning, and semen ejaculation.
Blood and urine studies are helpful in determining the cause of withdrawal. A physical examination and baseline laboratory studies (CBC, electrolyte and calcium levels, and renal and hepatic profiles) are important because I.V. drug abuse significantly increases the risk for medical complications, including AIDS, hepatitis, endocarditis, pneumonia, and tuberculosis. Staff members must take universal blood and body fluid precautions when handling body fluids of I.V. drug abusers.
The differential diagnosis of opioid withdrawal should exclude sedative-hypnotic and alcohol withdrawal. The clinician can make the diagnosis by testing the patient's blood and urine and by obtaining confirmation of drug use from relatives or friends.
A patient in opioid withdrawal is irritable and demanding. To avoid confusion during detoxification, only one clinician should deal directly with the patient. The clinician should explain that he will into minimize the patient's discomfort although withdrawal symptoms cannot be eliminated. Other staff members should establish a flow sheet of symptom severity.
A detoxification regimen should be started only when physical signs of withdrawal-such as lacrimation, dilated pupils, rhinorrhea, and piloerection - appear. The two commonly used approaches to opioid detoxification are methadone substitution and withdrawal and clonidine (Catapres) symptom blockade.
As described by Weiss and Mirin (1988), methadone treatment should be based on objective physical findings of withdrawal, including a pulse rate 10 beats/minute over baseline (or 90 beats/ minute without tachycardia), systolic blood pressure 10 mm Hg over baseline (or 160/95 mm Hg without hypertension), and other signs noted above. Treatment on the first day consists of 5 to 10 mg of methadone every 4 hours as needed for mild to moderate symptoms and 10 to 20 mg every 4 hours as needed for severe symptoms. On the second day, the total amount given during the first 24 hours should be administered in two equally divided doses. On subsequent days, the daily dosage is decreased by 5 mg each day until the patient is no longer receiving methadone.
Clonidine reduces the autonomic symptoms of withdrawal, but the craving, lethargy, insomnia, and restlessness remain. The average dose is 5 mcg/kg of body weight (0.35 mg for a 70-kg patient). The dosage is titrated against symptoms, with the average adult needing 0.3 mg four times daily, or 0.3 to 2 mg/day (Jaffee and Kleber, 1989). After the patient is stabilized, clonidine should be continued for 5 days, with the dosage decreased by 0.2 mg/day. Contraindications include hypotension, use of antihypertensive orantidepressant medication, a history of psychosis or cardiac arrhythmias, and pregnancy. Outpatients should not be given more than three doses of clonidine and must be cautioned about driving during the first several days, because clonidine can be sedating.
Educational interventions for opioid withdrawal are similar to those for stimulant abuse (see page 59).
Refer the patient to a methadone maintenance or drug rehabilitation program for further evaluation and treatment. Because opioid withdrawal is not life-threatening, the clinician should not dispense methadone in the emergency setting. Although most patients can be treated in an outpatient setting, hospitalization may be necessary if the patient is addicted to several substances, has a complicating medical illness, or has no family members, friends, or other support system.
Medicolegal considerations for opioid withdrawal are similar to those for stimulant abuse (see page 60).
Sedative-hypnotics form a class of drugs that includes benzodiazepines and barbiturates. Sedatives are typically used to control anxiety, whereas hypnotics are used to induce sleep. Sedatives and hypnotics are cross-tolerant and synergistic with alcohol and with each other. Abuse of these drugs in combination with alcohol is one of the most common drug-related causes of morbidity and mortality (National Institute on Drug Abuse, 1987).
Sedative-hypnotic intoxication is marked by impaired judgment, loquacity, mood lability, dreamlike feelings, and disinhibition of sexual and aggressive feelings.
Slurred speech, uncoordination, unsteady gait, nystagmus on lateral gaze, areflexia, muscle hypotonicity, hypotension, and hypothermia are common physical findings.
Baseline values for blood and urine toxicology, CBC, electrolyte levels, and renal and hepatic function should be established at the time of the initial evaluation.
The differential diagnosis of sedative-hypnotic intoxication includes conditions that mimic alcohol intoxication. Therefore, the differential diagnosis must rule out alcohol intoxication (alone or in combination with drugs), as well as hypoglycemia, diabetic ketoacidosis, subdural hematoma, cerebellar ataxia, multiple sclerosis. and Huntington's disease.
Provide clear instructions and information to the patient, identifying yourself as often as necessary and explaining any procedures that must be carried out. The patient usually responds to reassurance and acceptance; thus, friends or relatives can be a useful adjunct to treatment because of the support and familiarity they provide. Place the patient in a well-lighted room under constant supervision either by staffer family members, to prevent wandering or accidental injury.
Management of barbiturate intoxication is a complex medical inervention best left to clinicians who have experience in treating such cases (see Treatment of sedative overdose, page 74). Abuse of glutethimide (Doriden) poses a special problem because it is absorbed by adipose tissues and released gradually. Thus, the patient may wake up from a coma only to relapse as more of the drug is released from tissue stores.
Some patients indiscriminately abuse prescription sedative-hypnotics in combination with other substances; other patients intentionally abuse sedative-hypnotics as a form of self-medication. In the first case, consider the patient to be evidencing addictive disease, and follow the educational interventions for stimulant abuse on page 59.
Educational interventions differ for the patient attempting self-medication for anxiety, depression, or a psychotic disorder. After eliciting a history of a primary psychiatric disorder, explain to the patient that his symptoms must be controlled under strict medical supervision. Some patients, notably adult children of alcoholics, may overuse sedative-hypnotics to treat anxiety and depression. Because of the risk of addiction, do not administer a benzodiazepine to such patients. Instead, they may benefit from an antidepressant, such as fluoxetine (Prozac), or a nonsedating antianxiety drug, such as buspirone (Buspar). Educational interventions should focus on helping the patient to appreciate the dynamics of his drug abuse and encouraging him to consult a physician for a safer treatment.
Barbiturate overdose is a medical emergency. Most patients require admission to a medical intensive care unit for continued evaluation and treatment.
| Treatment of Sedative Overdose | |
| 1. | Establish airway. |
| 2. | Evaluate cardiovascular status and initiate advanced cardiac life support, if necessary. |
| 3. | Begin I.V. infusion with a large-gauge needle. |
| 4. | Establish means to measure urine output. |
| 5. | Start gastric lavage if the patient ingested oral medication during the last 4 to 6 hours. Administer 60 ml of castor oil via stomach tube, especially if fat-soluble drugs like glutethimide (Doriden) were taken. |
| 6. | Administer 12 to 20 g of activated charcoal suspended in water every 1 to 12 hours over the first 2 days. |
| 7. | Check for the possibility of narcotic overdose by giving natoxone (Narcan) 0.4 mg I.M. or IV. |
| 8. | Carry out a thorough neurologic and physical examination. |
| 9. | Draw blood for arterial blood gas analysis, general blood tests to evaluate liver and kidney functioning, blood counts, and toxicologic screen. |
| 10. | Establish flow sheet for vital signs, level of reflexes, urine output, I.V. fluids. |
| 11. | Consider forced diuresis with furosemide (Lasix) 40 to 120 mg, as often as needed to maintain urine output of 250 ml or more per hour. Or I.V. flush with enough saline and water with glucose to maintain urine output at 250 ml or more per hour. This is not needed for patients with stable vital signs or for those who have deep tendon reflexes. Forced diuresis rarely helps for overdoses of chlordiazepoxide (Ubrium) of diazepam (Valium). |
| 12. | Arrange for hemodialysis or peritoneal dialysis for patient in deep coma. |
| 13. | Evaluate need for antibiotics. Do not start prophylactically. |
| 14. | Do not use a central nervous system stimulant. |
| Source: Schuckit, 1989. Adapted with permission of the publisher. | |
Unlike the abuse of illegal drugs, such as cocaine and heroin, abuse of prescription sedative-hypnotics is sometimes perpetuated by duped, misguided, or dishonest physicians. Contributing to prescription abuse – intentionally or unwittingly-increases the patient's risk and magnifies your liability. Before refilling a patient's prescription for a controlled substance, perform a thorough examination, document the indication for treatment, contact the patient's prescribing physician, and limit the refill to a 3-day supply (see "Drug-Seeking Behavior" in Chapter 15, Difficult Situations!
Left untreated, sedative-hypnotic withdrawal can cause delirium, with significantly increased morbidity and risk for mortality. Additionally, withdrawal can be uncomfortable for the patient because all of its symptoms cannot be suppressed. For these reasons, the patient should be hospitalized.
Withdrawal symptoms do not follow an established pattern. Onset of symptoms correlates with the ingested drug's duration of action. For example, symptoms of pentobarbital (Nembutal) withdrawal begin 12 to 16 hours after the last dose, whereas those of chlordiazepoxide (Librium) withdrawal may not occur until 72 to 96 hours after stopping the drug (see Sedative-hypnotics and their duration of action, page 76). Barbiturates usually cause more severe symptoms, but with the advent of high-potency benzodiazepines, such as alprazolam (Xanax) and lorazepam, significant withdrawal symptoms can occur from antianxiety drugs.
The mental status findings in a patient undergoing withdrawal from a sedative-hypnotic are similar to those of a patient with alcohol withdrawal syndrome: anxiety, a strong desire for the drug, and. in severe cases, hallucinations and delusions.
The physical examination usually reveals tremors, nightmares, insomnia, increased pulse rate and respiration rate, hyperthermia, loss of appetite, nausea and vomiting, postural hypotension, seizures, and delirium. Suspect sedative withdrawal if the patient is agitated, has abnormal autonomic signs, and asks for a sedative. Examine the patient carefully; sedative abusers are at risk for many of the same medical problems that occur in opioid abusers, particularly infection and hepatitis.
| Sedative-Hypnotics and their Duration of Action | |
| BENZOUAZEPINES | |
| Long-acting: 20 hours or more | |
| · | diazepam (Valium) |
| · | clonazepam (Klonopin) |
| · | chtofdiazepoxide (Librium) |
| · | clorazepate (Tranxene) |
| · | fturazepam (Dalmane) |
| · | prazepam (Centrax) |
| Short-acting: 6 to 19 hours | |
| · | alprazolam (Xanax) |
| · | lorazepam (Ativan) |
| · | oxazepam (Serax) |
| · | temazepam(Restoril) |
| Ultra-short-acting: toss than 6 hours | |
|
· |
triazolam(Halcion) |
| BARBITURATES | |
| Long-acting: 20 hours or more | |
| · | mephobarbital (Mebaral) |
| · | metharbital (Gemonil) |
| · | phenobarbital (Barbita) |
| Intermediate-acting: 6 to 8 hours | |
| · | amobarbital (Amytal) |
| · | aprobartiital (Alurate) |
| · | butabarbilal (Butisol) |
| · | talbutal (Lotusate) |
| Short-acting: 3 to 4 hours | |
| · | pentobarbital (Nembutal) |
| · | secobarbital (Seconal) |
| Source: Smith et at., 1989. Adapted with permission of the publisher. | |
Toxicology screens are indicated to detect multisubstance abuse. A baseline CBC, hepatic and renal profiles, glucose and electrolyte levels, chest X-ray, electrocardiogram (ECG), and blood gas studies can help rule out many other possible causes of delirium.
The differential diagnosis for sedative-hypnotic withdrawal should exclude alcohol withdrawal and other causes of delirium.
Not all patients who are addicted to sedatives are hard-core addicts. Many patients unwittingly become addicted to sedatives prescribed by their physicians, and the addiction may go undiscovered until they are hospitalized for an unrelated medical evaluation or surgery. In this case, the best approach is to explain the addiction to the patient and family. Recommend a psychiatric evaluation to determine whether the patient has an underlying anxiety or sleep disorder. After the evaluation, the patient should be detoxified or referred to a psychiatrist knowledgeable about the specific addiction.
In contrast, hard-core addicts typically exhibit tough, demanding behavior as a defense against feelings of rejection and inadequacy (Renner, 1987), so expect an initial period of defensive hostility. Reassure the patient that you are concerned about him. Because many drug abusers have serious personality disorders, restrict visits to persons of known reliability. Individual and family counseling should start in the hospital, with the goal of enrolling the patient in a long-term program (Renner, 1987). (See also "Drug-Seeking Behavior" in Chapter 15, Difficult Situations.)
The clinician can choose from several pharmacologic approaches to withdrawing a patient from sedative-hypnotics. One method is effective when the patient's degree of drug use cannot be determined (see Sedative withdrawal procedure, page 78). Another method involves estimating the patient's daily sedative-hypnotic use during the month before treatment (based on the patient's reported history of drug use) and computing a detoxification schedule (see Phenobarbital conversion from benzodiazepines and sedative-hypnotics).
| Sedative Withdrawal Procedure | |||||||||||
| 1. | Test dose: Administer 200 mg of pentobarbital (Nembutal) orally and assess neurologic changes after 1 hour. The 24-hour pentobarbital requirement is estimated as follows:
If no signs of a drug effect appear, then repeat the test 3 to 4 hours later using a dose of 300 mg of pentobarbital. No response to the 300-mg dose suggests a habit of more than 1,600 mg/day. |
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| 2. | Use either pentobarbital or phenobarbital (Barbita) for withdrawal, but phenobarbital has the advantage of few variations of blood barbiturate level. If pentobarbital is used, divide the estimated daily requirement into four equal doses and administer them every 6 hours. If phenobarbital is used, calculate dose at the rate of 30 mg of phenobarbital/100 mg of pentobarbital. Divide the total dose into three equal doses, and administer every 8 hours. | ||||||||||
| 3. | Reduce both pentobarbital and phenobarbital at the rate of 10% each day. | ||||||||||
| 4. | If the patient is concomitantly dependent on an opiate, barbiturate detoxification should proceed first, to be followed by opiate withdrawal later. | ||||||||||
| Source: Shader, 197S, pp. 119-120. Adapted with permission of the publisher. | |||||||||||
| Phenobarbital Conversion from Benzodiazepines and Sedative-Hypnotics | ||
| DRUG | DOSE (mg) | PHENOBARBITAL WITHDRAWAL CONVERSION (mg)* |
| Benzodiazepines | ||
| alprazolam (Xanax) | 1 | 30 |
| chlordiazepoxide (Librium) | 25 | 30 |
| clonazepam (Klonopin) | 0.5 | 30 |
| clorazepate (Tranxene) | 15 | 30 |
| diazepam (Valium) | 10 | 30 |
| flurazepam (Dalmane) | 15 | 30 |
| halazepam (Paxipam) | 40 | 30 |
| lorazepam (Ativan) | 1 | 15 |
| oxazepam (Serax) | 10 | 30 |
| prazepam (Centrax) | 10 | 30 |
| temazepam (Restoril) | 15 | 30 |
| Barbiturates | ||
| amobarbital (Amytal) | 100 | 30 |
| butafaarbital (Butisol) | 100 | 30 |
| butalbital (Fiorinal) | 50 | 15 |
| pentobarbital (Nembutal) | 100 | 50 |
| secobarbital (Seconal) | 100 | 50 |
| Glycerols | ||
| meprobamate (Equanil, Miltown) | 400 | 30 |
| PIperldinediones | ||
| glutethimide (Doriden) | 250 | 30 |
| * Withdrawal doses of phenobarbital are sufficient to suppress most withdrawal symptoms but are not the same as therapeutic doses.
Source: Smith et al., 1989. Adapted with permission of the publisher. |
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Phenobarbital (Barbita) is used to wean patients from sedative hypnotics because its long half-life prevents a steep decline in blood levels and eases withdrawal. Patients who also abuse alcohol may need a higher dose of phenobarbital. The computed equivalence of phenobarbital is given daily, in three or four divided doses; maximum dosage is 500 mg/day.
After the patient has been stabilized for 2 days, decrease the daily dosage of phenobarbital by 30 mg each day. Before each dose is administered, staff members should check the patient for sustained horizontal nystagmus, slurred speech, and ataxia. If sustained nystagmus is found, the clinician should withhold the scheduled dose. If all three signs are present, the next two doses should be withheld and the total daily dose for the following day cut in half.
If the patient is already in acute withdrawal and in danger of having seizures, the clinician should administer 200 mg of phenobarbital I.M. to stabilize the patient's condition. The withdrawal schedule is then initiated based on one of the protocols described above. If nystagmus or other signs of intoxication develop after the phenobarbital injection, the patient is probably not dependent on sedative-hypnotics.
Educational interventions for sedative-hypnotic withdrawal are similar to those for sedative-hypnotic intoxication (see page 73).
Because this condition is life-threatening, the clinician should admit the patient for detoxification.
Medicolegal considerations for sedative-hypnotic withdrawal are similar to those for sedative-hypnotic intoxication (see page 74).
Hallucinogens comprise two groups of psychoactive substances that differ in chemical structure. The first group, structurally related to 5 hydroxytryptamine, includes lysergic acid diethylamide (LSD), dimethyl-4-phosphoryltryptamine (psilocybin), dimethyltryptamine (DMT), and peyote (mescaline). The second group, created by a series of ring substitutions on amphetamines, includes 2,5-dimethoxy-4methylamphetamine (DOM or STP), methylene dioxyamphetamine (MDA), methylene dioxymethamphetamine (MDMA), and DOB. a 4-bromo homolog of STP. LSD, mescaline, and the methoxylated amphetamines have a long duration of action (8 to 12 hours), whereas DMT and psilocybin have a shorter duration of action (2 to 6 hours). Hallucinogens cause no known withdrawal symptoms.
Hallucinogen intoxication is marked by perceptual, emotional, and cognitive changes (Cohen, 1989). With eyes closed, the patient "sees" colorful mobile displays of geometric patterns or complex human or animal forms. Colors become more intense. Fixed objects undulate and flow. The patient has a greater sensitivity to touch and an altered sense of taste and smell, sometimes experiencing synesthesia (an overflow of one sensory modality into another: for instance, the patient "hears" colors or "sees" music). Other perceptual changes include depersonalization, derealization, and body image distortions in which body parts seem to grow, shrink, or disappear.
Emotional alterations range from euphoria, elation, and bliss to tension and anxiety that culminate in a panic attack. The patient may laugh or cry for prolonged periods, usually at inappropriate times.
Cognitive alterations include a loosening of associations with unusual content, illogical and fantasy-laden thought sequences, paranoid grandiosity, and, less commonly, persecutory ideation.
Hallucinogens can cause elevated blood pressure and body temperature, dilated pupils, and hyperactive reflexes.
The clinician may order a drug toxicology screen.
The initial diagnosis is usually made by the patient or an accompanying person who verifies that the patient ingested a hallucinogen. Although the clinician typically makes the diagnosis from symptoms (especially the perceptual distortions), the differential diagnosis should rule out anticholinergic, PCP, or cannabis intoxication. A patient on PCP is usually drowsy rather than alert and exhibits such neurologic symptoms as nystagmus and ataxia. Dilated, unreactive pupils are common in anticholinergic intoxication.
Interpersonal intervention is crucial when the patient has a "bad trip"-a panic reaction with overwhelming anxiety as a result of the perceptional distortions he is experiencing. The primary intervention involves reassuring the patient that the drug's effects will wear off in several hours. When possible, involve friends and family members, who can help alleviate the patient's anxiety by maintaining a continuous dialogue in a supportive, nonthreatening environment.
The clinician should try to avoid pharmacologic intervention. If the patient's anxiety becomes overwhelming, he can be given 10 to 50 mg of diazepam P.O. or 2 to 4 mg of lorazepam I.M.
That the patient is in an emergency medical setting gives weight to the clinician's educational efforts. Initially, help the patient retain a sense of identity by reassuring him that his hallucinogenic intoxication, although a frightening experience, is nevertheless a drug effect that will subside. Once the patient is free of the drug's effects, focus on preventive measures. He will have already discovered the painful truth that hallucinogen use is far from a benign form of recreation. Remind him that such intoxication can lead to serious injury or death. Encourage the habitual user to participate in drug rehabilitation or counseling. If the patient is a child or adolescent, consider referral to family counseling, since hallucinogen abuse is a form of escape.
The effects of a "bad trip" usually remit within several hours, and the patient can be sent home, preferably in the company of family or friends. Arrange an immediate follow-up visit to address the drug problem and to rule out any psychiatric disorders.
Occasionally, a patient enters the ED because of "flashbacks" (recrudescence of symptoms experienced during previous hallucinogenic drug use). This response may appear days, weeks, or months after the last exposure. Treatment of flashbacks is the same as for a hallucinogen-induced panic reaction - reassurance, support, and administration of benzodiazepines to control extreme anxiety.
Although hallucinogen abuse does not carry as high a risk of violent behavior as PCP abuse, violent or self-destructive behavior is possible, especially when hallucinations are frightening. Thus. do not discharge a patient until the drug's effects wear off.
Failure to diagnose hallucinogen abuse-or mistaking it for schizophrenia-is a potential source of liability. Without a coexisting diagnosis of schizophrenia, hallucinogen intoxication does not warrant ongoing antipsychotic drug therapy.
Cannabis comprises hashish, bhang, marijuana, and purified delta9-tetrahydrocannabinol (THC). Abusers commonly use cannabis with other substances, particularly alcohol and cocaine. The most common methods of administration are smoking and eating: it is rarely used intravenously. The drug's effects develop 20 to 30 minutes after smoking, longer after oral ingestion.
A mildly intoxicated patient is euphoric and relaxed. Heightened sexual arousal and decreased social interaction are also typical signs. A patient who has ingested a moderate to heavy amount of cannabis becomes panicky, paranoid, suspicious, and disoriented and may also experience a loss of insight and hallucinations with paranoid delusions.
Physical findings of cannabis intoxication include fine tremor, a slight decrease in body temperature, reduced muscle strength, decreased balance and motor coordination, dry mouth, bloodshot eyes, nausea, and headache. A patient with epilepsy may have seizures.
Laboratory studies, such as a toxicology screen, may be ordered to rule out other causes.
The differential diagnosis should exclude intoxication from alcohol, sedative-hypnotics, and opioids.
The chief intervention for cannabis abuse is reassurance that the symptoms will clear within 4 to 8 hours. Keep the patient in a quiet room, and enlist family and friends to help comfort him.
A clinician would not usually prescribe psychotropic drugs for a patient with cannabis intoxication. However, if the patients anxiety and panic become severe, consider administering 10 to 30 mg of diazepam P.O. or 2 to 4 mg of lorazepam I.M. Rarely, paranoia or paranoid delusions warrant neuroleptic medication. Use these agents in small doses for brief periods. Haloperidol 2 to 5 mg P.O. every 24 hours in divided doses is usually adequate. The dosage will rarely need to be increased to more than 20 mg/day.
If a psychotic reaction lasts more than a few days, evaluate the patient for a major psychiatric illness. A patient with cannabis intoxication should not receive an indefinite regimen of neuroleptic medication unless he has an underlying psychiatric illness.
Educational interventions for cannabis intoxication are similar to those for hallucinogen intoxication (see page 83).
A cannabis-intoxicated patient can be managed in the ED, since the reaction remits within 4 to 8 hours. Discharge the patient in the company of a relative or friend, and refer him to a specialist in resolving drug problems. Further psychiatric evaluation is advised to rule out the possibility of coexisting psychopathology. As with hallucinogen abuse, flashbacks can occur with cannabis use. Treatment is similar to that for cannabis intoxication.
Medicolegal considerations for cannabis intoxication are similar to those for hallucinogen intoxication (see page 83).
Persons who abuse inhalants sniff toluene-containing glue, aerosols, cleaning solutions, nail polish remover, lighter fluids, paint thinner, and other petroleum products. Symptoms of abuse appear within 5 minutes and cease in 1 to 2 hours. An overdose can result in central nervous system depression, cardiac arrhythmias, bronchospasm, and ventricular fibrillation, any of which can lead to death. Inhalants have no known withdrawal syndromes.
Mental status findings include belligerence, assaultiveness, apathy, impaired judgment, and impaired social and occupational functioning.
Physical findings include dizziness, nystagmus, slurred speech, unsteady gait, depressed reflexes, tremors, blurred vision, diplopia, stupor, coma, rash around the nose and mouth, breath odors, residue on face, hands, and clothing, redness and swelling of the eyes, and irritation of the throat, lungs, and nose. Conduct a thorough physical examination because inhalants can interfere with normal functioning of most body systems. Major medical problems associated with inhalant abuse include cardiac arrhythmias, hepatitis, renal failure, bone marrow suppression (which can lead to aplastic anemia), impaired pulmonary functioning, and skeletal muscle weakness with muscle destruction (Schuckit, 1989).
In addition to a toxicology screen, baseline ECG, CBC, and renal and hepatic studies should be performed because of the potential for serious medical complications.
The differential diagnosis entails ruling out intoxication from alcohol or sedative-hypnotics. Other than results from a toxicology screen, the patient's breath odor or residue on his clothing may provide a clue to inhalant abuse.
Because inhalants have a short duration of action, panic reactions have usually subsided by the time the patient is seen by a clinician. The patient responds favorably to reassurance and support.
If the patient is in a state of panic on arrival at the ED, the clinician should prescribe 15 to 20 mg of diazepam P.O. or 1 to 2 mg of lorazepam P.O. to control the patient's anxiety.
Chronic, heavy use of inhalants can precipitate withdrawal symptoms within a few hours to several days after cessation of use. These symptoms include tremulousness, tachycardia, disorientation, hallucinations, delusions, agitation, and seizures (Westermyer. 198"). A patient experiencing withdrawal symptoms should be given a long-acting sedative, such as diazepam or phenobarbital (Luminal). in doses sufficient to produce a calm, seizure-free state (Westermyer. 1987). The physician should gradually withdraw the medication over 5 to 10 days.
Chronic inhalant abusers may have significant cognitive impairment, thus reducing the impact of educational efforts. Impress on the patient the seriousness of this form of substance abuse, and include a younger patient's parents in the discussion (many inhalant abusers are children or adolescents). Inform them that "huffing," even in moderation, can cause brain damage and that its use can hardly be considered recreational. Refer the patient for drug rehabilitation or counseling as indicated.
If a patient has a complicating medical problem, hospitalization may be warranted. Otherwise, discharge the patient. Schedule an immediate follow-up visit to assess him for underlying psychopathology and to ensure that he is referred to an appropriate treatment program.
Medicolegal considerations for inhalant abuse are similar to those for hallucinogen intoxication (see page 83).