Substance Abuse

Depressant

The most important concern in sedative-hypnotic (alcohol, benzodiazepines, and barbiturates) intoxication is maintenance of the airway.

The most important concern in sedative-hypnotic withdrawal is seizure prevention.

Alcohol

Signs of alcohol intoxication include:

• Sedation

• Ataxia

• Emotional lability

• Slurred speech

• Disinhibition

• Nystagmus

It is important to note that the disinhibition of alcohol intoxication can resemble hypomania/mania. Suspect alcohol intoxication in a patient with hypomanic symptoms, ataxia, normal pupillary findings, and normal BP.

Signs of alcohol withdrawal include:

• Tremulousness

• Tachycardia, hypertension

• Seizures

• Delirium tremens (DTs)

• Agitation

• Hallucinations

The first and most common sign of alcohol withdrawal is tremulousness.

Alcholic Hallucinosis

Alcoholic hallucinosis is a type of alcohol withdrawal syndrome characterized by an alert sensorium, predominantly visual hallucinations (although auditory and tactile hallucinations also occur) and relatively stable vital signs. It develops 12-24 hours after the last drink and usually resolves within 24-48 hours.

Benzodiazepines

Benzodiazepine use may resemble that of alcohol or barbiturates, which is likely due to their common action of agonizing GABA receptors. The presence of nystagmus is indicative of alcohol intoxication, rather than benzodiazepine intoxication.

Benzodiazepines intoxication can be differentiated from opioid intoxication by the presence of a lesser degree of respiratory depression and normal pupils in benzodiazepine use.

Additional information specific to benzodiazepines may be found on the benzodiazepine card.

Opioid

Opioid intoxication causes the triad of:

• CNS depression

• Respiratory depression

• Miosis

A relatively specific sign of opioid intoxication is significant respiratory depression (4-6 respirations/min). Pupils may not always be miotic in opioid intoxication due to ingestion of multiple illicit drugs or severe cerebral hypoxia from apnea.

While benzodiazepines and barbiturates can also cause respiratory depression, the prevalence of opioid use and the degree of depression it causes warrants a high clinical suspicion of opioids.

Opioid withdrawal is not life-threatening, but quite unpleasant. Signs and symptoms peak after 24-48 hrs. of onset and include:

• Restlessness, yawning

• Rhinorrhea, lacrimation

• Myalgias, arthralgias

• Nausea, vomiting, diarrhea

• Sweating, piloerection

• Dilated pupils

Meperidine

Is the only opioid that does not cause miosis.,

Opioid overdose is treated with naloxone, a short-acting opioid antagonist.

Patients that present with acute opioid withdrawal that is precipitated by an interruption in opioid use can be treated with methadone.

Cannabis/THC - Marijuana

Often associated with injected conjunctiva. Associated symptoms include euphoria, impaired judgement, increased appetite, and dry mouth.,

Stimulants/Hallucinogen

Emergent management of acute intoxication with both stimulants and hallucinogens centers around control of agitation. The first line medication choice is parenteral benzodiazepines. If inadequate sedation is achieved, antipsychotics may also be used.

Hyperthermia in the setting of intoxication arises from excessive muscle activity. Supportive measures such as IV fluids and cooling blankets should be used when necessary, and muscle paralysis with non-depolarizing neuromuscular blockers (e.g. rocuronium) can be added as well.

Notably, succinylcholine is contraindicated due to the risk of rhabdomyolysis and hyperkalemia.

Succinylcholine depolarizes AchR, causing Na influx and K efflux. When muscle no longer able to fire, K+ efflux continues, causing hyperkalemia. Rhabdomyolysis also contriutes to hyperkalemia.

Amphetamine

Amphetamine/cocaine intoxication is characterized by euphoria and grandiosity resembling mania or psychosis. The following signs are present:

• Tachycardia

• Hypertension

• Pupillary dilation

• Fever

• Insomnia

• Psychomotor agitation

Individuals often use cocaine in binges, taking the drug repeatedly over a short period to maintain their "high." Following abrupt cessation, a "crash" typically occurs. This initial period can include severe depression with suicidal ideation and psychomotor slowing with milder symptoms that resolve within 1-2 weeks.

Heavy use frequently causes marked weight loss, psychotic symptoms, and excoriations due to chronic skin picking. Severe dental problems ("meth mouth") can include brown discoloration, tooth decay, and cracked teeth due to severe clenching.

The diagnostic hallmark in this scenario is erythema of the turbinates and nasal septum, which is a common finding in individuals who snort cocaine. In severe cases, perforation of the nasal septum can occur.

Chronic use can cause tooth decay.

Amphetamine/cocaine withdrawal is not life-threatening, as opposed to that of sedative-hypnotics. It is characterized by the following:

• Depression/suicidality

• Hypersomnolence

• Increased appetite

• Psychomotor retardation

• Intense drug craving

Acute complications of stimulant use are:

• Myocardial infarction

• Stroke

• Arrhythmia

• Seizure

• All have decreased appetite

• Diagnosis of bulimia nervosa requires evidence of binge eating and compensatory behaviors

• Avoidant/restrictive food intake disorder involves lack of interest and avoidance of eating based on the sensory characteristics of food, with typical onset in infancy or early childhood. Cocaine use in adolescent

Ecstasy

Ecstasy is an amphetamine with hallucinogenic properties that is popular in dance parties ("raves"). Sequelae of intoxication include hyponatremia (seizures, altered mental status), heat exhaustion (hyperthermia), and serotonin syndrome (myoclonus). Other signs of amphetamine intoxication are possible as well.,

Inhalant

Commonly abused substances include glue, nitric oxide ("whippets"), toluene, and spray paints.

Inhalants may be abused by sniffing, huffing (inhaled from a saturated cloth), or bagging (bag over mouth or nose) to concentrate the inhaled substance.

Signs of acute intoxication may include brief transient euphoria and loss of consciousness and vary depending on the specific chemicals inhaled. Inhalants are highly lipid soluble and produce immediate effects that typically last 15-45 minutes. They act as central nervous system depressants and may cause death.

Dermatitis (glue sniffer's rash) due to chemical exposure can be seen around the mouth or nostrils. Inhalants are rapidly eliminated and are not included in most routine hospital toxicology screens. Liver function tests may be elevated with repeated use. Boys age 14-17 are at highest risk for inhalant abuse, which may go unnoticed because common household products are used and no drug paraphernalia is found.

Nicotine

Withdrawal causes irritability, headache, and increased appetite.,

Due to pharmacokinetics and chemical composition of the substances, certain hallucinogens (inhalants, mescaline, LSD) cannot reliably be detected on urine drug screen. Therefore, hallucinogen intoxication cannot be ruled out with a negative drug screen!

LSD

Hallucinogen characterized by perceptual distortion and subjectively intensified experiences. Patients may experience flashback hallucinations later in life after use.,

PCP

Angel dust is a hallucinogenic drug of abuse. The two features most suggestive of intoxication are nystagmus (rotatory, or simultaneous horizontal and vertical nystagmus, is highly indicative) and violence.,

Alcoholism

Wernicke-Korsakoff syndrome is caused by vitamin B1 (thiamine) deficiency secondary to alcoholism.

Wernicke encephalopathy is a triad of:

• Confusion

• Ophthalmoplegia

• Ataxia

Untreated Wernicke encephalopathy can progress to Korsakoff syndrome, which is characterized by anterograde and retrograde amnesia as well as confabulation.

Mamillary body atrophy on MRI is specific for chronic Wernicke encephalopathy and Korsakoff syndrome.

Wernicke encephalopathy is treated with IV thiamine.

Administration of glucose in patients at risk for thiamine deficiency should be preceded or accompanied by thiamine since Wernicke encephalopathy can be precipitated by glucose administration.

Delirium tremens

Delirium tremens is a life-threatening alcohol withdrawal syndrome which peaks 2-5 days after the last drink. It is characterized by delirium, hyperthermia, tachycardia, and seizures.

Alcoholic hallucinosis is a syndrome of alcohol withdrawal characterized by the onset of hallucinations (usually visual) within 12-48 hours of abstinence that resolve within 24 to 48 hours. In contrast to delirium tremens, patients experiencing alcoholic hallucinosis have stable vital signs.

Mallory-Weiss syndrome is characterized by longitudinal mucosal lacerations at the gastroesophageal junction caused by excessive vomiting. It presents as painful hematemesis in an alcoholic.

Esophageal varices are complications of portal hypertension that can also be a cause of bleeding in the setting of alcoholism. They present as painless hematemesis in an alcoholic.

Reference the following topics for further medical and pathological discussion of alcoholism:

• Liver Disease: Alcohol and Drugs

• Pancreatitis: Acute

• Pancreatitis: Chronic

Gambling

Gambling disorder, previously known as pathologic gambling, is defined as persistent and maladaptive gambling behavior that results in impairment or distress. The diagnosis is based on 4 or more of the following characteristics within the past 12 months: gambling when distressed, depressed or anxious; increased gambling to achieve the desired excitement; frequently returning to gambling to recover past losses; preoccupation with gambling; irritability and distress when trying to cut back on gambling; repeated unsuccessful attempts to cut back; trying to conceal the extent of behaviors; jeopardizing relationships or employment; and relying on others to make up for financial losses. The behavioral symptoms of gambling disorder appear to have commonalities with substance-related disorders (eg, anticipatory craving, chronic relapsing course).

Gamblers Anonymous is the most effective treatment. Comorbid conditions such as mood disorders or anxiety can be treated symptomatically.

Substance Use

The DSM-5 has integrated the DSM-IV categories of “substance abuse” and “substance dependence” disorders into one disorder called “substance use disorder.” The DSM-5 recognizes substance use disorders resulting from ten separate classes of drugs (i.e. tobacco use disorder, alcohol use disorder etc.), which all exhibit psychiatric, medical, and psychosocial complications to some extent.

Patients with substance use disorder exhibit some of the following characteristics:

• Social or occupational dysfunction due to substance use

• Inability to cut down

• Spending significant time getting, using, or recovering from the use of the substance

• Tolerance

• Withdrawal

Note: Always consider substance abuse in a child/adolescent with a relatively sudden change in behavior!

Lab findings that may suggest a substance use disorder include elevated mean corpuscular volume (alcohol), elevated liver enzymes (alcohol, hepatitis from re-using needles), and positive serology for hepatitis B or C.

Alcohol

Serum gamma glutamyltransferase (GGT) is a sensitive indicator of use.

Blood, breath, hair, saliva and sweat can all be tested for the presence of drugs of abuse. Urine testing is the most widely used because it is noninvasive.

Naltrexone is a first-line treatment of alcohol use disorder that has been shown to decrease alcohol craving, reduce heavy drinking days (defined as >5 drinks for men and >4 for women), and increase days of abstinence. It can be initiated while the patient is still drinking. Naltrexone acts as a mu-opioid receptor antagonist and decreases the reinforcing effects of alcohol use. It is contraindicated in patients taking opioids and those with acute hepatitis or liver failure. It can be used in mild liver dysfunction, as in this patient, to prevent worsening damage from chronic alcohol use.

Acamprosate, a glutamate modulator, is another first-line medication for alcohol dependence. It is initiated once abstinence is achieved and is used to maintain abstinence rather than to reduce drinking in nonabstinent patients. Naltrexone would be preferred in this patient who is actively drinking.

Disulfiram inhibits aldehyde dehydrogenase and is used as an aversive agent that discourages drinking by causing an unpleasant physiologic reaction when alcohol is consumed. Candidates for disulfiram must be abstinent and highly motivated.

Non-pharmacological treatments such as Alcoholics Anonymous are helpful to many patients.

The most effective pharmacological treatment for tobacco use disorder is varenicline. Other pharmacological treatment options include bupropion and nicotine (gum, patches, etc.).

Pharmacological treatment for opioid use disorder may involve methadone, buprenorphine, and naltrexone. Psychotherapy has a role as well.

Stages of Change

The "stages of change model" for behavioral change is a popular model for how health behavior change (including recovery from substance use) takes place.

It consists of five stages, the first being Pre-contemplation: not yet acknowledging that there is a problem.

The second stage is Contemplation: acknowledging the problem, but not yet ready or willing to change it.

The third stage is Preparation: preparing to change the behavior.

The fourth stage is Action: changing the behavior.

The fifth stage is Maintenance: maintaining the behavior change.

In addition to the five stages, patients may also experience termination (patients have no temptation and are sure they will not return to the behavior) or relapse (return from action or maintenance stages to an earlier stage).