Challenging Presentations of Substance Abuse

Educational Objectives

The goal of this program is to improve the management of challenging drug poisonings. After hearing and assimilating this program, the clinician will be better able to:

1. Create and utilize a general approach to treating poisoned patients.
2. Identify symptoms that correlate with use of long-acting or high-potency opioids.
3. List the mainstays of treatment for patients with amphetamine poisoning.
4. Effectively treat complications related to abuse of intravenous drugs.

Summary

Epidemiology of substance use: in 2008, death from drug poisonings exceeded deaths secondary to motor vehicle accidents; drug poisoning leading cause of injury-related death for first time since 1980; rise in poisoning-related deaths, which began in 1990s, likely related to opioid epidemic; currently, deaths due to use of opioid analgesics exceed those caused by use of any other drug; recent crackdown on use of opioid analgesics has led to increased use of heroin

Treatment: poisoned patients require care similar to that provided for any critically ill patient in emergency department (ED); supportive care most imperative; antidotes often not necessary; airway — primary cause of morbidity and mortality in poisoned patients; support respirations with intubation and airway adjuncts until intoxicants metabolized; breathing — assess and support respiratory rate and depth of respiration; circulation — assess perfusion and heart rate; establish adequate intravenous (IV) access; 3 “Ds” of intoxication (dextrose, drugs, and decontamination) — dextrose (always check blood glucose); drugs (any that may immediately reverse effects of current intoxication to prevent administration of naloxone or flumazenil); decontamination — consider activated charcoal for decontamination or whole-bowel irrigation

Hypoglycemia: masquerader; autonomic symptoms — tremor, tachycardia, sweating, pallor; may resemble sympathomimetic toxidrome or serotonin syndrome; neuroglycopenic symptoms — ataxia, seizures, focal neurologic deficit; metabolic and cardiovascular symptoms — hypothermia and bradycardia; hypoglycemia should always be ruled out as cause of altered mental status, especially when presenting with presumed intoxication

Naloxone: rapid onset, with short duration of action; negative effects — precipitating withdrawal; pulmonary edema; when treating hypoventilating patient, naloxone should not be held because of concern for side effects; short half-life — symptoms induced by ingestion of long-acting opioids may recur after naloxone wears off

Differential diagnosis of miosis: opiates often assumed to be cause of pin-point pupils; important to consider other drugs; sympatholytic drugs — eg, clonidine, benzodiazepines, sedative hypnotics; alpha-adrenergic blockers — quetiapine, chlorpromazine; may alter mental status; cholinergic agents — sarin gas; organophosphates; produce “SLUDGE” syndrome (salivation, lacrimation, urination, defecation, gastrointestinal distress, emesis); nontoxicologic causes — issues related to central nervous system (eg, subarachnoid hemorrhage, cerebellopontine infarct)

Pharmacology of various opioids: recurrent symptoms may indicate ingestion of opioid with longer duration of action; methadone — duration of action 6 to 12 hr; buprenorphine — long duration of action; hydrocodone bitartrate and acetaminophen — should not produce recurrent symptoms; poisoning should improve after single dose of naloxone; potency — higher-potency opioids require treatment with higher doses of naloxone (eg, fentanyl)

Urine toxicology screens: yield low overall; testable drugs often dependent on institution’s preference; opiates — those directly derived from opium poppy (eg, morphine, heroin, codeine) detectable on urine drug screen (UDS); at some institutions, hydrocodone and hydromorphone may not be detected on UDS; special testing generally required for detection of synthetic and semisynthetic opiates (eg, oxycodone, methadone, fentanyl, tramadol, buprenorphine); benzodiazepines — significant potential for false positives and negatives; commonly used benzodiazepines (eg, lorazepam, clonazepam) do not test positive on UDS; other drugs not detected on UDS — gamma-hydroxybutyrate, carisoprodol, some antidepressants, “designer” or novel psychoactive substances

Synthetic opioids: oral fentanyl — common example; pharmacokinetics not well understood; novel psychoactive substances — high potency; street names include W18, furanyl fentanyl, and acetyl fentanyl; may be introduced into counterfeit pills; may not test positive on UDS; require high doses of naloxone

Amphetamines: symptoms — agitation, hypertension, tachycardia, diaphoresis; main emergent side effect hyperthermia (should be focus of treatment); amphetamines cause sympathomimetic toxidrome; UDS — detects methamphetamine, amphetamine, ephedrine, and pseudoephedrine; many derivatives of amphetamine will not test positive (eg, 3,4-methylenedioxymethamphetamine [MDMA], 3,4-methylenedioxyamphetamine [MDA], methcathinone [“bath salts”]); false positives possible; hyperthermia — if prolonged, may cause brain damage, cardiovascular collapse, rhabdomyolysis, multi-organ system dysfunction, and disseminated intravascular coagulation; treat hyperthermia quickly, ideally in first 30 min of care; intubation, neuromuscular paralysis, and external cooling facilitate rapid cooling; benzodiazepines — first line of treatment for amphetamine poisoning; used to control agitation, psychosis, seizures, and hypertension; reducing agitation reduces risk of rhabdomyolysis; substituted amphetamines — structured similarly to methamphetamines; will produce different effects, depending on nature of substitution; presentation remains relatively consistent, but complications vary slightly; MDMA causes hyponatremia; addition of bromine group to dimethoxybromo-amphetamine (DOB) may cause intense vasospasm and gangrenous extremities

Black tar heroin: thick, tar-like heroin injected IV or subcutaneously; common in Mexico and certain areas of US; skin popping — IV drug users (IVDU) who have exhausted usable veins often resort to injecting drugs into subcutaneous tissue; scarring lesions occur at sites of injection

IVDU and wound botulism: dramatic increase in wound botulism seen in late 1990s in association with injection of black tar heroin; botulinum spores germinate and release toxin, causing wound botulism; gram-positive spore-forming bacillus creates toxin, which inhibits release of acetylcholine at presynaptic nerve terminals, leading to paralysis; weeks to months required to regenerate vesicles that release acetylcholine at nerve terminal; symptoms of botulism — acute descending paralysis that begins at bulbar muscles; progresses to dysarthria; decreased respiratory rate or respiratory paralysis may ensue; differential diagnoses include myasthenia gravis, Guillain-Barré syndrome, and paralytic shellfish poisoning; consider diagnosis of wound botulism for any IVDU presenting with weakness

Nontoxicologic soft-tissue complications of IV drug abuse: causes of skin abscesses and cellulitis — skin popping; booting (blood drawn out of vein and reinjected); speedballs (cocaine combined with heroin and injected); necrotizing fasciitis — IVDU at risk for rapidly spreading infections; symptoms include fever, systemic toxicity, marked edema, and swelling; may lead to compartment syndrome and myonecrosis; surgeons should be involved early for debridement and/or fasciotomy; mortality rate ≈25%

Cocaine: UDS specific for cocaine (no false positives or negatives); levamisole — antihelmintic agent and immunomodulator; prevalent contaminant of cocaine in some regions of the United States; causes reticular, bullous lesions on extremities, cheeks, and ears; associated with arthralgias and neutropenia in 60% of patients; treatment cessation of cocaine use and (sometimes) trial of steroid; may cause significant necrosis of tissue; other adulterants of cocaine — contaminants include benzocaine, lidocaine, and caffeine

Methemoglobinemia (MetHb): signs — syncope, tachycardia, cyanosis, clear breath sounds on examination; presence of saturation gap (hypoxia on pulse oximetry but normal partial pressure of oxygen [PaO2] on arterial blood gas); cyanosis disproportionate to other findings on physical examination; on venipuncture, blood appears chocolate brown; pathophysiology — iron in hemoglobin (Hb) oxidized from Fe2+ to Fe3+, which impairs Hb’s oxygen-carrying capacity; treatment — methylene blue 1 to 2 mg/kg IV over 5 min (reduces Fe3+ in Hb back to Fe2+); symptoms improve over 1 hr; methylene blue used when MetHb levels in blood >20%; may cause hemolysis, worsening condition in patients with glucose-6-phosphate dehydrogenase deficiency; oxygen saturation may drop after administration of methylene blue, which may affect function of pulse oximetry probe; causes — local anesthetics (eg, proparacaine hydrochloride spray); phenazopyridine (Pyridium); aniline dyes; benzene derivatives; well water contaminated with nitrites; “poppers” (room odorizers that contain butyl nitrite or amyl nitrite)

Tetrahydrocannabinol (THC): psychoactive component of marijuana; symptoms of intoxication — dizziness, nausea with or without vomiting, fatigue, hallucinations, palpitations, tachycardia, hypertension, and tachypnea; symptoms generally resolve within 4 to 6 hr; “edibles” — THC incorporated into edible or drinkable products; packaging and candies may be attractive to children; concentrated THC — called “earwax” or “shatter”; butane filtered through marijuana and heated to semisolid; process has caused unintentional fires and burns; may be sold as oil (butane hash oil), hash butter, or “earwax”; highly concentrated (≈90% THC); pediatric exposure — may increase with increasing legalization; symptoms include ataxia, rigidity, seizures; parents may not be forthcoming with information

Summary: treatment for poisoning — supportive care needed; treatment similar to that of critically ill patient; remember airway, breathing, circulation; remember “3 Ds” of dextrose, drugs, decontamination; check blood sugar (hypoglycemia masquerades as many toxidromes); stimulants — potential to present with severe hyperthermia and agitation; wound botulism — possible complication of skin popping with black tar heroin; levamisole — common contaminant of cocaine; recurrent use may cause necrosis of skin; MetHb — may present secondary to use of amyl nitrate poppers; consider with saturation gap or cyanosis; edible marijuana — UDS helpful for pediatric patients

Readings

Hedegaard H et al: Drug Overdose Deaths in the United States, 1999-2016. NCHS Data Brief. 2017 Dec;(294):1-8; Kiyatkin EA et al: MDMA, Methylone, and MDPV: Drug-Induced Brain Hyperthermia and Its Modulation by Activity State and Environment. Curr Top Behav Neurosci. 2017;32:183-207; Rubin, R: Illicit Fentanyl Driving Opioid Overdose Deaths. JAMA. 2017 Dec 12;318(22):2174; Vo KT et al: Cannabis Intoxication Case Series: The Dangers of Edibles Containing Tetrahydrocannabinol. Ann Emerg Med. 2017 Nov 3. pii: S0196-0644(17)31657-8; Yuan J et al: Recurrent wound botulism among injection drug users in California. Clin Infect Dis. 2011 Apr 1;52(7):862-6.

Disclosures

For this program, members of the faculty and planning committee reported nothing to disclose.

Acknowledgements

Dr. Smollin was recorded at High Risk Emergency Medicine Hawaii, presented by the University of California, San Francisco, School of Medicine and its Office of Continuing Medical Education. For information about upcoming CME conferences from the University of California, San Francisco, School of Medicine, please visit http://meded.ucsf.edu/cme. The Audio Digest Foundation thanks the speakers and the sponsors for their cooperation in the production of this program.

CME/CE INFO

Accreditation:

The Audio- Digest Foundation is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.

The Audio- Digest Foundation designates this enduring material for a maximum of 0 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Audio Digest Foundation is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center's (ANCC's) Commission on Accreditation. Audio Digest Foundation designates this activity for 0 CE contact hours.

Lecture ID:

EM350701

Expiration:

This CME course qualifies for AMA PRA Category 1 Credits™ for 3 years from the date of publication.

Instructions:

To earn CME/CE credit for this course, you must complete all the following components in the order recommended: (1) Review introductory course content, including Educational Objectives and Faculty/Planner Disclosures; (2) Listen to the audio program and review accompanying learning materials; (3) Complete posttest (only after completing Step 2) and earn a passing score of at least 80%. Taking the course Pretest and completing the Evaluation Survey are strongly recommended (but not mandatory) components of completing this CME/CE course.

Estimated time to complete this CME/CE course:

Approximately 2x the length of the recorded lecture to account for time spent studying accompanying learning materials and completing tests.