Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
The Poisoned Patient: A Medical Student Review William Beaumont Hospital Department of Emergency Medicine Introduction • All chemicals, especially medicines, have the potential to be toxic • 2006 TESS data – 2.7 million exposures – 19.8% were treated in a healthcare facility – 21.6% of those had more than minor outcomes including death • Over half of poisonings occur in children less than 5 years of age The Initial Approach • • • • • • • • Always consider poisoning in differential dx IV, O2, monitor Accucheck – in all pts with altered mental status D50 +/-Thiamine or Naloxone as indicated Decontamination, protect yourself Enhanced elimination Antidotal therapy Supportive care History • • • • • • Name, quantity, dose and route of ingestant(s) Time of ingestion Any co-ingestions Reason for ingestion – accidental, suicidal Other medical history and medications EMS – inquire what they saw at the scene, notes left, smells, unusual materials, pill bottles, etc. Pupils • Dilated – anticholinergic or • • • • sympathomimetic Constricted – Cholinergic Pinpoint – Opiods Nystagmus – horizontal – ethanol, phenytoin, ketamine Nystagmus – rotatory or vertical - PCP Skin Hyperpyrexia – anticholinergic, sympathomimetic, salicylates Hypothermic – Opiods, sedative-hypnotics Dry skin – anticholinergics Moist skin – cholinergics, sympathomimetics Color – cyanosis, pallor, erythema Overall exam • Stimulants – everything is UP – temp, HR, BP, RR, agitated – Sympathomimetics, anticholinergics, hallucinogens • Depressants – everything is DOWN – temp, HR, BP, RR, lethargy/coma – Cholinergics, opioids, sedative-hypnotics • Mixed effects: Polysubstance overdose, metabolic poisons (hypoglycemic agents, salicylates, toxic alcohols) Laboratory studies • Accucheck • Chemistries (BUN, Cr, CO2) • Urinalysis – Calcium oxalate crystals in • • • • • ehtylene glycol poisoning Drugs of abuse and comprehensive drug screen Acetaminophen, aspirin and ethanol levels Urine HCG if warranted EKG ABG, serum osmolality, Toxic Alcohol screen, LFTS if warranted General Decontamination • Remove all clothing, wash away any external toxic substances – If suspect transmittable contaminant, perform in special decontamination area • If ocular exposure – flush eyes copiously with at least 2 L NS using lid retractors, until pH 7 – 7.5 GI Decontamination • Three methods – Gastric emptying – Bind the toxin in the gut – Enhance elimination • Always consider the patient’s mental status, risk of aspiration, airway security and GI motility before attempting any method Orogastric Lavage • Indications – life threatening ingestions who • • present one hour within ingestion With the patient in the left lateral decub position, a 36 fr tube is passed oral - gastric to evacuate gastric contents and lavage with room temperature water until effluent is clear Studies show little benefit (may remove as little as 35% of the substance), the need of a secure airway and relatively high complication rate Activated Charcoal • Adsorbs toxin within the gut making it • • • unavailable for absorption 1 g/kg PO or via NGT Contraindications: bowel obstruction or perforation, unprotected airway, caustics and most hydrocarbons, anticipated endoscopy Not effective for alcohols, metals (iron, lead), elements (magnesium, sodium, lithium) Multi-dose Activated Charcoal • • • • • • • MDAC Large doses of toxin Slow release toxins Enterohepatic or enterenteric circulation Toxins that form bezoars “gastrointestinal dialysis” Phenobarbital, theophylline, carbamazepine, dapsone, quinine Cathartics • 70% Sorbitol 1g/kg, administered with • • • charcoal Decreased transit time of both toxin and charcoal through the GI tract Typically only used with the first dose if MDAC Do not use in children under 5, caustic ingestions, or possible bowel obstruction Whole Bowel Irrigation (WBI) • Go-Lytely via PO or NGT at a rate of 2L/hr (500 ml/hr in peds) • Typically used for those substances not bound by Activated Charcoal • Do not use in patients with potential bowel obstruction Hemodialysis • Useful for Salicylates, Methanol, Ethylene Glycol, Lithium, Amanita mushrooms, Isopropyl alcohol, Chloral hydrate • Patients must be hemodynamically stable and without bleeding disturbances • Charcoal hemoperfusion – essentially HD with a charcoal filter in the circuit – Barbituates, Carbamazepine, Phenytoin, Methotrexate, Theophylline and Amanita poisonings Toxin • • • • Acetaminophen Anticholinergic agent Benzodiazepines Beta blockers or calcium channel blockers • Carbon monoxide • Cardiac glycosides • Cyanide Antidotes • • • • N-Acetylcysteine Physostigmine Flumazenil Glucagon, calcium • Oxygen • Digoxin-specific Fab fragments • Amyl nitrate, sodium nitrate, sodium thiosulfate, hydroxycobalamin Toxin • • • • • • Ethylene glycol Heparin Hydrofluoric acid Iron Isoniazid Lead Antidote • • • • • • 4-Methylpyrazole, ethanol Protamine sulfate Calcium gluconate Desferoxamine Pyridoxime (Vit B6) BAL or DMSA, Calcium disodium EDTA • Mercury, arsenic, gold • BAL • 4-Methylpyrazole, ethanol • Methanol • Nitrites (Methemoglobin) • Methylene blue Toxins • Opiates, • • • propoxyphene, lomotil Organophosphates Sulfonylureas Tricyclic antidepressants Antidote • Naloxone (Narcan) • Atropine, pralidoxime • Glucose, octreotide • Sodium bicarbonate, benzodiazepines Case One 56 y/o male found unconscious in a basement. He has snoring respirations, frothing at the mouth, and rales on pulmonary exam. His pupils are pinpoint. He wakes up swearing and swinging at staff after a little narcan. What could it be? The Toxidromes - Opioid • Heroin, Morphine, fentanyl • CNS depression, lethargy, confusion, coma, • • • • respiratory depression, miosis Vital signs: temp, HR, RR, +/- BP Pulmonary edema, aspiration, resp arrest Check for track marks, rhabdomyolysis, compartment syndrome Tx: Naloxone 0.4 - 2 mg iv/im/sc slowly • May result in severe agitation • Monitor closely and re-dose if necessary The Toxidromes Sympathomimetic • Cocaine, amphetamines (speed, dex, ritalin), Phencyclidine (PCP), methamphetamines (crank, meth, ice), MDMA (Ecstasy, X, E) – Stimulant: Meth > amphetamines > MDMA – Hallucinogen: MDMA > Meth > amphetamines • Agitation, temp, HR, BP, mydriasis • Seizures, paranoia, rhabdomyolysis, MI, arrythmias Toxidromes Sympathomimetics • Management - primarily supportive - Benzo’s, • • • IV hydration, cooling if hyperthermic Treat HTN with benzodiazepines, nitrates, phentolamine MI – avoid beta blockers Bodystuffers (small amount, poorly contained) – Asymptomatic - AC, monitor for toxicity – Symptomatic - AC, WBI, treat symptoms • Bodypackers (lg amount, well contained) – Asymptomatic - WBI followed by imaging – Symptomatic - Immediate surgical consultation The Toxidromes - Cholinergic • Organophosphates – Insecticides, nerve gas (Sarin, Tabun, VX) – Irreversible binding to ACHe – “aging” • Carbamates – Insecticides (Sevin) – Reversible binding to ACHe – short duration • Physostigmine, Edrophonium, Nicotine • All increase Ach at CNS, autonomic nervous system and neuromuscular jx The Toxidromes - Cholinergic • Common Clinical Findings – SLUDGE Syndrome • Parasympathetic hyperstimulation • Salivation, Lacrimation, Urinary Incontinence, Defecation, GI pain, Emesis – Killer B’s • Bradycardia, Bronchorrhea, Bronchospasm – Bronchorrhea and respiratory failure is often the cause of death – Miosis, garlic odor, CNS ( MS, seizures, muscle fasciculations and weakness, resp depression, coma The Toxidromes - Cholinergic • Diagnose – RBC or plasma cholinesterase level • Management – Decontamination – protect yourself – Supportive therapy – Atropine - competitive inhibition of ACH • Large doses required - 2-5 mg q 5 minutes • End point is the drying of secretions – Pralidoxime (2-PAM) - breaks OP-ACHe bond • Start with 1-2 g IV over 30 minutes, give before “aging” • Adjust dose based on response, ACHe level Case 2 22 y/o F presents with decreased urine output. She is febrile, confused, flushed and has dilated pupils on exam. You also notice a linear, vesicular rash on her lower legs. What do you want to know? Case 2 • Meds – She has been using oral benadryl and topical caladryl lotion for the poison ivy What is her toxidrome? The Toxidromes - Anticholinergic • Agents – Antihistamines: diphenhydramine, loratadine, meclizine, prochlorperazine – Antipsychotics: chlorpromazine (Thorazine), Thiroidazine (Mellaril), – Belladonna Alkaloids: Jimsonweed, deadly nightshade, mandrake, atropine, scopolamine – Cyclic Antidepressants: amitriptyline (Elevil), nortriptyline (Pamelor), fluoxetine (Prozac) – OTC’s: Excedrin PM, Actifed, Dristan, Sominex – Muscle Relaxants: Orphenadrine (Norflex), cyclobenzaprine (Flexeril) – Amanita mushrooms The Toxidromes - Anticholinergic The Toxidromes - Anticholinergic • Common Clinical Findings – Dry as a bone - lack of sweating, dry skin and mucous membranes – Red as a beet - flushed, vasodilated – Hot as Hades - hyperthermia, may be agitation induced – Blind as a bat - mydriasis – Mad as a hatter - anticholinergic delirium, hallucinations – Stuffed as a pipe - hypoactive bowel sounds, ileus, decreased GI motility, urinary retention – VS: temp, HR, BP The Toxidromes - Anticholinergic • R/O psychiatric disorders, DTs, • • sympathomimetic toxicity Dry skin and absent bowel sounds indicate likely anticholinergic toxicity Management – – – – Sedation with high dose benzodiazepines AC (esp if BS), temp control Treat widened QRS and dysrhythmias with bicarb Physostigmine • far more effective but use only in clear cut cases • 0.5 to 2.0 mg IVP, every 30-60 minutes • Monitor for excess cholinergic response - SLUDGE The Toxidromes - Salicylate • Aspirin, oil of wintergreen, OTC remedies • Altered mentation, tinnitus, diaphoresis, nausea • • • and vomiting, tachycardia Metabolic acidosis and respiratory alkalosis Dx: + anion gap, salicylate level > 30mg/dl Treatment – Multidose AC – Alkalinize urine – HD if levels > 100 mg/dl, altered MS, renal failure, pulmonary edema, severe acidosis or hypotension The Toxidromes Serotonin Syndrome (SS) • SSRI’s: fluoxetine (Prozac), sertraline (Zoloft), paroxetine (Paxil), fluvoxamine (Luvox), citalopram (Celexa), escitalopram (Lexapro) • MAOI’s, meperidine, tricyclics, trazadone, mertazapine, dextromethorphan, LSD, lithium, buproprion, tramadol • SS may be caused by any of the above, but usually occurs with a combination of agents, even if in therapeutic doses The Toxidromes Serotonin Syndrome (SS) • altered MS, mydriasis, myoclonus, hyperreflexia, tremor, rigidity (especially lower extremities), seizures, hyperthermia, tachycardia, hypo or hypertension • Citalopram and escitalopram - prolonged QT and QRS • No confirmatory tests – diagnosis is based on clinical suspicion The Toxidromes Serotonin Syndrome Treatment • Supportive care • Single dose AC (ensure airway control) • Benzodiazepines to treat discomfort, muscle • • • contractions or seizures) and cooling measures Treat prolonged QT with magnesium Treat widened QRS with Bicarb Cyproheptadine (antiserotonin agent) - 4 to 8 mg PO. Dose may be repeated in 2 hrs. If positive response, give 4 mg PO q 6 hrs for 48 hrs. Acetaminophen Poisoning • Common Clinical Findings – Stage I 0-24 hrs, nausea, vomiting, anorexia – Stage II 24-72 hrs, RUQ pain, elevation of AST and ALT, also elevation of bilirubin and PT if severe poisoning – Stage III 72-96 hrs, peak of AST, ALT, bilirubin and PT, possible renal failure and pancreatitis – Stage IV > 5 days, resolution of hepatotoxicity or progression to multisystem organ failure Acetaminophen Poisoning RummackMathew nomogram acetaminophen levels vs time Plot 4 hr level Useful for single acute ingestion only Acetaminophen Poisoning • Management – AC assume polypharmacy OD – NAC - N-acetylcysteine (NAC) indicated if • patient ingested over 140 mg/kg OR toxic • • level on nomogram IV dose: 150mg/kg IV load, 50 mg/kg over 4 hrs, then 100mg/kg over 16 hrs PO dose: 140 mg/kg load, then 70 mg/kg q 4 hrs x 17 – Draw baseline LFTs and PT CASE: UNKNOWN LIQUID 17 y/o M brought in by family for acting “drunk.” He is lethargic, confused, disoriented. Vitals: 130, 90/60, 16, 37 C. Labs: Etoh 0, CO2 12 What else do you want to know? CASE UNKNOWN LIQUID Accucheck: 102 Serum Osmolality 330 Na 140, K 4.0, Cl 100, CO2 12, glucose 90 BUN 28, Cr 2.0 UDS, APAP, ASA are all negative U/A has calcium oxalate crystals What are we hinting at? Toxic Alcohols • Typical Agents – Ethanol – Isopropanol – Methanol – Ethylene glycol (EG) • All toxic alcohols cause an osmolar gap • Methanol and EG cause an anion gap acidosis Useful Equations • Anion Gap (mEq/L) Na - (Cl + HCO3) • Calculated Osmolarity (mosm/L) 2Na + BUN/2.8 + Glu/18 + ETOH/4.6 Toxic Alcohols - Isopropanol • Rubbing alcohol > solvents, antifreeze, • • • • disinfectants It is the second most commonly ingested alcohol Isopropyl alcohol has twice the CNS depressing potency and up to 4 times the duration as ethanol Toxic dose of 70% isopropanol is 1ml/kg Lethal dose is as little as 2ml/kg Toxic Alcohols - Isopropanol • Metabolized by alcohol dehydrogenase to • • • • acetone Fruity breath, ketonuria, + osmolar gap, no acidosis Clinically may appear similar to ethanol intoxication with greater CNS depression Hypotension, respiratory depression, coma Nausea, vomiting, abdominal pain and upper GI bleeding secondary to hemorrhagic gastritis Toxic Alcohols - Methanol • Typical agent is wood alcohol, used in • • • solvents, paint removers, antifreeze and windshield washer fluid. Also may be found in bootleg liquor. Is rapidly metabolized to toxic formaldehyde and formic acid Can cause permanent retinal injury and blindness as well as parkinsonian syndrome if not treated promptly May have a long latent period (12 to 18 hours), especially if co-ingested with ethanol Methanol diagnosis • Common Clinical Findings – Lethargy, nausea, vomiting, abd pain – Visual symptoms seen in 50% - blurring, tunnel vision, color blindness – HR, RR, BP (poor prognosis if present) – CNS - head ache, seizures or coma • Wide anion-gap metabolic acidosis with osmolar gap • Toxic alcohol screen to confirm Toxic Alcohols - Ethylene Glycol • Typical agent is antifreeze • Often seen in alcoholics, suicide attempts and • • • • children Colorless, odorless and sweet Metabolism and treatment similar to methanol Is rapidly absorbed and converted to toxic acids responsible for clinical signs and symptoms Lethal dose is as low as 2 ml/kg Toxic Alcohols - Ethylene Glycol • Common Clinical Findings – Three phases • 1-12 hours - CNS Depression: inebriation, • • vomiting, seizures, coma, tetany (hypocalcemia) 12-24 hours - Cardiopulmonary Phase: hypotension, tachydysrhythmias, tachypnea and ARDS 24-72 hours - Nephrotoxic Phase: Oliguric renal failure, ATN, flank pain, calcium oxylate crystalluria Toxic Alcohols - Ethylene Glycol • Additional findings – Hypocalcemia secondary to precipitation with oxylate, excreted as urinary calcium oxylate crystals – Urine may also fluoresce secondary to fluorescence dye in antifreeze – EKG: QT prolongation (hypocalcemia) and peaked T’s (hyperkalemia) – Myalgias, secondary to acidosis and elevated CPK Diagnose Ethylene Glycol (EG) Always consider EG in an inebriated patient without alcohol breath, an anion-gap metabolic acidosis, osmolar gap and calcium oxylate crystalluria Treatment of EG and Methanol • Supportive, especially airway • Correct acidosis with IV bicarb, • • • • 1meq/kg IV Benzo’s if seizures develop Folic acid 50mg IV q 4 hrs for both Pyridoxine 100 mg IV q 6 hrs, Thiamine 100mg IV q 6 hrs, Magnesium for EG Ca gluconate 10 ml of 10% IV – to correct hypocalcemia – EG only Treatment of EG and Methanol • Block production of toxic metabolites – Ethanol infusion or oral administration • Load 10% in D5W at 10 ml/kg over 30 min • Infuse 10% in D5W at 1.5 ml/kg to maintain ETOH level at > 100 mg/dl – Fomepizole - preferred method • 15 mg/kg over 30 minutes, then 10 mg/kg q 12 hrs x 4 • Has 8000 times the affinity for ADH as ETOH without CNS depression and hypoglycemia • Or 4-MP (4-methylpyrazole) Treatment of EG and Methanol • Hemodialysis indicated if – Serum level > 50 mg/dl – Signs of nephrotoxicity (EC) or CNS or visual disturbances (Methanol) – Severe metabolic acidosis Tricyclics • Agents – Amitriptyline (Elevil), desipramine (Norpramin), imipramine (Tofranil) and nortriptyline (Pamelor) – Narrow therapeutic index – Have returned to popularity with nondepression indications such as chronic pain, migraines, ADHD and OCD Tricyclics • Common Clinical Findings – CNS - decreased LOC • Confusion, hallucinations, delirium, seizures – Cardiovascular - arrhythmias and hypotension • QRS > 100 msec, conduction delays • Arrhythmias such as V-tach & Torsades may develop as QRS widens and QT prolongs – Anticholinergic Toxidrome • Tachycardia, mydriasis, hyperthermia, anhydrosis, urinary retention, decreased bowel sounds Tricyclics • EKG during TCA toxicity and after treatment with bicarb. Note wide QRS, prolonged QT and terminal R’s > 3mm in AVR Treatment of tricyclic overdose • AC • Na Bicarb – to treat QRS prolongation > 100 msec and hypotension refractory to IV fluids • Benzo’s to treat seizures and hyperthermia (avoid physostigmine) • Magnesium and Lidocaine for Ventricular arrythmias refractory to Bicarb • Magnesium for QT prolongation or Torsades CO • Sources – Fossil fuel combustion (car exhaust), smoke, kerosene or coal heaters, steel foundries – Methylene chloride vapor • Found in bubble Christmas tree lights and in paint strippers • CO binds to hemoglobin with 230 times the affinity to oxygen, decreasing it’s ability to transport oxygen CO • Common Clinical Findings – Organs with high O2 demand become dysfunctional – Nausea, malaise, headache, decreased mental status, dizziness, paresthesias, weakness, syncope – May progress to vomiting, lethargy, coma, seizures, CVA , MI or respiratory arrest – Need a high index of suspicion – multiple family members with flu like symptoms without fever, winter months CO • COHb level may not represent the severity of the poisoning • Pulse oximetry also may be misleading • Half-life of COHb – 4 hours on room air – 60 minutes breathing 100% normobaric O2 (NBO) – 15 to 23 minutes breathing 100% hyperbaric O2 (HBO) at 2.5 atmospheres CO treatment • 100% O2 via NRB for 4 hrs minimum if mild symptoms (nausea, heachache, malaise) CO • 100% O2 and transfer to a hyperbaric center if any of the following • Altered mental status or coma • History of LOC or near syncope • History of seizure • Hypotension during or after exposure • MI • Pregnant with COHb > 15% • Arrythmias • +/- COHb > 25-40% • Only absolute contraindication to hyperbaric chamber is pneumothorax References • Tintinalli, J., Kelen, G.D., Stapczynski, J.S., Emergency Medicine, A • • Comprehensive Study Guide, Sixth Edition 2004, McGraw-Hill, New York, pp 1015-1172 Flomenbaum, N., Goldfrank, L., et al., Goldfrank’s Toxicologic Emergencies, Eighth Edition 2006, McGraw-Hill, New York, pp 37-140, 523-614, 1070-1098, 1118-1162, 1447-1468, 1497-1512 Ziad, N.K., Roberge, R.J., A Toxicology Handbook, American Academy of Emergency Medicine