Presentation Transcript

1. Adult Poisonings

   Brannon Marshall and Lauren Walker Georgetown University
2. Objectives Discover the prevalence of poisonings in the United States Understand the primary assessment of the patient with a poisoning including the diagnostic work-up Learn about the clinical manifestations of the top two substances of intoxication Review the appropriate pharmacologic and therapeutic management of poisoning and Review the above findings with a case study
3. Prevalence of Poisonings 2-5 million poisonings and drug overdoses annually in the US 60 poison control centers: 2,384,825 exposures Females > Males Ages: 20-29 most prevalent: exposures decline with age 965 active generic codes: 541- non-pharmaceutical, 424 pharmaceutical 61 national poison centers take over 4 million calls
4. Hospital Prevalence Poison exposures account for 5-10% of all ER visits Greater than 5% of all adult ICU admissions Annual incidence of poisoning is increasing with a 4.6% increase in cases noted in 2000-2001 Routes of poisoning: Ingestion 83.5%, dermal, inhalation/nasal, ocular. Burns, M. (2006). General approach to drug poisoning in adults. Retrieved June 28, 2012, from https://vcuhsra.mcvh-vcu.edu/f5-w-687474703a2f2f7777772e7570746f646174652e636f6d$$/contents/general-approach-to-drug-poisoning-in-adults?source=search_result&search=poisoning&selectedTitle=1%7E150
5. Other Statistics 95 percent of episodes caused minor or no effects 92 percent were due to acute rather than chronic ingestions 92 percent involved a single substance 85 percent were unintentional 59 percent of poison fatalities occurred in individuals aged 20 to 49 52 percent of exposures occurred in children younger than 6 years 47 percent involved pharmaceuticals Burns, M. (2006). General approach to drug poisoning in adults. Retrieved June 28, 2012, from https://vcuhsra.mcvh-vcu.edu/f5-w-687474703a2f2f7777772e7570746f646174652e636f6d$$/contents/general-approach-to-drug-poisoning-in-adults?source=search_result&search=poisoning&selectedTitle=1%7E150
6. Top 25 Substances Most Frequently involved with poisonings Vitamins Bites and environmental Antimicrobials Hormones and hormone antagonists Plants Gastrointestinal preparations Stimulant and street drugs Anticonvulsants Hydrocarbons Chemicals Arts/crafts/office supplies Fumes/gases/vapors Electrolytes and minerals Analgesics Cosmetics/personal care Cleaning susbstances (household) Sedative/hypnotics/antipsychotics Foreign bodies/toys/misc Topical preparations Antidepressants Cardiovascular drugs Antihistamines Pesticides Alcohol Cold and cough preparations
7. Substances most frequently involved in adults Analgesics Sedative/hypnotics/antipsychotics Antidepressants Cleaning substances (household) CV drugs Alcohol
8. Patient Assessment
9. Diagnostic Work-up
10. Antifreeze PoisoningMethanol and Ethylene Glycol Inflict self-harm, by accident, illicit distillation ("moonshine") or occult substitution for ethanol Rapidly and completely absorbed after oral ingestion Peak serum alcohol concentrations reached within 1-2hrs. Ingestion of approximately 1 g/kg of either methanol or ethylene glycol is considered lethal serious toxicity has been reported following ingestions of as little as 8 g of methanol. Methanol and ethylene glycol are relatively nontoxic, and cause mainly central nervous system (CNS) sedation. However, profound toxicity can ensue when these parent alcohols are oxidized
11. S/S of Antifreeze Poisoning May present with mild CNS effects (inebriation and sedation) similar to ethanol intoxication Methanol metabolite formulate and the ethylene glycol metabolites accumulate causing: End-organ Damage, Visual Blurring Central Scotomata and Blindness
12. Ethylene glycol metabolism Metabolites target the kidney andl/t reversible acute renal failure primarily due to glycolate-induced damage to tubules, although tubule obstruction from crystals Oliguriaand hematuria Hypocalcemia from calcium oxalate formation cranial nerve palsies and tetany
13. Methanol Metabolite Retinal injury with optic disc hyperemia Retinal edema Permanent blindness Ischemic or hemorrhagic injury to the basal ganglia
14. Coma, seizures,kussmaulrespirations and hypotension all suggest a substantial portion of the parent alcohol has been metabolized to its toxic byproducts. Acidemiaincreases the ability of the toxic metabolites to penetrate cells further depressing CNS function and causing a rapid downward spiral of hypoxia and acidemia
15. Clinical ManifestationAcetaminophen Available in both IR and SR formulations Therapeutic dose: 325 to 1000 mg/dose Q4-6 hrs with a max daily dose 4 g in adults (new rec. say 1-2 grams) Therapeutic serum concentrations range from 10- 20 mcg/mL Unlikely to result from a single dose of less than 7.5 to 10 g for an adult Likely to occur with single ingestions greater than 250 mg/kg or those greater than 12 g over a 24-hour period Absorbed from the GI tract Metabolized by liver Peak serum conc. are reached within 4 hrs after OD Elimination ½ life range from 2-4 hrs
16. Acetaminophen Therapeutic doses: 90% is metabolized to sulfate and glucuronide conjugates excreted in the urine Remainder is metabolized via the hepatic CYP450 into NAPQI Appropriate dose produces a small amount of NAPQI:rapidly conjugated and excreted in the urine. NAPQI reacts with hepatocytes, and injury ensues = oxidative injury and hepatocellularcentrilobular necrosis Cytokine release may l/t a secondaryinflammatory response from Kupffer cells = more hepatic injury
17. Acetaminophen Clinical Manifestations Stage I (0.5 to 24 hours) N/V, diaphoresis, pallor, lethargy, and malaise. Some remain asymptomatic. Laboratory studies are typically normal. Initially symptoms may resolve and appear toimprove clinically while subclinical elevations of hepaticAST, ALT occur Stage II (24 to 72 hours) clinical and laboratory evidence of hepatotoxicity and some nephrotoxicity RUQ pain, with liver enlargement and tenderness. The initial manifestations are often mild and nonspecific and don’t reliably predict hepatotoxicity
18. Tylenol Manifestations Cont. Stage III(72 to 96 hours) — LFT abnormalities peak from 72 -96 hours after ingestion. The systemic symptoms of stage I reappear with jaundice and encephalopathy Stage IV(4 days to 2 wks) — Patients who survive stage III enter a recovery phase that usually begins by day 4 and is complete by 7 days after OD Renal function spontaneously returns to the previous baseline within 1to 4 wks, although dialysis may be required during the acute episode
19. Management
20. Case Study Scenario: 49 y/o male ingested a gallon of antifreeze in a suicide attempt. EMS transported him to the ED Laboratory Data: In the ED: methanol 0, ABG pH 7.05/pCO2 26/pO2 313, BE 24 Na 150, K 4.7, Cl 110, HCO2 5, BUN 13 CR 1.4 GLU 100
21. Laboratory Data in the ED:Methanol 0,ABG pH 7.05/pCO2 26/pO2 313, BE 24Na 150, K 4.7, Cl 110, HCO2 5, BUN 13 CR 1.4 GLU 100
22. Clinical Course He was intubated and sedated, gastric lavaged returned 1200 ml of fluid with the appearance of antifreeze. Fomepizole and CVVHD were initiated. Bicarb bolus was given in ER. HR 73, BP 133/71, NSR. He was able to follow commands. Day 2 he became unresponsive. Head CT showed bilateral subarachnoid hemorrhaging. Family decided to institute comfort measures and he expired on Day 4
23. Autopsy Findings: Many polarizable crystals were present in the kidneys consistent with calcium oxalate. Cause of death: ethylene glycol intoxication Bronstein, A., Spyker, D., Cantilena, L., Green, J., Rumack, B., & Dart, R. (2011). 2010 annual report of tehamerican association of posion control centers' national posion data system (NPDS): 28th annual report. ().Informa Healthcare USA, Inc. doi:10.3109/15563650.2011.635149
24. Patient Pearls Poison control centers are free, confidential and open 24 hours a day, seven days a week and 365 days a year.  Some medicines are dangerous when mixed with alcohol Keep potential poisons in their original containers. 
- DO NOT use food containers such as bottles to store household and chemical products
25. References American association of poison control centers: Poison prevention tips for adults. (2012). Retrieved June 26, 2012, from http://www.aapcc.org/dnn/poisoningprevention/adults.aspx Bronstein, A., Spyker, D., Cantilena, L., Green, J., Rumack, B., & Dart, R. (2011). 2010 annual report of tehamerican association of posion control centers' national posion data system (NPDS): 28th annual report. ().Informa Healthcare USA, Inc. doi:10.3109/15563650.2011.635149 Burns, M. (2006). General approach to drug poisoning in adults. Retrieved June 28, 2012, from https://vcuhsra.mcvh-vcu.edu/f5-w-687474703a2f2f7777772e7570746f646174652e636f6d$$/contents/general-approach-to-drug-poisoning-in-adults?source=search_result&search=poisoning&selectedTitle=1%7E150 Burns, M., Friedman, S. & Larson, A. (2011). Acetaminophen (paracetamol) poisoning in adults: Pathophysiology, presentation and diagnosis. Retrieved June 28, 2012, from https://vcuhsra.mcvh-vcu.edu/f5-w-687474703a2f2f7777772e7570746f646174652e636f6d$$/contents/acetaminophen-paracetamol-poisoning-in-adults-pathophysiology-presentation-and-diagnosis?source=search_result&search=acetaminophen+poisoning&selectedTitle=3%7E48 Pierzak, M., Kuffner, E., Morgan, D., & Tomasgewski, C. (1999). Clinical policy for the initial approach to patients presenting with acute toxic ingestion or dermal or inhalation exposure. Analysis of Emergency Medicine, 33(6), 735-761. Sivilotti, M., & Wichhester, J. (2012). Methanol and ethylene glycol poisoning. Retrieved June 2, 2012, from https://vcuhsra.mcvh-vcu.edu/f5687474703a2f2f7777772e7570746f646174652e636f6d$$/contents/methanol-and-ethylene-glycol-poisoning?source=search_result&search=antifreeze+posioning&selectedTitle=1%7E55#H2 Watson, I. (2002). Laboratory analyses for poisoned patients: Joint position paper. The Association of Clinical Biochemists, 39, 328-339.