Transcript Assessment and management of the adult poisoning

Adult Poisonings
Brannon Marshall and Lauren Walker
Georgetown University
Objectives
 Discover the prevalence of poisonings in the
United States
 Understand the primary assessment of the patient
with a poisoning including the diagnostic workup
 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
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- nonpharmaceutical, 424 pharmaceutical
61 national poison centers take over 4 million calls
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 20002001
• 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.mcvhvcu.edu/f5-w-687474703a2f2f7777772e7570746f646174652e636f6d$$/contents/general-approach-to-drug-poisoning-inadults?source=search_result&search=poisoning&selectedTitle=1%7E150
Other Statistics
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95 percent of episodes caused minor or no effects
92 percent were due to acute rather than chronic ingestions
92 percent involved a single substance
85 percent were unintentional
59 percent of poison fatalities occurred in individuals aged
20 to 49
• 52 percent of exposures occurred in children younger than
6 years
• 47 percent involved pharmaceuticals
Burns, M. (2006). General approach to drug poisoning in adults. Retrieved June 28, 2012, from https://vcuhsra.mcvhvcu.edu/f5-w-687474703a2f2f7777772e7570746f646174652e636f6d$$/contents/general-approach-to-drug-poisoning-inadults?source=search_result&search=poisoning&selectedTitle=1%7E150
Top 25 Substances Most Frequently
involved with poisonings
• Analgesics
• Cosmetics/personal care
• Cleaning susbstances
(household)
• Sedative/hypnotics/antipsychot
ics
• Foreign bodies/toys/misc
• Topical preparations
• Antidepressants
• Cardiovascular drugs
• Antihistamines
• Pesticides
• Alcohol
• Cold and cough preparations
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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
Substances most frequently
involved in adults
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Analgesics
Sedative/hypnotics/antipsychotics
Antidepressants
Cleaning substances (household)
CV drugs
Alcohol
Patient Assessment
Diagnostic Work-up
Antifreeze Poisoning
Methanol 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
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
Ethylene glycol metabolism
• Metabolites target the kidney and l/t
reversible acute renal failure
– primarily due to glycolate-induced damage to
tubules, although tubule obstruction from
crystals
• Oliguria and hematuria
• Hypocalcemia from calcium oxalate
formation
– cranial nerve palsies and tetany
Methanol Metabolite
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Retinal injury with optic disc hyperemia
Retinal edema
Permanent blindness
Ischemic or hemorrhagic injury to the basal
ganglia
• Coma, seizures, kussmaul respirations and
hypotension all suggest a substantial portion
of the parent alcohol has been metabolized
to its toxic byproducts.
• Acidemia increases the ability of the toxic
metabolites to penetrate cells
– further depressing CNS function and causing a
rapid downward spiral of hypoxia and acidemia
Clinical Manifestation
Acetaminophen
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
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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
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 hepatocellular centrilobular necrosis
– Cytokine release may l/t a secondary
inflammatory response from Kupffer cells = more hepatic
injury
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 to
improve clinically while subclinical elevations of
hepatic
AST, 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
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
Management
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
Hours after arrival
Ethylene glycol (mg/dL)
Osmolar Gap
0.5
1282
235
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770
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554
122
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
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
• 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 teh american association
of posion control centers' national posion data system (NPDS): 28th annual report. ().Informa Healthcare USA, Inc.
doi:10.3109/15563650.2011.635149
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
References
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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 teh
american 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$$/contents/generalapproach-to-drug-poisoning-in-adults?source=search_result&search=poisoning&selectedTitle=1%7E150
Burns, M., Friedman, S. & Larson, A. (2011). Acetaminophen (paracetamol) poisoning in adults: Pathophysiology,
presentation and diagnosis. Retrieved June 28, 2012, from https://vcuhsra.mcvh-vcu.edu/f5-w687474703a2f2f7777772e7570746f646174652e636f6d$$/contents/acetaminophen-paracetamol-poisoning-in-adultspathophysiology-presentation-anddiagnosis?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), 735761.
Sivilotti, M., & Wichhester, J. (2012). Methanol and ethylene glycol poisoning. Retrieved June 2, 2012, from
https://vcuhsra.mcvh-vcu.edu/f5687474703a2f2f7777772e7570746f646174652e636f6d$$/contents/methanol-andethylene-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.