poising in the ER

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decontamination techniques:
inhaled poisons
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decontamination techniques:
inhaled poisons
give oxygen by mask or water aerosol to dilute inhaled irritants in the nasophoarynx - make sure to check for stridor, hoarseness, and singed nasal hairs and be alert for delayed development of obstruction or pulmonary edema
decontamination techniques:
contaminated eyes
wash immediately with plain water or normal saline DO NOT sue neutralizing solutions
consider ophthalmic proparacine, an eyelid retractor, and irrigation lens to inc compliance and efficacy
if material was acidic or basic - tears may be check with pH paper
decontamination techniques:
hydrofluoric acid burns
following irrigation, promp application of 10% calcium gluconate gel OR quaternary ammonium salt solution
decontamination techniques:
ingested poisons
activated charcoal is the preferred method - others include emesis, gastirc lavage, and catharsis
*contraindicated if those unable to protect airway/protective reflexes are absent
indications include: large ingestion of modified-released products, chemicals poorly absorbed to charcoal such as lithium or other metals, and ingestion of foreign bodies or drug-filled packets
- technique utilizes a balanced electrolyte polyehylen glycol solution (goLYTELY) to flus out the entire tract
whole bowel irrigation
most common findings:
- CNS depression, miosis, respiratory depression, dec bs
additional signs/symptoms:
- hypothermia, brady, death may result from respiratory arrest, pulmonary edema
Potential interventions:
- ventilation or naloxone
opioid- heroin, morphine
most common findings:
- psychomotor agitation, mydriasis, diaphoresis, tachy, HTN, hyperthermia
additional signs/symptoms:
- seizures, rhabdomyolysis, MI. death may result from seizures, cardiac arrest, hyperthermia
Potential interventions:
- cooling, sedation w/ benzodiazepines, hydration
sympathomimetic: cocaine, amphetamine, cathinones
most common findings:
- salivation, lactrimation, diaphoresis, N/V, urinarion, defecation, muscle fasciculations, weakness, bronchorrhea
additional signs/symptoms:
- brady/tachy, rales, miosis, mydraisis, seizures, respiratory failure, paralysis deathmay result from respiratory arrest 2ry to paralysis and/or bronchorrhea, seizures
Potential interventions:
- airway protection and ventilation, atropine, pralidoxime, dizepam
cholinergic: organophosphate insecticides, carbamate insecticides
most common findings:
- AMS, mydriasis, dry/flushed skin, urinary retention, dec bs, hyperthermia, dry MM
additional signs/symptoms:
- seizures, dysrhythmias, rhabdomyolysis
- death may result from hyperthermia and dysrhythmias
Potential interventions:
- physostigmine, sodium bicarbonate for wide QRS benzodiazepines, cooling, supportive management
anticholinergic: scopolamine, atropine, diphendydramine
most common findings:
- AMS, respiratory alkalosis, metabolic acidosis, tinnitus, hypercapnea, tachy, diaphoresis, N/V
additional signs/symptoms:
- low-grade fever, ketonuria
- death may result from pulmonary edema, cardiorespiratory arrest, cerebral edema, herniation
Potential interventions:
- MDAC, sodium bicarbonate, potassium repletion, hemodialysis, hydration
salicylates: asa, oil of wintergreen
most common findings: - *AMS, diaphoresis, tachy, HTN* additional signs/symptoms: - *paralysis, slurring of speech, bizarre behavior, seizures* - *death may result from seizures, altered behavior* Potential interventions: - *IV glucose, PO feedings if able, frequent blood for glucose measurements, octreotide if recalcitrant*hypoglycemia: sulfonyureas, insulinmost common findings: - *AMS, inc muscle tone, hyperreflexia, hyperthermia* additional signs/symptoms: - *"wet dog shakes"" (intermittent whole body tremor)* - *death may result from hyperthermia* Potential interventions: - *cooling, sedation w/ benzodiazepines, supportive management, theoretical benefit - cyproheptadine*serotonin syndrome: meperidine/dextromethorphan + MAOI, SSIR+TCA, SSRI/TCA/MAOI + amphetamine, SSRI overdosedetermined by subtracting the calculated serum osmolarity from the measured serum osmolalityosmolar gapwhich drugs and toxins may be radiopaque? mnemonic is CHIMPSchloral hydrate "heavy metals" (iron, arsenic) iodine psychotropics (phenothiazine, tca) salicylates modified-released preparationsin an overdose, pathways of elimination are often saturated, and first-order kinetic elimination becomes zero-order (fixed amount) elimination at higher concentrations...this is known as?Michaelis-Menten kineticsthis is the apparent volume into which the toxin is distributed after absorption based on the dose and resultant serum concentrationsvolume of distributiondrugs demonstrating inc clearance with MDAC (multiple-dose activated charcoal) Mnemonic: "these pts should drink charcoal quickly"theophylline phenobarbital salicylates dapsone, digitoxin carbamazepine quinidineantidotes: - acetaminophenacetylcesteineantidotes: - anticholinergicsphysostigmineantidotes: - anticholinesterases (organophsphates, carbamates, physostigime)atropine pralidozime (2PAM)antidotes: - benzodiazepinesflumazenilantidotes: - b-blockersglucagon, calcium, high-dose insulin, lipid emulsionantidotes: - calcium channel blockerscalcium, high-dose insulin, lipid emulsionantidotes: - carbon monoxide100% oxygen, hyperbaric oxygenantidotes: - cyanidesodium nitrite (or amyl nitrite if no IV access)antidotes: - digoxindigoxin-specific antibodiesantidotes: - heavy metalschelating agents: succimer for lead, arsenic, mercury deferoxamine for ironantidotes: - isoniazidpyridoxine (vit B6)antidotes: - methanol, ethylene glycolfomepizole, folate, pyridosine, thiamine, ethanolantidotes: - opiodsnaloxoneantidotes: - tca - salicylatessodium bicarbonateantidotes: - warfarinvit Kantidotes: - methotrexatefolinic acidantidotes: - sulfonyureasoctreotideantidotes: - local anestheticslipid emulsionantidotes: - valprioc acidl-Carnitinewhat drugs can cause hyperthermia?1. salicylates 2. antipsychotics 3. seizures or hyeractivity 4. anticholinergic propertiesPatient may be asymptomatic early after acute ingestion or present with anorexia, nausea, and right upper quadrant pain. Obtain 4-hour postingestion concentrations, and use the nomogram (Figure 47-1) to predict hepatocellular injury following acute ingestion. Chronic toxicity should be assessed through clinical examination, an acetaminophen concentration, and liver function tests. NAC therapy is antidote if indicated.acetaminophenAll drugs in this class are CNS stimulants. Predominant symptom is sympathetic hyperactivity. Treatment is supportive, including liberally titrated benzodiazepines and active cooling PRN.amphetamines and related stimulantsIngestion produces many symptoms prompting the phrase "blind as a bat, hot as Hades, red as a beet, dry as a bone, and mad as a hatter." Treatment is primarily supportive, although physostigmine can be used in life-threatening situations or to confirm the diagnosis.anticholinergicsAverage toxic dose is 5 mg/kg. Anticholinergic symptoms range from mydriasis, agitation, and tachycardia to seizures and coma. Cardiovascular manifestations are often life threatening and include QRS widening, profound hypotension, atrioventricular blocks, and ventricular dysrhythmias.antidepressantsSulfonylureas potentiate insulin release in the presence of glucose; hypoglycemia may be resistant to parenteral glucose administration. Oral feeding is preferred for lucid patients; octreotide may prevent recurrent hypoglycemia. Metformin overdose results in mitochondrial injury, profound lactic acidosis, and hypothermia or coma. Hemodialysis may correct acidosis without metformin clearance.antideiabetic agentsAcute extrapyramidal side effects include dystonia and akathisia. Sedation, miosis, tachycardia, and hypotension are common. Coma, seizures, and ventricular dysrhythmias may occur with large doses.antipsychoticsIngestion of a large amount of β-antagonists primarily affects the cardiac system. Symptoms of ingestion include hypotension, bradycardia, and coma. Glucagon and/or calium can be used to treat hypotension if IV fluids are unsuccessful; refractor cases often respond to high-dose insulin euglycemia therapy (HIET).b-adrenergic antagonistsIngestion of a large amount of calcium channel blockers can cause hypotension, bradycardia, and hyperglycemia; CNS depression is a late finding. Treatment is calcium and high-dose insulin euglycemia therapy.calcium channel antagonistsa colorless, odorless gas that binds avidly to hemoglobin. Manifestations of tissue hypoxia include headache, nausea, syncope, and end-organ injury. Carboxyhemoglobin concentrations correlate acutely with severity of symptoms and should be used to guide treatment. Treatment is with 100% oxygen; hyperbaric oxygen can also be used in certain circumstances.carbon monoxideThese cardiotoxic drugs cause conduction disturbances, dysrhythmias, and occasionally severe hyperkalemia. Digoxin concentrations in combination with serum potassium are indicative of the degree of poisoning in the acute overdose. Patients with severe dysrhythmias or hyperkalemia may benefit from digoxin antibodies to reverse toxicity.cardiac glycosidesIncludes both acids and alkalis. Ingestion can result in coagulative (acids) or liquefactive (alkalis) necrosis of tissue. Attempted dilution may be ineffective; neutralization is harmful; enteral perforation requires surgery; treatment is otherwise supportive. Endoscopy is recommended to assess degree of damage in symptomatic patients and safely place a feeding tube past severe injuries.causticscauses sympathetic hyperactivity and can result in severe hypertension, hyperthermia, myocardial ischemia, and even aortic dissection. Sodium bicarbonate improves wide QRS due to sodium channel antagonism; otherwise liberal benzodiazepine doses negate most of cocaine's effects.cocaine intoxicationcauses initial CNS excitement and seizures, followed by CNS depression and cardiovascular collapse. Lipid emulsion can completely reverse local anesthetic poisoning.Overdose of local anestheticsacts as a cellular asphyxiant that inhibits the use of oxygen by mitochondria. Symptom onset is rapid and ultimately results in hypotension. In very mild cases, supportive care including 100% oxygen is adequate. If poisoning is severe, a CN antidote kit of sodium nitrite, amyl nitrite, and sodium thiosulfate should be used; alternatively, hydroxocobalamin may be administered. CN concentrations are not readily available and should not be used to determine treatment; acutely elevated lactate (>8 mmol/L) in the appropriate clinical situation (eg, fire) is sensitive and specific for CN poisoning. All patients with CN intoxication should be hospitalized.cyanideMethemoglobin cannot bind oxygen. Symptoms correlate with the degree of methemoglobinemia and can include asymptomatic cyanosis, dyspnea, and severe CNS depression. Treatment includes methylene blue, which can reduce methemoglobin concentrations in less than 1 hour.drug-induced methemoglobinemiaLow-viscosity liquids may be aspirated when swallowed, resulting in pneumonitis. Physical findings and infiltrates on chest X-ray may be delayed 4-6 hours. Halogenated hydrocarbons may induce tachydysrhythmia, frequently in the prehospital setting.hydrocarbonsHypoxia may result from displaced O2, lung injury, hemoglobinopathy, or mitochondrial injury. Irritants may simply inflame conjunctiva and upper airway or cause chemical pneumonitis and pulmonary edema.inhalants (toxic gases and vapors)Signs and symptoms of iron poisoning can vary widely and include all major organ systems. Concentrations can be obtained and may guide treatment. Chelation with deferoxamine is most effective early in iron poisoning (sometimes before "iron studies" have returned).ironcauses lactic acidosis via seizures, sometimes status epilepticus. Seizures may be refractory to standard management (benzodiazepines), but resolve with pyridoxine (vitamin B6).isoniazidCommon findings are nausea/vomiting, tremor, slurred speech, and ataxia; seizure and coma are rare. Chronic toxicity is often unintentional and seen with diuretic therapy or dehydration. Toxic lithium concentrations greater than 2 mEq/L chronically or greater than 4 mEq/L acutely. Most patients improve with IV saline; CNS injury or renal impairment warrant consideration of hemodialysis.lithiummiosis, decreased bowel sounds, sedation, and respiratory depression; some cases will also manifest hypotension, bradycardia, and hypothermia. Naloxone administration may be diagnostic or therapeutic.opiod toxidrome"SLUDGE M and the Killer Bs": salivation, lacrimation, urination, diaphoresis, gastrointestinal hypermotility, emesis, miosis, bronchorrhea, bronchospasm, and bradycardia. Serially doubled doses of atropine may reverse otherwise fatal pulmonary findings; a 10-mL dropper of 1% ophthalmic atropine can supply the 100 mg sometimes required to adequately dry airway secretions.muscarinic overdosemnemonic the days of the week "MTWHFSS": muscle paralysis, tachycardia, weakness, hypertension, fasciculations, sweating, and seizures. 2PAM may restore normal cholinesterase function and decrease the subsequent doses of atropine needed; some patients require benzodiazepines, and intubation.nicotinic overdose signsSymptoms may fluctuate unpredictably from severe agitation to quiet stupor. Agitation may lead to hyperthermia, rhabdomyolysis, and acute renal failure. Vertical and horizontal nystagmus are common.phencyclidine and ketamineDelayed onset of symptoms (gastrointestinal irritation) of 6-12 hours suggests a toxic mushroom ingestion. Mushrooms containing amatoxins may produce fatal hepatic necrosis.posonous mushroomsToxicity generally occurs at concentrations greater than 150 mg/kg. Early manifestations include nausea, vomiting, and hyperventilation. Initial respiratory alkalosis is often followed by a severe metabolic acidosis, creating a mixed acid-base status. Hypoglycemia is prominent in children.salicylatesAlthough the typical toxidrome is coma with normal vital signs, symptoms may include nystagmus, respiratory depression, hypotension, and hypothermia. Sedative-hypnotics such as γ-hydroxybutyric acid (GHB) may be associated with symptoms ranging from respiratory depression and coma to seizure-like activity with aggressive behavior.sedative-hypnoticsMild symptoms include nausea and vomiting, tremor, anxiety, and abdominal cramping. Severe symptoms include dysrhythmias and seizures.theophylline and methylxanthinesThe blood pressure and pulse rate are elevated, though with severe hypertension reflex bradycardia may occur. The temperature is often elevated, pupils are dilated, and the skin is sweaty, though mucous membranes are dry. Patients are usually agitated, anxious, or frankly psychotic. Examples: Amphetamines, cocaine, ephedrine, pseudoephedrine, synthetic cathinones and cannabinoidssympathomimetic syndromeThe blood pressure and pulse rate are decreased and body temperature is low. The pupils are small or even pinpoint. Patients are usually obtunded or comatose. Examples: Barbiturates, benzodiazepines and other sedative hypnotics, gamma-hydroxybutyrate (GHB), clonidine and related antihypertensives, ethanol, opioids.sympatholytic syndromeStimulation of muscarinic receptors causes bradycardia, miosis, sweating, and *hyperperistalsis* as well as bronchorrhea, wheezing, excessive salivation, and urinary incontinence. Nicotinic receptor stimulation may produce initial hypertension and tachycardia as well as fasciculations and muscle weakness. Patients are usually agitated and anxious. Examples: Carbamates, nicotine, organophosphates (including nerve agents), *physostigmine.*cholinergic syndromeTachycardia with mild hypertension is common, and the body temperature is often elevated. Pupils are widely dilated. The skin is flushed, hot, and dry. Peristalsis is decreased, and urinary retention is common. Patients may have myoclonic jerking or choreoathetoid movements. Agitated delirium is frequently seen, and severe hyperthermia may occur. Examples: Atropine, scopolamine, other naturally occurring and pharmaceutical anticholinergics, antihistamines, tricyclic antidepressants.anticholinergic syndromePatients often have minimal and nonspecific symptoms of toxicity, such as anorexia, nausea, vomiting, and malaise. *Hypokalemia and metabolic acidosis* may be seen during the first 24 hours and correlate with a high 4-hour acetaminophen concentration.stage 1 - first 24 hours after exposure - acetaminophen toxicitySymptoms seen in stage 1 often improve, but clinical signs of hepatotoxicity may occur, including right upper quadrant abdominal pain and tenderness, with elevated serum transaminases. Even without treatment, most patients with mild to moderate hepatotoxicity recover without sequelae.stage 2 - days 2-3; acetaminophen toxicitySome patients will progress to fulminant hepatic failure. Characteristic stage 3 findings include metabolic acidosis, coagulopathy, renal failure, encephalopathy, and recurrent GI symptoms. Patients who survive the complications of fulminant hepatic failure begin to recoverstage 3 - days 3-4; acetaminophen toxicityPatients who survive the complications of fulminant hepatic failure begin to recover over the next 2 weeks (stage 4), with complete resolution of hepatic dysfunction in survivors after 1 to 3 months.stage 4 - 1-2 weeks; acetaminophen toxicityassociated with the altered sensorium and a metabolic acidosis with an elevated lactate that can occur in the absence of either liver failure or hypotension.massive doses of acetaminophen (4 hour concentration of > 800 microgram/mL)this predominates in the developed word.....where as this is common in developing countries?alkaline in DEVELOPED acid in DEVELOPINGwhat is the first priority in tx caustic substances? if impaired, what should you do?airway maintenance ; oral intubation with direct visualization - blind nastotracheal intubation is CIthis is contraindicated if caustic substance is the only ingestionactivated charcoalwhat are some indications for emergency laparotomy s/p a caustic ingestion?esophageal perforation, peritoneal signs, or free intraperitoneal air - signs of shock, respiratory distress, persistent lactic acidosis, ascites, and pleural fluid (surgical exploration)usually fever, hyperventilation, and altered mental status with volume depletion, acidosis, and severe hypokalemia. Renal failure may be a significant complication, but pulmonary edema is unusualsalicylates toxicity in childrenThe typical clinical presentation includes nausea, vomiting, tinnitus, hearing loss, sweating, and hyperventilation. Patients with tinnitus or hearing loss following an acute ingestion usually have an elevated serum salicylate value CNS dysfunction manifests as agitation, lethargy, confusion, seizure, or coma. CNS dysfunction leading to cerebral edema is an ominous development and a sign of severe toxicity, requiring rapid and aggressive treatmentsalicylates intoxication in adultsoften presents with neurologic abnormalities such as lethargy, altered mental status, irritability, and hallucinations, particularly in the elderly. include hyperventilation, tremor, papilledema, agitation, paranoia, bizarre behavior, memory deficits, confusion, and stupor.chronic salicylate intoxication in adultssalicylates tx:- activated charcoal - sodium bicarbonate - +/- hemodialysisconsidered the extracorporeal technique of choice for the treatment of serious salicylate toxicity because hemodialysis can correct acid-base and electrolyte abnormalities while rapidly reducing the body salicylate burden *consider for salicylism requiring respiratory and ventilatory support*hemodialysisdescribe the effects of the inhibition process in digoxininc INTRAcellular sodium and inc EXTRAcellular potassiumwhat is the classic description of digoxin toxicity?viewing yellow-green halos around objects, termed *xanthopsia*tx of digitalis toxicity- supportive - continuous cardiac monitoring and frequent reevaluations - IV magnesium - atropine - digoxin-Fab - *TOC* for acute w/ hyperkalemiatx of anticholinergic toxicity?- obesrvation, monitoring, and good supportive care - temp monitoring - activated charcoal within 1 hour - bezos for agitation - IV sodium bicarbonate for wide complex tachydysrhythmias - *physostigmine* antidotethese inhibit the enzyme cholinesterase which leads to *cholinergic crisis* manifested as central and peripheral clinical toxidromeorganophosphate and carbamate compoundsSkin irritation (dermatitis) Respiratory tract irradiation (Wheezing) CNS symptoms of cholinergic excess anxiety, restlessness, emotional lability, tremor, headache, dizziness, mental confusion, delirium, hallucinations, and seizures. Coma with depression of respiratory and circulatory centers may result. *Miosis and muscle fasciculations are considered reliable signs*acute organophosphate poisoningantidote for significant organophosphate poisonings Competitive antagonist of acetylcholine at central and peripheral muscarinic receptors, will reverse the effects secondary to excessive cholinergic stimulation. Nebulized atropine or ipratropium may be used to improve pulmonary symptomsatropineused to displace organophosphates from the active site of acetylcholinesterase, thus reactivating the enzyme reverses muscle paralysispralidoximecauses chemical pneumonitis by direct toxicity to the pulmonary parenchyma and alteration of surfactant function Hyperthermia of ≥39°C (≥102.2°F) is likely and may occur initially or 6 to 8 hours after exposure.hydrocarbon aspirationthis has been used to tx acute lung injury from hydrocarbon aspirationsurfactant therapywhat should NOT be given with hydrocarbon toxicity?- catecholamines such as dopamine, NE, and epi - no benefit in gastric lavage - activated charcoal does not workwhat is the most clinically significant metalloidarsenicwhat is the MC cause of chronic metal poisoning and remains a major environment containmentlead poisoningEncephalopathy, a major cause of morbidity and mortality, may begin dramatically with seizures and coma or develop indolently over weeks to months with decreased alertness and memory progressing to mania and delirium GI and hematologic manifestations occur more frequently with acute than with chronic poisoning, and the colicky abdominal pains may be associated with concurrent hemolysis. Patients may complain of a metallic taste and, with long-term exposure, have *bluish-gray gingival lead lines*lead poisoning clinical findingsabdominal or neurlogic dysfunction with hemolysis should raise suspicion for???? also consider this in all children presenting w/ encephalopathylead toxicityedetate calcium disodium (sometimes abbreviated CaNa2-EDTA)dimercaprol - chelating agent(also known as dimercaptosuccinic acid)succimer - chelating agentSevere gastroenteritis with nausea, vomiting, and cholera-like diarrhea is the hallmark of acute poisoning and may last several days to weeks, frequently necessitating hospitalizationacute toxicity of arsenicHypertension, peripheral vascular disease, diabetes mellitus, epidermoid cancer, respiratory tract cancer, hepatic angiosarcoma, and, possibly, leukemia. Dermatologic manifestations are prominent and include hyperpigmentation, hyperkeratosis of the palms and soles, Bowen's disease, and squamous and basal cell carcinomaschronic toxicity from arsenic d/t low-level occupation or environment exposurewhat is the chief cause of death with arsenic poisoning and how should it be managed?hypotension and dysrhythmias - tx with crystalloid volume replacement, and vasopressors with dopamine or NEAcute symptoms following inhalation of elemental mercury vapor include shortness of breath, fever/chills, cough, nausea, vomiting, diarrhea, metallic taste, headaches, weakness, and blurry vision. In severe cases, patients may develop acute lung injury and severe respiratory distress. In severe cases, patients may develop ataxia, muscle rigidity and spasticity, blindness, hearing deficits, and dementia HIGH SEAFOOD DIETmercury poisoningmay improve motor function in methyl mercury-poisoned patients by improving acetylcholine levels at the neuromuscular junctionneostigminethe smell of *bitter almonds* supports this diagnosis? how is it tx?cyanide poisoning - 2 antidoes are in a kit (nitrites and thiosulfate) and hydroxocobalamin + 100% oxygen, crystalloids, and vasopressurescharacterized by abdominal pain, vomiting, and diarrhea.Iron is directly irritating and corrosive to the GI tract and typically induces vomiting within the first few hours following ingestioniron poisoning stage 1This stage is a 6- to 24-hour interval following ingestion during which GI symptoms may resolve and falsely reassure the patient and physicianiron poisoning stage 2Systemic toxicity from iron-induced disruption of cellular metabolism with resultant shock and lactic acidosis. Iron-induced coagulopathy may worsen bleeding and hypovolemia.iron poisoning stage 3Hepatic stage, develops 2 to 5 days following ingestion It results from iron uptake by the reticuloendothelial system with local lipid peroxidation; it manifests as elevation of aminotransferase levels and may progress to hepatic failure.iron poising stge 4Delayed sequelae, including gastric outlet obstruction secondary to the corrosive effects of iron on the pyloric mucosa. Delayed sequelae are rare and occur 4 to 6 weeks after ingestioniron poisoning stage 5Indicated in the iron-poisoned patient with systemic toxicity, persistent emesis, metabolic acidosis, progressive symptoms, or a serum iron level predictive of moderate to severe toxicitydeferoxamine