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58 Cards in this Set
- Front
- Back
- 3rd side (hint)
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Ataxia
ophthalmoplegia confusion and impairment of short-term memory resulting from inadequate intake or absorption of thiamine (Vitamin B1) often but not always results from prolonged alcohol amphetamine or methylphenidate |
Wernicke's encephalopathy
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Typically are helpful in establishing a diagnosis when the exposure is not well defined
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Toxidrome
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Single substance
identified no signal words on label known route of exposure and amount no symptoms follow up is available |
Non-toxic ingestion
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Substance that adversely affects the function of any system within that organism.
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Poison
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Integral part of managing exposures
specialists trained in management of poisoning have reference material and immediate access to medical toxicologists can help focus diagnosis and treatment and may reduce costs and unnecessary hospitalizations. |
Poison control center
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5 routes of exposure to poisons
Which one is the most common? (hint: IIIICM) |
Most common is ingestion
inhalation insufflation injection cutaneous mucous membrane |
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Toxins outside the body must be washed away and toxins inside the body must be either bound within the gut lumen to make them unavailable for absorption or
have their elimination enhanced from the gut blood or tissues. |
GI decontamination
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Can be given to children and adults and about 90% of pts vomit within 20 mins of first dose
May be used at home. |
Ipecac
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Contraindicated in pts with ingestions that have the potential for alter mental status;
active or prior vomiting; caustic ingestion; a toxin with more pulmonary than GI toxicity; and ingestions of toxins that have the potential for inducing seizures. |
Ipecac
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Indications for this procedure are limited to ingestion of a life threatening toxin that requires ventilator support
immediate return of small pills or pill fragments |
Gastric Lavage
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What percent of drug removal is possible with gastric lavage?
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Only about 35% to 56 %
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The most appropriate agent to decontaminate the GI tract
works by adsorbing the toxin within the gut lumen making the toxin less available for absorption into the tissues. |
Activated charcoal
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The benefits of this procedure include its ability to decontaminate the gut without requiring invasive procedures
its rapid administration and its proven safety in both adults and children |
Activated charcoal
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When should you not use activated charcoal for safety reasons?
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If esophageal or
gastric perforation are suspected or if emergency endoscopy might be needed. |
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When will activated charcoal be ineffective?
+h |
Iron
lead lithium ingestion |
I
L L |
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Generally considered when certain toxins have been ingested
such as: 2-4-D (herbicide); Phenobarbital; chlorpropamide; Salicylates and Methanol. |
Urinary Alkalinization
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Urine alkalinization is a treatment regimen that increases poison elimination by the administration of intravenous sodium bicarbonate to produce urine with a pH > or = 7.5. Experimental and clinical studies confirm that urinary alkalinization increases salicylate elimination, although the mechanisms by which this occurs have not been elucidated. The conventional view is that ionisation of a weak acid, such as salicylic acid, is increased in an alkaline environment. Since the ionisation constant (pKa) is a logarithmic function then, theoretically, a small change in urine pH will have a disproportionately larger effect on salicylate clearance. Hence, elimination of salicylic acid by the kidneys is increased substantially in alkaline urine. |
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Generally reserved for specific toxins that must both be potentially life-threatening and amenable to removal by this method
Drugs include: Salicylates; Methanol Ethylene glycol lithium theophylline Amanita (mushrooms). |
Hemodialysis
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Potentially useful for the toxins:
Phenobarbital Phenytoin Ethchlorvynol but in practice this method is only commonly recommended for Theophylline OD. |
Hemoperfusion
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What methods do you use for removal of toxins that are already absorbed from the gut;
removal of substances that do not adhere to activated charcoal and the ability to remove both the parent compound and the active toxin metabolites. |
Enhancing elimination-
urinary alkalinization hemodialysis hemoperfusion |
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Intravenous bolus of 1 to 2 meq/kg sodium bicarbonate
followed by either intermittent boluses of sodium bicarbonate or a continuous intravenous infusion to achieve a urinary ph of 7.5 to 8.0. info + |
Urinary Alkalinization
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Urine alkalinization is a treatment regimen that increases poison elimination by the administration of intravenous sodium bicarbonate to produce urine with a pH > or = 7.5. Experimental and clinical studies confirm that urinary alkalinization increases salicylate elimination, although the mechanisms by which this occurs have not been elucidated. The conventional view is that ionisation of a weak acid, such as salicylic acid, is increased in an alkaline environment. Since the ionisation constant (pKa) is a logarithmic function then, theoretically, a small change in urine pH will have a disproportionately larger effect on salicylate clearance. Hence, elimination of salicylic acid by the kidneys is increased substantially in alkaline urine. |
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When performing urinary alkalinization
what is the upper limit of serum ph? what electrolyte disorder can occur when using this technique and must be aggressively treated? |
7.5-7.55
hypokalemia |
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Much less effective when the toxin ingested has a large volume of distribution (>1 L/kg)
has a large molecular weight (more than 500 Da) or is highly protein bound. |
Hemodialysis
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Involves placing a filter filled with activated charcoal
into the circuit of the Hemodialysis machine Toxins removed by this method must adsorb well to -activated charcoal -have a small volume of distribution. |
Hemoperfusion
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A mild lactic acidosis may be seen
However significant acidosis should never be attributed to |
Alcohol intoxication
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The symptoms of ??
poisoning may not appear for up to 12 to 18 h after ingestion because of the time it takes for it to be metabolized to its toxic metabolites. |
Methanol
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The most appropriate fluid is D5NS
This fluid addresses volume issues as well as glycogen depletion Hypoglycemia should be excluded |
Alcohol intoxication
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Visual disturbances
abdominal pain nausea and vomiting and wide-anion-gap metabolic acidosis. |
Methanol
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Visual disturbances are seen in approximately 50 percent of patients: diplopia
blurred vision decreased visual acuity photophobia descriptions of "looking into a snow field " constricted visual fields and blindness. |
Methanol
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Potent mucosal irritant
severe abdominal pain as well as nausea and vomiting. |
Methanol
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Treatment: 1) supportive care
2) correction of acidosis 3) administration of fomepizole or ethanol to decrease conversion to toxic metabolites and 4) dialysis to eliminate the _______? |
Methanol
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Use of fomepizole or
alcohol does not alter the indications for |
Dialysis.
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Duration of symptoms and signs is longer and central nervous system depression may be more profound because of the formation of acetone.
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Isopropanol
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symptoms 30 to 60 min
w peak effects in a few hours Nystagmus Hemorrhagic gastritis secondary to gastric irritation appears early Hypoglycemia secondary to Depressed gluconeogenesis. |
Isopropanol
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Establish IV access
Bedside testing for blood glucose and give thiamine and naloxone no utility to performing gastric lavage Hemodialysis is indicated when hypotension is refractory to conventional therapy. |
Isopropanol
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appear inebriated
Slurred speech ataxia without no ethanol on breath...?????? hey Blue its a Clue! Hallucinations coma Sz death may also occur |
Ethylene glycol phase 1
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The optic fundus is usually normal
differentiating from methanol poisoning although nystagmus and ophthalmoplegia may be observed. |
Ethylene glycol
phase 1 |
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12 to 24 h after ingestion
Tachycardia mild hypertension and tachypnea are common; congestive heart failure acute respiratory distress syndrome cardiomegaly and circulatory collapse are also observed Myositis may be seen. |
Ethylene glycol phase 2
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24 to 72 h after ingestion
Early symptoms consist of flank pain and CVA tenderness Oliguric renal failure and acute tubular necrosis ensue Two forms of urinary calcium oxalate crystals may be identified on microscopic evaluation of the urine. |
Ethylene glycol phase 3
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Has been shown to be a cofactor in the metabolism of toxic metabolites and should be given if patients are deficient
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Magnesium
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Competitive inhibition of alcohol dehydrogenases breakdown of ethylene glycol with fomepizole or
ethanol should be initiated in the ED when overdose is suspected or confirmed |
Methanol and ethylene glycol
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Which routine labs
should be ordered in a poisoned patient? |
blood screening
& Urine Utility of toxicologic tests in many circumstances is very limited |
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In which poisoned patient is a psychosocial evaluation indicated
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Children
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CNS depression
miosis respiratory depression maybe hypothermia bradycardia respiratory arrest acute lung injury What Toxidrome? What antidote? |
Opioid OD
Ventilation or Naloxone |
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Psychomotor agitation
mydriasis diaphoresis tachycardia hypertension hyperthermia maybe rhabdomyolysis MI seizures death from any of these What Toxidrome? What antidote? |
Stimulant
(sympathomimetic). Hydration Cooling -Benzodiazepines |
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Salivation
Lacrimation N&V Urination defecation muscle fasciculations weakness bronchorrhea maybe bradycardia miosis/mydriasis seizures respiratory failure paralysis Death from any of these What Toxidrome? What antidote = two Rx? +h |
Organophosphate Poisoning
Airway protection Ventilation -Atropine -Pralidoxime |
A....
Pra..... |
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This Poisoned state creates
an Altered mental status Mydriasis Dry/flushed skin Urinary retention Decreased Bowel Sounds Hyperthermia Dry Mucous Membranes seizures Dysrhythmias Rhabdomyolysis What Toxidrome? what antidote? |
Anticholinergic-
cooling supportive management -physostigmine -sedation w benzodiazepines |
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Altered mental status
diaphoresis tachycardia hypertension Maybe paralysis slurring of speech bizarre behavior seizures What Toxidrome? What antidote? |
Hypoglycemia
glucose |
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The four empiric antidotes
("coma cocktail") administered on arrival to ED Identify Dosing |
O2
Naloxone Adults = 50 ml D50W {Children = 1 g/kg glucose} + Adults = 100 mg thiamine |
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Absorption from the GI tract may be slowed because of the inhibitory effect on gastric emptying and the impaired dissolution in gastric fluids at high concentrations.
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ASA poisoning
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Acute ingestion of less than 150 mg/kg may produce "mild" toxicity
with nausea vomiting and GI irritation but significant toxicity is not expected. |
ASA poisoning
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Above 30 mg/dl
Most patients have a mixed acid-base disturbance of respiratory alkalosis and metabolic acidosis Patients with mixed ingestions have a normal anion-gap metabolic acidosis 40 percent of the time. |
ASA overdose
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Hyperpyrexia appears to be an adverse prognostic indicator
and death is usually preceded by a predominant metabolic acidosis and neurologic deficits. |
ASA overdose
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The main goals of therapy are immediate resuscitation;
maintenance of airway breathing and circulation; correction of volume depletion and metabolic derangements; GI decontamination with activated charcoal |
ASA overdose
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Hepatic metabolism through glucuronidation and sulfation is easily saturated
Therefore a larger proportion is metabolized by cytochrome P450 to NAPQI depleting glutathione NAPQI binds to other hepatic macromolecules and hepatic necrosis occurs. |
Acetaminophen OD
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Presents in four stages
1 is nonspecific nausea etc 2 is RUQ pain and elevated enzymes 3 is fulminant hepatic failure and 4 is recovery. |
APAP overdose
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Treatment consists of GI decontamination
(activated charcoal orally or through nasogastric tube); the timely use of the antidote N-acetylcysteine (NAC); and supportive care. |
APAP overdose
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Withdrawal produces yawning
tears diarrhea abdominal cramping piloerection and rhinorrhea. |
Opiate withdrawal
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A medical emergency and should be treated on an inpatient basis
disorientation fever and visual hallucinations tachycardia diaphoresis anorexia and insomnia. |
ETOH withdrawal
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