Poisoning and Ingestions - Exam 3 Flashcards
What is super important in the management of a poisoned pt?
Gross decontamination prior to assessment!!!
Avoid self-exposure to toxin
Fully disrobe patient for exam
What are some common poisons that would cause a prolonged QRS interval?
Antidepressants
antipsychotics
antihistamines
organophosphate insecticides
What are some common poisons that would cause SVT?
Sympathomimetics and Anticholinergics
What are some common poisons that would cause Ventricular tachycardia?
Sympathomimetics and TCA
What are some common poisons that would cause bradycardia?
Cholinergics
opioids
sedative-hypnotics
What is the tx for seizures in the poisoned pt? What is the seizure persists?
IV Diazepam (Valium) 5mg Repeated and doubles every 5 to 10 minutes as needed
If the seizure persists - IV phenobarbital and prepare to intubate
What is the tx for a seizure due to Isoniazid?
pyridoxine
What 3 things are used to help classify the patient into either a state of physiologic excitation or depression?
mental status
vital signs
pupillary examination!!!
What are some potential causes of a mydriasis (dilated pupil)?
anticholinergics and sympathomimetics
What are some potential causes of a miosis (constricted pupil)?
cholinergics
opioids
What are some potential causes of a nystagmus?
Ethanol, phenytoin, ketamine, PCP
What are some potential causes of a excessive lacrimation?
cholinergics
When would you want to order an abdominal xray?
if you suspect “body packers” of cocaine/heroin packs
bezoar formation -> most likely causes by ASA
What is the recommendation with regards to UDS in a poisoned pt?
Unnecessary in patients who presents with a non-intentional ingestion and are asymptomatic or have clinical findings that are consistent with the medical history
What 3 common ingestants can you order a concentration level on? Especially in those pts who present with AMS
Acetaminophen
ethanol
salicylate
What is the UA finding associated with ethylene glycol (antifreeze) poisoning?
Calcium oxalate crystals may be present
What are your gastric decontamination options? Which one is preferred?
activated charcoal** preferred method
gastric lavage
whole bowel irrigation
What are the indications for activated charcoal? What 3 substances is it NOT good for?
indicated if ingestion of a toxic substance within 1 hour prior to arrival
metals, corrosives or alcohols
What are the CI to activated charcoal?
Unable to protect airway (high risk for aspiration/pneumonitis) aka cannot use in any unstable pts
poorly absorbed toxin (Iron, lithium, alkali, mineral acids, alcohols)
intestinal obstruction
When can you use activated charcoal AFTER the 1 hour mark?
can be used after 1 hour if toxins that slow GI transit (anticholinergics) and those that form bezoars (salicylate)
What are the indications for a gastric lavage?
ingestion has occurred < 1 hour prior to presentation
there is no antidote
toxin has a poor response to supportive care
What is the risk of gastric lavage?Describe the pt who would be a good candidate for gastric lavage
High risk of aspiration!!!
avoid unless patient is INTUBATED or airway protective reflexes are intact
aka good for intubated pts!!
What is the procedure to perform a gastric lavage?
Insert 36F-40F orogastric tube
Lie patient in left lateral decubitus with head of bed tilted down
200 ml of warm tap water instilled into stomach and removed via gravity or suction
What are the indications for a whole bowel irrigation? What are the CIs?
ingestion of chemicals poorly adsorbed to charcoal (such as lithium, iron, lead) and ingestion of drug-filled packets
CI: absent bowel sounds or suspected ileus or obstruction
What are the procedure steps for a whole bowel irrigation?
Instil a electrolyte polyethylene glycol solution (GoLYTELY) to flush out the entire intestinal tract
Administer via NG tube, 1–2 L/h (400–500 mL/min in children)
Continue until the rectal effluent is clear (3–5 hours or more)
What are the indications for multi-dose activated charcoal? What is considered multi-dose?
ingestion of toxic levels of carbamazepine, dapsone, phenobarbital, quinine, and theophylline
MORE than 2 doses of oral activated charcoal to enhance elimination toxins
What are the CIs of multi-dose activated charcoal? What is the caution?
unprotected airway
absent bowel sounds
Caution in ingestions resulting in reduced gastrointestinal motility
What is happening in urinary alkalinization? What is the indication?
ionizes acidotic toxins preventing resorption back across the renal tubule
Indications: moderate-severe salicylate toxicity
What do you need to monitor for when utilizing urinary alkalinization?
hypokalemia will reduce the alkalinity of the urine
need to check K every 2 hours
What is the procedure for urinary alkalinization? What is the K range? When should you assess urine pH? What is the pH goal?
IV administration of sodium bicarb (+/-) potassium chloride
monitor serum potassium and bicarb every 2-4 hours to ensure both are staying within normal limits
Serum potassium should be maintained in the 4.0 to 4.5 mEq/L range
assess urine pH every 15-30 minutes with a pH goal of 7.5-8.5
_____ is more effective at clearing highly protein-bound drugs and lipid-soluble drugs
hemodialysis
______ is more effective at clearing
water-soluble low molecular weight substances
hemoperfusion
When are hemodialysis and hemoperfusion used?
Both require critical care setting and are expensive and invasive leading to high risk of complication
What are your tx options for enhanced elimination?
multidose activated charcoal
urinary alkalinization
Extracorporeal removal - hemodialysis and hemoperfusion
How do antidotes reduce or reverse poison effects?
Prevent absorption
Bind and neutralize poisons directly
Antagonize end-organ effects
Inhibit conversion to more toxic metabolites
What are the indications for an antidote? How common are they?
exposure to toxin in which an antidote exists
the severity of the toxicity warrants use
benefits outweigh its associated risk
no contraindications
only used in a small percentage of patients
What is the antidote for acetaminophen?
acetylcysteine
What is the antidote for anticholinesterases (organophosphates, carbamates, physostigmine)?
atropine
What is the antidote for B-blockers?
glucagaon
calcium
high dose insulin
What is the antidote for cyanide?
sodium nitrite
What is the antidote for isoniazid?
pyridoxine (vit B6)
What is the antidote for warfarin?
vit K
What is the antidote for TCA?
sodium bicarb
What is the antidote for salicylates?
sodium bicarb
What is the antidote for methotrexate?
folinic acid
What is the antidote for sulfonylureas?
octreotide
What is the tx for an inhaled poison? What 2 things do you need to watch for?
Administer oxygen
Water aerosol inhalation may help to dilute irritants in the nasopharynx
Be alert for delayed upper airway obstruction or pulmonary edema
What is the tx for contaminated eyes? When do you assess pH?
Irrigate eyes immediately with copious amounts of plain water or NS
Assess pH of eye after 2 L of irrigated fluid
What is the tx for contaminated skin?
Wash the skin immediately with plenty of water and dilute soap solution
Discard contaminated clothes in a marked plastic bag.
What is the number for poison control? What are 4 things they can help with?
1-800-222-1222
Obtain information on unknown pills or chemicals found at scene
Provide immediate assistance in selecting appropriate laboratory or toxicity tests
Recommend preferred methods of decontamination, patient-specific care recommendations, or the use of antidotes
Advise on patient disposition
What is the disposition for a poisoned pt?
Asymptomatic patients with non-toxic exposures may be discharged after a short period of observation, providing they have access to further consultation and a safe discharge destination
What 3 questions do you need to ask to determine a non-toxic exposure?
- Was the exposure unintentional and a clearly identified single substance?
- How much of the agent was ingested or amount of exposure?
- Can the Poison Control Center (or other reliable information source) confirm the substance as nontoxic in the reported dose?
What is the mainstay of therapy for a poisoned pt?
supportive care!!!
If a poisoned pt is HTN and agitated can administer _______
BZD
If a poisoned pt is HTN and at risk of a end-organ damage, want to tx with what medications? What do you want to avoid?
tx with: CCB, phentolamine, labetalol or nitroprusside
avoid: BB in sympathomimetic toxicity
Why do you avoid BB in sympathomimetic toxicity?
due to unopposed a-adrenergic stimulation resulting in vasoconstriction
If a PP (poisoned patient) has a cardiac arrhythmias what treatments will most likely fix the arrhythmias?
correction of hypoxia
metabolic/acid–base abnormalities
administration of an antidote
_____ is beneficial for wide QRS tachyarrhythmias in a PP
sodium bicarb
What are the 3 routes naloxone can be administered? What can giving too large of a dose result in?
administered IV, IM or intranasal both dx and therapeutic
large doses may induce vomiting and aspiration, acute opioid withdrawal, or an uncooperative, agitated patient
What is considered hyperthermia? What is the tx? What are the 3 complications?
core body temp >39°C (>102.2°F)
aggressive cooling
complications include - rhabdomyolysis, end-organ failure, and DIC
When do you need to consider rewarming a pt due to hypothermia?
Indications for re-warming is a core temp <32°C (<90°F)
What is the formula to calculate the anion gap? What is a normal AG?
AG = Na - (Cl + HCO3)
Normal AG is <10-15 mEq/L
What are the big things that can cause anion gap metabolic acidosis?
C - cyanide, carbon monoxide
A - alcoholic ketoacidosis
T - toluene
M - methanol, metformin
U - uremia
D - diabetic ketoacidosis
P - propylene glycol
I - inborn errors, iron, isoniazid, infection
L - lactic acid
E - ethanol, ethylene glycol
S - salicylates, starvation ketoacidosis
What is the management plan (in order) for a pt with anion gap metabolic acidosis?
What are the 7 basic toxidromes?
Opioid
Sympathomimetic
Cholinergic
Anticholinergic
Sedative/hypnotic
Serotonin Syndrome
Hallucinogenic
What is the classic presentation of an opioid toxidrome? What is the tx?
What symptom of the classic opioid presentation will be lacking in meperidine?
will NOT cause miosis
What is the MOA behind sympathomimetic toxidromes? What substances fall under this category?
mimic the effects of endogenous agonists of the sympathetic nervous
Cocaine, Caffeine, Amphetamines, Cathinones
What are the presenting s/s of sympathomimetic toxidromes? What is the management?
M: Mydriasis, muscle cell death
A: Agitation, arrhythmia, angina
T: Tachycardia
H: Hypertension, hyperthermia, hyperactive bowel sounds
S: Seizure, sweating
External cooling
BZD for agitation, HTN and seizure
IV fluids
What is CI in the management of a sympathomimetic toxidrome?
do NOT give BBs!! for HTN if caused by sympathomimetic
What is the MOA behind cholinergic toxidromes? What are common substances?
blocks acetylcholinesterase resulting in an excessive amount of acetylcholine
think insecticides and farming communities
What is the presentation of a cholinergic toxidromes?
crying all over!!
Salivation, lacrimation, diaphoresis, bronchorrhea, increased urination and defecation, N/V, muscle fasciculations, weakness
may also have bradycardia, rales, seizures, miosis/mydriasis, respiratory failure, paralysis
What is the tx for cholinergic toxidromes?
protect airway!!
atropine!! or Pralidoxime AND atropine
diazepam for seizures and muscle fasciculation
Why do you use atropine in cholinergic poisoning?
blocks Ach receptors at the muscarinic receptors
Why is pralidoxime used in cholinergic toxidromes?
reactivate cholinesterase at both muscarinic and nicotine receptors
What is the MOA behind anticholinergic toxidromes?
block the acetylcholine muscarinic receptors resulting in inhibition of parasympathetic nerve impulses¹ (involuntary movements of smooth muscles)
What medications fall under the anticholinergic toxidrome?
Scopolamine
Atropine
Antihistamines
TCA’s
Antiparkinson agents
Antispasmodics/Muscle relaxants
What are the s/s of an anticholinergic toxidrome?
hyperthermia
tachycardia
no secretions/sweating (dry)
AMS
urinary retention
mydriasis (blind as a bat)
flushed, dry skin
**How are anticholingeric and sympathomimetic s/s different?
Differs from sympathomimetic toxicity by dry skin and decreased bowels sounds
**What is the antidote used in anticholinergic poisoning? How does it work? When is it indicated?
Physostigmine
a cholinesterase inhibitor increases the concentration of Ach at the cholinergic receptor
indicated if conventional therapies fail
What do you need to do first in an anticholinergic poisoning?
address the possible complications
then physostigmine if conventional therapies fail
What is the disposition for an anticholinergic poisoning?
Discharge home if symptoms resolve after 6 hours of observation
Admit patients with more significant symptoms or those receiving physostigmine
What are the 3 classes that fall under sedative/hypnotic toxidromes?
Benzodiazepines
Non-BZD’s: carisoprodol, alcohol, hypnotics
Barbiturates
How will a sedative/hypnotic toxidrome present?
slurred speech , lethargy, CNS depression, respiratory depression, confusion
What is the management for a sedative toxidrome?
supportive care!! vent, intubate, fluid, activated charcoal
What should you do for barbiturates that do NOT respond to supportive care measures?
Consider enhanced excretion methods
What is the tx for a confirmed BZD overdose with respiratory depression? Why does it need to be confirmed?
flumazenil - do not use empirically
it may precipitate seizures
What is the disposition for a sedative toxidrome?
Admit if symptomatic after 6 hours of management
Consult psych for intentional overdoses
What is the MOA behind serotonin syndrome toxidromes? What medications?
increased serotonergic activity in the CNS
MAOI’s, SSRI’s, meperidine (Demerol), dextromethorphan, TCA’s, L-tryptophan
What is the presentation of serotonin syndrome? What is the MC cause of death?
H : hyperthermia, hypertension
A : altered mental status, agitation
T : tremor, tone (increased muscle tone), tachycardia, tachypnea
S : seizures
hyperthermia
What is the tx for serotonin syndrome?
vent support as needed
EXTERNAL cooling
BZD: for agitation, tremors, seizures
Identify and discontinue serotonergic drug
What should you do in serotonin syndrome if BZD and supportive care fails? What is the disposition?
use serotonin receptor antagonist:
cyproheptadine (histamine 1 receptor antagonist)
admit all pts
What are examples of hallucinogenic toxidromes? What are the s/s?
LSD, PCP, mushrooms (psilocybin), ecstasy, dextromethorphan, ketamine
Disorientation, hallucinations, anxiety, seizures, agitation, muscle tension, N/V,
Hypertension, tachycardia, tachypnea, hyperthermia, mydriasis
What is the tx for hallucinogenic toxidromes?
External cooling for hyperthermia
BZD for agitation, hyperthermia, seizures, tachycardia and HTN
aggressive IV fluids
What is the tx for refractory HTN in hallucinogenic toxidromes? What is the disposition?
Nitroprusside or phentolamine for refractory HTN
Admit patients for persistent symptoms after adequate treatment
What groups of people are at an increased risk for APAP toxicity?
chronic alcohol use, AIDS, anticonvulsant and anti-tuberculosis therapy
What is considered a toxic exposure to APAP in a pt 6 years and older?
> 10 grams or 200 mg/kg as a single ingestion or over 24 hour
> 6 grams or 150 mg/kg per day for at least 2 consecutive days
What is considered a toxic exposure to APAP in a pt less than 6 years old?
200 mg/kg or more as a single ingestion or over an 8-hour period
150 mg/kg per day for at least 2 consecutive days
What are the 4 stages of APAP toxicity?
When should you check a serum APAP level? When does serum concentration levels peak?
levels should be assessed even in asymptomatic patients due to delay in symptoms with toxicity
peak serum concentration 30-120 minutes after acute ingestion
When do liver enzymes rise and peak in APAP toxicity?
Liver enzymes (rise at 24hr, peak at 72hr)
In APAP toxicity, the _____ is utilized to determine clinical outcomes ______ between _____ post ingestion
Rumack-Matthew nomogram
only after acute ingestion
4-24 hours post ingestion
need to treat if above dotted line
What is the tx in APAP toxicity?
activated charcoal
acetylcysteine
or
Extracorporeal excretion (dialysis or similar)
What is the MOA of acetylcysteine and when does it need to be given?
prevents metabolite from binding to hepatic cells (if given within 8 hr of exposure) and diminishes hepatic necrosis
When is extracorporeal excretion utilized in APAP toxicity?
utilized only in patients with severe intoxication who present too late to remove the drug and in patients who have hepatic encephalopathy
What is the disposition in APAP toxicity?
Admit all patients requiring acetylcysteine therapy
Discharge after 4-6 hours of observation if acetylcysteine isn’t needed
Consider looking at this again
What are the s/s of alcohol toxicity? Alcohol inhibits ______
ataxia, slurred speech, depressed sensorium, and nystagmus
vasodilation leads to orthostatic hypotension and hypothermia
hypoglycemia
gluconeogenesis
What are the complications of alcohol toxicity?
trauma, respiratory depression, pulmonary aspiration, coma
What labs should you order in alcohol toxicity?
Blood Alcohol Concentration (BAC)
glucose level
UDS
labs to assess organ damage/dysfunction
What BAC level indicates a high possibility of death?
> 0.50
What is the tx for alcohol toxicity?
supportive care and observation
IV dextrose if hypoglycemic
IV thiamine: if concerned for chronic alcohol use and Wenicke’s encephalopathy
What is the disposition for alcohol toxicity?
uncomplicated ethanol intoxication - observe in ED until sober
if no suicidal or homicidal ideations - d/c home
Admit patients who have associated conditions that require admission
What does ASA hydrolyze into after absorption? What does this lead to? What are they at risk for?
aspirin is hydrolyzed to salicylic acid (salicylate)
In large amounts this creates an acidic environment
can lead to acute and chronic toxicity
At risk for bezoar formation due to salicylate impairing gastric emptying
What are the s/s of a ASA toxicity?
fever, hyperventilation, and altered mental status with volume depletion, acidosis, and severe hypokalemia
tinnitus, hearing loss, dizziness, N/V
What level of ASA toxicity?
<150 milligrams/kg
tachypnea, hyperpyrexia, diaphoresis, ataxia, anxiety
What level of ASA toxicity?
150–300 milligrams/kg
abnormal mental status, seizure, heart/lung/renal failure, shock
What level of ASA toxicity?
> 300 milligrams/kg
What is the salicylate level therapeutic range? What is considered toxic?
15-30 mg/dL
> 30 mg/dL is toxic
When does the salicylate level peak concentration level occur? How often do you need to monitor?
peak concentration in acute ingestion may not occur for 4-6 hours
repeat levels every 1-2 hours until peak has been reached then every 4-6 hours
also should monitor electrolytes, renal/liver function and glucose by ordered CMP and mag
How will ASA toxicity present as a acid/base disorder?
In the early stages of ASA (aspirin/salicylate) toxicity, patients typically present with respiratory alkalosis due to hyperventilation, which is a compensatory mechanism to counter the developing metabolic acidosis with anion gap
What labs and imaging should you order in ASA toxicity?
labs: ASA and toxicology to check for any coingestants
CXR and EKG assessing signs of end organ damage
Abdominal imaging if bezore is suspected
When should a bezoar be suspected in ASA toxicity?
Suspect if salicylate level continue to rise despite treatment with gastric lavage or activated charcoal
What is the management for an ASA toxicity? ______ is considered first line in pts with moderate/severe ASA toxicity. When is hemodialysis indicated?
Systemic/urinary alkalinization with sodium bicarbonate
indicated in severe toxicity not responding to above treatments or evidence of renal impairment
