Emergency Flashcards
what is most common overdose ingestion in the US?
tylenol
what is most common cause of acute liver failure?
tylenol
minimum toxic dose of tylenol
150mg/kg; hepatotoxicity at 250mg/kg
Presentation tylenol OD in first 24 hours
often asymptomatic or nausea/vomiting/dehydration
-LFTs start to elevate
Management Tylenol OD
- unspecified dose: level initial and at 4 hours with CMP
- activated charcoal in first 4 hours
- NAC per protocol within 24 hours of ingestion; prevents hepatotoxicity if first 8 hours
Classic Lab changes in salicylate poisoning
- anion gap metabolic acidosis
- respiratory stimulation causes respiratory alkalosis and alkauria
- -so will see acidosis with respriatory alkalosis
- hypokalemia
First 12 hours Salycilate poison
- tinnitus
- hyperthermia and CNS change
- hyperventilation
Management of Salycilate
- can add ferric chloride to UA
- ABG, CMP, UA
- salicylate blood: initial, ever 2 hours until peak then every 4 to 6 until resolution
- peak usually 4 to 6 hours
- activated charcol
- whole bowel irrigation if enteric coated
- can consider alkalinizatino of blood and urine with bicarb
- HD if severe (>100 at 6 hours)
What is antifreeze?
ethylene glycol
Presentation ethylene glycol ingestion
- increase in glyoxilc acid and oxalic acid which are toxic and combine with Calcium–>hypocalemia, calcium oxalate crystals
- first 12 hours: they seem drunk and with metabolic acidosis
- 12 to 24 ours: tetany, muscle pain, arrhythmia 2/2 hypocalcemia
- beoynd heart failure, renal failure, cerebral edema, seizures
Management Ethylene glycol
- can screen by mixing fluorescein and urine
- estimate levels by osmol gap (NOT serum levels)
- charcol doesn’t work
- alklainize with na bicarb
- fomepizole!!! (inhibit aldehyde dehydrogenase)
What is the most frequent toxic exposure in the US
carbon monixde
Who is most at risk from CO poisoning?
very young, fetuses (fetal hgb binds tighter), very old, chronically ill
-note if intentional then higher mortality
Pathophys CO poisonining
-shift dissociation curve to the left (hgb can’t carry oxygen); interrupts cellular respiration, makes free radicals, increases inflmmatory response, DIC, vasolidation, myocardial depression
Pulse ox in CO poisoning
normal because carboxy-Hgb read same; spectrophotometer can tell difference
Most common long term complication of CO poisoning
neuro and neuropsych sequelae
Management CO poisoning
- ABG for acid base status (PaO2 will be normal)
- do spectrophotometer
- asymtpomatic with < 10% go home
- mild symtpoms: 100% O2 x 4 hours; follow up 24 to 48 hours and a month for delayed neuro findings
- 100% oxygen!
- do not correct acidosis
- CMP, CK, UA, CBC, CXR with pulm, coags, trops, ECG
Most common morbidity 2/2 organophosphate?
respiratory failure
Pathophys organophosphate
- inactivates cholinesterase so accumulate Ach resulting in nicotinic and muscarinic effects
- -nicotinic: skeletal depolarization and fasciculations
- -muscarinic: smooth muslce contractions, cardiac conduction delay
Presentation Organophosphate
SLUDE: salivation, lacrimation, urination, defecation, GI, emesis
- -conduction issues
- -HTN
- -wheezing, pulmonary edema, respiratory muscle weakness
- -CNS: AMS!!!!!!!! seizures
Tx organophosphate
- can measur eRBC cholinesterase level if want to document exposure
- ATROPINE for muscarinic effects
- Pralidoxime for nicotinic receptors (first 18 hours or else may be irreversible)
- benzos for seizures
Complications of Hydrocarbons
- resp: hypoxia, ARDS
- CV: arrhythmias, myocardial damage, coronary vasospasm
- neuro: AMS, peripheral neuropathy
- heme: hemolysis, bone marrow toxicity
- hepatic and renal failure
- RTA