Emergency Flashcards
1
Q
what is most common overdose ingestion in the US?
A
tylenol
2
Q
what is most common cause of acute liver failure?
A
tylenol
3
Q
minimum toxic dose of tylenol
A
150mg/kg; hepatotoxicity at 250mg/kg
4
Q
Presentation tylenol OD in first 24 hours
A
often asymptomatic or nausea/vomiting/dehydration
-LFTs start to elevate
5
Q
Management Tylenol OD
A
- 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
6
Q
Classic Lab changes in salicylate poisoning
A
- anion gap metabolic acidosis
- respiratory stimulation causes respiratory alkalosis and alkauria
- -so will see acidosis with respriatory alkalosis
- hypokalemia
7
Q
First 12 hours Salycilate poison
A
- tinnitus
- hyperthermia and CNS change
- hyperventilation
8
Q
Management of Salycilate
A
- 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)
9
Q
What is antifreeze?
A
ethylene glycol
10
Q
Presentation ethylene glycol ingestion
A
- 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
11
Q
Management Ethylene glycol
A
- 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)
12
Q
What is the most frequent toxic exposure in the US
A
carbon monixde
13
Q
Who is most at risk from CO poisoning?
A
very young, fetuses (fetal hgb binds tighter), very old, chronically ill
-note if intentional then higher mortality
14
Q
Pathophys CO poisonining
A
-shift dissociation curve to the left (hgb can’t carry oxygen); interrupts cellular respiration, makes free radicals, increases inflmmatory response, DIC, vasolidation, myocardial depression
15
Q
Pulse ox in CO poisoning
A
normal because carboxy-Hgb read same; spectrophotometer can tell difference
16
Q
Most common long term complication of CO poisoning
A
neuro and neuropsych sequelae
17
Q
Management CO poisoning
A
- 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
18
Q
Most common morbidity 2/2 organophosphate?
A
respiratory failure
19
Q
Pathophys organophosphate
A
- inactivates cholinesterase so accumulate Ach resulting in nicotinic and muscarinic effects
- -nicotinic: skeletal depolarization and fasciculations
- -muscarinic: smooth muslce contractions, cardiac conduction delay
20
Q
Presentation Organophosphate
A
SLUDE: salivation, lacrimation, urination, defecation, GI, emesis
- -conduction issues
- -HTN
- -wheezing, pulmonary edema, respiratory muscle weakness
- -CNS: AMS!!!!!!!! seizures
21
Q
Tx organophosphate
A
- 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
22
Q
Complications of Hydrocarbons
A
- resp: hypoxia, ARDS
- CV: arrhythmias, myocardial damage, coronary vasospasm
- neuro: AMS, peripheral neuropathy
- heme: hemolysis, bone marrow toxicity
- hepatic and renal failure
- RTA
23
Q
Management of Hydrocarbon Exposure
A
- CXR: initially normal and must get at 6 hours
- symptomatic must admit and observe
- no charcoal, no inducing emesis
- gastric lavage if CHAMPS (camphor, halogenated hydro, aromatic hydro, heave metal hydro, pesticide contatining hydro)
24
Q
Most common cause of iron overdose
A
children less than 6 who take a bunch of pediatric MVNs
–worst if < 3 years old
25
Pathophys of Iron OD
- mitochondrial disurption
- GI corrosion, hepatocellular injury
- anion gap metabolic acidosis
- coagulopathy
26
Presentation first 6 hours after iron OD
hemorrhagic vomiting, diarrhea, and abdominal pain; may lead to shock
27
Presenation 6 to 12 hours after iron OD
if mild may recover; but if moderate+ temporary recovery as iron distributes through body followed by lethargy, tachy, and tachypnea
28
Presentation 12 to 24 hours after iron OD
```
metabolic acidosis
coagulopathy
shock
arrhythmias
CNS
```
29
When does hepatic injury happen in iron OD
2 to 3 days
30
When does scarring of the GI tract occur after iron OD
2 to 6 weeks
31
Labs Iron OD
- serum levels 2 hours after
| - abdominal XR
32
Tx Iron OD
- whole bowel irrigation
| - deferoxamine
33
Tx TCA OD
- first hour can gastric lavage
- activated charcoal
- ECG (at least 6 to 8 hours if asymptomatic)
- alkalinize
34
Clinical Presentation TCA OD
- first anticholinergic: dry skin, mydriasis, urinarty retension, decreased GI motiligy, myoclonic twitching
- followed by CNS
- vasodilation with hypotension, heart block
35
3 different pharm effects of cough syrups
-antihistamine: anticholingergic
-cathetolamines
0serotnergic
36
Management Cough Syrup Ingestion
- charcoal best in 1 hour
- dystonia: if 2/2 antihistmain use diazepam; if no antihistamin benadryl
- seizure: lorazepam
- serotonins syndrome: cyproheptaidine
37
Most common cause of pediatric death period
unintentional injury
38
most common unintential injury overall
MVA
39
most common unintentional dath less than 1
suffocation
40
most common unintentional death 1 to 4
drowning
41
most common unintentional death 5+
MVA
42
pathophys saltwater drowning
- inactivation of surfactant leads to ARDS
- fluid shifts cause hypernatremia and hemoconcentration
- DI
43
pathophys of freshwater drwoning
-washout of surfactant causing ARDS
-hyponatremia and hemodilution
0intravascular hyperkalemia, hemoglobinuria, renal tubular damage
-SIADH
44
Drowning when to actively re-warm
if temp is < 32 C
45
Most common pathogens dog bites
- staph aureus
| - pasteurella
46
Tx Dog Bite
- Augmentin (azithro if allergic)
- must consider tetanus and rabies
- do not suture if > 24 hours or infected; face must be within 6 hours
- delay closure of hand wounds
- cultures if > 8 hours, infection, severe, or immunocompromised
47
Tx Cat bite
- must get anerobic and aerobic cultures
- augmentin
- suture if less than 24 hours (6 for face); delay closure for hands
- tetanus and rabies
48
Tx Human Bite
- augmentin
- aerobic and anaerobic cultures in all
- consier hepatitis B
49
most common pathogen human bite
-anerobe
50
Do you ice or tourniquet poisonous snake bite?
no becaue increase risk of ischemia; just immobilize
51
Side Effects of Antivenin
- anaphylaxis
| - delayed hypersensitivity (serum sickness; 5 to 21 days later)
52
When to give antivenin
- rattlesnakes
- best within 4 hours; not effective after 12
- coral snakes have neurotoxin so give as soon as possible
53
Symtpoms of black widow bite
- within 1 hour dull cramping pain; includes chest and abdomen (boardlike)
- hypertension and agitation
- resolves within 24 to 48 hours
54
Management Black Widow Bite
-opiates and benzos
| 0antivenin if severe with autonomic instabililty (acetycholine and norepi is released)
55
Symptoms of brown recluse
- characterized by local necrosis due to hyaluronidase and sphinomyelinase
- -hemorrhagic blister
- -can cause hemolysis
56
Management Brown Recluse
- typically just symptomatic
| - admit for significant pain; increased risk of hemoglobinuria
57
Management of Scorpion Bite
- if severe antivenin
- ice and anlgesics
- -autoimmune dysfunction can happen in 1 hour with salivation, blurred vision, hypotension, nystagmus, and muscle twitching
