Environmental Injuries & Toxic emergencies Flashcards
1
Q
Approach to the poisoned patient
A
Assess ABCs:
Airway, Breathing, Circulation
Vitals signs
Supportive care
2
Q
Information to obtain in poisened patient
A
PACT -
Product - what did they take?
Amount - how much (when was pill bottle filled?)
Coingestion - does pt have anything else on board?
Time - how long ago did he/she take it?
3
Q
Physical Exam components possible poisoning
A
VENAS -
Vitals Eye exam Neuro exam Abd exam Skin exam
4
Q
Eye exam findings - what to look for
A
Pupil size (pinpoint = opioid) Nystagmus (can = ketamine) Reactivity to light? Scleral discoloration? Ptosis? Ophthalmoplegia?
5
Q
Skin Exam Assessment
A
Temperature Moisture Flushed Cyanotic Pale Track marks/abscesses
6
Q
ABD Exam Assessment
A
Bowel sounds?
Ileus?
Abd cramping?
Diarrhea?
7
Q
Neuro Exam Assessment
A
Mental status - A&Ox3
Gait
Reflexes
Clonus - shaking/seizing
8
Q
Anti-Cholinergic Toxidrome
A
"Hot as hare" (hyperthermia) "Dry as bone" (dry mm) "Red as a beet" (flushed) "Mad as hatter" (Confusion) "Seizing like squirrel" (seizures) "Full as flask" (Urinary retention) "Tachy as lesiure suit" (tachy) "Blind as bat" (mydriasis, blurred vision)
Absent bowel sounds - ileus/constipation.
9
Q
Agitated delirium w/ visual hallucinations & mumbling speech, tachycardia, dry flushed skin, mydriasis, myoclonus, urinary retention, dec bowel sounds
Which Toxidrome?
A
Anticholinergic
Similar to simpathomimetic except simpathomimetic OD (cocaine) = DIAPHORESIS not dry skin & also HYPERTENSION
10
Q
Sympathomimetic Toxidrome Symptoms
A
Delusions, agitation Paranoia Tachycardia Hypertension Hyperpyrexia Diaphoresis Piloerection Hyper-reflexia
Severe: Seizures/dysrhythmias
Caffeine & Theophyline OD present similarly but don’t have the organic psych manifestations
11
Q
Causes of Anticholinergic OD
A
Antihistamines Anti-parkinsonism meds Atropine Scopolamine Amantadine Antipsychotics Antidepressants Antispasmotics Skeletal muscle relaxants Many plants - Jimson weed
12
Q
Causes of Sympathomimetic OD
A
Cocaine
Methamphetamine, MDMA
OTC decongestants (pseudoephidrine, phenylpropanolamine)
13
Q
Opiate/Sedative OD CP
A
- Depressed mental status
- Respiratory depression
- Miosis
= classic triad for opioids
Bradycardia Hypotension Dec bowel sounds Hyporeflexia Needle marks
14
Q
Causes of opiate/sedative OD
A
Narcotics
Barbiturates
Benzos
Z-drugs (zolpidem, zopiclone, zaleplon)
GHB Carisoprodol (Soma)
15
Q
Cholinergic Toxidrome
A
Confusion
CNS de pression
Weakness
SLUDGE BBB
Salivation, lacrimation, urination, diarrhea, GI cramping, emesis, bronchorrhea (pulmonary edema), bronchospasm, bradycardia
16
Q
Causes Cholinergic toxidrome
A
Organophosphate & carbamate insecticides
Physostigmine, edrophonium (MG, alzheimer’s meds)
Some mushrooms
17
Q
Serotonoergic Toxidrome
A
SHIVERS
S hivering, one of the neuromuscular symptoms unique to SS, helps distinguish it from other hyperthermic syndromes
H yperreflexia and myoclonus are frequently seen in mild to moderate cases and are especially notable in the lower extremities; muscular rigidity occurs only in more severe cases
I ncreased temperature, although variable in SS and usually observed in severe cases, is likely caused by muscular hypertonicity
V ital sign instability can present as tachycardia, tachypnea, and/or labile blood pressure
E ncephalopathy—characterized by mental status changes such as agitation, delirium, confusion, and to a lesser extent obtundation—can develop from hyperthermia
R estlessness and incoordination are common because of excess serotonin activity
S weating (diaphoresis) is an autonomic response to excessive serotonin stimulation; by comparison, anticholinergic toxicity usually manifests with hot, dry skin
18
Q
NMS
A
Similar to SS (SHIVERS) - but develops/progresses over 1-3 days instead of <12 hrs in SS. Also caused by different medications
NMS = HALA
Hyperthermia, AMS, Autonomic instability, Lead-pipe rigidity
19
Q
Diagnostic Testing in possible overdose - 4 things to order right away
A
Remember - assess ABCs FIRST..then do…
- 12-lead EKG
- Glucose (AMS)
- CMP (anion gap)
- ABG/VBG (pH)
Also order:
ASA/APAP level
Pregnancy test
Urine/serum tox screen
20
Q
Causes of anion gap / metabolic acidosis
A
MUDPILES
Methanol Uremia DKA Propylene glycol, propofol Isoniazid, iron, infection Lactic acidosis Ethylene glycol Salicylates, starvation ketosis, sympathomimetics
Analgesics (ibuprofen, asa, apap), carbon monoxide, cyanide
21
Q
What causes QRS interval prolongation in OD’s?
A
Agents blocking cardiac fast Na+ channels (QRS >100ms)
22
Q
What causes QT interval prolongation in ODs?
A
Agents that block cardiac K+ efflux channels
QTc > 440 men
QTc > 460 women
23
Q
Sedative overdoses mimic which condition which you must rule out first?
A
Intracranial hemorrhage - rule out with CT
24
Q
Treatment strategies for OD (3)
A
- Prevent absorption:
Emesis, gastric lavage, activated charcoal, cathartics, whole bowel irrigation - Enhance elimination:
Hemodialysis, urine alkalinization - Block effects
25
When to use emesis as method of preventing GI absorption
Not clinically used 2/2 risk of aspiration
26
When to use gastric lavage as method to prevent GI absorption of toxin
Not clinically used very often
Only used if life-threatening dose/ingestion of substance <1 hr ago for which reliable tx options are limited. Not shown to affect clinical outcomes
Increases risk of aspiration, laryngospasm, and esophageal injury
27
When to use cathartics as method of preventing GI absorption
Theory: Speeding up GI transit time = dec absorption - in reality, cathartics = vomiting, abd pain, electrolyte abormalities & do not dec drub absorption or improve outcomes so DO NOT USE
28
When to use whole bowel irrigation in preventing GI absorption
MOA: Use PEG to rapidly flush chemicals thru GIT
Indications: Used when pt ingests extended release tabs, radio-opaque tabs/chemicals, substances not well absorbed by charcoal (Lithium, iron, heavy metals), or large packets of street drugs (cocaine bags etc)
Problems: Unless pt is awake & oriented, there is risk of vomiting & aspiration & massive amounts of diarrhea in bed
29
When to use activated charcoal
Activated charcoal = most widely used GI decontaminant in OD. Decreases drug absorption Has not been shown to affect clinical outcomes.
Use w/in 1 hour of ingestion. Or longer if ER formulations or very large ingestion.
30
Drugs not well absorbed with charcoal decontamination
Lithium, heavy metals, iron, alcohols
31
When is use of charcoal contraindicated?
After ingestion of hydrocarbons (won't help & inc risk of vomiting & aspiration pneumonitis)
After ingestion of alkali/acidic substances - major concern w/ these is mucosal injury not GI absorption so won't help
Patients w/ trivial or small ingestions (risks of activated charcoal > benefits) or pt that ingested it >1 hour ago
Patients who are not able to protect their own airway
32
Does forced diuresis help in the treatment of acute poisoning?
Probably not - few drugs are excreted unchanged in the urine so increasing urine flow is unlikely to help
HOWEVER - if some cases if we manipulate urine pH AND urine flow - we can increase excretion - examples = salicylates & phenobarbitol (called alkaline diuresis) --> contraindicated if pulmonary or cerebral edema
Use of high volume Ns to treat Li intoxication also common - unclear whether forced saline diuresis for lithium is of extra benefit over simply ensuring normal renal flow
33
When to use hemodialysis to enhance elimination of a drug?
Drugs that are LMW w/ low volume of distribution, are water soluble & not protein bound - ie if a drugs has rapid and thorough tissue distribution, then HD won't work - needs to be in vessels unbound (or if highly protein bound, then protein saturation = free amts of toxin that can be removed (valproic acid))
MC used w/ Lithium
Others: ASA, methanol, ethylene glycol, and sometimes theophylline
Benefits: Corrects metabolic acidosis and fluid/electrolyte abnl as it removes the drugs
34
How can dx of drug overdose be made when pt is unconscious?
Do bedside glucose or administer glucose - positive response = dx hypoglycemia
Miosis, resp depression - administer naloxone - positive response = definitive dx opioid OD
Examine pill bottles, review medical records (medication list), interview family & friends - call pharmacists where prescriptions were filled - dates
Needle track marks - IV ipioid, crack cocaine, or amphetamine
Physical examination - DRY w/ mydriasis = anticholinergic realm. DIAPHORESIS, HTN, hyperthermia - possible sympathomimetic. Tremor - possible SS.
35
Antidote suspected anticholinergic toxidrome
Physostigmine (SOS -help!)
Do not use in TCA overdose or suspected TCA overdose (QRS widening)
36
Antidote cholinergic poisoning
Atropine and pralidoxime (2-PAM)
Atropine dries up pulmonary secretions - direct inhibitor of Ach receptor (direct parasympatholytic)
2-PAM prevents skeletal muscle toxicity by preventing maturing of organophosphate bond
37
Antidote for methanol or ethylene glycol overdose
Ethanol or fomepizole (F-MP)- alcohol dehydrogenase blocking agents - aka prevent metabolism of methanol/ethylene glycol to toxic metabolites
38
Antidote Digoxin OD
Digibind, DigiTAb = DIgoxin immune Fab
MOA: Sequesters all digoxin - can rapidly reverse dysrhythmias and hyperkalemia - full response takes 20 minutes
39
CP Methanol or ethylene glycol poisoning
CP Methanol/ethylene glycol OD = CORGI- dogs often drink b/c tastes sweet
C = CNS toxicity -
HA, AMS, confusion
O = Ocular toxicity -
Decreased visual acuity, retinal edema, hyperemia of disc - can progress to blindness & osmol gap (occurs early, but can be normal)
EG also = Oxalate crystaluria
R = Renal failure (late) -
PROFOUND METABOLIC ACIDOSIS = multi-organ failure, kidneys first
GI symptoms - N/V/ ABD pain
40
Treatment methanol/ethylene glycol OD
Remember - ABCs ALWAYS first - protect airway if decreased level of consciousness
Gastric lavage & charcoal - not effective b/c sm volume & rabid absorption
Acidosis (pH < 7.2) - treat rapidly w/ sodium bicarb or HD
Antidotes: Ethanol, 4-MP (preferred 2/2 ease of use, less ADRs but slows 1/2 life of EG/M so need to be given over period of days)
Inc final step of metabolism to nontoxic substance - pyridoxine (vit B6) & thiamine for ethylene glycol, folate for methanol
41
Toxic dose of methanol
| Toxic dose of ethylene glycol
Methanol - 15-30ml (1-2 Tbsp)
| Ethylene glycol - 1-2ml/kg
42
Indications for hemodialysis in methanol or ethylene glycol OD
HD is most definitive therapy
b/c clears all ethylene glycol/methanol & toxic metabolites from blood & corrects any metabolic acidosis
Indications: Serum pH < 7.2, signs of end organ toxicity (seizures, coma) and renal failure
43
Sx of ASA or salicylate OD
ASPIRIN acronym
Agitation, convulsions, delirium, hallucinations, convulsions etc
Sodium bicarb = tx, spots (petechiae) on eyelids
Pyretic (fever)
Increased anaerobic metabolism = lactic acidosis
Rapid breathing (hyperventilation --> respiratory alkylosis - pulmonary edema
Intestinal irritation - vomiting
Noise in ears - ringing/tinitis
Last three (RIN) = classic salicylism
44
Tx Salicylate OD
Activated charcoal + cathartic +/- lavage - ASA has zero order kinetics - metab at same rate no matter how much you ingest - repeated charcoal may be necessary even > 1 hr - help prevent gastric concretions w/ ongoing absorption
Alkaline diuresis - Sodium bicarb bolus then infusion - reduces fraction of non-ionized salicylate & increases pH gradient with the CSF (prevents entry into CNS) - make blood more basic so acid is pulled from tissues & into blood stream
Correct for hypokalemia (give 20-40mEq) -
Consider hemodialysis in pt who cannot tolerate volume load
45
Salicylate OD - which lab tests to order?
Salicylate level q2 hrs until decreasing trend w/ final level < 20 & pt is asx w/ normal RR
CBC, BMP (look at electrolytes (hypokalemia), BUN/Cr), glucose level, and UA, quantitative APAP level
Consider: PT/INR (coags) and ABG
46
Explain why you could have decreasing serum salicylate and increasing clinical toxicity
Serum salicylate levels do not reflect tissue distribution of the drug
Acidic blood means the salicylate remains unionized and can easily penetrate the BBB = CNS toxicity
Therefore salicylate levels should be interpreted in light of the pt;s clinical condition and a concurrent blood pH - an acidotic pH is a/w toxicity regardless of the salicylate level
47
Indications for hemodialysis in salicylate OD
Persistent, refractory metabolic acidosis (arterial pH < 7.1), renal failure w/ oliguria, cardiopulmonary dysfunction (pulmonary edema, dysrhythmias, cardiac arrest), CNS deterioration (seizures, coma), serum salicylate level >100 at 6hr mark
CONSULT NEPHROLOGY EARLY if pt ingests > 300mg/kg - predictor of severe toxicity - will probably need HD
48
How do you treat respiratory compromise in pt w/ opioid OD?
Resuscitation takes precedence over naloxone administration
Support ventilation w/ bagged mask until naloxone can be administered
Intubate the cyanotic or apneic patient if no response to naloxone
Obtain serum glucose, administer oxygen
49
Which over the counter cold remedy is sometimes abused by teenagers?
Dextromethorphan (DM) is the d-isomer of codeine - metabolite stimulates release of serotonin - which accounts for abuse as a hallucinogen
APAP = common co-ingredient in these meds - should get tylenol level
50
CP Sedative hypnotic intoxication
Slurred speech, ataxia, loss of coordination
Moderate-severe w/ greater CNS depression, respiratory depression (8-10 breaths/min, esp if mixed w/ opioids/ethanol),
51
Treatment of pt w/ toxicity from stimulants
3 C's - take cocaine - tx = calm, cool, uncover complications
Treat agitation/seizures w/ benzos. Treat chest pain after cocaine w/ benzos (NO BETA BLOCKERS= unoppposed alpha agonism = WORSE HTN & coronary artery vasospasm)
Cool (to treat hyperthermia) with evaporation, cooling blankets, and cool IV fluids)
Complications = rhabdo, pyrexia, acidosis, ICH, pneumomediastinum, abd ischemia, & injection-related complications (abscess, endocarditis, cellulitis) - evaluate for thru history, physical exam, and testing - cocain = more likely to cause complications b/c causes direct vasoconstriction
52
How do you treat HTN from stimulant toxicity?
Most HTN from stimulant toxicity is short-lived - treat w/ benzos - if true HTN emergency then add nitroglycerin
53
Which toxic ingestion would cause bradycardia with hypotension (no QRS widening)?
Alpha-agonists:
Cclonidine, guanfacine, oxymetazoline, tetrahydrolozine) - inhibit sympathetic outflow in CNS resulting in hypotensino, bradycardia, pinpoint pupils, and somnolence
Beta blockers w/o sodium channel effects, CCBs, cardiac glycosides (digitalis)
Sedative-hypnotics:
Decrease CNS sympathetic outflow - opioids, benzos, barbiturates - usually minimal brady/hypo unless moderate-severe OD
54
Which toxic ingestion would cause bradycardia with hypotension and WIDE complex QRS?
Quinidine, procainamide, dispropyramide (class 1a antiarrhythmics)
Lidocaine, tocainide (class 1b anti-arrhythmics)
Propafenone, fecainide (class 1c antiarrhythmics)
BB w/ Na+ channel effects (propanolol, metoprolol)
Severe CCB OD = ventricular escape arrhythmias
Hyperkalemia from cardiac clycosides, BBs, and K-sparring diuretics
55
Which toxic ingestion(s) would cause tachycardia & HTN?
Sympathomimietics (amphetamines, cocaine, ephedrine, pseudoephedrine)
Anticholinergics (diphenhydramine & atropine) - decreased vagal tone & agitation from delirium
56
Tachycardia w/ hypotension & wide complex QRS?
TCA - amitriptyline, imipramine, cyclobenzaprine (flexeril)
57
Sx of pt w/ BB/CCB toxicity
BBs compete w/ endogenous catecholamines for receptor sites = blunts normal adrenergic response = bradycardia, AV blocks, hypotension (decreased heart contractility) - similar to CCB overdose
Propanolol = lipid soluble - crosses BBB and can cause seizures & AMS
Some BBs antagonize sodium channels = widened QRS - propanolol, acebutol)
Sotalol = QT prolongation
CCB toxicity also causes hyperglycemia
58
Signs/sx of TCA overdose
MOA: TCA inhibits reuptake of NE & 5HT. Also has anti-histamine, anti-adrenergic, anti-muscarinic and Na+-channel blocking activity
TCA OD si/sx think that the C stands for CARDIAC toxicity & A stands for AMS leading to seizure
Cardiac - tachycardia, prolonged QRS & QT, & PR intervals = torsades (rare), AV block, RBBB, hypotension & myocardial depression --> GET SERIAL EKGs!!!!
Seizures managed w/ benzos
59
Tx TCA Overdose
QRS prolongation - sodium bicarb- sodium overwhelms that Na+ receptor to un-do the TCA blocking effects
Torsades - Mg sulfate
Seizures - benzos
Severe TCA OD - Intravenous lipid emulsion therapy
60
Initial treatment BB/CCB OD
ABCs - airway, breathing, circulation
Symptomatic bradycardia - atropine or pacing
Hypotension - 2L fluid bolus
Refractory brady/hypotension - GI decontamination
Calcium gluconate or chloride (requires central access 2/2 venous necrosis but is 4x more powerful)
Vasopressors (epinephrine)
Glucagon (activates beta-cells)
HDI (high dose insulin)
ILE (intralipid emulsion therapy)
= "Lipid sink" - only works on highly lipid soluble drugs (amiodorone, amitryptiline, fluoxetine, fentanyl, verapamil, amiodipine, propanolol) - binds offending toxin thereby reversing toxicity
61
Uses of digoxin & MOA
Used for CHF and to control ventricular response in atrial tachydysrhythmias
MOA: Inhibits Na+/K+ ATPase - promotes Ca2+ influx via the Na+/Ca2+ exchange pump = increased force of myocardial contraction (positive inotrope)
62
Digitalis toxicity CP
Acute dig intoxication -
N/V/ABD pain, confusion, weakness, hyperkalemia
Chronic dig intoxication -
insidious onset of weakness, anhedonia, loss of apetite, N/V/ABD pain, delirium, confusion, drowsiness, HA, hallucinations, seizure, visual disturbances
Also xanthopsia - blurred, yellow-tinted vision/halos
63
Digitalis toxicity EKG changes
Sinus bradycardia
High degree AV block (AV dissociation)
ST depression - "reverse check" or "salvador dali"mustache
Signs of hyperkalemia
64
What are the indications for DigiFab?
Symptomatic bradycardia, complete heart block, ventricular tachycardia, ventricular fibbrilation
Pt's who seek tx after acute ingestion w/ hyperkalemia or hemodynamically significan dysrhythmias
Give 10-20 vials empirically if critically ill & unknown amt ingested
