Toxicology Flashcards
outline
- basic approach
- toxidromes
- decontamination
- diagnostics
- acetaminophen basics (APAP)
- observation
- toxicology consultation
General approach
- ABCs
- history
- physical examination
- labs, imaging
- diagnosis, antidotes
- disposition
REASSES
-frequently!!
history
- what, when, how, much, why?
- Rx. OTC. herbals, supplements, vitamins
- talk to family, friends, EMS
- pill bottles, needles, beer cans, suicide note
- call pharmacy
- comorbidities
- allergies, medical problems
physical examination
- vital signs: BP, HR, RR, temp, O2 sat
- mouth- odors, mucous membranes
- pupils
- breath sounds
- bowel sounds
- skin
- urination/defecation
- neurologic exam
essential laboratory tests
- electrolytes:
- hyponatremia – lithium intox from DI, amitriptyline
- hypokalemia – theophylline, B2 agonist, acidosis
- glucose- BB, caffeine, theophylline – can cause hyoglycemia
- propanol, insulin, salcylates – can cause hyperglycemia
- BUN and creatinine- renal
- LFTs- tylenol, arsenic, ethanol, iron, valproic acid
- CK- rhabdo, rigidity, arrhythmias - PCP, cocaine, amphetamines
- urinalysis, urine drug screen- hemoglobinuria, myoglobinuria, crystalluria
- Etoh, alcohol screen
- acetaminophen, salicylates
- specific drug levels
- pregnancy tests
prolonged QRS
- TCAs (tricyclic antidepressant)
- phenothiazines
- calcium channel blockers
sinus bradycardia/AV block
- beta blockers, calcium channel blocker
- TCAs
- digoxin
- organophosphates
ventricular tachycardia
- cocaine, amphetamines
- chloral hydrate
- theophylline
- digoxin
- TCAs
acetaminophen **
antidote- N-acetylcysteine
- usually IV
- common overdose with pediatrics
organophosphates **
antidote- atropine (anticholinergic)
- pupils dilated, lacrimation, vomiting (everything coming out)
- chemicals, hazmat
anticholinergic **
-antidotes- physostigmine
benzodiazepines **
-antidote- flumazenil
beta blockers**
- antidote- glucagon
- beta blockers are BP medications -> BP will be too low
calcium channel **
-antidote- calcium
carboxyhemoglobin **
antidote- 100% O2
opioids
- antidote- naloxone (narcan)
- IV, up nose
- fentanyl
- pale, pinpoint pupils, altered
- decompensate
- oxycodone
salicylate (ASA)**
-antidote- alkalization
TCAs ** (tricyclic antidepressants)
- antidote- sodium bicarbonate
- respiratory distress
warfarin**
-antidote- FFP, vitamin K
diagnosis
- may not identify ingested substances
- provide ABCs and supportive care
- give antidote when appropriate
- call regional poison control center
unconscious unresponsive patient in the EM…
- ABCs
- blood work
- urinalysis (catheter)
- call friends, family, pharmacy, neighbors, primary MD
- just by look at a pill you can google it
- be skeptical if patient is lying (especially suicidal)
establish a pattern to his symtpoms
- toxic syndrome
- aka TOXIDROME
toxidrome
not every drug fits into a broad based category
- lots of meds have unique effects not easily grouped
- 5 basic toxidromes:
- sympathomimetic
- optiate
- anticholinergic
- cholinergic
- sedative hypnotic
toxidromes: sympathomimetic
- cocaine
- methamphetamine/amphetamines
- ecstasy (MDMA)
- ADHD meds like Ritalin, Adderall
- ephedrine
- caffeine
- excessive sympathetic stimulation involving epinephrine, norepinephrine, and dopamine
- excessive stimulation of alpha and beta adrenergic system
- tachycardia
- arrhthmias
- hypertension
- ICH
- confusion with agitation
- seizures
- rhabdomyolysis- renal failure can result
sympathomimetic treatment
- supportive care- monitor airway, diagnose ICH, rhabdo
- IVF for insensible loses and volume repletion
- Benzos!!!!
- BP management if severe
- CNS excitation -> behavioral agitation -> cardiac excitation ->
toxidrome: opiate
opiate- derived directly from the opium poppy
- morphine and codeine
- much broader class of agents that are capable of producing opium like effects or of binding to opioid receptors
- deadly- respiratory, cardiac arrest
- heroin
- methadone
- hydrocodone
- oxycodone
- fentanyl
risks of opiates
- coma
- miosis
- respiratory depression
- peripheral vasodilation
- orthostatic hypotension
- flushing (histamine)
- bronchospasm
- pulmonary edema
- seizures
opioid treatment
- competitive opioid antagonist- naloxone
- goal of return of spontaneous respirations sufficient to ventilate the patient appropriately
- may have to re-dose as opiates may act longer than antagonist
- there are other longer acting opioid antagonists such as nalmefene and naltrexone but these are not often used
toxidrome: anticholinergic
- ACh receptors are either nicotinic or muscarinic
- the anticholinergic drugs just block the muscarinic receptors (SLUGEM)
- some have argued that the anticholinergic poisoning syndrome should be called the antimuscarinic poisoning syndrome because you do not see anti-nicotinic symptoms
what does wrong with anticholinergics
- CNS muscarinic blockage:
- confusion
- agitation
- myoclonus
- tremor
- picking movements
- abnormal speech
- hallucinations
- coma
- peripheral muscarinic effects:
- mydriasis
- anhidrosis
- tachycardia
- urinary retention
- Ileus
anticholinergics treatment
- supportive care- IVF to replace insensible losses from agitation, hyperthermia
- benzos to stop agitation
- physotigmine:
- induces cholinergic effects
- short acting
- may help with uncontrollable delirium
- do not use if ingestion not known -> danger with TCAs
toxidrome: cholinergic
- D- diarrhea
- U- urination
- M- miosis
- BBB- bradycardia, bronchorrhea, bronchospasm
- E- emesis
- L- lacrimation
- S- salivation
- S- salivation
- L- lacrimation
- U- urination
- D- diaphoresis
- G- gastrointestinal upset- vomiting, diarrhea
- E- eye- miosis
toxidrome- cholinergic treatment
- antagonize muscarinic symptoms- atropine
- stop aging of enzyme blockage- 2-PAM
- prevent and terminate seizures- diazepam
- supportive care
toxidrome- sed-hypnotic
different agents have different mechanisms
-may interfere in the GABA system
sed-hypnotic- what goes wrong
- CNS depression
- lethargy
- can induce respiratory depression
- can produce brady cardia or hypotension
sed-hypnotic treamtent
- supportive care
- be wary of the benzo “antidote” flumazenil
- is an antagonist at the benzo receptor
- RARELY INDICATED
- if seizures develop either because of benzo withdrawal, a co-ingestant or metabolic derangements, have to use 2nd line agents, barbiturates, for seizure control
agitated, pupils 8 mm, sweaty, HR 140s, BP 230/130
-sympathomimetic
unarousable, RR 4, pupils pinpoin
-opiate
confused, pupils 8mm, flushed, dry skin, no bowel sounds, 100 cc output with foley (not urinating a lot)
-anticholinergic
vomiting, urinating uncontrollably, HR 40, Pox 80% from bronchorrhea, pupils 2mm
-cholinergic
lethargic HR 67, BP 105/70, RR 12, pupils midpoint
-sedative hypnotic
basic approach
- airway, breathing, circulation
- establish IV, O2 and cardiac monitor
- consider coma cocktail- D50, Narcan
- evaluate history and a thorough physical exam
- look at vitals, pupils, neuro, skin, bowel sounds
- gives you hints regarding the general class of toxins
- guides your supportive care
- draw blood/urine for testing
- time to consider decontamination options
ordering diagnostic studies
- acid base status
- renal function
- liver function
- cardiac conduction- EKG
- drug levels- based on history or clinical findings
- any toxin specific findings- CK for cocaine, etc.
EKG
- evaluate QRS and QTC presence of blocks, rhythm
- QTc > 450 and a QRS > 100 can be concerning for toxin induced (eg TCAs) cardiac abnormalities
specific toxins
- acetaminophen- tylenol
- salicylates- aspirin
- tricyclic antidepressants (TCA)
acetaminophen (apap)
- max dose- 4g/day for adults
- 90 mg/kg day kids
- peak serum levels- 4 hours after overdose
- toxicity- 140mg/kg acute ingestion*****
- direct hepatocellular toxicity (liver)*
- can also have renal damage and pancreatitis
stages of tylenol toxicity
- 1 (0-24 hours): n / v, but most asymptomatic
- 2 latent stage (24-48 hours): subclinical increase in ast/alt/bilirubin
- 3- hepatic stage (3-4days): liver failure, ruq pain, vomiting, jaundice, coagulopathy, hypoglycemia, renal failure, metabolic acidosis
- IV recovery stage (4days-2weeks): resolution of hepatic dysfunction
- dont really need to know
need 4 hour level (peak) and N-acetylcysteine (NAC)
- Dx- 4 hour level compared to the Rumack and Matthews nomogram
- 150ug/ml at 4 hours
- Rx- NAC 140mg/kg** then 70mg/kg every 4 hours for 17 doses
- we have PO and IV dosing
- only useful for one time ingestion (not chronic ingestion)
- if time of ingestion unknown, drawl level immediately and again at 2-4 hours
- labs- LFTs (liver function-> bilirubin), coags, lytes, aspirin, ETOH, tox screen
N-acetylcysteine (NAC) indications
- ingestion with potential toxicity
- late presentations with potential or ongoing toxicity
- chronic overdose with evidence of hepatic damage
Acetaminophen (APAP) levels
- if your patient is toxic on the nomogram- start NAC
- if your patient does not have a known time of ingestion- start NAC
- if your patient took multiple rounds of APAP- start NAC
- if you have any question about the history…start NAC
Tylenol overdose disposition
- admit if…
- known toxicity / potential toxic levels
- lab evidence of hepatic damage
- unknown time of ingestion and sx consistent with toxicity
- unknown ingestion time with measurable acetaminophen levels
salicylates (asa)
- aspirin
- weak acid, rapidly absorbed
- messes up acid base balance
- enteric coated has delayed absorption
- toxic dose- 160 mg/kg
- lethal dose 480 mg/kg
- mixed respiratory alkalosis- metabolic acidosis
- stimulates respiratory drive causing hyperventilation, but limits ATP production -> metabolic acidosis
salicylates symptoms
- tachypnea, tachycardia, hyperthermia
- resp alkalosis-metabolic acidosis
- altered serum glucose
- AG metabolic acidosis (MUDPILES)
- dehydration (vomiting, tachypnea, sweating)
- Abd pain/ n/v
- tinnitus, hearing loss
- lethargy, seizures, altered mental status
- noncardiogenic pulmonary edema
evaluation of ASA overdose
- lytes, ABG, LFTs, CBC, preg test, urine pH
- bicarbonate, CO2 levels -> acid base levels
- serum salicylate levels (toxicity at 25mg/ dl)
- toxicity correlates POORLY with levels
- evaluation with DONE nomegram based on single ingestion of regular ASA at levels drawn 6 hrs after ingestion
- underestimates toxicity in cases of severe acidemia or chronic ingestion
therapy for ASA overdose
- ABCs
- activated charcoal
- urinary alkalinization (start if serum level is greater than 35mg/dl)
- 3 amps bicarbonate in 1 L D5W at 150 ml/hr
- neutralize acid base imbalance
- by increasing urinary pH to greater than 8, ASA gets trapped in tubes and cannot be reabsorbed
- dialysis for severe acidemia, volume overload, pulmonary edema, cardiac or renal failure, seizures, coma levels > 100 mg/dl in acute ingestion, or > 60-80 mg/dl in chronic ingestion
disposition for ASA overdose
- pt gets charcoal and remain asymptomatic after 6-8hours = possible D/C
- sustained release requires longer observation period
- pts with toxic levels, symptomatic, or develop symptoms = admission
TAC (tricyclic antidepressants)
- leading cause of death by intentional overdose
- blocks sodium channels
- respiratory depression
- death by cardiovascular dysrhythmias and cardiovascular collapse
- most TCAs have anticholinergic effects- dry skin, blurry vision , hot
- severe OD- hypotension, ,seizures, respiratory depression
- in severe cases- ARDS, rhabdomyolysis, DIC
treatment of TCA overdose
- Get an EKG
- Sodium Bicarbinate
- Initial bolus of 2 amps
- Drip 3 amps in 1 L D5W at 150 ml/hr
- Titrate for serum pH of 7.45-7.5
- IV fluids
- Lidocaine for perisistent arrhythymias
other tox labs
- Strongly consider ASA on every overdose
- Not as silent as APAP can be but initial signs can be subtle
- Urine drug screen -Little benefit but makes consultants feel better
- EtOH level - Poor form to miss something as common as too much beer
- Specific drug or toxin levels as indicated:
- Know what you are looking for and how to order it
- There is no such thing as a comprehensive drug screen
observation period
- Normal labs, normal EKG, normal exam, no history of extended release drug
- Approximately 6 hours
- Extended release medications, buprorion, oral hypoglycemics involved
- Depending on agent, 12-24 hours