toxicology Flashcards

(42 cards)

1
Q

activated charcoal

Activated charcoal administration, whole bowel irrigation,
urinary alkalinization, and hemodialysis - Recall the indications for poison management

A

CHARCOAL:
-direct binding -> doesnt affect anything in blood (alcohol)
-do within 1 hour of ingestation
- useful in: acetaminophen, TCA, salicylates, barbituates, SSRIs, digoxin, warfarin/rat poison
- complication: aspiration
-CI: AMS, ileus, obstruction
-Poorly binds: Heavy Metals:
(iron, lead, mercury), Lithium, Cyanide, Hydrocarbons (pesticides), Liquids (Alcohols, Alkali / Acids, Caustics)

🦑 Activated Charcoal
📌 Mechanism
Adsorbs toxins in the GI tract, preventing absorption.

Does not enter the bloodstream — only works in the gut.

⏱️ Indication
Use within 1 hour of ingestion of a known toxic substance.

Best for:

Acetaminophen

Aspirin (salicylates)

Many prescription drugs (e.g., TCAs, antiepileptics)

❌ Does NOT bind well to:
(Memory aid: CHILLS = Charcoal Hates Iron, Lithium, Lead, Solvents)

Cyanide

Hydrocarbons (e.g., gasoline, pesticides)

Iron

Lithium

Lead

Solvents (alcohols, alkalis, acids, caustics)

🚫 Contraindications
AMS without protected airway (risk of aspiration)

GI obstruction or ileus

Caustic ingestion (can obscure endoscopy and worsen injury)

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2
Q

whole bowel irrigation, chelating agents

A

WHOLE BOWEL IRRIGATION:
-MC
-flush out GI with diarrhea
-polyethylene glycol (miralax)
-Good for sustained release like iron, lithium, lead, drug packers
-CI- ileus or obstruction

chelating agents:
* Used for heavy metal poisoning
* Combines with metallic ions to form complexes that are easily excretable
* Examples:
* Dimercaprol (BAL): Arsenic, mercury, lead
* Dimercaptosuccinic acid (DMSA): lead, arsenic, mercury
* Penicillamine: Copper toxicity, occasionally gold or arsenic
* Ethylenediaminetetraaceticacid (EDTA): Lead poisoning
* Deferoxamine: Iron poisoning*

🚽 Whole Bowel Irrigation (WBI)
📌 Mechanism:
Rapid GI cleansing by inducing diarrhea using polyethylene glycol (PEG) (e.g., GoLYTELY, MiraLAX).

✅ Indications:
Sustained-release or enteric-coated drugs

Heavy metals (iron, lithium, lead)

Body packers (drug smugglers)

Drugs poorly adsorbed by charcoal

❌ Contraindications:
Ileus

Bowel obstruction

GI bleeding

Unstable patients or compromised airway

⚛️ Chelating Agents
📌 Purpose:
Used for heavy metal poisoning

Chelators bind metals → form water-soluble complexes → excreted in urine or bile

🧪 Key Chelators & Indications:
Agent Used For Notes
Dimercaprol (BAL) Arsenic, Mercury, Lead IM injection, used with EDTA for lead
DMSA (Succimer) Lead, Arsenic, Mercury Oral; preferred in kids with lead
Penicillamine Copper toxicity (e.g., Wilson’s disease)
Also used for gold or arsenic Oral, rarely used due to side effects
EDTA (CaNa2EDTA) Lead poisoning IV or IM, often with BAL
Deferoxamine Iron poisoning IV/IM; urine turns orange (“vin rose”)

🎯 Quick Associations:
Iron → Deferoxamine

Lead → EDTA + BAL (or DMSA in mild/moderate cases)

Arsenic/Mercury → BAL or DMSA

Copper → Penicillamine

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3
Q

urine alkalinization and hemodialysis: indication for poison management, CI

A

URINE ALKALINIZAITON:
-things already been absorbed
-indications: SALICYLATES! (ASA), phenobarbital, INH**
-urine goal pH 7-8
-sodium bicarb infusion
-CI- renal failure, pulmonary edema, cerebral edema, volume overload

HEMODIALYSIS:
-good for low protein binding, low molecular wt, small volume of distribution, water solubles
-drugs that already absorbed
-works for most things
-I-STUMBLED:
-!Isopropyl alcohol, iron, INH
-!Salicylates
-Theophylline
-Uremia
-Methanol
-Barbiturates
-Lithium
-!Ethanol/ethylene glycol
-Depakote (valproic acid)

💧Urinary Alkalinization
✅ What it is:
Alkalinizing the urine with IV sodium bicarbonate to enhance renal excretion of weak acids.

📌 Indications (Best for weak acids):
Mnemonic: “PI-S”

Phenobarbital

Isoniazid (some sources)

Salicylates (most important – aspirin)

🎯 Goal urine pH: 7.5–8.0
❌ Contraindications:
Renal failure – can’t excrete bicarbonate

Pulmonary edema or volume overload

Cerebral edema – alkalosis can worsen swelling

🩸 Hemodialysis
✅ When to use it:
For drugs that are:

Low molecular weight

Low protein binding

Small volume of distribution (Vd)

Water-soluble

💡 These characteristics make toxins easier to remove from the blood.

📌 Mnemonic: I STUMBLED
Letter Toxin
I Isopropanol, Iron, INH (Isoniazid)
S Salicylates
T Theophylline
U Uremia (ESRD, not poison but indication)
M Methanol
B Barbiturates
L Lithium
E Ethylene glycol, Ethanol
D Depakote (Valproic acid)

These are all absorbed poisons — dialysis removes them from blood, unlike charcoal.

❌ Hemodialysis Contraindications (relative):
Hemodynamic instability (though sometimes tolerated)

Severe coagulopathy (bleeding risk from HD access)

High protein-binding or large Vd toxins (e.g., TCAs, digoxin)

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4
Q

gastric decontamination - Recall the indications for poison management

A

Gastric decontamination = functionally removing an ingested toxin from the GI tract in order to decrease its absorption

May be beneficial in the following patients:
* Early ingestion ( <1 hour from ingestion benefit the most)
* Delayed release products
* Not fully absorbed yet

Most patients will not benefit from gastric decontamination:
* Time of presentation is past the window of potential benefit
* Ingestion of non-toxic substances
* Ingestion of non-toxic amounts of toxic substances

options:
- activated charcoal
- whole bowel irrigation: good for sustained release products
- chelating agents: heavy metal poisoning (BAL - dimercaprol; (DMSA))
- urine alkalinization: enhances elimination
- hemodialysis: good for low protein binding drugs, LMW, small volume distribution, water soluble

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5
Q

Anticholinergics overdose signs and sx, EKG findings and their tx

  • [ ] Recognize the signs and symptoms of anticholinergic toxicity
    - [ ] Recognize the medications or exposures that can cause anticholinergic toxicity
    - [ ] What are the ECG findings in TCA toxicity and its treatment? If refractory?
A

-MCC- ANTIHISTAMINES, antidepressants (TCAs), anti-psychotics
-atropine, phenothiazines, parkinsonian drugs, scopolamine, jimsonweed
-!Blind as a bat, mad as a hatter, red as beet, dry as a bone, hot as Hades”
-Blurry vision, delirium, FLUSHED BUT DRY SKIN, hyperthermia, dry mucus membranes
-mydriasis (dilated pupils!), hypoactive bowel, URINARY RETENTION, agitation, seizures

ECG:
- sinus tachy (common)
- wide complex tachycardias: tx = SODIUM BICARB**
- ventricular dysrhythmias: tx = lidocaine,amiodarone
- torsades de pointes: MAGNESIUM
-Wide QRS >100ms, terminal R wave, right axis deviation

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6
Q

anticholinergics OD tx and EKG finding tx

  • [ ] Be able to determine when first- and second-line medications for anticholinergic toxicity are required, and what those medications are.
A

-supportive- fluids and COOLING
-mainstay of tx = BENZODIAZEPINES
-second line: physostigmine!! for refractory sx of seizures, hyperthermia, dysrhythmias
-> CI in heart block and TCA overdose

ekg:
-ventricular dysrhythmias -> lidocaine, amiodarone
-torsades -> Mg
-wide complex tachy -> sodium bicarb!!!

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7
Q

Tricyclic antidepressants (TCA): MOA, drug names, sx

A

-self poisoning ANTICHOLINERGIC
-drugs: Amitriptyline, nortriptyline, cyclobenzaprine
-MOA: Inhibits reuptake of norepinephrine and serotonin, sodium, histamine, muscuarinic, alpha 1, potassium, GABA
-Blood or urine TCA
->5mg/kg – average toxic dose
->10-20mg/kg- severe

Anticholinergic effects
-!!3 C’s = Cardiac abnormalities, Convulsions, Coma*
-CV effects: hypotension, tachy, wide QRS, V-tach, torsade’s
-!!!!ECG - most useful in determining severity
-!sinus tachy
-!wide QRS >100ms (seizures)
-prolonged QT
-!Wide terminal R wave in aVR
-hypotension

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8
Q

tca od tx

A

-ABCs
-intubation bc LOC
-NG tube -> charcoal!
-QRS >100ms, ventricular dysrhythmia -> !!!Sodium bicarb IV bolus -> infusion! -> lidocaine! if refractory + arryhthmia
-hypotension -> crystalloids! + norepinephrine (reverse alpha1 blockage)
-seizures -> (GABA-A inhibition) -> BENZOS!! (diazepam, phenobarbital) -> !!!physostigmine!!! if refractory

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9
Q

Cholinergic: sx

  • [ ] Recognize the signs and symptoms of cholinergic toxicity
    - [ ] Recognize the exposures or medications that can cause cholinergic crisis
    - [ ] Order the correct treatment for cholinergic crisis
A

sx:
-!!!Killer Bs: BRADYCARDIA, Bronchospasm, and BRONCHORHEA (frothy mouth)
-weakness, fasciculations, resp failure, wheezing
-people that work with chemicals or landscapers (insecticides)
-VERY WET PTS
-SLUDGE- saliva, lacrimation, urinartion, diarrhea, GI dysmotility, emesis
-DUMBBELLS- DIAPHORESIS, urine, miosis, bradycardia, emesis, lacrimation, lethargy, salivation
-nictoinic effects- FASCICULTIONS, weakness, paralysis

-Causes: !Organophosphate poisoning (insecticides)!, chemical warfare agents (nerve gas like sarin)

Tx:
-!Decontamination -> use PPE
-ABCs
-elevate head of the bed
-Antidotes: ATROPINE! and 2-PAM (PRALIDOXIME)!
-Atropine -> reduce muscarinic effects
-2-5 mg q 5-10 min until !secretions are dry!
-Increases HR
-Pralidoxime or 2-PAM -> reverse paralysis and fasciculations

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10
Q

cholinergics: causes and tx

  • [ ] Recognize the signs and symptoms of cholinergic toxicity
    - [ ] Recognize the exposures or medications that can cause cholinergic crisis
    - [ ] Order the correct treatment for cholinergic crisis
A

-Causes: !Organophosphate poisoning (insecticides)!, chemical warfare agents (nerve gas like sarin)

Tx:
-!Decontamination -> use PPE
-ABCs
-elevate HOB
-Antidotes: ATROPINE! and 2-PAM (PRALIDOXIME)!

Atropine -> reduce muscarinic effects
-2-5 mg q 5-10 min until !secretions are dry!
-Increases HR

Pralidoxime or 2-PAM -> reverse paralysis and fasciculations

sx:
-!!!Killer Bs: Bradycardia, Bronchospasm, and Bronchorrhea
-weakness, fasciculations, resp failure, wheezing
-people that work with chemicals or landscapers (insecticides)
-VERY WET PTS
-SLUDGE- saliva, lacrimation, urine, diarrhea, GI dysmotility, emesis
-DUMBBELLS- diaphoresis, urine, miosis, bradycardia, emesis, lacrimation, lethargy, salivation
-nictoinic effects- fasciculations, weakness, paralysis

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11
Q

Opioids oD: cause, sxs

A

Causes: morphine, heroin, fentanyl, Demerol, codeine, diphenoxylate (Lomotil), propoxyphene (Darvon), hydrocodone (Vicodin), Percocet (careful of Tylenol addition), etc.
-Caution: Clonidine can mimic opioid overdose (pinpoint pupils and hypoventilation) -> also reversed with high dose naloxone (10mg)

sx:
-PINPOINT pupils + not breathing = opioids
-Resp depression! (<12) -> respiratory arrest!!!
- BRADYCARDIA*
- miosis
- lethargy
- hypotension
- coma
- noncardiogenic pulmonary edema
- N/V in opioid naïve patients
- ileus
-some cause agitation and dilated pupils such as dilaudid, Demerol, diphenoxylate
-Death by apnea!

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12
Q

opiods OD: PE, dx, tx

A

PE:
- Pinpoint pupils, lethargy, RR<12 breaths/min
- Look for circumstantial evidence of opioid use: needle marks, drug paraphernalia (undress), tourniquets, fentanyl patches (mucus membranes), witnesses

Dx- urine can be positive 2-4 days after

Tx:
-NALOXONE (opiod antagonist)
-Intranasal: 1mg each nostril (total 2mg)
-IV start with 0.4mg if mild-moderate depression, 2mg if apneic
-repeat q 2-3 mins up to 10mg due to opioid longer half life
- may cause an ALI that resolves within 24 hrs

discharging someone with opiod use disorder:
Addiction medicine referral
Fentanyl test strips
Naloxone
Buprenorphine
Suboxone
Methadone

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13
Q

opiod withdrawal

A
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14
Q

toxidrome chart summary:
- sympathomimetic
- anticholinergic
- cholinergic
- sedative/hynotic
- opiod

A
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15
Q

full toxidrome charts: opiods and sympathomimetics and cholinergics

A
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16
Q

full toxidrome charts: anticholinergics and salicylates

A
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17
Q

hypoglycemia and serotonin syndrome toxidrome chart

18
Q

toxic alcohol: METHANOL
causes, sx, tx

A

Anion gap metabolic acidosis + increased osmolal gap

-paint thinner, car window wash, wood alcohol, gas tank additive
-sx delayed 12-18 hrs
-!BLINDNESS from disc hyperemia!, seizures, resp failure, N/S, pancreatitis, visual changes, ataxia, AMS

Tx:
-1. !!Fomepizole (4-methylpyrazole)
-excretes via kidneys
-temporizing until dialysis
-2. !Ethanol- competitive inhibition
-!!Dialysis and bicarbonate if severe acidosis + refractory to 4-MP or ethanol therapy

19
Q

-ETHYLENE GLYCOL:

A

-ANTIFREEZE, moonshine, paints, solvents, windshield wiper fluid
-will have NO SMELL BUT APPEAR INTOXICATED

-oxalic acid -> forms calcium oxalate crystals! -> acidosis and kidney injury
-<12 hrs: Intox + CNS depression!! w/o odor
-12-24 hrs: Tachy, HF/pulm edema
-24-72 hrs: ATN, anuria, flank pain, hypocalcemia, hematuria
-Wood’s lamp - green glowing urine, d/t calcium oxalate crystals

Tx:
-FOMEPIZOLE - inhibits alcohol dehydrogenase
-HEMODIALYSIS if severe
-THIAMINE & PYRIDOXINE
-Both are consumed in the metabolism of ethylene glycol and need supplementation

20
Q

-ISOPROPYL ALCOHOL:

A

-Rubbing alcohol (mouthwash, ginseng shots, NyQuil)
-CNS depression worse than ethanol
- Hallmark: Normal anion gap, increased osmolar gap , Ketosis with normal glucose**
-!Hemorrhagic gastritis, pulmonary edema, hypoglycemia
-Severe hypotension

tx:
-Supportive care, don’t give alcohol
-Hemodialysis (if severe)

21
Q

flowchart of toxic alcohol ingestion

22
Q

toxic alcohol overview: when to consider it and how to calculate the osmolol gap

A

Toxic metabolites produced by alcohol dehydrogenase which can be inhibited by ethanol or fomepizole. These all cause inebriation.

Consider toxic alcohol if there is an unexplained anion gap or ↑ osmolar gap

Methanol and Ethylene glycol will produce an anion gap. Isopropyl alcohol will NOT.
-Ethanol < isopropyl alcohol < ethylene glycol < methanol (order of increasing alcohol toxicity)
- Drunk + Anion gap metabolic acidosis + osmolol gap = ethylene glycol or methanol poisoning
- Drunk + osmol gap = isopropyl

23
Q

acetaminophen (paracetamol) overdose overview pathophys and labs to order, when can you use the normogram

pathophysiology of acetaminophen toxicity

A

-!toxic dose = >150mg/kg
-Hepatic metabolism via CYP450 to NAPQI –> highly toxin that damages liver
-Normally, NAPQI combines with thiols to produce non-toxic metabolites
-In overdose -> thiol stores are depleted -> NAPQI accumulates

Dx:
-!LFTs (serial)
-Coagulation profile (PT/PTT/INR)
-CBC
-anion gap, ABG
-Renal study
-APAP LEVEL
-!>140u/mL 4 hours after ingestion is TOXIC -> tx with NAC
-Rumack-Mathew normogram -> for !Acute SINGLE ingestion ONLY within 4-24hrs and NON-extended release product -> need to know exact timing

24
Q

acetaminophen 4 stages of injury - what sx

A

-NO characteristic PE findings
-stage 1- first 24hrs -> N/V, abdominal pain
-stage 2 (latent)- 24-48hrs, GI sx resolve (asymptomatic!), hepatic/renal dysfunction begins (high AST/ALT bilirubin INR)
-stage 3- 3-4 days, LFTs peak, coagulopathy, renal failure, fulminant hepatic failure, encephalopathy, sepsis, coma, death
-stage 4: 4 days-2wks, recovery if survive stage 3

25
acetaminophen OD tx
-ABCs -activated charcoal within 8-12 hrs Antidote: !N-acetyl-cysteine (NAC)! -> Dose: 140mg/kg!, Detoxes and decrease NAPQI -Very effective when given EARLY – !within 8hrs of ingestion! -Equally effective at 1hr vs 7hrs post ingestion -still indicated in late presentations >24hrs - safe in pregnancy - charcoal does not inhibit effectiveness Dialysis (rare): severe (>1000mg/L), AMS, metabolic acidosis, elevated lactate Transplant = liver failure Discharge pt if unintentional, no hepatotoxicity, downtrending APAP levels that nontoxic after tx (<150 @ 4hrs or below nomogram)
26
NAC indications
-Significant reported ingestions (single ingestion >150mg/kg) -4 hour level (or more) APAP lies above the nomogram cutoff (>140mcg/mL) -APAP ingestion presenting close to the 8hr cut off -Evidence of hepatotoxicity presumed to be from APAP -A serum APAP >10mcg/mL and unknown ingestion time -There is technically no “cut off” time to start NAC
27
alcohol intoxication
-NOT toxic -CNS depressant- down regulates GABA and upregulates NMDA -!intox level - 80-100mg/dL -always r/o other causes of AMS -> POC glucose, consider head CT, fx (trauma), other drugs, electrolytes, ammonia, etc. -!Ataxia, slurred speech, horizontal nystagmus, alcohol on breath (AOB) Tx- supportive
28
Wernickes encephalopathy vs Korsakoff syndrome (not on test) ## Footnote Know Wernicke’s encephalopathy, Korsakoff syndrome
Wernicke- -B1 (thiamine) deficiency from chronic alcoholism and poor nutritional intake -tachy, HTN, tremor, hallucination, seizures, delirium tremens -triad = oculomotor abn (CN6 palsy), ataxia, global confusion - reversible -COAT- confusion, oculomotor abnormalities (nystagmus, CN 6 plasy), ataxia, thiamine def -tx- IV thiamine for 3 day Korsakoff syndrome: -untreated wernickes and untreated thiamine deficiency - irreversible -RACK- retrograde amnesia, anterograde amnesia, confabulation (fabricated memories to fill in gaps), korsakoff psychosis
29
alcohol withdrawal (also benzos and barbs) sx (whats the withdrawal timeline)
benzos, booze, barbs withdrawals = fatal sx: CNS hyperexcitation -TACHYCARDIA, HTN, AGITATION - diarrhea, mydriasis, insomnia, cramps, diaphoresis, piloerection -6-12 hrs: early uncomplicated -> minor sx- anxiety, intention hand tremors that dont fatigue, tongue fasciculations, insomnia -> ASK WHY -tx- benzos -12-24hrs: hallucinosis -> hallucinations (tactile > auditory or visual) -24-48hrs: seizures -> generalized tonic-clonic convulsions -chronic alc (not binge) -r/o head trauma/bleed, poisoning, epilepsy, CNS infection, metabolic -tx- benzos only -48-72hrs: delirium tremens -> !disorientation/confusion! - must have disturbances in CONSCIOUSNESS OR COGNITION, hallucinations, hyperthermia, hyperreflexia, tachycardia, resp alk - low K and Mg and hypovolemia -mortality 5% -if A&O = not delirium tremens - tx = benzos - valium
30
alcohol withdrawal dx and tx
Dx- CIWA score; higher score = more severe withdrawal; done hourly Tx - BENZOS: diazepam, lorazepam, midazolam, chlordiazepoxide - if severe: titrate benzo to achieve state of sedation with arousability to minimal stimulation - phenobarbital (if resistant) - propofol if intubation - clonidine: HTN, tachycardia - IV fluids with dextrose, thiamine, multivitamins, Mg replacement
31
alcohol withdrawal: early phase
* Ask- WHY did they stop drinking? * Tremulous, anxious, agitated * Intention hand tremor, that is constant and does not fatigue * Tongue fasciculations are more sensitive * Early as 6 hours, Peaks at 24-36 hours, resolves at 2-3 days Treatment: * Benzodiazepines * Assess readiness for rehab * Reassess with CIWA score * <8 can be managed outpatient
32
alcohol withdrawal seizures
* 1-48 hours after decrease/cessation of alcohol consumption * Usually 1-6 seizure episodes * Generalized tonic-clonic w/ shorter post-ictal time (few minutes) * Prolonged seizures, localizing findings, focal seizure, or status epilepticus – look for other cause!!! * Low threshold to scan, and look for other trauma (CT head noncontrast) * Usually chronic alcoholics (not binge drinkers) Treat: - benzos to reduce recurrent AWDS - No role for antiepileptics unless hx of epilepsy
33
alcohol withdrawal syndrome: delirium tremens vs hallucinosis (not on test - Differentiating between alcoholic hallucinations and delirium tremens)
12-24 hrs: alcohol hallucinosis (TACTILE > auditory, visual) - feeling things that aren't there (bugs on skin) 48-72 hrs: delirium tremens - DISORIENTATION/CONFUSION** - hallucinations - hyperthermia - tachycardia - mortality up to 50%
34
delirium tremens overview, management
* Late occurrence: 2-4 days after stopping/decreasing alcohol * 1-15% mortality rate * Symptom complex: * Must have disturbance in CONCIOUSNESS or COGNITION ** * (if they are awake and alert its not DT) * Accompanied by tremor, agitation, delusions, hallucinations, fever, tachycardia, diaphoresis, seizures, hyperreflexia * Respiratory alkalosis from hyperventilation * Hypovolemia common * Hypokalemia and hypomagnesemia common Management: * R/O other causes of AMS * head bleed, infxn, GIB, Liver dz, neuro * General measures (can be applied to any alcoholic): * IVF * Thiamine 100mg IV * Multivitamin PO/IV * Magnesium 2-4g IV * Dextrose if needed 1st line medical option: Benzodiazepines (used for all alcohol withdrawals) - GABA agonist: sedates the patient - Valium (diazepam): Fastest onset 1-5 minutes; 5-10mg IV diazepam - Ativan (lorazepam) - Versed (midazolam) - Librium (chlordiazepoxide): PO only, 50-100mg, slow onset and long half life, ideal for outpatient setting Phenobarbital: Barbiturate for benzo-resistant alcohol withdrawal Propofol is preferred induction agent if intubating
35
ASA overdose tx
-ABCs, O2 PRN, monitor -IV fluids with glucose for CNS hypoglycemia (D5W) -!Decon: Activated charcoal -!Urine alkalinization with !SODIUM BICARB! infusion (urine pH > 8) -check K -> hypokalemia prevents alkalinization -DONT do in CHF or renal failure pts bc of volume load -goal serum pH of 7.45-7.55 or a urine pH of 7.50-8.0 Hemodialysis!: -!!pulmonary edema, cerebral edema (severe confusion/AMS, seizure, coma), renal failure, acidemia, level >100mg/dL (acute) or > 60mg/dL (chronic)
36
ASA overdose overview where is it found, toxic dose, sx, lab orders, what is the COD RECOGNIZE SX OF ACUTE VS CHRONIC TOXICITY
-Aspirin, Oil of WINTERGREEN, Bengay, Air fresheners, mouthwash -Toxic dose = 300mg/kg -!Acute toxicity: N/V, DIAPHORESIS, FEVER, TACHYCARDIA, TACHYPNEA! ** -> RESPIRATORY ALKALOSIS with AG metabolic acidosis -!Chronic toxicity: TINNITUS, GI irritation, AMS*** (think elderly w long term salicylate use with ear ringing, GI sx, AMS, NO HYPERVENTILATION) -Severe: Cerebral and pulmonary edema, HYPOGLYCEMIA causing seizure Labs: - ABG/VBG!!!: -!!Primary resp alk + Anion gap metabolic acidosis****** - -E.g. ↑ pH 7.44 | ↓ PCO2 26 | ↓ HCO3 18 - ASA level: ≥ 30mg/dL - Acetaminophen level, - BMP, - LFTs - POC: hypoglycemia - UA: urine pH LOW (goal: 7.5-8) - Chest xray: check for ARDS and pulmonary edema COD: Cerebral edema (seizure), pulmonary edema (ARDS), metabolic acidosis / resp alk
37
ASA OD tx
- ABCs, IV fluids with GLUCOSE for CNS, O2, monitor - ACTIVATED CHARCOAL and URINE ALKALINIZATION with sodium bicarbonate infusion (goal urine pH of 7.5-8) - hemodialysis: if sevewhy re - pulmonary edema - cerebral edema - renal failure - acidemia - altered mental status - level >100mg/dL (acute) or > 60mg/dL (chronic)
38
hemodialysis is indicated in salicylate toxicity in what cases?
- pulmonary edema - cerebral edema - renal failure - acidemia - altered mental status - level >100mg/dL (acute) or > 60mg/dL (chronic)
39
common trauma from alcoholism
- chronic subdural hematoma - acute SDH - TBI - MVC
40
Agents and antidotes
-beta blocker OD -> glucagon, insulin + dextrose, intralipid fat emulsion therapy if refractory -iron- GI upset, kids -> IV crystalloid, antiemetics, whole bowel irrigation, DEFEROXAMINE (severe) -rat poison = warfarin -> lavage, charcoal, vitamin K, FFP, PCC -benzo -> flumazenil* -heparin -> protamine
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key overview when OD what are the ABCs and hx qs
DECON Airway, Breathing, Circulation Dextrose Elimination Find an antidote (if available) Get a good history if possible WHAT, WHEN and WHY Which drug, dose, amount, immediate vs extended release, co-ingestions Exact time of exposure/ingestion Where they any immediate symptoms? Establish if exposure is acute vs. chronic, history of suicide attempts, illicit drug use, past medical history, other drug use or medication changes Corroborate with EMS, friends, family, neighbors, psych, primary care doctor, pharmacy Comprehensive physical exam  identify toxidrome Vital signs Neurologic: delirium, hyperactivity, obtunded, comatose Eye: pupillary response, nystagmus, lacrimation Skin: Wet or dry/hot GI: Bowel sounds Diagnostic tests should include: POC glucose! - Typical agents that can cause hypoglycemia: - Salicylates - Acetaminophen - Insulin - Oral hypoglycemics - Alcoholism CMP to calculate anion gap and osmol gap VBG for acid-base disturbances Urine or blood drug screen (qualitative , false ±, timeliness) Specific drug levels (APAP, salicylate, dig, anti-seizure, alcohols) ECG Xray - The following are radio-opaque and can sometimes be seen on a KUB Chloral hydrate / cocaine packets Heavy metals Iron Potassium Enteric coated tabs Slow-release forms Poisons have an unpredictable onset and duration of symptoms and toxicity due to many factors: Absorption, elimination, half rate, saturation, metabolism Get help! Call regional poison center (1-800-222-1222) to ensure correct management New York (1-800-764-7667 or 1-800-POISONS)
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antidote