toxicology Flashcards
A 20-year-old presents with agitation and combativeness. Emergency medical services (EMS) reports they were called for a combative male who was screaming and threatening bystanders. He is emotionally labile and appears to be responding to internal stimuli.
A 22-year-old woman presents with agitation and combativeness. EMS reports they arrived on scene to find her wandering through traffic, beating on cars, and screaming at drivers. Her medical record indicates she has been admitted to the ED multiple times for substance use. Her companion indicates she was behaving normally 2 hours prior to arrival.
An 83-year-old man with a history of memory loss is admitted for syncope. After boarding in the ED for several hours, he becomes agitated and less directable. He is currently trying to climb out of his bed and striking out at staff members.
acute agitation (NOT ON TEST)
-Safety first
-Identify if mild, moderate, severe
-Verbal de-escalation
-Show of concern
-Treat underlying medical problem
-Restraints: sparingly and only to protect pt/staff from harm, in the least restrictive manner
-PO meds preferred
-IM/IV meds (2nd generation anti-psychotics)
-Respect personal space
-Do not be provocative
-Establish verbal contact
-Be concise
-Identify wants and feelings
-Listen closely to what the patient is saying
-Agree or agree to disagree
-Lay down the law and set clear limits
-Offer choices and optimism
-Debrief the patient and staff
Pharm option in the older agitated pt
-Avoid benzos
-Elderly patients are at increased risk of respiratory depression and delirium from benzodiazepines. Experts recommend avoiding benzodiazepines whenever possible, the exception being alcohol/sedative-hypnotic withdrawal.
-Use antipsychotics (consider atypicals)
-Haldol 0.5mg IM is a reasonable first line medication for the agitated older patient. Consider atypical antipsychotics such as risperidone, quetiapine or olanzapine starting at the lowest dose and titrating slowing to effect.
-Start low go slow
-calm someone down- antipsychotics
-withdrawal- benzo
-if on a stimulant- benzo
severely agitated pts (she didnt go over)
-First few minutes
-1. Place the patient in a resuscitation room and apply cardiorespiratory monitoring, capnography and oximetry
-2. Place 1-2 large bore IV lines
-3. Assess for and start to treat:
-Hypoxia – place supplemental O2
-Hyperthermia – obtain rectal temperature and initiate cooling measures
-Hypoglycemia – obtain capillary glucose and administer D50W
-Hypovolemia – most severely agitated patients will be volume depleted and acidotic; initiate crystalloid 1L bolus on speculation
-B) Next few minutes
-Hyperkalemia and acidemia – send a blood gas with lytes and consider calcium gluconate, insulin with glucose and sodium bicarb
-CNS lesions – CT head
-Monitoring – ideally vitals q5min for the first 30 mins
-C) Next hour
-Consider primary diagnoses such as: sepsis, neuroleptic malignant syndrome, thyrotoxicosis, meningitis/encephalitis
-Rule out consequences of agitation: rhabdomyolysis, traumatic injuries
toxicology
-Poisoning = any illness caused by exposure to a toxic substance
-Recreational use of a drug or alcohol
-Occupational or environmental exposure
-Chemical weapon exposures
-Self harm
-Accidental ingestion
principles of toxicology management
-Reduce the exposure
-Reduce the absorption
-Increase elimination
-Know when to intervene
-Give supportive care with DABCDEFGH
-DECON
-Airway, Breathing, Circulation
-Dextrose
-Elimination
-Find an antidote (if available)
key points
-Primary survey and supportive measures (ABCDEFGH)
-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!
-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?
-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)
metabolic acidosis with AG
M = methanol, metformin
U = Uremia
D = DKA
P = paraldehyde
I = INH, Iron
L = lactate
E= ethylene glycol
S= salicylates
C = CO, cyanide
T= toluene
causes of AMS- AEIOUTIPS
-A- alcohol, acidosis, ammonia, arrythmia
-E- electrolytes, endocrine, epilepsy
-I- infection (sepsis, meningitis)
-O- overdose, O2, opiates
-U- uremia
-T- temperature, trauma, thiamine
-I- insulin (hypoglycemia)
-P- psychiatrics, poisoning
-S- stroke, seizure, syncope, space occupying lesions, shunt (VP) malfunction, SAH
AMS? Overdose?
-check glucose level in all overdoses and AMS pts
-Typical agents that can cause hypoglycemia:
-Salicylates
-Acetaminophen
-Insulin
-Oral hypoglycemics
-Alcoholism
common agents and their antidotes
-know the common ones
-everything else- call poison control
when do we image in overdose
-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
-remember there are always exceptions to these rules
gastric decontamination
-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
Activated charcoal (AC)
-Prevents absorption of the drug through direct binding, very little risk
-does not affect anything in blood (alcohol)
-Greatest benefit within one hour
-Up to 4 in large acetaminophen ingestion
-Dose 1-2g/kg PO (max 100g)
-Potential complication: Aspiration
-Contraindications: decreased level of consciousness, ileus, obstruction
-Poorly binding:
-Heavy Metals:
(iron, lead, mercury)
-Lithium
-Cyanide
-Hydrocarbons (pesticides)
-Liquids:
-Alcohols
-Alkali / Acids
-Caustics
Whole bowel irrigation (WBI)
-Whole bowel irrigation
-Probably the most used
-Goal is to flush out the GI system by inducing diarrhea
-Polyethylene glycol (Miralax)(Golytely)
-Good for: sustained release products such as iron or lithium, lead poisoning, drugs packers, sustained release tablets
-Contraindications: Ileus or obstruction
chelating agents
-Used for heavy metal poisoning
-Combines with metallic ions to form complexes that are easily excretable
-Examples: (know these)
-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
urine alkalinization
-for things that have already been absorbed
-Enhances elimination
-Indications: Salicylates! (aspirin), phenobarbital, INH
-Urine goal pH 7-8
-Sodium bicarb infusion
-Contraindications:
-Renal failure, pulmonary edema, cerebral edema, or other cases of volume overload
hemodialysis
-Good for drugs that are low protein binding, low molecular weight, have a small volume of distribution, and are water soluble
-for drugs that are already absorbed
-works for most things
-Mnemonic I-STUMBLED!
-!Isopropyl alcohol, iron, INH
-!Salicylates
-Theophylline
-Uremia
-Methanol
-Barbiturates
-Lithium
-!Ethanol/ethylene glycol
-Depakote (valproic acid)
labs/imaging in the poisoned pt
-consider in everyone:
-EKG
-POC glucose
-CMP
-lipase
-coags
-acetaminophen and salicylate levels
-ETOH levels
-Add as indicated:
-osmolality
-ethylene glycol and methanol levels
-carboxyhemoglobin (found in comprehensive VBGs)
-UDS
-specific drug levels
-head CT
-CXR
formulas: anion gap metabolic acidosis
-NA - (Cl+HCO3)
-Normal gap is < 12
-MUDPILES
-Methanol, Metformin, Massive ingestions, Uremia, DKA, Paraldehyde, Iron, INH, Lactic acidosis (CO, CN), Ethylene glycol, Salicylates
formulas: osmolol gap
-Gap = measured osmolol – calculated
-Calculated = 2 Na+BUN/2.8, Glu/18+ ETOH/4.6
-Increased gap (>10)= acetone, isopropanol, methanol, ethylene glycol, mannitol, ketaoacidosis, ETHANOL MC
urine drug screens
-Urine drug tests screen for drugs of abuse and are unreliable
-False positives:
-Amphetamines: pseudoephedrine, labetalol, Ritalin
-TCAs: cyclobenzaprine, carbamazepine, phenothiazines, diphenhydramine
-PCP: ketamine, dextromethorphan, Benadryl, doxylamine
-Benzodiazepine: Zoloft
-False negatives:
-Dilute urine
-Adulterants
-Different versions or metabolites (GHB, rohypnol)
drug levels
-Quantitative blood tests should be limited to those drugs for which levels can predict subsequent toxicity or guide specific therapy
-e.g. iron, lithium, acetaminophen, ASA, theophylline, digoxin
-Levels mean different things if acute ingestion vs. acute on chronic ingestion
-Cannot use a nomogram if underlying chronic consumption
-Levels require THOUGHT
20 year old man “found down” in the street. He is unresponsive, and there is white powder around mouth and nose . How do you approach the assessment and management of this pt?
Decontaminate – protect yourself with PPE
Airways
Often obtunded and unable to protect airway
Breathing
Monitor O2 and ETCO2
Support as needed (nasal cannula, NIPPV, BVM, intubation)
Circulation
Cardiac monitor and frequent BP checks, vascular access
Iv fluids or pressors for shock / hypotension
Manage dysrhythmias
Disability (neurologic)
GCS, pupil check, 4-extremity movement
Check glucose!
approach to the posisoned pt
-decontaminate- protect urself
-airways/breathing- intubate as needed -> monitor O2 and ETCO2
-circulation- hypotension -> IV fluids, pacers, vasopressors PRN
-EKG- wide QRS -> sodium bicarb; long QT -> give magnesium
-disability:
-GCS, pupil check, 4 extremity movement, check glucose
-neuro depression- consider naloxone, glucose, thiamine
-seizure- POC glucose, benzos
-counter C collar
-exposure- hyperthermic or agitated- benzos, cooling
toxidrome
-There are TOO many drugs!
-Impossible to have a drug-by-drug approach
-Classify most drugs by TOXIDROME (pattern of symptoms)
-Sympathomimetics
-Anticholinergics
-Cholinergics
-Opioids
-Sedative-hypnotics
-Classifying toxidromes rely on looking at: Eyes, Skin, Secretions, Vital signs
sympathomimetics
-Caused most often by:
-Cocaine
-Amphetamines (including MDMA – ecstasy)
-PCP
-“Bath salts”
-Caffeine
-Pseudoephedrine
-Diet pills
-Methylphenidate
-CNS excitation: Hyperactivity, agitation, paranoia/psychosis, HTN, hyperthermia!!, tachycardia, tachypnea, dilated pupils, diaphoresis, coronary vasospasm
-Lab testing can include:
-POC glucose, CBC, CMP, Troponin, BNP, CPK, U/A, Urine toxicology screening, ECG
-Imaging can include:
-CXR
-KUB (suspected body packer)
-head CT (if AMS)
sympathomimetics tx
-mostly supportive, no specific antidotes
-Decrease external stimulation (dim room lights), active cooling, IV fluids
-!!Benzodiazepines for agitation, HTN and seizures
-!!Beta-blockers are (theoretically?) contraindicated in amphetamine and cocaine use due to unopposed alpha stimulation which can cause worsening hypertension, ischemia, and vasoconstriction
-Labetolol has alpha/beta mixed properties
cocaine (sympathomimetic)
-Overdose has a high mortality rate
-Can be snorted, swallowed, injected, smoked
-Half life about 1 hour
-Causes alpha and beta stimulation -> increased myocardial oxygen demand and vasoconstriction for hours after use
-Common to have co-ingestions (alcohol)
-Common to have neuropsychiatric and social problems: Bipolar disease, schizophrenia, other drug abuse, HIV, homelessness, uninsured
-Injections can be associated with: PTX, thrombosis, pseudoaneurysms of central vessels, AV fistulas, abscesses, thrombophlebitis, tetanus, necrosis
-Cocaine associations: abruptio placentae, prematurity, status epilepticus, CVA, MI, rhabdomyolysis
anti-choloinergics
-Common causes: Antihistamines! (diphenhydramine/Benadryl), antidepressants (TCAs), anti-psychotics
-Also atropine, phenothiazines, anti-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 skin!, dry skin, hyperthermia
-Others: mydriasis (dilated pupils!), hypoactive bowel sounds, urinary retention, confusion, agitation, delirium, seizures
-ECG: sinus tachy (common), wide complex tachycardias, ventricular dysrhythmias, torsades de pointes
-Wide QRS >100msec, terminal R wave , right axis deviation
-Treat QRS complex widening with sodium bicarb
anti-cholinergics tx
-!Mainly supportive: Fluids & cooling
-!Mainstay of treatment: Benzodiazepines!*
-Consider physostigmine!! for refractory symptoms of seizures, hyperthermia, dysrhythmias -> Contraindicated in heart block and TCA overdose
-ECG management:
-Ventricular dysrhythmias: lidocaine, amiodarone
-Torsades de pointes: Magnesium
-Wide complex tachycardia: Sodium bicarb!
tricyclic antidepressants (TCA)
-Were a leading cause of pharmacologic self poisoning
-Now decreased since SSRIs are more common for depression tx
-Examples: Amitriptyline, nortriptyline, cyclobenzaprine
-Inhibits reuptake of norepinephrine and serotonin, sodium channel blockade, antagonizes histamine, muscuarinic, alpha 1, sodium channel, potassium channel, GABA receptors
-Blood or urine TCA
->5mg/kg – average toxic dose
->10-20mg/kg severe poisoning
-!!3 C’s = Cardiac abnormalities, Convulsions, Coma
-Anticholinergic effects: flushed skin, dry mouth, mydriasis, decrease bowel sounds, urinary retention
-CNS effects: drowsiness, confusion, ataxia, delirium, ↓ LOC, seizures
-CV effects: hypotension, tachycardia, wide QRS, V-tach, torsade’s
-!!!!ECG is the most useful in determining severity
cardiac effects of TCA
-!Sinus tachycardia
-!Widened QRS >100ms (seizures)
-Prolonged QT
-!!Wide terminal R wave in aVR
-Hypotension
TCA tx
-!!ABCs: Cardiac monitor, IV access, oxygen
-Patients often need intubation! due to ↓ LOC
-NG tube activated charcoal!
-Focused therapy:
-ECG changes (QRS>100msec, ventricular dysrhythmias)
-!!*Sodium bicarb IV bolus 1-2meq/kg bolus -> infusion! -> lidocaine! if refractory + arrythmia
-!!Treat !hypotension with crystalloids! + norepinephrine (reverse a1-receptor blockade)
-!!Treat seizures (GABA-A inhibition) with benzos! e.g. diazepam, phenobarbital -> physostigmine! if refractory
anticholinergic vs sympathomimetic
cholinergics
-The counterpart to anti-cholinergics, this is mostly parasympathetic
-Causes: !Organophosphate poisoning (insecticides)!, chemical warfare agents (nerve gas like sarin)
-!!!“Killer Bs”: Bradycardia, Bronchospasm, and Bronchorrhea
-Muscle weakness, fasciculations, respiratory failure, wheezing
-people that work with chemicals or landscapers (insecticides)
-VERY WET PTS = CHOLINERGICS
cholinergics: amcronims
-SLUDGE:
-Secretions / Salivation
-Lacrimation
-Urination
-Defecation/diarrhea
-GI dysmotility
-Emesis
-DUMBBELLS:
-Diaphoresis
-Urination
-Miosis
-Bradycardia
-Emesis
-Lacrimation
-Lethargy
-Salivation
-NICTOINIC EFFECTS:
-fasciculations
-muscle weakness
-paralysis
cholinergic tx
-!Decontamination, use PPE
-ABCs and elevate the head of the bed
-Antidotes: ATROPINE! and 2-PAM (PRALIDOXIME)!
-Atropine will reduce muscarinic effects.
-Keep giving 2-5 mg q 5-10 min until !secretions are dry!
-Increases heart rate
-Pralidoxime or 2-PAM will reverse the muscle paralysis and fasciculations
-2g IV followed by 24 hour infusion
opioid use
-Death by apnea!
-pinpoint pupils + not breathing = opioids
-Symptoms: Respiratory depression, miosis, lethargy, hypotension, coma, noncardiogenic pulmonary edema, nausea/vomiting in opioid naïve patients, ileus
-Most universally cause miosis, however some can cause agitation and dilated pupils such as dilaudid, Demerol, diphenoxylate
-Causes: morphine, heroin, fentanyl, Demerol, codeine, diphenoxylate (Lomotil), propoxyphene (Darvon), hydrocodone (Vicodin), Percocet (careful of Tylenol addition), etc.
-Caution: Clonidine can mimic opioid overdose (causes pinpoint pupils and hypoventilation) which is also reversed with high dose naloxone (10mg)
opioids PE, dx, tx
-Physical exam:
-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
-Urine drug screen can be positive 2-4 days after single use
-Acute opioid OD treatment: NALOXONE (opioid antagonist) 0.4 to 2 mg
-Intranasal (NARCAN): 1mg each nostril (total 2mg)
-IV start with 0.4mg if mild-moderate depression, 2mg if apneic
-May repeat doses every 2 to 3 minutes up to 10mg due to opioid long half life
-Can start IV infusion in long acting opioids or body packers
-May cause an ALI that resolves within 24 hours
opioid withdrawal
-Withdrawal: abrupt discontinuation of opioids or naloxone use:
-“Cold turkey” symptoms begin ~6 hours after last dose, peaks on day 3, resolves by day 6
-Anxiety, tremors, irritability
-Nausea, vomiting, diarrhea
-Cramping
-Yawning
-Rhinorrhea
-Piloerection
-Symptoms are uncomfortable but rarely fatal
sedative hypnotics
-Sedation and somnolence are the hallmark findings
-Loss of airway protective reflexes in severe cases
-Causes: Benzodiazepines, barbiturates, melatonin, Z drugs
sedative hypnotics: barbiturates (DONT NEED TO KNOW)
-Not so common anymore
-Treats anxiety, insomnia, seizures
-Phenobarbital, pentobarbital
-Miosis, hypotension, CNS depression
-!Cutaneous bullae = bad prognosis
-Renally excreted and dialyzable:
-Treatment: Lavage, charcoal, urine alkalinization if long acting, hemodialysis
sedative hypnotics: benzos
-Quite common
-Lorazepam (Ativan), alprazolam (Xanax), diazepam (valium), chlordiazepoxide (Librium)
-Date rape drug Rohypnol
-Respiratory depression, ataxia, hypotension, hypothermia, coma
-THIS IS ALL YOU NEED TO KNOW:
-Treatment: Supportive mostly
-!!!!!!bc you cant die from overdose but you can from withdrawal
-Can give antidote Flumazenil!!, but benzo withdrawal is more life-threatening than overdose (can cause seizures and death, esp in chronic overuse)
22man found down in a shed at work. Works as landscaper. White powder on face and clothing. Began vomiting during exam
VITALS: T 35.9F (96.6F), P 55, RR 24, BP 108/55, SPO2 85% on RA
Gurgling respirations with pooled secretions in oropharynx
Pupils 2mm (normal 2-4mm)
Skin cool and diaphoretic
-killer bees
summary charts
toxic alcohols
-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.
must know osmolal gap calculation
-This may be the only clue in an isopropyl alcohol ingestion
-!!!Osmolal Gap = measured osmolarity – calculated osmolarity
-Measured is given to you on a BMP
-Calculated = (2 Na) + (BUN/2.8)+ (Glu/18) + (ETOH/4.6)
-IF GAP IS >10 consider:
-Toxic alcohols: Isopropyl alcohol, methanol, ethylene glycol
-Ethanol
-Mannitol
-DKA/HHS
-Drunk + Anion gap metabolic acidosis + osmolol gap = ethylene glycol or methanol poisoning
Drunk + osmol gap = isopropyl
methanol poisoning
-Sources: paint thinner, car window washing solvent, wood alcohol, gas tank additive
-Methanol itself is nontoxic, but alcohol dehydrogenase forms the toxic metabolite
-Formaldehyde -> broken down by the formaldehyde dehydrogenase into -> formic acid
-!!!!!!!Anion gap metabolic acidosis + increased osmolal gap
-Symptoms are often delayed 12-18 hours: !Blindness from disc hyperemia!, seizures, resp failure, N/S, pancreatitis, visual changes, ataxia, AMS
-Treatment:
-!!Fomepizole (4-methylpyrazole) (antizol)
-An alcohol dehydrogenase inhibitor
-Allows methanol to be excreted intact via the kidneys without being broken down into its toxic metabolites
-Usually, a temporizing measure until you can get dialysis
-!Ethanol
-Occupies alcohol dehydrogenase to limit breakdown of methanol into its toxic metabolites
-Ethanol is preferentially metabolized by alcohol dehydrogenase over methanol and ethylene glycol
-!!Dialysis and bicarbonate if severe acidosis refractory to 4-MP or ethanol therapy
ethylene glycol poisoning
-Ingestion of antifreeze, moonshine, paints, solvents, windshield wiper fluid
-Ethylene glycol metabolizes into oxalic acid -> combines with calcium -> forms calcium oxalate crystals! -> acidosis and kidney injury
-!!Intox + CNS depression, heart failure/pulm edema, ATN+anuria
-Labs: !Anion gap acidosis, increased osmolar gap!, hypocalcemia, renal failure, hematuria
-Wood’s lamp might show green glowing urine, d/t calcium oxalate crystals
-Treatment:
-FOMEPIZOLE loading dose of 15 mg/kg IV
-Fomepizole inhibits alcohol dehydrogenase activity
-HEMODIALYSIS if severe
-THIAMINE 10 mg IV & PYRIDOXINE 50 mg IV
-Both are consumed in the metabolism of ethylene glycol and need supplementation
isopropyl alcohol poisoning
-“Rubbing alcohol” (mouthwash, ginseng shots, NyQuil)
-CNS depression greater than ethanol
-Metabolism: in liver >50% metabolized to acetone
-!!Hallmark: Normal anion gap, increased osmolar gap , Ketosis with normal glucose,
-Hemorrhagic gastritis, pulmonary edema, hypoglycemia
-Severe hypotension
-Supportive care, don’t give alcohol.
-Hemodialysis (if severe)
TOXIC ALCOHOL CHART
sympathomimetics get
BENZOS
ethanol (alcohol)
-NOT A TOXIC ALCOHOL
-Found in: Wines, spirits, beers, mouthwash, cologne, perfume
-CNS depressant = Downregulates GABA and upregulates NMDA
-Many presentations:
-Intoxication
-Withdrawal
-Physical changes: liver disease, varices, SBP, cirrhosis, trauma!
-Intoxication: 80-100mg/dL (0.08 - 0.100 g/dL)
-!!Supportive care management
-Always search for other causes of AMS in the intoxicated patient
-Check blood glucose
-Consider CT head and c-spine
-Look for fractures or other trauma
-Look for other evidence of drug use
-Evaluate for electrolyte abnormalities
-Ethanol serum level, ammonia levels, CBC, BMP+LFTs, VBG, CPK, consider levels for other drugs such as Tylenol or salicylates
wenickes encephalopathy
-Chronic alcoholism can result in B1 (thiamine) deficiency due to poor nutritional intake, causing Wernicke’s encephalopathy
-Tachycardia, tremors, hypertension, agitation, Hallucinations, Seizures, Delirium tremens
-Classic triad
-1. Oculomotor abnormalities (CN VI palsy, nystagmus)
-2. Ataxia
-3. Global confusion
-Treatment: IV thiamine 500mg q8hours for 3 days
-Followed by 250mg daily for 3-5 more days
fatal withdrawals: alcohol
-Alcohol, barbiturates, benzodiazepines
-CNS depressants
-Abuse, dependence, and acquired tolerance
-Drug intake abruptly stopped = withdrawal symptoms
-Withdrawal will cause CNS hyperexcitation!
-Tachycardia, hypertension, agitation, diarrhea, mydriasis, insomnia, cramps, diaphoresis, piloerection
-Treatment: benzodiazepines, clonidine
-Overdose with benzos, booze and barbs is rarely life threatening unless associated with co-ingestion of other CNS depressants such as alcohol, opioids, barbiturates, first-generation antihistamines
CIWA scores
-Clinical institute for withdrawal assessment (alcohol, revised)
-Validated scoring tool for alcohol withdrawal
-Done hourly
-Asks about various areas including !nausea, vomiting, anxiety, tremors, hallucinations !
-High scores = severe withdrawal
alcohol withdrawal syndrome timeline
-6-12 hrs: early uncomplicated withdrawal -> minor sx- anxiety, tremors, insomnia
-12-24hrs: alcohol hallucinosis -> hallucinations (tactile > auditory or visual in 7%)
-24-48hrs: alcohol withdrawal seizures -> generalized tonic-clonic convulsions
-48-72hrs: delirium tremens -> !disorientation/confusion!, hallucinations, hyperthermia, tachycardia, mortality 5%
EARLY alcohol withdrawal
-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
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
-Usually chronic alcoholics (not binge drinkers)
-Treat with benzos! to reduce recurrent AWDS
-No role for antiepileptics unless hx of epilepsy
-Differentials for new onset seizures!:
-Head trauma
-Intracranial bleed
-Metabolic derangement
-Acute poisoning
-Epilepsy
-CNS infection
delirium tremens
-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
delirium tremens: 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
-For severe withdrawals, titrate the benzodiazepines to achieve a state of sedation with arousability to minimal stimulation
antabuse (disulfiram) reaction
-!Alcohol + Antabuse (disulfiram)
-!Alcohol + metronidazole (flagyl)
-Flushed face, neck, trunk
-Marked diaphoresis
-Nausea, vomiting, headache
-Severe reactions:
-Hypotension
-Seizures
-Dysrhythmias
acetaminophen (paracetamol) overdose
-!Toxic dose: Single ingestion >150mg/kg
-Mechanism:
-Hepatic metabolism via CYP450 to NAPQI –> highly toxic free radical that causes damages liver
-In normal doses, NAPQI combines with thiols to produce non-toxic metabolites
-In overdoses, thiol stores are depleted, and NAPQI accumulates
-Predisposing factors: chronic alcohol use, malnutrition, older age, meds that utilize the CYP450 pathway (anticonvulsants, anti-TB meds)
acetaminophen overdose: 4 stages of injury
-stage 1- first 24hrs -> N/V, abdominal pain
-stage 2- 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, hepatic failure, encephalopathy, sepsis, coma, death
-stage 4: 4 days-2wks, recovery phase for those who survive stage 3
acetaminophen labs
-Serum Studies
-!LFTs (serial)
-Coagulation profile (PT/PTT/INR)
-CBC baseline and calculate anion gap acidosis
-ABG/VBG to confirm acidosis levels
-Renal study
-APAP LEVEL
-Serum concentration >140u/mL 4 hours after ingestion is considered TOXIC and treatment with NAC should be initiated
