inservice review toxicology n.
Download
Skip this Video
Loading SlideShow in 5 Seconds..
Inservice Review: Toxicology PowerPoint Presentation
Download Presentation
Inservice Review: Toxicology

Loading in 2 Seconds...

play fullscreen
1 / 45

Inservice Review: Toxicology - PowerPoint PPT Presentation


  • 161 Views
  • Uploaded on

Inservice Review: Toxicology. Gerry Maloney, DO Attending Physician, Emergency Medicine and Medical Toxicology CWRU/MetroHealth Medical Center. APAP 140 mg/kg toxic dose for single acute ingestion (200 mg/kg peds) Rumack-Mathews nomogram only for single acute ingestion

loader
I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
capcha
Download Presentation

PowerPoint Slideshow about 'Inservice Review: Toxicology' - jatin


An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.


- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
inservice review toxicology

Inservice Review: Toxicology

Gerry Maloney, DO

Attending Physician, Emergency Medicine and Medical Toxicology

CWRU/MetroHealth Medical Center

analgesics
APAP

140 mg/kg toxic dose for single acute ingestion (200 mg/kg peds)

Rumack-Mathews nomogram only for single acute ingestion

NAC can be given with charcoal (no need to adjust dose)

PO NAC: 140 mg/kg load, then 70 mg/kg q 4 h for 72 h

IV NAC: 150 mg/kg LD, then 50 mg/kg over 4 h, then 100 mg /kg over 16 h

APAP

Liver injury usually takes 24 h to develop for acute OD

Elevated AST & detectable APAP treat with NAC

Refer for transfer: elevated INR, encephalopathy, acidosis, renal failure

Analgesics
analgesics1
Analgesics
  • ASA
    • Toxic dose 140 mg/kg
    • See respiratory alkalosis first, then mixed metabolic acidosis/resp alkalosis
    • Cause of AGMA
    • Treatment is IV bicarb
    • HD for: level > 60 chronic or > 90 acute, esp if mental status changes
opiates
Opiates
  • Heroin: short-acting
  • Methadone: long-acting
  • Narcan: lasts approx 25-45 min
  • Can see seizures from demerol/propoxyphene
  • Wide QRS and hypotension with propoxyphene
  • Pulmonary edema can be seen with all
alcohols
Alcohols
  • EtOH: zero-order kinetics
  • IsoOH: osmole gap, may be serum/urine ketones, gastritis, no metabolic acidosis
  • MeOH: blindness, severe acidosis; windshield-washer fluid
  • Ethylene Glycol: antifreeze; Ca Ox crystals in urine, flourescent urine; renal failure, metabolic acidosis
  • If double gap (osmole and anion) is present, think MeOH or EG
  • MeOH/EG treated with IV EtOH or fomepizole; hemodialysis for acidosis, levels > 25 mg/dL
  • Anion: Na-Cl + HCO3; Osmole: 2(Na) + BUN/2.8 + Glu/18 + EtOH/4.6
anesthetics
Anesthetics
  • Know the dose and effects of your procedural sedation drugs (versed, ketamine, fentanyl, propofol) and when not to use them
  • Classic question is lidocaine allergic pt who need local anesthesia; what can you use?
    • Lidocaine is an amide; amides have 2 i’s
    • So look for the answer with one i, or can also use benadryl
autonomic agents
Autonomic Agents
  • Know cholinergic, anticholinergic, sympathomimetic toxidromes
  • Cholinesterase inhibitors (OP agents, nerve agents)
    • Treatment is atropine 1st (endpoint is secretions, not heart rate or atropine dose)
    • Then 2-PAM (to prevent aging, ie irreversible binding of OP to cholinesterase enzyme)
    • DUMBELS is mnemonic
autonomic agents1
Autonomic Agents
  • Anticholinergic
    • Dry skin/mouth or decreased bowel sound is clue
    • Treatment is benzo first; can consider physostigmine (though NOT if tricyclic on board)
    • Jimson weed or benadryl are classic agents
autonomic agents2
Autonomic Agents
  • Sympathomimetics
    • HTN, tachy, dilated pupils, moist skin
    • Cocaine can cause Na channel blockade and wide QRS
    • Treatment for all sympathomimetics is lots of benzos
    • Avoid β blockers in cocaine
    • Ecstasy-see bruxism and hyponatremia
anticoagulants
Anticoagulants
  • Most children with rat poison (brodifacoum) asymptomatic
  • FFP is first-line for severe bleeding
  • IV vitamin K is associated with allergic reactions
  • Make sure you give K1 (activated vit K)
anticonvulsants
Anticonvulsants
  • Dilantin
    • Iv infusion: hypotension (from propylene glycol) that is rate-related, necrosis if IV infiltrates
    • PO: OD sees ataxia/nystagmus, may be obtunded late
    • Normal level is 10-20
    • Load is 17 mg/kg IV
anticonvulsants1
Anticonvulsants
  • Carbamazepine
    • Level is 4-12
    • Has active metabolite that is also toxic (10,11 epoxide)
    • Can cause seizure in OD, cross react with TCA on urine tox
    • Treat with multi-dose AC
  • VPA
    • Hyperammonemia in absence of toxic level or abnl LFT
    • Need serial levels in OD (irregular absoprtion)
    • Normal is 50-100
    • Can use MDAC, hemodialysis (level >1000) or carnitine
antidepressants
Antidepressants
  • TCA: hypotension, seizure, anticholinergic sx; wide QRS on EKG (look at aVR); treat with bicarb
  • QRS > 120 predicts increased risk of szr
  • Trazodone: priapism, orthostatic hypotension
  • Buproprion: wide QRS, seizure, SND reuptake
  • Citalopram: cardiotoxic
  • SSRI or MAOI think serotonin syndrome, may be delayed if MAOI involved
antipsychotics
Antipsychotics
  • Can see QT prolongation and orthostatic hypotension with all
  • EPS/akathisia decreased with use of benadryl/cogentin
  • NMS vs SS: NMS has slow onset, lead pipe rigidity, hyperthermia; SS rapid onset, reflexes and muscle tone LE>UE
  • Stop offending agent, benzos, may consider cyproheptadine (SS) or dantrolene (NMS)
slide16
CO
  • Know half life of CO (RA 3-4 h, 100% 90 min, HBO 23 minutes)
  • Know classic presentation (HA, vomiting, winter, whole family sick)
  • Refer for HBO: level > 40% (15% if pregnant), syncope, MI, mental status change, neuro deficits
  • CNS lesion: bilat globus pallidus
cardiac meds
Cardiac Meds
  • Digoxin
    • Level > 2 ng potentially toxic
    • Classic EKG is bidirectional VT or PAT with block
      • Most common finding is PVC’s
    • K > 5 serious toxicity
    • Digibind: empiric treatment is 5-10 vials (acute OD), 3-5 vials (chronic OD)
    • Can calculate if level is known (dig level x wt in kg/100= # of vials)
cardiac meds1
Cardiac Meds
  • Beta blockers
    • Glucagon is antidote
    • Propranolol causes seizures
  • CCB
    • See metabolic acidosis and hyperglycemia (DKA like picture)
    • Most ER so need prolonged observation
    • “pill can kill” in kids
    • Treatment: calcium, pressors, HIE
  • Clonidine
    • Looks like opioid, narcan sometimes reverses effects
caustics
Caustics
  • No vomiting, no charcoal
  • Alkali: liquefactive necrosis deeper burn
  • Acid: coagulation necrosis stops burn
  • Can have severe esophageal injury w/o intra-oral injury
  • Steroids not generally helpful
cn hs
CN/HS
  • CN: rapid BP fluctuations, metabolic acidosis (elevated lactate)
  • Affects Cytochrome aa3
  • Treatment: amyl nitrate/sodium nitrite, then sodium thiosulfate
  • See “arterialization” of venous blood (high venous O2 sat)
  • HS: rapid knockdown with rotten egg smell
metals
Metals
  • AC binds poorly to all metals (works for strychnine)
  • Li: causes ataxia; HD if level > 2.5 (chronic) or 4 (acute); can treat with IVF/WBI
  • As: see vomiting early, then neuropathy/multi-organ failure/prolonged QT, Mee’s lines
  • Lead:
    • level > 70 needs parenteral chelation.
    • Give BAL and EDTA.
    • Peanut allergy is contraindication to BAL.
    • > 10 is action level
herbicides pesticides rodenticides
Herbicides/pesticides/rodenticides
  • Many are arsenical
  • Also see superwarfarins or organophosphates
  • Paraquat: need to decrease FiO2
hydrocarbons
Hydrocarbons
  • Determinants of aspiration risk:
    • Surface tension
    • Viscosity
    • Volatility
  • Never induce vomiting
  • May see delayed pneumonitis (esp in kids)
  • Sniffers/huffersmyocardial sensitization to catecholamines, can have sudden death
hypoglycemics
Hypoglycemics
  • Insulin: not much
  • Sulfonylurea: prolonged hypoglycemia; octreotide is antidote
    • May be delayed in kids, generally need 24 hour OBS
  • Metformin: lactic acidosis, esp in renal failure
inhalational
Inhalational
  • Water solubility determines toxicity
    • High-immediate irritation to eyes/MM
    • Medium (like Cl) some upper and lower airway stuff
    • Low: all the way into the lungs, delayed pulm edema (phosgene)
  • Bleach + acids/ammoniachlorine or chloramine gas
  • CS: riot control agent
slide26
Iron
  • See phases (Phase 1: immediate GI sx; phase 2: quiescent; phase 3: acidosis, liver injury, GI bleed; phase 4: recovery)
  • Know different preps have different amounts (FE fumarate>sulfate>gluconate)
  • Deferoxamine (DFO)is antidote
  • Vin rose urine is sign DFO is working
slide27
INH
  • Inhibits pyridoxal phosphateprevents creation of GABA
  • Clinical picture is intractable sz
  • Causes profound lactic acidosis (“I” in MUDPILES or METALACIDGAP)
  • Treatment is pyridoxine (1 g of B6 for every G of INH ingested, or 5 g empiric dose)
methemoglobin
Methemoglobin
  • Change in oxidation of iron in heme molecule (Fe++ to Fe+++ )
  • Chocolate brown coloration of blood
  • Also the MOA of nitrates in the CN antidote kit
  • Treatment (if levels >20% or severe sx) is methylene blue 1 mg/kg
  • High-risk persons include those susceptible to oxidative stress (G6PD)
shrooms plants
Shrooms/Plants
  • Shroom you most need to know: amanita phalloides
  • Delayed GI sx (>4 h) after ingestion is associated with toxic mushrooms (delayed sx bad)
  • Liver failure is result of A. phalloides
  • coprinus antabuse reaction
  • Gyromitra (false or brain morel) intractable sz (INH-like, treated like INH)
  • Amanita muscaria (red shroom)-anticholinergic
  • Psilocybin (little brown shroom)-hallucinogen
shrooms plants1
Shrooms/Plants

a. phalloides

gyromitra

coprinus

a. muscaria

psilocybin

shrooms plants2
Shrooms/Plants
  • Plants
    • Cardiac glycosides (yew, oleander, lily of the valley, foxglove) dig-like toxicity
      • Can treat with digibind
    • Poison Ivy: 3 shiny leaves; blistering rash; type IV allergic reaction
    • Jimson weed: anticholinergic
    • Castor bean: ricin; inhibits RNA, MOSF
shrooms plants3
Shrooms/Plants

jimson

foxglove

Poison ivy

ricin

neuroleptics
Neuroleptics
  • EPS responds to cogentin/benadryl
  • Can decrease EPS when giving phenothiazines by pretreating with benadryl
  • NMS: gradual onset, hyperthermic, AMS, lead pipe rigidity, rhabdo; treat with benzos, +/- dantrolene, stop agent
  • SS: more rapid onset, similar clinical picture except LE more rigid than UE; consider cyproheptadine
nonprescription drugs
Nonprescription drugs
  • Cough & cold preps
    • Dextromethorphan: can x-react with PCP on U Tox; see nystagmus and AMS/ataxia
    • Pseudoephedrine: sympathomimetic, methamphetamine precursor
    • Vitamins: know Fe content
    • Imidazolines (afrin): look like clonidine
    • Oragel: benzocaine, can cause methemoglobin
    • Lido patches: seizures
recreational drugs
Recreational Drugs
  • Cocaine
    • Sodium channel blockade
    • Sympathomimetic toxidrome, may see widened QRS
    • Metabolite in urine: benzoylecgonine
    • EtOH + coke cocaethylene, which may be more toxic than plain coke
    • Treat with benzos, avoid β-blockers
recreational drugs1
Recreational Drugs
  • Heroin-already covered
  • Ecstasy hyponatremia
  • GHB: comatose, then wakes up suddenly and yanks out ETT
  • Ketamine: dissoc anesthetic, emergence reactions, intact airway reflexes
  • PCP: hallucinations, rotary nystagmus
sedative hypnotics
Sedative-hypnotics
  • Benzos
    • Dec LOC, generally need to mix with EtOH to have sig toxicity
    • Rohypnol: ultra rapid metabolizer, does not x-react on standard U Tox
  • Barbiturates
    • Skin bullae, coma, hypothermia; can treat phenobarb with MDAC/urinary alkalinization/HD
  • Soma
    • Meprobamate, may cause bezoar/radio-opague
strychnine
Strychnine
  • Increase in excitatory neurotransmission
  • Pseudo seizure activity (rigid, opisthotonus, awake)
  • Marked lactic acidosis
  • Rat poison is culprit
environmental toxicology
Environmental Toxicology
  • Arthropods
    • Black Widow
      • Presentation is severe abd cramping mimicking acute abd with normal labs
      • Key: may have been working in garage/reaching into pile of lumber
      • Treatment: supportive, may try calcium gluconate; antivenin not generally available
    • Brown recluse
      • Small wound that develops into ulcer
      • Treatment: wound care; dapsone has been advocated before but not used widely d/t risk of MetHb
environmental toxicology1
Environmental Toxicology
  • Scorpions
    • Centuroides only significantly venomous species in US
    • Neurotoxin that cause paresthesias/vomiting/cramping, treatment is supportive
  • Tick
    • Tick paralysis= neurotoxin by dermocentor sp usually
environmental toxicology2
Environmental Toxicology
  • Marine
    • Scombroid: large fish (tuna, mahi-mahi, swordfish), excess histamine in flesh; flush/cramping/diarrhea/hypotension
    • Ciguatera: also larger fish, hot/cold reversal in extremities
    • Jellyfish: treat with ammonia or urine (not fresh water)
    • Lionfish: hot water immersion
environmental toxicology3
Environmental Toxicology
  • Snakes
    • Pit viper: diamond shaped head, pits anterior to eyes, fangs
    • Crofab: used instead of Wyeth antivenin; less risk of anaphylaxis/serum sickness
    • Pit vipers (rattlers, cottonmouth, copperhead) have hemotoxin (low plt, coagulopathic) and cause tissue swelling +/- compartment syndrome
    • Elapids (coral snake, cobras) are neurotoxic
    • Mojave rattler is only NA pit viper with primary neurotoxin