Mini-Tox: Liberia
Management of common and
commonly problematic
toxicological emergencies
Andrew Shannon, MD MPH
Jacobi Medical Center Emergency Medicine Residency
Albert Einstein College of Medicine, Yeshiva University
Objectives and Outline

Brief overview of important initial steps in managing
intoxications






History
Toxicological physical exam and adjuncts
Toxidromes
Gastric decontamination
Approach to coma
Specific poisonings






Acetaminophen (APAP)
Salicylates
CO / CN
Caustics / Iron
Alcohols
Drugs of abuse




Special psychiatric
overdoses
Toxic bradycardia
Pesticides
Heavy Metals
Helpful Resources









Poison Centers in the US: 1-800-222-1222
Vaults of Erowid: www.erowid.org
Lycaeum: www.lycaeum.org
MMWR: www.cdc.gov/mmwr
Medwatch: www.fda.gov/medwatch
Emergency Preparedness and Response: www.bt.cdc.gov
Household Products Database:
http://housholdproducts.nlm.nkh.gov
Cornell Univ. Poisonous Plants Informational Database:
www.ansci.cornell.edu/plants
Dartmouth Toxic Metals Research Program:
www.darmouth.edu/~toxmetal
History

Pts p/w ingestions may
not be reliable




AMPLE Hx

SI/HI



who called EMS? why?
altered mental status
(AMS)
Family
EMS (check ACR!)
MiSys- prior visit/med hx

allergies, medications (recent
changes), procedures, last po
intake, what led up to incident
Ingestion Hx


chemicals/meds available to pt? (ie
Soc Hx)
how much, when, why?



SI/HI, accidental med OD,
abuse/Munchausen by proxy
paraphernalia/bottles at scene
last time Pt noted to be at baseline?
Physical Exam

HEENT


ABC’s

GCS - not prognostic

Dry if wet, warm if cold, cool if hot
Re-address decon and staff
safety/contamination
Vital Signs (VS)


do not rely on a “Nurses’ 20” for
RR
If you can’t get a BP, there
probably isn’t one
FSBG is 6th VS!
Skin






rales
Abd


diaphoresis; piloerection
cyanosis
track marks
CV
Chest

Count/repeat yourself



“E” – Exposure/(EKG)



“D”- Disability/(Dextrose)



signs of trauma
MMM; burns
nystagmus, pupils
bowel sounds
Neuro



MS (O x ?); gag
gait
tremor, fasciculation, DTRs
Adjuncts to Physical Exam

FSBG


Lab tests




Arrhythmias
Intervals
End-organ effects (ischemia)
CXR/AXR



Aspiration
Free-air / perforation
Radio-opaque ingestants




Order:

EKG


by now you’ve realized this is
important

body packers/stuffers
halogenated hydrocarbons
Fe, K, I or heavy metal compounds
enteric coated preparations

APAP / ASA level
bHCG
Consider:








anion gap
anti-convulsant level
CO level
EtOH level
CPK
ABG / VBG / lactate
NH4
osmolality
“Toxidromes”

Sympathomimetic






Hyperthermia
Tachycardia
Hypertension
Mydriasis
Diaphoresis
AMS – agitated/combative,
hallucinations, seizure

Narcotic




Pinpoint pupils (variable)
AMS – obtundation
Decrsd RR
Sedative/Hypnotic


AMS – obtundation
Normal VS!
CAUTION: toxidromes are generalities, and intoxications may not
present classically, especially in mixed ingestions
“Toxidromes”

Cholinergic

Muscarinc – “leaky”




Anti-cholingergic

SLUDGE: salivation,
lacrimation, urination, diarrhea,
GI cramps, emesis
“Terrible B’s”: bradycardia,
bronchorrhea, bronchospasm





Nicotinic


Autonomic: diaphoresis,
mydriasis, tachycardia, HTN
Neuromuscular: fasciculation,
weakness, paralysis


hyperthermia
tachycardia/HTN
dry/flushed skin; dry MM
mydriasis
decrsd bowel sounds
urinary retention
AMS – agitation,
hallucination, seizure
“Red as a beet, dry as a
bone, hot as hell, blind as
a bat, mad as a hatter”
Classically, cholinergic toxidrome includes constricted pupils
(miosis), but this is variable (agent; predominating effect)
Gastric Decontamination

Ipecac



~20 min to V onset
No role in ED setting
Gastric lavage


Consider if <1 hr, critical toxin, protected airway
Contraindicated: caustics, large or sharp FBs



L lat decub/Trendelenberg, suction, intact gag or ETT
Measure nose to xiphoid, confirm position, lavage until clear
36-40 Fr in adults; 22-24 Fr min in children
“critical toxin” = a small decrease in toxin burden may have large
impact on clinical status; i.e. TCAs, CCBs, colchicine, Li…
Activated Charcoal

Adsorbs many toxins


MDAC (multi-dose)

optimal charcoal: toxin ratio 10:1
Initial dose in unkn ingst




1 g/kg
Must mix slurry well! (actual
charcoal is in bottom of bottle)
NOT USEFUL in…



small molecules (Li, Fe, Pb)
hydrocarbons, alcohols
when endoscopy indicated
(caustics)



phenobarb, dapsone,
theophylline, digitoxin,
phyentoin, carbamazepine
ensure cathartic only w/ 1st
dose!
Cathartics

sorbitol (0.5g/kg), Mg citrate
or sulfate
AC contraindicated:


gut perforation or ileus
sig aspiration risk
Whole Bowel Irrigation

Rarely indicated




metaclopramide; NGT; dose of AC
minimum 1.5-2 L/hr (adult) or 25 mL/kg/hr (child) PEG




large burdens poorly adsorbed (AC) agents (Li, Pb, Fe, Zn)
or SR/ER preps
In consultation w/ GI for body-packers (“mules”)
Golytely, Nulytely, Colyte
until rectal effluent is clear (? rectal tube)
re-dose AC
Contraindications

No bowel sounds; obstruction or perf; unstable pt;
unprotected compromised airway
Coma

Care of the undifferentiated coma patient is EM
distilled
‘As a rule,’ said Holmes, ‘the more bizarre a thing is the less mysterious it
proves to be. It is your commonplace, featureless crimes which are really
puzzling, just as a commonplace face is the most difficult to identify.’

ATLS / ACLS / PALS protocols are key



C-spine stabilization? HCT to r/o chronic subdurals? Roll the patient
so you don’t miss the bullet hole…
Infxn, SAH, CVAs, MIs, Ao dissections leading to CVAs
can all affect a Pt’s “responsiveness”
Coma due to toxins should be treated in the same way,
with emphasis placed on above measures and
observations
Coma “Cocktail”

Thiamine


100 mg iv prior to dextrose
Dextrose


0.5-1.0 g/kg
D50 – “1 amp” (50cc of 5% dextrose = 25 g)



D10 in children
Narcan



0.05-0.1 mg IVP initially; textbook dose (0.01 mg/kg)
Indicated when RR < 11 & AMS
½ life 60-90 min


4 kcal/g = ~100kcal (less than ½ a candy bar! Food is next!)
duration of action 20-90 min; less than most opiates
Flumazenil (?)

Risk of precipitating seizure severely limits routine use
Acetaminophen (APAP)

N-acetyl-para-aminophenol; aka paracetamol


peak serum lvls 30-60 min; hepatic metabolism


#1 cause acute liver failure in US; #1 cause tox fatalities
in OD, NAPQI metabolite becomes toxic as glutathione is depleted
APAP lvls are sent on unknown ingestions/SAs





toxic, treatable, time dependent, commonly co-ingested,
ASYMPTOMATIC
½-24 hrs: N/V, no sxs, (? APAP OD interferes w/ FSBG)
24-48 hrs: RUQ pain, elevated LFTs, PT/INR, bilirubin
48-96 hrs: hepatic dysfxn, acidosis, coagulopathy, LFTs
peak, hypoglycemia, jaundice, cerebral edema  death
4-14 days: resolution
APAP

Hx- time of ingestion & amnt






150 mg/kg : potentially toxic dose (~
7.5 g adults) within 24 hr
Rumack-Matthew nomogram: acute
ingestions only
obtain 4-hr level (or as soon after as
possible)
in unknown time frame, if initial lvl is
zero, the 4hr lvl will not rise to toxic
AST sens for hepatic injury
prognostic markers in acute injury
PT/INR, CO2/pH, lactate, renal
function, phosphate
“extended relief” APAP: sequential release in same pill
if 4 hr lvl above nomogram, treat; if not, repeat in another 4 hrs

APAP

N-acetylcysteine (NAC) “mucomyst”

multiple mechanisms



charcoal (AC) binds po NAC, but likely not significant
po load 140mg/kg



maint dose 70mg/kg q 4hrs x 17doses; 1330mg/kg/72hrs
antiemetics, sweetners, etc.; ? po in asthmatics/anaphylactoid rxn risk
iv load 150mg/kg in 200cc D5W ovr 1hr



greatest benefit if started < 8 hrs; benefit for late start
then 50mg/kg in 500cc x 4hrs; 100mg/kg in 1L x 16hrs
separate protocol for children <40kg 2/2 fluid concerns; or give po
Indicated in




h/o ingestion presenting >8hrs out while awaiting lvl
chronic large ingestions (>4g/day; >120mg/kg/day)
high APAP lvl (nomogram)
late (>24hrs) presentations w/ detectable APAP or high LFTs
Salicylates


ASA (acetylsalicylic acid)
Methyl salicylate - “oil of wintergreen”


max serum lvls ~ 1hr; in OD, ~ 4-6 hrs


Michaelis-Menten (“saturation”) kinetics: from 1st to 0 order elimination
initial resp alkalosis 2/2 direct stim of medulla


1 mL 98% m.s. = 1.4 g salicylate; 5 mL potentially fatal in 2 yo
not present in young children, so present later w/ severe acidosis
AG met acidosis 2/2 dcrsd renal excret of acids & uncoupling
of oxidative phosphorylation, et al.

resp acidosis superimposed on 10 mixed resp alk/met acidosis when
ventilation fails-- from fatigue or ASA induced ALI

Pre-terminal event
“Salicylism”

N/V, ALI, tachy, tinnitus, vertigo, cerebral edema, hepatitis,
dehydration, hypoglycemia, hypokalemia

ASA lvl






MDAC 2-4 doses; IVF for dehydration
RSI & subsequent impairment of hyperventilation may worsen
acidosis
Urine alkalinization: goal urine pH 7.5-9.0, ABG 7.45-7.55


>30mg/dL = s/sxs present : >100mg/dL requires HD
repeat lvl hourly during Rx
for symp salicylism, lvl > 40 mg/dL
Hemoperfusion removes salicylate most efficiently
HD can also correct lytes, H+ status

ALI, AMS, coagulopathy, ARF, unable to tol IVF, acute lvl > 100 mg/dL
Carbon Monoxide (CO)

colorless, odorless tasteless gas



mild exposure– HA, N, malaise
sig exposure– chest pain, focal neuro signs, dysrhythmias, syncope
venous carboxyhemoglobin (CO-Hb) lvl, beta-hcg


?EKG, ?CPK, ?UA, ?chem-7
nml CO-Hb 1-2%; smokers 5-10%







poor correlation w/ sx’s
ME uses >50% lvl is min lvl for lethality – “CO poisoning death”
CO-Hb dcrs’s O2 carrying capacity
shifts curve to the left (dcrsd O2 offloading to tissues)
binds myoglobin inducing cardiac/skeletal muscle hypoxia
binds cytochrome oxidase, blocking (not uncoupling!) mitochondrial
oxidative phosphorylation
induces CNS lipid peroxidation
CO

Rx


O2 therapy at highest conc possible
Hyperbaric O2 (HBO2): best effect if within 6 hrs


primarily to prevent delayed neurological sequelae
absolute indications for HBO2




pregnant w/ lvl >10% or fetal distress (3rd trimstr)
CO-Hb > 25%
unconscious/syncope on scene or ER, AMS, cerebellar signs,
seizure or confusion
end-organ ischemia (EKG chngs, chest pain, pH < 7.1)

Asymp Pts or those asymp in 4-6 hrs w/ (-) lab/EKG
findings  d/c home

Ongoing study to correlate CO finger sensor and blood levels!
Cyanide (CN)

suicide, homocide, nitroprusside, jewelry production, fumigants, combustion
of inorganic materials, artificial nail remover


blockade of electron transport chain  anaerobic metabolism  lactic
acidosis


high AG, lactate, & central venous O2 sat
CN antidote kit



suspect in acidotic CO poisonings w/ high lactate (ie >10mmol/L)
1) induce methemoglobinemia to bind CN: 20-30% metHb tolerable
 amyl nitrite pearls – inhaled while awaiting iv access
 sodium nitrite (3%) - 0.33 mL/kg to max 10mL ovr 2-4min
2) sodium thiosulfate (25%) – 1.65 mL/kg to max 50mL (adults); may repeat dose
Cyanokit – hydroxycobalamin 5g (70mg/kg) ovr 15 min



cyanocobalamin (B12) formed, chelating CN
initial hypotn possible; subsequent dosing uses longer infusion (6-8hrs)
CO & CN poisoning

avoid metHb in setting of CO-Hb; use only the sodium thiosulfate and HBO2
Caustics



Acid – H+ donator – pH < 3; coagulation necrosis
Base – H+ acceptor – pH >11; liquefactive necrosis
Pts w/ sx’s require w/u incld bloods & CXR (r/o perf)

endoscopy



intentional ingestions, stridor, pain, vomiting, drooling
within 12 hrs, no later than 24
Grade I – hyperema/edema, w/o ulceration



Grade IIa/IIb – submucosal lesions, exudates not/near-circumferential
Grade III - deep ulcers/necrosis into peri-esophageal tissues



med clear if can eat/drink; no incrsd risk for stricture/CA
IIa; soft diet as tol; NGT under direct visualization prn
IIb/III; risk for perf/infxn (days to wks); all form strictures; ?Surg consult
airway

inspection (direct/fiberoptic laryngoscopy); ?ETT, ? dexamethasone
Caustics

Gastric decon contraindicated except

large acid ingestions, ZnCl2, HgCl2

? gastric emptying w/ narrow NGT if < 30 min



bleach (sodium hypochlorite, NaOCl)
ammonia (ammonium hydroxide, NH4OH); 3-10% household, 28% industrial str



severity of systemic absorption may outweigh risks
lrg industrial str exposures or those w/ sx’s require w/u
otherwise clear if tol po
Ophthalmic exposures



immediate high vol irrigation for at least 15 min
check pH (UA, litums paper, nitrazine paper), goal pH 7.4
?ant chamber irrigation; d/w Ophtho
Iron

Direct GI irritant, vasodilator, neg ionotrope, disrupts
electron transport chain & aerobic metabolism
 Min/no sxs- observe 6 hrs; if no sxs, d/c
 Mild/mod tox- emesis, mild tachy, mild acidosis



local effects N/V/D onset < 6 hrs from ingestion
Rx if: Fe on KUB, persistent clin toxicity (>4 episodes emesis),
acidosis, serum Fe > 350 mcg/dL, estimate of elemental Fe >2060mg/kg
 sulfate 20% eFe; gluconate 12%, fumarate 33%
Severe tox – GIB, acidosis, AMS, hypotn, coagulopathy


IVF, RBCs, lavage/WBI if feasible; ICU admission
iv deferoxamine: start 5mg/kg/hr, titrate up to 15mg/kg/hr as BP allows
 obtain pre-Rx and 4-6hr post-Rx UA
 when urine color returns to baseline, no more free Fe is being
chelated
 DFO Rx should stop @ 24hrs; safe in pregnancy
Alcohol Intoxication

“Intoxicated” is a clinical diagnosis

1 g/kg EtOH = serum lvl 100mg/dL ~ 1 hr later





12 oz beer (5%EtOH) x (30 mL/oz) x 0.8 g/mL = 14.4 g EtOH
5 oz wine (12%EtOH) = 14.4 g EtOH
1.5 oz liquor (40%EtOH) = 14.4 g EtOH
“proof” ~ 2 x %EtOH
unhabituated patients eliminate EtOH 1520mg/dL/hr

alcoholics avg 25-35 mg/dL/hr
Alcohol Intoxication

Withdrawal from EtOH

6-24 hrs after last drink - "the shakes“


4-24 hrs – hallucinosis


persecutory auditory, visual, tactile hallucinations w/o delirium
6-72 hrs – “rum fits”


tremor, tachycardia, diaphoresis, anorexia, insomnia
generalized seizures
3-10 days - delirium tremens (DT)

disorientation, fever, visual hallucinations
Managing Alcohol

High incidence of infection/trauma


?HCT, ?c-collar & c-spineCT, ?LP, ?CXR
Dehydration w/ osmolar gap


VS, FSBG, ?chem-7, ?CPK, ?EtOH lvl (prognostic), ?osms
“Banana bag”/“Osler bag”/“Rally pack” – expensive


D5NS or ½NS, 2g MgSO4, 10mL MVI, 1mg folate, 100mg
thiamine
thiamine only vitamin affecting outcome (dcrsd incidence DTs)
Alcohol Withdrawal

diazepam 10mg ivp


lorazepam 2mg ivp





no active metabolites (liver pts)
phenobarbital 130 mg iv (up to 390mg)


shorter time to peak onset of action
failure to respond to benzos (200mg / 40mg) in first 3-5 hrs
prepare for intubation; arrange ICU admission
IVF, MgSO4
phenytoin – no role in w/d sz’s unless a proven focus
chlordiazepoxide – mild/early w/d



50-100 mg/d single or divided dose
Elderly/debilitated: Initial 10 mg PO/IV/IM
Detox: 25 mg PO q6h for 1 d, q8h for 1 d, q12h for 1 d, qhs for 1 d
Toxic Alcohols

Ethylene glycol – antifreeze, coolants; “sweet” tasting

LD 1-1.5 mL/kg






cardiac depression, ATN (Ca oxalate crystals in UA), AG acidosis, hypo-Ca
UA can fluoresce under UV (Wood’s lamp) light; poor Sens/Spec
Glycolic acid (metabolite) may cross-react with some lactate assays!
Detox cofactors - pyridoxine (B6) 50mg q6hr; thiamine (B1) 100mg q6hr
HD indications – serum lvl >25mg/dL, acidosis, pulm edema, renal failure, VS instability
Methanol – “wood alcohol” solvents, windshield washer fluid, paints/removers,
varnishes, “canned heat”

LD 15-30mL; metabolized into formaldehyde/formic acid




Ocular toxicity “snowstorm” vision, ARF/myoglobinuria, CNS dep & seizures, N/V
Optic disc hyperemia
Detox cofactors – folic or folinic (leucovorin) acid 1 mg/kg up to 50 q 4-6 hrs iv
HD – serum 20-50mg/dL, acidosis, visual impairment, renal failure, VS instability
Toxic Alcohols


NaHCO3 to alkalinize urine may enhance metabolite
excretion
Fomepizole – ADH competitive inhibitor




witnessed ingestion/strong history; lvl >25mg/dL; lrg osmol gap w/
suspicion; significant unexplained AG acidosis
load 15mg/kg over 30 min; 10mg/kg q 12 for 48hrs; then 15mg/kg q 12
reload post-HD
Isopropyl alcohol – “rubbing alcohol” solvent, disinfectant, window
cleaners, skin/hair products


LD (70% soln) 1 mL/kg
metabolized to acetone  significant ketosis w/ minimal acidosis



CNS dep, unstable VS, N/V, ATN, hemolytic anemia, myoglobinuria
HD indications- uncorrectable hypotn, deep coma, VS instability, serum lvl > 400-500mg/dL
supportive care
Drugs of Abuse

Opiates (natural); Opioids (semi-/synthetic)

CNS,CV & respiratory depression, histamine release



Lomotil (diphenoxylate) and Imodium (loperamide)


poorly absorbed, may give acute toxicity
Narcan (naloxone)- typically needed if RR < 11



miosis common, not universal (esp. w/ coingestant)
hypoventilation, rhabdomyolysis, hypothermia, concomitant APAP
toxicity, lung injury (talc pneumonitis, ALI ?2/2 naloxone)
0.05mg test dose, escalate prn, lowest effective dose q 2-3min
If infusion needed, use 2/3 of dose giving a response / hr
Clonidine overdose may appear identical

50% pediatric clonidine ODs may respond to naloxone
Opiates

Withdrawal – if iatrogenic, do not give opioid!

unpleasant, not dangerous


Methadone- 10mg IM; 20mg po (dissolved)




piloerection, mydriassis, incrsd BS, yawning, diaphoresis,
larcimation, N/V
effective regardless of abuse pattern
use antiemetics prn
DO NOT give full methadone maint dose, esp if unverified
 if diverting, “prescribed” dose potentially an acute OD
Clonidine 0.1mg-0.3mg po q1hr until sx’s improve


? maint dose 0.3mg bid/tid
watch for hypotn
Sympathomimetics

Cocaine, amphetamines

CVA, szs, MI, hypo-/hypertn, hyperthermia, bronchospasm,
pneumothorax/mediastinum, rhabdomyolysis, quinidine effect
(dysrhythmias, interval prolongation), placental abruption (2nd/3rd
trimester)





Chest pain
 AMI risk in 1st hr after cocaine use 24x normal
 6% pts w/ cocaine CP have CE elevations
 EKGs less sens/spec for MI in recent cocaine users
 cocaine prothombotic
“Crack lung” 1-48hrs s/p smoking - hypersensitivity pneumonitis
 acute pulm infiltrates, pain, eosinophilia
benzos (diazepam 2.5mg), external cooling
nitroglycerin, ASA, ?CCBs in pts w/ concern for ACS
withdrawal – lethargy, dysphoria
Benzodiazepines

“Coma with normal vital signs”


RR should be normal
DDx: head trauma, stroke, hypoglycemia, CO poisoning, multisubstance ingestion


ABCs: ?ETT




EKG, FSBG, bHCG, EtOH lvl
“Anyone who can tolerate a nasopharyngeal airway probably deserves
one”
if awake, activated charcoal
most pts are arousable within 12-36 hrs w/ supportive care
Flumazenil: use only to avoid an intubation!


0.5mg slow IVP 1-2 hrs to max 5.0 mg
w/d similar to EtOH


predictable based on pharmacokinetics
chronic use of long-acting agents (diazepam) may delay w/d 4-10 days
Psychiatric Overdoses

TCAs: NE/DA/5-HT reuptake blockade


anti-cholinergic effects, antihistamine effect, Na channel
blockade
ABCs; orogastric lavage if < 1 hr; AC 1-2 doses (q4hrs)

EKG as screen: QRS




<100ms = no toxicity
>100ms = 1/3 pts w/ szs: ADMIT, think about ICU
>160ms = ½ pts w/ ventricular dysrhythmia: ADMIT to ICU
NaHCO3 2 amps (1-2mEq/kg) bolus – observe response on
rhythm strip




3 amps in 1 L D5W @ 2-3x maint; goal narrow QRS or max pH 7.55
replete Mg, K
consider 24 hr tele admission for pts w/ persistent HR > 120, or QTc >
480
No Sz, nml EKG (exept tachy that resolves)  observe 6 hrs to clear
terminal 40 ms R axis deviation: aVR R wave > 3mm (~ 81% PPV for
poisoning) w/ R/S ratio in aVR > 0.7 ; deep slurred S wave in I & aVL

long
QT, sinus tach
Mood Stabilizers

Lithium

precipitants- dehydration, renal dysfunction, preeclampsia, Na
depletion, thermal stress, drug interactions

NSAIDs, carbamazepine, ACE-Is/ARBs, metronidazole, antipsychotics,
diuretics

tremor, slurred speech, ataxia, hyperreflexia/clonus, sz, CV collapse, EPS
 acute- dilute urine, prolonged QT, hypothyroid, inc WBCs
 chronic- nephro DI, interstitial nephritis, aplastic anemia, dermatitis

IVF; WBI if SR preparations ingested


repeat Li lvl 2 hrs after initial draw in acute (6 hrs in chronic) OD
HD: call nephrologist w/ 2nd lvl value

S/Sxs neurotoxicity (AMS); unable to eliminate Li (ARF); unable to tol
IVF load (CHF); Li lvl > 4.0mEq/L (acute) or > 2.5mEq/L (chronic)

“re-bound”- tissue redistribution requires post-HD lvl and again 6 hrs later
Mood Stabilizers

Valproic acid (VPA)

carnitine depletion leads to hyperammonemia



11% pts w/ asymp chemical hepatitis
risk for (rare) fulminant hepatic failure, hypoglycemia
OD usually benign, self-limited drowsiness






> 30mg/kg  coma, respiratory depression
poor correlation w/ serum lvls; repeat in 2-3 hrs for downward trend
consider NH4 lvl, lytes, lactate if AMS
MDAC in lrg acute OD w/ rising lvls
HD: deterioration, hepatic dysnfxn, rising lvls, VPA > 1000mg/L
carnitine supplement: VPA-induced hepatotoxicity, NH4 > 35
micromol/L, peds <2 yo or on ketogenic diets


100mg/kg (max 6g) ovr 30 min iv
100mg/kg/day (max 3g) divided q6hrs po
Toxic Bradycardia

CCBs

rapid onset 1-2 hrs IR, SR 12-18 hrs



BBs


CHF, low HR, bronchospasm, hyper K, hypoglycemia
(children)
early onset of effect (<6hrs); peak 1-4 hrs


verapamil – nodal (HR, CO)
nifedipine – peripheral (SVR)
(sotalol may delay >24hrs)
Clonidine


onset 30-60 min; peak 2-3 hrs
naloxone, IVF, atropine, pressors
Toxic Bradycardia

atropine 0.5-1.0mg (0.02mg/kg) q2-3min, max 3mg



CaCl2 10-20 cc 10% soln (1-2 amps); slow IVP ovr 3-5min






3-6 amps Ca gluc
q 15-20min; up to 5 gms w/o serial Ca, PO4
peds 10-20 mg/kg Ca gluc (10% soln ~ 0.1cc/kg)
glucagon 2-5mg slow IVP, q5-10min; 10mg max; BB>CCBs


hypotn 2/2 myocard dep, not incr vagal tone
slows gut in pts receiving WBI
gtt to follow; mg/hr = effective initial dose mg
peds 50-150 mcg/kg; gtt 50mcg/kg/hr
pressors (NE)
pacing – often ineffective
Pesticides

200,000 deaths/yr



leading cause of suicide/unintentional poisonings
Vomiting, diarrhea  resp distress  LOC
Cholinesterase inhibitors

cholinergic toxidrome (miosis, SLUDGE, “killer ‘B’s”)


organophosphates



bradycardia is muscarinic, but bronchorrhea/constriction induced
hypoxia may cause tachycardia
penetrate latex/vinyl; leather is reservoir; 0.5% hypochlorite bleach or
alcohol based soap for dermal decon
“age” – irreversible inactivation of AChE
carbamates


reversible binding- no aging
muscarinic > nicotinic effects
Pesticides

atropine

0.5-1.0 mg (0.02 mg/kg) initial; double dose q2-3min




pralidoxime (2-PAM)




titrate to drying of bronchial secretions
0.5mg min adult dose (0.1mg peds) 2/2 paradoxical brady
no effect on nicotinic neuromuscular junction (paralysis)
frees un-”aged” AChE
1-2 g in 100 cc NS (25mg/kg, max 1 g) ovr 15-30min; then q6-12hr
WHO regimen: 30 mg/kg iv bolus; then > 8mg/kg/hr gtt
glycopyrrolate/ipratropium

periph-acting/inhaled anti-muscarinics may be considered as
adjuncts to atropine for clearing lung secretions
Pesticides

Sxs usually unlikely if not developed in 6-12 hrs


exceptions: fenthion, VX gas (nerve agent) ~ 24 hrs
Sequelae of organophosphate/carbamates

“Intermediate Syndrome”

acute prox/resp muscle wkns; cranial neuropathy




24-96 hrs following poisoning; up to 1st few wks
unpredictable occurrence
supportive care; pralidoxime/atropine as indicated
persistent sensory/motor neuropathy occasionally
Pesticides

Organochlorines

DDT, benzene hexachloride (Lindane), aldrin, etc.


Pyrethrins and Pyrethroids

permethrin, deltamethrin, fenvalerate


supportive Rx for agitation, szs; decon
supportive Rx; paresthesias self-limited (top vit E)
Nicotine/neonicotinoids

nithizaine, dinotefuran, thiacloprid


irritant, szs, resp dep
decon (skin), supportive care
Marine toxins

Ciguatera

tropics/subtropics; reef dwelling tropical fish



barracuda, moray eel, amberjack, grouper, mackerel, parrot
fish, red snapper
GI (N/V), CNS (palsies, paresthesias, hot/cold
reversal), CV (heart block, brady), fatigue/malaise
Scombroid



tuna, mackerel, skip-jack, bonito, mahi mahi, bluefish,
amberjack
flushing, rash, palpitations, tachycardia
anti-H1,2, epinephrine, beta-agonists
Heavy Metals

Multi-system toxicity

Acute






GI: N/V/diarrhea – most metal salt ingestions
Renal: proteinuria, aminoaciduria, ATN
CV: response to volume loss, dysrhythmia, congestive CM
CNS: dMS; periph neuropathies in hours to days
Hair/skin/nail changes: lag days -wks behind acute exposure
Chronic





CNS/PNS: predominate
Heme: anemias, cytopenias
Renal: CRI/CRF
CA: various
Skin: rashes, colored lines on nails/gums
Heavy Metals

Arsenic


ABCs, gastric emptying/AC

KUB to r/o residual GI content


inhaled dusts; copper/lead/zinc ore smelting; pesticides/herbicides;
naturally occurring well water
IM Dimercaprol (BAL) if can’t take po; ?add DMSA (meso-2,3dimercaptosuccinic acid) when GI tract clear
Mercury




Elemental- medical, Ore processing, mining, jewelry/battery making
Inorganic salts- batteries, calomel, dyes, fireworks
Organic- antiseptics, fungicides, by-products
supportive/ABCs; AC for HgCl



Milk, NAC, egg whites- may bind salts in gut
BAL: acute (esp GI) tox- not in organic Hg
DMSA: organic Hg, chronic or mild tox, when tol po
Heavy Metals

Lead


wrist-drop (PNS effects); Fanconi-like nephropathy;
plumbism-gout



crystal, solder, glaze, batteries, traditional meds
ABCs/supportive care
R/o GI burden; DMSA for sxs or elevated levels; BAL followed by Ca
EDTA if encephalopathy present
Thalium:



semi-conductors, insecticide/rodenticide, jewelry
salts; elemental/organic v. rare
GI absorp; ~ 1 g lethal dose in adults


MDAC likely helpful
Prussian Blue enhances gut elimination via K exchange
 BAL, EDTA, etc. not effective
References


New York City Poison Control Center. An intensive review course in clinical
toxicology; March 13-14, 2008. All Rights Reserved.
Toxicology and Pharamacology. In Emergency Medicine: A comprehensive study
guide, 6th ed. Tintinalli JE, Kelen GD, Stapczynski JS Eds. McGraw-Hill Companies,
Inc. 2004