Clinical Side of Tox Flashcards
most common route of exposure for POISON
ingestion (83%)
inhalation next with 7%
fundamental approach to the poisoned patient
airway
breathing
circulation
decontamination or avoid abs
elimination or enhance excretion
find an antidote
airway can be in danger due to:
- sedation = low airway smooth muscle tone
- inhalation of toxin or vomit (ASPIRATION)
- increased secretions
protect airway early and continually assess!!
if breathing effort poor but patient’s airway is open =
sedation
aspiration
if breathing is poor, you or machine must breathe for the poisoned pt
mouth to mouth
bag-valve mask ventilation (BVM)
advanced airway
how to position for ventilation
head tilt, chin lift
jaw thrust
circulation assesses for signs of..
poor perfusion
- heart rate, BO, skin temp, pulses, urine output
- establish vascular access early in poisoned pt
where to check for pulse
carotid or radial pulse
CPR is as easy as …
Compression = push hard and fast on victim’s chest
Airway = tilt victim’s head and lift chin to open airway
Breathing = give mouth-to-mouth rescue breaths
signs of POOR perfusion
- tachycardia
- tachypnea
- hypotension
- mottled skin
- altered mental status
- weak pulses
- delayed capillary refill
- cool skin
treatment for poor perfusion
IV fluids
meds to increase BP = inotropes = epi, norepi, dopamine, dobutamine
what is the goal of decontamination
to prevent or minimize absorption
options for decontamination
activated charcoal
emesis
whole bowel irrigation
gastric levage
when is gastric lavage ideally performed
in first 4 hrs
complications of gastric lavage
aspiration pneumonitis
GI tract perforation
when do we ideally give activated charcoal for decontam?
within first hour
- complications: aspiration, small bowel obstruction
when will activated charcoal fail?
PHAILS
pesticides
hydrocarbons
acids and alkali
iron
lithium
solvents
how does whole bowel irrigation help with decontamination?
decrease absorption by decreasing transit time
uses PEG through nasogastric tube
greatest utility of whole bowel irrigation
iron
lead
lithium OD
sustained release tablets
only the sickest or those w potential for severe deterioration do we use THIS technique
ELIMINATION
elimination techniques
urine alkalization
hemodialysis
urine alkalization
- NAHCO3 intravenously to produce urine pH >/=7.5
urine alkalization increases urine elimination of:
chlorpropamide (type II DM)
2,4-dichlorophenoxyacetic acid and Mecoprop (herbicides)
fluoride
methotrexate (chemotherapy)
phenobarbital (antiseizure)
salicylate
medication properties of hemodialysis
low Vd (<1L/kg)
single compartment kinetics
low endogenous clearance (<4 ml/min/kg)
MW <500 daltons
water sol
not bound to plasma proteins
examples of hemodialysis
salicylates
theophylline
uremia
methanol
barbiturates
lithium
ethylene glycol
antidote: acetaminophen
N-acetylcysteine (NAC)
antidote: anticholinergic
physostigmine
antidote: benzodiasepines
flumazenil
antidote: CO
oxygen
antidote: cyanide
hydroxocobalamin, sodium nitrite, sodium thiosulfate
antidote: digoxin
digoxin-specific Fab
antidote: ethylene glycol
ethanol, fomepizole
antidote: iron
deferoxamine
antidote: methanol
ethanol, fomepizole
antidote: methemoglobinemia
methylene blue
antidote: opioids
naloxone
antidote: organophosphates
atropine, pralidoxime
4 key questions in history taking
what
when
how much
what is patient’s weight?
tox physical exam (5)
vital signs = HR, BP, R, T, O2 sat
skin
pupils
bowel sounds
neuro exam
other clues?
miotic
little pupil
mydriatic
big pupil
bitter almonds toxin
cyanide
carrots smell toxin
water hemlock
fishy smell toxin
zinc or aluminum phoshide
fruity smell toxin
ethanol, acetate, isopropyl alcohol, chloroform
garlic smell toxin
arsenic
DMSO
organophosphates
yellow phosphorus
glue smell toxin
toluene, solvents
pear smell toxin
paraldehyde
chloral hydrate
rotten egg smell toxin
hydrogen sulphide
DMSA
N-acetylcysteine
shoe polish smell toxin
nitrobenzene
wintergreen smell toxin
methyl salicylate
T or F. Everys ingle tox patient gets an ECG
T
common toxidromes
sedative/hypnotic
opioids
cholinergic
antichloniergic
sympathomimetic
Quaaludes
sedative/hypnotic
methaqualone
sed/hypnotic drugs
quaaludes
benzos
barbiturates
ethanol
effects of sed/hypnotic drugs
- general anesthesia
- complete loss of awareness and reflex
- mixing common here = dangerous!!
sed/hypnotic signs
pupil = normal
RR = decreased
BP,HR = slightly decreased
Skin = normal
mental status = sedated
bowel sounds = normal
antidote for sed/hypnotic
flumazenil for benzo but need t be cautious
opioids drugs
heroin
morphine
codeine
oxycodone
fentanyl
opium
hydromorphone
Percocet (Tylenol and oxy)
tramadol
triad of symptoms in opioid overdose
pinpoint pupils
uconsciousness
respiratory depression
T or F. pronounced resp depression in opioid intake
T! RR often diminished before decreases in BP/HR occur
opioid symptoms
pupil = small, fixed or pinpoint
RR = decreased
BP,HR = slightly decreased
Skin = normal
mental status = euphoria to coma
bowel sounds = decreased
antidote for opioids
naloxone
these are common in terrorist attacks
cholinergic
what arecholinergic drugs
organc phosphorus compounds = pesticides, nerve gases such as sarin gas
carbamates
mushrooms = boletus, Clitocybe sp, Inocybe sp
RARE
foundation of nerve agents
cholinergic
Cholinergic drugs can harm these healthcare workers
first responders!!! giving mouth-to-mouth
symptoms of cholinergic toxidrome
pupil = small, fixed, lacrimation
RR = normal/increased
BP,HR = increased/decreased
Skin = wet
mental status = conusion/drowsiness to coma, seizures
bowel sounds = increased
other = SLUDGE and killer B’s, pulmonary edema, fasciculations,
weakness -> paralysis
antidote for cholinergic
atropine, pralidoxi,e (2-PAM) = cholinesterase regenrator
this toxidrome is due to massive discharge of parasymp nervous system
cholinergic
killer B’s
bronchorrhea
bronchospasm
bradycardia
cholinergic
SLUDGE
cholinergic
salivation
lacrimation
urination
diarrhea
GI distress
emesis
anticholinergic drugs
anticholinergic
antihistamines
antipsychotics
antidepressants
Jimson weed
symtoms of anticholinergic toxidrom
pupil = big, fixed, blurred vision (CARTOON-like)
RR = normal
BP,HR = HR increased
Skin = dry, hot, flushed
mental status = delirium, coma, seizures
bowel sounds = decreased
other = urinary retention (sometimes can’t communicate so insert catheter to decrease pt agitation)
anticholinergic memory aid
mad as a hatter, hot as hades, red as a beet, dry as a bone, blind as a bat. the bowel and bladder lose their tone and the heart goes on alone
sympathomimetic drugs
stimulants
amphetamines
cocaine
ephedrine (Ma Huang)
meth
phenylpropanolamine (PPA’s)
pseudoephedrine
sympathomimetic symptoms
pupil = large, reactive
RR = increased
BP,HR = increased
Skin = wet
mental status = agitation, delirium, psychosis
bowel sounds = increased
other = tremor, myoclonus, increased temp
antidote for sympathomimetic
none but benzos for agitation
antidote for anticholinergic drugs
consider phygostigmine
massive sympathomimetic overdoses symptoms
cardiovascular collapse = hypotension
shock
dysrhythmias
piloerection may be seen in this toxidrome
sympathomimetic
blood gases
pH
hemoglobin
lytes
glucose
lactate
CO level
methemoglobin level
look at each result then calculate AG and OG
a normal pH and anion gap rules out many ingestions
ASA
cyanide
toxic alcohols
metabolic acidosis with resp alkalosis
salicylates
metabolic acidosis with increased lactate
metformin
anion gap
cations - anions
sodium - (bicarb + chloride)
if AG is >____, this implies unmeasured ______ from a toxic or metabolic source
12; anions
elevated AG is strongly suggestive of this
metabolic acidosis
high anion gap metabolic acidosis drugs
MUDPILES
methanol
uremia
diabetic ketoacidosis, etc.
paraldehyde
iron, isoniazid
lactic acidosis
ethylene glycol
salicylates
osmolal gap
measured - calc osmoles
- should be 0-10 (-12 to 1)
- unaccounted osmoles (elevated OG) may signify a toxic alc ingestion
= but not sensitive enough to rule out
calculated osmoles
2(Na+) + urea + glucose
290-300
these caused increased OG
SAGMMAP
sorbitol
alcohols
glycerol
maltose
mannitol
acetone
polyethylene glycol, propylene glycol
what is the tox screen?
urine screen for various drugs of abuse
= rarely results in ID of ingestion agent
= results not usually available until hrs/days after most of acute treatment decisions are made
= very expensive!
one pill can kill
cardiac medications
antidepressants
antimalarials
isoniazid
iron
sulfonylureas
rec sympathomimetic drugs
opiates
oil of wintergreen
ASA toxic dose
150-200 mg/kg
severe intoxication of ASA
300-500 mg/kg
what do we initially see after ASA ingestion?
resp alkalosis
- direct stimulation of medulla/breathing center
then develop elevated AG metabolic acidosis
- impaired renal function due to acid production
- interference w Krebs
- uncoupling oxidative phosphorylation
clinical presentation of ASA ingestion
vomiting
hyperpnea (increase depth and breathing rate)
lethargy
tinnitus
mixed resp alk and metabolic acidosis
severe ASA intoxication presentation
coma
seizure
hypoglycemia
hyperthermia
pulmonary edema
ASA decontam
gastric decontam : activated charcoal and consider whole bowel irrigation if enteric coated
elimination for ASA
urinary alkalization
- indicated when symptomatic, acute salicylate level >2.5 mmol/L or rising, significant acid-base disturbance
hemodialysis
- indicated when >7mmol/L, chronic >3.5, altered mental status (coma, seizure), intubation, pulmonary edema, renal or hepatic failure, failure of urinary alkalinization
acetaminophen toxic dose
> 150 mg/kg
overdose PK of acetaminophen
sulfation and glucuronidation pathways become saturated, shunting acetaminophen towards P450 pathway resulting in increased NAPQI production
detox of NPQI depletes glutathione
glutathione below 30% = NAPQI binds non-specifically to intracellular proteins resulting in cell dysfunction
phases of acetaminophen poisoning
phase I (<24h)
- anorexia, nausea/vomiting, malaise
phase II
- most symptoms resolve
- right upper quadrant abdominal pain
- start seeing abnormal labs such as high AST/ALT, high bili, high INR
phase III
- sequelae of hepatic necrosis = jaundice, coagulopathies, encephalopathy, hypoglycemia
- renal failure
myocardial dysfunction
phase IV
- 4d-2wk
- after hepatic failure
- complete resolution of injury; no residual liver dysfunction
- need for urgent liver transplantation
- death
this is available to help decide if treatment is needed for acetaminophen level
nomogram
- indicated only in acute ingestions
- need time of ingestion
NAC
N-acetylcysteine
- glutathione precursor/substitute
- enhances sulfation
- free radical scavenger
- enhances hepatic oxygen delivery
- decreases cerebral edema and hypotension
- initiate within 8hrs
- 21hr protocol
- oral or IV dosing
Decontam and antidote for Acetaminophen
charcoal
NAC
what does CO bind with?
hemoglobin (250x greater affinity than O2)
myoglobin
cytochrome oxidase
induces lipid peroxidation also
what causes CO poisoning?
incomplete combustion of fossil fuels
> fires
> engine exhaust
> propane-powered vehicles
> home heating, gas stoves, dryers, water heaters
methylene chloride (paint strippers)
T or F. CO shifts oxygen dissociation curve to right
F! shits to left
Rate of elimination for CO depends on …
rate of dissociation
clinical symptoms of CO
CNS:
headache, nausea, blurred vision, altered LOC, ataxia, seizures, coma
CVS:
dyspnea, weakness, angina, palpitations, hypotension, MI, dysrhythmias
this percentage of CO is rapidly fatal
> 80&
60-70% = seizures/death
this percentage of CO is normal
1-5%
5-10% in smokers
management for CO poisoning
remove from source
ABCs
F: 100% supplemental O2 = hyperbaric O2 if indicated
labs
- COHb level by co-oximetry (NOT PULSE)
- assess end-organ damage
- preg test
T or F. Ethanol is not a toxic alcohol
T! b/c metabolite not toxic
- CNS depression, resp depression and hypoglycemia due to inhibition of gluconeogenesis
clinical presentations of ethylene gkycikl
stage I: acute neurologic, slurred speech, ataxia, vomitting
stage II: cardiopulmonary: hypertension, tachycardia, tachypnea, ARDS, CV collapse
III: renal; flank pain, hematuria, proteinuria, oliguria => anuria
labs for eth glycol
elevated OG
high AG metabolic acidosis without signifcant lactates/ketones
hypocalcemia from formation of oxylate
this is used in gas line antifreeze and windshield washer fluid
methanol
clinical findings for methanol
inebriation
visual changes
abdominal complaints
labs for methanol
high AG metabolic acidosis without significant lactate or ketones
pH <7.2 predictive of impaired visual acuity
elevated OG
treatment for toxic alcohol ingestion
block alc dehydrogenase (ADH)
> ethanol or Fomepizole
> risk of hypotension, tachycardia, CNS/resp depression, hypoglycemia, electrolyte derangement, gastritis
sodium bicarb to correct acidosis
adjuncts (folate, pyridoxine, thiamine)
dialysis to remove parent alc and metabolites
what is fomepizole?
competitive inhibitor of ADH
benefits over alcohol:
- no increased sedation or resp depression
- avoid hypoglycemia
BUT EXPENSIVE!
indications for hemodialysis
met acidosis
renal failure
deterioration despite other treatments
electrolyte disturbances
visual disturbance (methanol)
methanol level >15 mmol/L
ethylene glycol >8 mmol/L
elim for toxic alcs
hemodialysis
adjuncts for toxic alcohols
folate, pyridoxine, thiamine
sodium bicarb
