Case 24: 2yo - toxic ingestion Flashcards
mnemonic for altered mental statsu
AEIOU TIPS
A lcohol (other toxins) E pilepsy, encephalitis, endoctrine, electrolytes I nfection O verdose, opiates, O2 deprived U remia (renal failure)
T rauma, temp
I nsulin
P sychosis
S trike, shock, space-occupying lesions
physical exam findings for toxic ingestion: cholinergic
==> organophosphates
DUMBBELLS
D iaphoresis, diarrhea U urination M iosis == blurred vision B radycardia B ronchorrhea, bronchospasm E mesis L acrimation L oss of muscle (twitching and weakness) S alivation, seziures, coma
physical exam findings for toxic ingestion: anticholinergic
EKG
==> diphenhydramine, TCAs, atropine, pralidoxine
- blind as a bat ==> mydriasis (dilated)
- dry as a bone ==> dry skin, constipation, ileus, urinary retention
- mad as a hatter ==> delirium, seizures
- red as a beet ==> red skin (flushed), tachycardia
- hot as Hades ==> fever
EKG
- irregular irregular rhythm
- small P waves
- widened QRS ==> risk of dysrrhythmia, seizures, coma,hypotension
- prolonged QT
physical exam findings for toxic ingestion: sedative-hypnotic
v. opiates?
==> benzos, barbituates
- blurred vision (miosis / mydriasis)
- hypotension
- apnea, bradycardia
- hypotonia
- hypothermia
- sedation/confusion/delirium/coma
v. opiates ==> does NOT cause respiratory depression
physical exam findings for toxic ingestion: opiates
v. benzos?
==> codeine, morphine, heroin
- miosis (small)
- respiratory depression
- bradycardia, hypotension
- hypothermia
- sedation/confusion/delirium/coma
v. benzos = does NOT cause mydriasis
physical exam findings for toxic ingestion: sympathomimetics
==> cocaine, amphetamines, pseudophedrine
- mydriasis
- fever, diaphoresis
- tachycardia
- agitation, seizures
identify the drug that the kid took:
- decreased HR
- diaphoretic
- constricted pupils
- hyperactive abdomen
cholinergic
WET
closed eyes, open abdomen (PNS effects)
identify the drug that the kid took:
- decreased HR, hyperthermia
- dry skin
- dilated pupils
- hypoactive abdomen
anticholinergic
DRY
open eyes, closed abdomen (SNS effects)
identify the drug that the kid took:
- decreased HR, BP, RR
- altered sensory exam
- hypoactive abdomen
DOWNER
benzos
identify the drug that the kid took:
- decreased HR, BP, RR, hypothermia
- constricted pupils
- hypoactive abdomen
THE EYES
opiod
identify the drug that the kid took:
- increased HR, BP, RR, hyperthermia
- diaphoretic
- dilated pupils
- hyperreflexia
- hyperactive abdomen
everything is up
sympathomimetics == loosen the bowels
what are typical accidental ingestions in toddlers
iron supplements
acetaminophen
management of toxic ingestion
- considerations on whether to initiate decontamination
- methods of decontamination
considerations on whether to initiate decontamination
- amount and timing of ingestion
- nature of substance ingested
- patient sxs == mental status, airway security
methods of decontamination
- syprup if ipecac ==> secondary agent
- activated charcoal ==> for ingestions not due to small molecules or heavy metals; may need more if slow GI motility (NOT for pt with loss of protective airway reflexes, ? intubation)
- gastric lavage ==>
- cathartics ==> + activatedcharcoal
- hemodialysis ==>
- hemoperfusion ==>
- urinary alkalinization ==>
toxicity in a 2yo of nortiptyline (TCA)
- how much needs to be taken to cause toxicity:
- peak effect time post-ingestion:
- presentation
- mechanism of toxicity
- treatment
- how much needs to be taken to cause toxicity: > 2.5mg/kg (2 pills)
- peak effect time: 7-8h
-presentation == AMS, anticholinergic, HYPOTENSION, dysrrhythmia, seizure
- mechanism
1) inhibition of NorE, Seretonin
2) antagonism of muscarinic acetylcholine receptors and peripheral alpha receptors ==> peripheral vasodilation
3) blocked Na channels, GABA receptors ==> direct myocardial depression
treatment = activated charcoal + catharsis
- cardiac monitoring for 6h
- serum alkalinization, Na loading = hypertonic HCO3 (1mEq/kg) q3-5min until QRS narrows, hypotension improves. Continue for 12-24h after EKG normalizes d/t drug redistribution from tissues. goal pH = 7.5-7.55
- pH monitoring
- antiarrhythmia
- hypotension == voume expansion, serum alkalinization, Na loading (+/- norE)
- anti-seizure (benzos, barbiturates, propofol)
toxicity in a 2yo of glipizide
- how much needs to be taken to cause toxicity:
- peak effect time post-ingestion:
- how much needs to be taken to cause toxicity: 10mg tablet (hypoglycemia)
- peak effect time: 2-3h, lasting 24h
diffdx of ingestion causing altered mental status and mydriasis
- presentation:
- amount needed to cause sxs:
TCAs
- presentation: + agitation, cardiac (hypotension), anti-chol
- amount needed to cause sxs: 1-2 pills (>2mg/kg)
SSRIs
- presentation: diaphoresis, agitation, fever, AMS, diarrhea, myoclonus
- amount needed to cause sxs: SIGNIFICANT
Anti-histamine==> presentation (like TCAs) w/out cardiac problems
Decongestant (phenylphedrine) ==> presentation (SNS) =tachycardia, HTN, agitation, sweating, fever, mydriasis, seizures
Iron ==> severe abd pain, shock
beta-blocker ==> bradycardia
acetaminophen ==> GI problems, then liver toxicity
WITHOUT MYDRIASIS
- aspirin ==> agitation, tachycardia
- opioid ==> sedation, miosis
evaluation of altered mental status
- CBC ==> infection
- electrolytes ==> metabolic acidosis +/- AG (aspirin/NSAID)
- glucose ==> hypoglycemia
- calcium ==> abn levels can affected cardiac
- blood gas ==> metabolic acidosis +/- AG
- toxicology screen (urine, blood)
- acetaminophen levels == initially presents with minimal sxs
- EKG ==> dysrrhythmias
treatment of glypizide or insulin overdose
1) maintenance dextrose
2) octreotide (somatostain analog) == inhibit insulin release
why is it so easy to miss acetaminophen overdose?
while it’s one of the most common toxicities, it starts with minimal sxs
management of child with altered mental status
1) CAB + DFG (glucose)
2) then more info + hx + physical exam + tests
3) evaluation via tests +/- lumbar puncture
immediate treatment of hypoglycemia, hypotension, and tachycardia
1) boluses of 20cc/kg NS
2) 25% dextrose
3) MIVF of D10W + NS + KCl
is NGT indicated for toxic ingestion
NO == no clinical benefit
also technically difficult to pass a tube large enough in a 2yo kid
is syrup of ipecac indicated as first-line therapy for toxic ingestion?
NO –> d/t potential side effects (cardiac, seizures)
CONTRAINDICATED if risk of aspiration due to altered mental status
what are the top 5 in initial assessment of altered mental status?
What should be the steps in your initial assessment? (Select the top five.)
Multiple Choice Answer: A Obtain more history from the mother B Assess the patency of her airway C Observe for cyanosis or respiratory depression D Check the vital signs E Order a CT scan of the head F Check for evidence of circulatory compromise G Order a serum drug screen H Perform a complete neurological exam I Obtain a fingerstick blood glucose
B Assess the patency of her airway
C Observe for cyanosis or respiratory depression
D Check the vital signs
F Check for evidence of circulatory compromise
I Obtain a fingerstick blood glucose
ABC DFG
Which of the following medications would cause mydriasis (dilated pupils)? (Select all that apply.)
Multiple Choice Answer: A Diphenhydramine B Aspirin C Codeine D Pseudoephedrine E Lorazepam F Acetaminophen
what else?
antihistamines (anticholinergic)
pseudoephedrine (SNS)
TCAs
SSRIs
Which of the following medications would cause miosis (constricted pupils)? (Select all that apply.)
Multiple Choice Answer: A Diphenhydramine B Aspirin C Codeine D Pseudoephedrine E Lorazepam F Acetaminophen
which causes neither miosis or mydriasis
codeine (opiate)
cholinergics (organophosphates)
NEITHER
lorazepam
acetaminophen
aspirin
most common cause of death from TCA overdose
refractory hypotension
toxicity in a 2yo of iron
- how much needs to be taken to cause toxicity:
- peak effect time post-ingestion:
- presentation
- mechanism of toxicity
- labs
- complication:
- tx
- peak effect time post-ingestion: 6h
- presentation
1) GI hemorrhage == mucosal cell nephrosis ==> hematemesis, melena, GI edema, ulceration +/- infarction, necrosis
2) metabolic acidosis == mitochondrial toxicity –> inhibited Krebs, uncoupled ==> lethargy, tachycardia, metabolic acidosis oxidative phosphorylation ==> lethargy, tachycaria
3) shock == direct vasodilitation, negative ionotropy, hemorrhage ==> lethargy, hyperventilation, seizures, coma
4) coagulopathy == inhibited thrombin
5) hepatotoxicity - mechanism of toxicity: oxidative stress –> loss of cellular integrity ==> INCREASED Fe absorption
- labs == AG metabolic acidosis; anemia; high serum iron; elevated glucose/WBC
- tx
1) GI decontamination = polyethylene glycol
2) deferoxamine - complication: gastric outlet obstruction (2-8w) d/t strictures, scarring
indications for deferoxamine use
- Metabolic acidosis
- Repetitive vomiting
- Lethargy or toxic appearance
- Hypotension or signs or shock
- Serum iron concentration > 500 mcg/ml
indications for serum alkalinization for TCA toxicity
CARDIOTOXICITY == conduction delays, dysrrhythmias, hypotension
- QRS > 100 msec
- R wave in AVR > 3mm
- Wide-complex tachycardias
- Fluid-refractory hypotension
- Seizures
==> hypertonic HCO3 (1mEq/kg) q3-5min until QRS narrows, hypotension improves. Continue for 12-24h after EKG normalizes d/t drug redistribution from tissues. goal pH = 7.5-7.55
indications for serum alkalinization for TCA toxicity
CARDIOTOXICITY == conduction delays, dysrrhythmias, hypotension
- QRS > 100 msec
- R wave in AVR > 3mm
- Wide-complex tachycardias
- Fluid-refractory hypotension
- Seizures
==> hypertonic HCO3 (1mEq/kg) q3-5min until QRS narrows, hypotension improves. Continue for 12-24h after EKG normalizes d/t drug redistribution from tissues. goal pH = 7.5-7.55
what pressors are contraindicated in TCA toxicity?
beta-adrenergic agonists
dopamine
d/t effects on the heart
NorE is okay b/c it mostly works on vasoconstriction (not heart)
what anti-seizure meds are contraindicated in TCA toxicity?
phenytoin ==> cardiac toxicity
A 2-year-old female with normal birth and developmental history presents with increased agitation and decreased arousability. Her father suffers from chronic pain secondary to a back injury, and her mother found an open container of pills on the bed. Vitals reflect bradycardia, bradypnea, hypotension, and slight hypothermia. On physical exam, she exhibits somnolence, constricted pupils, hypoactive bowel sounds, and hyporeflexia. What substance was most likely ingested?
Single Choice Answer: Please select one answer. A Iron B Amitriptyline C Insecticides D Hydromorphone
D
decreased HR, RR, BP, Temp
constricted pupils
slowed bowels
Opioids such as hydromorphone can cause respiratory depression, bradycardia, hypotension, hypothermia, constipation, nausea, vomiting, sedation, confusion, and/or miosis.
A 2-year-old male presents to the ED with a 5-hour history of hyperactivity, fever, and sweating. His BP is 160/90 mmHg, HR 130 bpm, RR 30 bpm. On exam, he has dilated pupils, cool skin, and hyperreflexia. What is his most likely accidental medication ingestion?
Single Choice Answer: Please select one answer. A Pseudoephedrine B Codeine C Iron pill D Acetaminophen E Propranolol
A
increased HR, T, BP, RR
diaphoresis
mydriasis
vasoconstriction
SNS
Ingestion of a sympathomimetic like pseudoephedrine stimulates the beta and alpha adrenergic receptors, causing elevated HR, RR, BP and hypothermia along with diaphoresis, dilated pupils, hyperreflexia, and hyperactivity.
toxicity in a 2yo of acetaminophen
- how much needs to be taken to cause toxicity:
- peak effect time post-ingestion:
- presentation
- mechanism of toxicity
- labs
- complication:
- tx
- how much needs to be taken to cause toxicity: 150mg/kg
- peak effect time post-ingestion: <1h
- presentation: (1) N/V, malaise, diaphoresis –> (2) hepatotoxicity, AST elevated first, PT prolonged next, (3) fulminant hepatic failure, coaguopathy
- mechanism of toxicity: metabolized in the liver ==> depleted glutathione, accumulation of NAPQ1
- labs: acetaminophen levels (4h post); AST
- complication:
- tx (indicated when elevated AST)
1) control of N/V
2) charcoal 1g/kg
3) NAC (esp within 8h)
You are working in the pediatric ED when a 3-year-old girl, Jenny, presents with altered mental status for the past six hours. Her mother reports that the babysitter called her at work today after Jenny started acting agitated and “looking very sick.” The mother reports “she feels so warm, I think she has a fever and has become dehydrated.” On exam, the patient is agitated and anxious with dilated pupils. Her skin is warm and dry. Vitals reveal tachycardia and hypotension. You suspect the child may have accidentally ingested one of her mother’s medications. An overdose of which of the following medications could cause Jenny’s symptoms?
Single Choice Answer: Please select one answer. A Tricyclic antidepressant B SSRI C Decongestant D Acetaminophen E ACE inhibitor
A
6 hours ago
mydriasis = TCA
NOT SSRI, decongestant (SNS), acetaminophen, ACEI
increased HR
decreased BP
TCA toxicity presents with agitation, tachycardia, hypotension, dilated pupils, and hot, dry skin from the anticholinergic effects of TCAs.
B. SSRI is incorrect, because serotonin syndrome will usually present with a fever and sweaty, not dry, skin. Also, serotonin syndrome usually does not present with hypotension.
C. Decongestant is not the correct answer. Decongestant overdose will elicit a sympathomimetic response, including agitation and tachycardia. However, unlike TCA overdose, decongestant overdose will cause hypertension, constricted pupils, fever/sweating. Additionally, severe overdose of decongestant may cause seizures.
D. Acetaminophen is not the correct answer. Acetominophen overdose will produce mild and nonspecific symptoms and include right upper quadrant pain, with elevation in liver enzymes, resulting in liver failure at toxic levels.
E. ACE inhibitor is not the correct answer. The typical adverse event for ACE inhibitors is cough.
A 2-year-old male is brought into the ED by his mother because of vomiting and altered mental status. He has pinpoint pupils and seems to be drooling and sweating uncontrollably. His heart rate is 60 bpm, his respiratory rate is 45 bpm, and he seems to have difficulty breathing. Which ingestion is the most likely cause of his symptoms?
Single Choice Answer: Please select one answer. A Organophosphates B Tricyclic antidepressant C Barbiturates D Codeine E Pseudoephedrine
A
vomiting, AMS
pinpoint pupils + WET (drool, sweat)
== cholinergic
Increased RR, SOB (bronchorrhea, bronchospasm)
Organophosphates cause cholinergic effects, such as miosis, sweating, lacrimation, salivation, urination, increased gastric mobility (vomiting, diarrhea), muscle twitching, bronchospasm, bradycardia, and seizures. A good mnemonic is SLUDGE (salivation, lacrimation, urination, defecation, GI mobility, emesis).
