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Likely Environmental
Most Likely Environmental
Culprit?
Carbon Monoxide
Carbon Monoxide
What tests?
Carboxyhemoglobin concentration
What about O2 Saturation?
Patients was 99% (room air)
Carbon Monoxide Poisoning
Remember colorless and odorless
Why did our patient get better in the
hospital?
Why wasnt Dad symptomatic?
What do you do as the health care
provider?
Case 2
10 month old little boy, brought by EMS in
December 2010
Presents with increased work of breathing
for 1 day and vomiting x 4
Past medical history: asthma, gastro-
esophageal reflux, developmental delay
Physical Exam
HR 186, RR 72, BP 92/56, Temp 38.3C,
Sat 100%
Mental Status: appears dazed and sleepy
HEENT: sunken eyes, dry lips
Chest: rapid breathing, almost panting,
equal BS bilaterally, no audible wheezing
Abdomen: soft, slightly distended
Skin: cool, mottled extremities; no
evidence of trauma
Progression
Albuterol nebulizer started by nurse
Intravenous access obtained
Electrolytes sent
20 mL/kg bolus initiated
Continuous monitoring
Ill-appearing!
Evaluation
Airway: patent
Breathing: almost panting
Circulation: capillary refill (> 4 sec)
Disability/Dextrose: 168 mg/dL
Exposure: no bruising
iSTAT 8: Na, K, Cl, bicarbonate, serum
urea nitrogen and creatinine
Differential Diagnosis?
Infection
Trauma
Toxin
Neoplasm
Severe Sepsis
Salicylate Poisoning
Progression
More thorough history suspecting an
inborn error of metabolism??
Miscarriages?
Medications?
Ingestions?
Over the counter preparations?
Only Maalox for his GE reflux
Tell Me More About the
Maalox
Well it was on sale at the pharmacy and
we had a coupon. I asked his
gastroenterologist if I could use the
Maalox Maximum Strength and she said
okay
I am giving 2 tablespoons every 4 hours
Poison Control Center
1-800-222-1222
Maalox Maximum Strength contained
bismuth subsalicylate 525 mg/15ml
Receiving 30 ml each 4 hours,
235-320 mg/kg for days
His salicylate level was 98 mg/dL
Most Important Intervention???
Hemodialysis
Pharmacokinetics
Salicylate is rapidly absorbed from the GI
tract (predominantly the jejunum)
Metabolized by the liver (first order
kinetics: glucuronidation, oxidation,
glycine conjugation)
In an overdose, switches to zero order
kinetics, so at increased doses the half-life
is greatly increased up to 30 hours
Mechanism of Action
Activation of the respiratory center of the
medulla
Uncoupling of oxidative phosphorylation
leads to metabolic acidosis, hyperpyrexia,
fluid loss
Inhibition of tricarboxylic acid leads to
metabolic acidosis
Clinical Manifestations
Intoxication may be acute, chronic or acute-on-
chronic (our patient)
Fatal salicylate intoxication may occur with as
little as 3 grams in children
Death is usually from severe CNS toxicity and
loss of function of the cardiorespiratory center
Hallmarks of salicylate overdose include:
hyperpnea, metabolic acidosis, and tachycardia.
Severe overdose can cause altered mental
status, coma, non-cardiac pulmonary edema and
death.
Case 3
Previously well 4 year old boy
On way back from New York (car trip)
Difficult to arouse in back seat of car
VS: T 37C HR 90, RR 6-14, BP 90/60
Three sibs are fine: ages 1, 3 and 6 yrs
FHx: Mom, history of anxiety, Dad nil
Parents say no meds available to him
Arrives at Community Hospital
Very sleepy, difficult to arouse, no external
evidence of trauma
RR 6-12, with stimulation higher
HR 64-66
BP 82/54
Pupils 1-2mm
Approach?
Approach
Airway
Breathing
Circulation
Disability/Dextrose
Exposure
Differential Diagnosis
CNS Depression - AEIOU TIPS
Alcohols
Epilepsy: partial, complex, status, or post-ictal
Ingestion
Opiates
Uremia (chronic, not acute)
Fever Infection