NJ Poison Information

• Regionally certified Poison & Drug Information center
• Responds to poison and medication information questions from
– Health professionals
– Public

• Participate in other health related hotlines upon request:
• Corona virus
• Flu on call
• Ebola hotline
• Zikia hotline
• Lead hotline

1-800-222-1222

• Aspirin, acetylsalicilc acid, ASA

• Combination products
– ASA + opioid

• Other salicylates
– Methylsalicilate (e.g. Icy Hot, Bengay, Wintergreen Oil)
• 1 ml 98% methylsalicylate = 1.4 gm

– Topical products (can still be lethal)

Can be very slow orally;
– stomach and proximal intestine
– pH dependent
• ASA is a weak acid
• Stomach relatively acidic environment

Small intestine absorbs aspirin more than stomach does at pH ~6.5

• Protein binding
– Highly protein bound

• Protein binding influences
– where it distributes in the body
– removal by dialysis

> free drug vs bound in an OD situation $\rightarrow$ More amenable to dialysis

• Salicylic acid is a weak acid
– Exists primarily in the ionized state at physiologic pH
– Not permeable to cell membranes when ionized
– Becomes un-ionized as pH falls
– More permeable to cell membranes when un-ionized

1st order elimination
– $T_\frac{1}{2}$ ~ 2-4 hrs
– Conjugated with gluculrinic acid & glycine in liver
– Small % eliminated via urine

– N/V
– Abdominal pain
– Tinnitus
• vasoconstriction of auditory microvasculature

– Respiratory effects: fast, deep breathing = increased blood pH; respiratory alkalosis

• Respiratory alkalosis
$\uparrow$
• Direct stimulation of respiratory center in CNS (medulla)
– Increased rate and depth
– May not be seen in young children
– May be missed if the patient presents late

– uncoupling mitochondrial oxidative phosphorylation causes an increase in O2 consumption and CO2 production
• Enhances respiratory stimulation
• Heat loss

– Uncouples oxidative phosphorylation
• Disruption in cellular energy production
• Disruption of mitochondrial respiration
• Increases O2 consumption
• Increased CO2 production

• Increased pyruvic and lactic acid production
– Increased acidosis

• Disrupts Kreb’s cycle
– Accumulation of pyrivic and lactic acids

• Disrupts glycolysis
– Increased gluconeogenesis and lipid breakdown
• Increased ketone formation

– Inhibits liver lactate elimination
– Enhances insulin release
– decreases glucose utilization

Initially respiratory alkalosis $\rightarrow$ anion gap metabolic acidosis

• GI
– N/V/abdominal pain

• Pulmonary
– Tachypnea, hyperpnea, lung injury

• Cardiovascular
– Tachycardia
• Dehydration, hyperpyrexia

• Fluid and electrolytes
– kidneys excrete bicarbonate, sodium and potassium
• Bicarbonate loss contributes to metabolic acidosis

– Hypokalemia
• K loss in urine
• Intracellular movement from alkalosis
– From treatment

Insensible loss
Vomiting
Diaphoresis
Fever
Renal

• Manifestation of significant toxicity
– Agitation, confusion, irritability, and restlessness are early findings.
– lethargy then coma
– Seizures
• Acidemia
• Cerebral edema

• potentially toxic acute dose : >150 mg/kg

• serious toxicity possible : 300 to 500 mg/kg is ingested
• ~one adult tablet/kg

Fluids
• Need to be aggressive
• Most patients are dehydrated by the time they come in
• 1-2 Liters fluid to start
• 3-5 cc urine/kg/hr

Benzos - may be considered for agitation, but will make patient more acidotic. Need to understand the implications

• Large volumes of fluid with bicarb (get patient to stop absorbing aspirin) - alkalinize pt. urine to trap salicylates
– 3 Liters to start
– 2 amps bicarb push

1–2 mEq/kg of NaHCO3 IV bolus

• Follow with NaHCO3 drip to keep pH at 7.45-7.55 and output at 3-5 cc/kg/hr

• Add potassium as needed
– hypokalemia prevents alkalinization of urine

• Consider when?
– Levels > 80-100 mg/dl
• > 60 mg/dl in the chronic exposure
– Renal failure
– Altered mental status
– CHF
– Poor response