Posters IV - The American Academy of Clinical Toxicology

contracture of the right face and received lorazepam 2 mg. Pupils were equal and sluggishly reactive. She
withdrew to pain. Heart, lungs, and abdomen were unremarkable. She was intubated for airway protection.
Initial labs were significant for arterial pH 7.12, pCO2 41, pO2 220, Na 138 mmol/L, K 3.6 mmol/L, Cl
104 mmol/L, CO2 16 mmol/L, AG 18, BUN 7 mg/dL, creatinine 0.6 mg/dL, glucose 198 mg/dL, Ca 9.2
mg/dL, ALT/AST 31/51 U/L, lactate 5.1 mmol/L, CK 91 U/L, ketones negative, urine: no crystals, ECG:
ST 111, QRS 82, QTc 413. Ethanol, acetaminophen, salicylate, methanol, and ethylene glycol were
undetectable. Head CT, CSF cell counts and chemistries were normal. After transfer to a children's
hospital, EEG showed diffuse slowing, consistent with encephalopathy. A bicarbonate infusion was begun
for acidemia, and stopped 2 days later when the patient was extubated. Family found a bottle of ibuprofen
800 mg in her room with 70 pills (56 g) missing. Serum ibuprofen level was > 250 mcg/mL (therapeutic
10-50). The patient developed transient hyperrnatremia to 159, which resolved by hospital day 2. At
transfer from the ICU, she had uncoordinated movements of all extremities. By post-ingestion (PI) day 3,
mental status had normalized, but she was unable to ambulate due to ataxia. She received physical therapy
twice daily. On PI day 4 she could ambulate with assistance. On PI day 6, she was able to tandem walk
without deficit. She recovered fully and was transferred to a psychiatric unit. Discussion: Acidosis,
seizure, and CNS depression have been reported with large ibuprofen overdoses. In this case, a previously
unreported finding of gait ataxia was prominent, requiring physical therapy and prolonging hospital stay.
Ataxia resolved by PI day 6, making anoxic injury an unlikely etiology. Comprehensive drug screening
was not done, but according to the patient, her family, and pharmacy, she had no access to other
medications. Although the mechanism is unclear, other etiologies of ataxia seem unlikely. Conclusion:
Ataxia may be a previously unrecognized complication of severe ibuprofen toxicity. Further study is
warranted to elucidate the mechanism.
306
Acute Acepromazine Overdose: Clinical effects and toxicokinetic evaluation
D. Adam Algren, Amber Ashworth
Background: Acepromazine, a phenothiazine derivative, is used as sedative in veterinary medicine. Cases
of acepromazine overdose are infrequently described and toxicokinetic data has not been previously
reported. We report a case of intentional acepromazine overdose resulting in central nervous system
(CNS)/respiratory depression and hypotension with confirmatory toxicokinetic data. Case Report: A 54
year old woman reported intentionally ingesting 950mg of her dog's acepromazine. She denied other coingestants.
Her past medical history was significant for depression, anxiety, and hypothyroidism. She
denied current medication use. She was evaluated in an emergency department within 1 hour of her
ingestion and was alert with normal vitals signs. Physical examination was unremarkable. Activated
charcoal was administered. CBC, electrolytes and LFT's were normal. Serum acetaminophen, salicylate
and alcohol were undetectable. Urine drug screen was negative for drugs of abuse. An EKG demonstrated
normal intervals. Over the proceeding two hours the patient developed increasing somnolence, tachycardia
and hypotension. The HR ranged from 100-130/min and the systolic BP was 70 mmHg. ABG
demonstrated a mild respiratory acidosis. Bipap and a norepinephrine drip were instituted. Clinically she
improved over the next 12 hours at which time the Bipap and norepinephrine were discontinued. Repeat
laboratory studies and EKG's remained normal and the patient was transferred to a psychiatric facility the
following day. Serial plasma acepromazine levels were determined using GC/MS. The initial
acepromazine level (1 hour post-ingestion) was 63 ng/ml. Follow up levels at 8, 10.5 and 13.5 hours post
ingestion were 7.6 ng/ml, 8.9 ng/ml and 6.3 ng/ml, respectively, resulting in an elimination half-life of 3.1
hours. Case discussion: Acepromazine is structurally similar to chlorpromazine. It is used in dogs and