Case Report
A 29-year-old white female with a previous history of bipolar disorder and multiple previous suicide attempts was brought to a local emergency room by her boyfriend for evaluation and treatment of abnormal behavior. Reportedly, a dispute had occurred between the patient and her boyfriend the evening before admission, and she subsequently had ingested an unknown amount of prescription medications possibly 2 hours prior to her early morning arrival in the emergency department (ED). A review of her medications revealed that she had been taking acetaminophen/propoxyphene 650/100, diphenhydramine, diazepam, and Depakote (divalproex). Shortly after her arrival in the ED, she was given 50 g of activated charcoal orally.
On examination, the patient smelled of alcohol and was disoriented. Her temperature was 98.7°F, pulse was 140 beats/minute, respiratory rate was 32 breaths/minute, and blood pressure was 158/87 mm HG. Pupils were equal at 2 cm and slowly reactive to light. The neck showed no evidence of thyromegaly, jugular venous distension, or adenopathy. The cardiovascular examination revealed a regular rhythm with notable tachycardia without murmurs. The lungs were clear. The abdomen had positive bowel sounds, was soft, nontender, with no hepatosplenomegaly. The extremities revealed no clubbing, cyanosis, or edema, and no IV tracks were noted. Skin revealed multiple tattoos, but no rashes or lesions were noted. Neurologically, the patient was disoriented and unable to obey commands but freely moved all extremities with downgoing plantar reflexes (Glasgow Coma Scale [GCS] 11).[4]
Initial laboratory studies revealed a serum ethanol level of 79 mg/dL, an acetaminophen level of 138.7 ug/mL, a VPA level of 336.9 ug/mL, a negative salicylate level, and a urine drug screen that was positive for THC. Her serum B-HCG level was negative. Serum sodium was 138 meq/L, potassium 3.2 meq/L, chloride 109 meq/L, bicarbonate 17 meq/L, BUN 12, creatinine 0.9, and glucose 116 mg/dL. The white blood cell count was 11.1 103 uL, hemoglobin 14.6 g/dL, hematocrit 42.2, and platelets 243 103 uL. Liver function tests showed an albumin of 4.8 g/dL, total bilirubin of 1.0 mg/dL, direct bilirubin of less than 0.2 g/dL, alkaline phosphatase of 62 IU/L, aspartate aminotransferase of 26 IU/L, alanine aminotransferase of 13 IU/L, and total protein of 7.4 g/dL. Cardiac enzymes were normal. Electrocardiogram revealed sinus tachycardia with no ischemic changes. Her initial chest x-ray was unremarkable. The patient was admitted to the ICU during the early morning hours.
After arrival in the ICU, an attempt for placement of a nasogastric tube was made, but due to combative behavior, 2 mg of intravenous midazolam were given for sedation. N-acetylcysteine via nasogastric tube was initiated per protocol[5] due to uncertainty about time of the polysubstance ingestion and the patient's risk factors for hepatic toxicity with the acetaminophen overdose. During the late afternoon hours, the patient was noted to be unresponsive. The neurologic examination revealed that the she was in a deep coma; she had an absent corneal reflex with no response to painful stimuli (GCS 3). The patient was subsequently intubated and placed on mechanical ventilation for airway protection. A stat magnetic resonance imaging scan of the brain revealed no abnormality or cerebral edema. Her arterial blood gas prior to intubation showed a metabolic acidosis with a superimposed respiratory acidosis (pH 7.16, PO2 85 mm Hg, PCO2 57 mmHg). Her serum VPA level was rechecked and had significantly increased to 904.0 mcg/mL.
Naloxone 0.4 mg intravenously times 2 doses was given to the patient, with notable improvement of her neurologic exam. Specifically, she regained her corneal and gag reflexes, would respond to painful stimuli, and would move in response to her name and briefly open her eyes (GCS 8). A second dose of activated charcoal was then given to the patient per her nasogastric tube. Supportive care and monitoring was continued. Hemodialysis was considered as a possible therapeutic intervention to decrease her serum VPA level. After consultation, however, the Renal Service did not feel that this had any proven benefit.
By day 2, her morning arterial gas showed a worsening metabolic acidosis. The patient's serum chemistries showed evidence of pancreatic dysfunction, hypocalcemia, hypokalemia, hypernatremia, lactic acidosis, and hyperammonemia, but her renal function remained stable ( Table ). The serum VPA level had decreased to 458.0 uG/mL and acetaminophen to 102.4 uG/mL. She was also found to be hepatitis B core antibody and hepatitis C antibody positive. The patient also developed a fever and elevated white blood cell count of 14.1 103 uL. Her urinalysis was positive for bacteria and white blood cells. A chest x-ray showed a new right lower lobe infiltrate and sputum; blood and urine cultures were obtained. In consultation with the Pulmonary/Critical Care Service, the decision was made to add bicarbonate to her IV fluids. We also initiated IV ampicillin-sulbactam for probable aspiration pneumonia. L-carnitine at 100 mg/kg/day was begun via nasogastric tube.
By day 3, her white blood cell count had decreased, serum electrolytes began to normalize, her metabolic acidosis had resolved, and serum VPA and acetaminophen levels continued to decrease along with improvement of her amylase and lipase levels. The patient's condition continued to improve, and she was extubated. Her mental status improved and level of consciousness returned to normal. Psychiatry evaluated the patient and recommended continuing inpatient therapy since she was still suicidal.
By day 6, the patient's laboratory values had completely normalized ( Table ) and she displayed no signs of residual health problems as a result of her drug overdose. The patient was transferred to an inpatient psychiatric facility for continuing therapy.
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Cite this: Valproic Acid Overdose: A Case Report and Review of Therapy - Medscape - Jan 15, 2003.
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