P0899 - Still in Shock: A terrifying tale of refractory hypotension

Initial History/Presentation:
Previously healthy 12 year old female presenting after a witnessed 2 minute syncopal event in the setting of 1 week of nausea and abdominal pain.

Physical exam:
By ED arrival, she had returned to full consciousness. She was afebrile, mildly tachycardic with a HR of 109, and hypotensive to 84/43. Her exam was normal other than mild tenderness over the left scapula and epigastrium.

Diagnostic Evaluation:
Her lab work was significant for an elevated lactate, mild leukocytosis, bicarbonate of 19, creatinine of 1.06, hyperglycemia (224), negative urine toxicology, and negative blood and urine cultures. Aggressive fluid resuscitation did not improve her blood pressure. Ceftriaxone and vancomycin were empirically given for 48 hours. Blood pressures remained critically low, and she was started on continuous dopamine, epinephrine, norepinephrine and vasopressin. She was also started on an insulin drip for persistent hyperglycemia. Over the next several days, her symptoms self-resolved and she was able to wean off of all support. She was transferred to the general floor at her baseline, however without a source of her presentation. Due to the self-resolution of symptoms and negative workup for other causes, toxicologic causes were added to the differential. Discussion with a toxicologist revealed that the presentation was highly consistent with a calcium-channel blocker (CCB) overdose. On further investigation, 16 pills were found missing from mom’s bottle of prescribed amlodipine. The patient eventually admitted to taking these pills intentionally in a suicide attempt.

Diagnosis:
This presentation of syncope, non-fluid responsive shock, acidosis, acute renal failure, and hyperglycemia was consistent with CCB overdose.

Discussion/

Conclusion:
CCBs are among the most commonly prescribed medications in the United States and the most lethal when overdosed, in particular amlodipine due to its long half-life of 30-50 hours. CCB intoxication is challenging to diagnose, as the clinician must rely only on signs and symptoms with no rapid blood level test available. CCBs cause peripheral vasodilatation, suppress pancreatic insulin release, and decrease fatty acid uptake by cardiac myocytes, and when consumed in excess can lead to profound non-fluid responsive hypotension, hyperglycemia, and acidosis. Treatment can include calcium gluconate, or glucagon to reverse the calcium channel blockade, as well as pressors for hypotension, and insulin drip for hyperglycemia. Earlier identification of CCB intoxication may have decreased the patient’s 5-day course in the Intensive Care Unit, and led to earlier psychiatric intervention.