Failure of high-dose insulin and intravenous fat emulsion in two patients with poison-induced cardiopulmonary arrest after 2-CE use [abstract #55] Abstract uri icon
  • Background: High Dose Insulin (HDI) and Intravenous Fat Emulsion (IFE) are promising therapies for the treatment of Poison-Induced Cardiogenic Shock (PICS). The American College of Medical Toxicology recently published a position that IFE is "a reasonable consideration for therapy, even if the patient is not in cardiac arrest." We describe 2 cases of PICS that died despite early aggressive therapy with IFE and HDI. In both situations IFE was given while the patient still had a pulse and immediate cardiac arrest ensued.
    Case 1: A 50-year-old woman presented after an overdose (OD) of 80 total tabs of metoprolol 50 mg and bupropion XL 150 mg. She had profound bradycardia and hypotension refractory to IV fluids, 41 mEq of Ca 2, 10 mg of glucagon, and a HDI infusion of 10 U/kg/hr. With a pulse of 40 bpm and mean arterial pressure (MAP) of 30 mmHg, a bolus of 1.5 mL/kg of 20% IFE was given. Within 30 seconds she had a bradyasystolic arrest. Pulses returned after 4 min of CPR. Despite catecholamines, a transvenous pacemaker (TP), and an intra-aortic balloon pump (IABP), the patient died on hospital day (HD) 4 of multi-system organ failure (MSOF). Post-mortem drug levels were: bupropion 130 ng/ml, hydroxybupropion 480 ng/ml.
    Case 2: A 53 yo man presented after an OD of a one-month supply of diltiazem SR 120 mg and propranolol 20 mg. He had profound hypotension and bradycardia that was refractory to IV fluids, 32 mEq of Ca 2 , a HDI infusion of 10 U/kg/hr, 2 mg each of epinephrine and atropine, and a dopamine drip. With a pulse of 30 bpm and a MAP of 40 mmHg a bolus of 1.5 mL/kg of 20% IFE was given. Within 1 minute he had a bradyasystolic arrest. Pulses returned after 5 min of CPR. Despite 4 vasopressors, TP and IABP, the patient died on HD 7 of MSOF. A propranolol level on HD 2 was 53 ng/ml (therapeutic range 30-100); a diltiazem level on HD 5 was 100 ng/ml (therapeutic range 100-200).
    Discussion: In severe cases of PICS clinicians may consider the use of both HDI and IFE. IFE has been described to work by the "lipid sink" mechanism. The relationship between IFE and HDI is unclear, but it is possible our patients were dependent upon HDI for inotropic support and IFE rendered HDI ineffective. It is also possible the brief lack of oxygen in the lipid-laden blood circulating in the coronary vessels contributed to the arrests. The arrests also could have occurred without influence from a HDI/IFE interaction or the IFE alone. However, the temporal relationship of the arrests following IFE in these cases is difficult to ignore.
    Conclusion: We report 2 cardiac arrests after use of HDI followed by IFE. An interaction between IFE and HDI must be contemplated. Additionally, these cases should be considered with caution when using IFE in pre-arrest scenarios.

  • publication date
  • 2011
  • Research
  • Drugs and Drug Therapy
  • Emergency Medicine
  • Poisoning
  • Additional Document Info
  • 49
  • issue
  • 6