Intravenous lipid emulsion for intentional Chloroquine poisoning

To the Editor:

Intravenous lipid emulsion (ILE) has successfully been used in local anesthetic toxicity and in poisonings with several other lipophilic drugs.¹ There is evidence supporting the use of ILE for cardiotoxic effects due to poisonings with lipophilic agents. Until now, data on the use of ILE for Chloroquine poisoning has been limited. Chloroquine poisoning is exceptional, but with potentially fatal consequences.² Two cases were described with little or no benefit attributed to ILE.³ In one case ILE therapy was initiated more than 11 h post-ingestion. The other case describes ingestion of 20 g of Hydroxychloroquine, a dose that greatly diminishes any chance of survival. The lipophilic character of Chloroquine implies the efficacy of ILE for this type of poisoning.

We treated a 24-year-old male for voluntary ingestion of several drugs including a high dose of Chloroquine. The ambulance crew found him unconscious on the floor. Ingestion of 58 tablets of Chloroquine 250 mg, 20 tablets of Midazolam 7.5 mg, 5 tablets of Domperidon 10 mg and 10 tablets of Ondansetron 4 mg were suspected, and the time of ingestion was unknown. Clinical exam revealed a Glasgow Coma Scale (GCS) of 6/15 (E1V1M4), normal breathing, a junctional rhythm and a blood pressure of 70/40 mmHg. A rapid evolution to ventricular fibrillation (VF) occurred and resuscitation was initiated. The evacuation of the patient out of his flat required fire fighter assistance, resulting in a long “at the scene time” of approximately 1 h, during which standard advanced life support (ALS) was continued using a Lund University cardiac arrest system (LUCAS) device.

At arrival in the emergency department (ED), pulseless electrical activity (PEA) was observed. Active charcoal was given through a gastric tube. Infusion of 500 ml Human Albumin 5% was started in addition to standard volume resuscitation and ILE treatment was also initiated. A bolus of Intralipid 20% was administered in the dosage of 1.5 ml/kg followed by a continuous infusion of 0.25 ml/kg/min.

We observed an evolution of PEA to a shockable rhythm for which a DC shock of 200 J was administered. Conversion to sinus rhythm was reached for the first time. Blood pressure rose to 120/90 mmHg. After about 10 minutes, however, a recurrent ventricular tachycardia (VT) occurred for which again a DC shock of 200 J was given, with no response.

At this point an arterial blood sample demonstrated an inadequate oxygenation despite 100% oxygen administration. Given the prolonged resuscitation with only short-term beneficial hemodynamic effect, a veno-arterial extracorporeal membrane oxygenation (ECMO) was installed. Hereafter he was delivered to the intensive care unit. Over the following days the hemodynamic situation stabilized gradually, but the patient was declared brain dead after 5 days.

Chloroquine is a highly lipophilic substance having a lipid/ aqueous partition coefficient (log P 4.3) that is comparable to that of local anesthetics, thus ILE seemed justified because standard resuscitation was insufficient.4 Moreover, Chloroquine has an extremely high volume of distribution, due to ion trapping (pKa =10.3).

Stabilization of hemodynamic parameters and conversion to sinus rhythm occurred within minutes after initiation of ILE therapy. The irreversible neurologic damage was a result of the prolonged resuscitation.

There was no interference with the ECMO therapy. Blood sample analysis, however, did pose a problem, specifically for determining the coagulation parameters.

ILE therapy for poisonings with lipophilic substances, other than local anesthetics, is still under debate. However, we strongly support the use in distinct cases of life-threatening poisonings with lipophilic drugs, such as Chloroquine. This case adds to the increasing series of case reports on ILE therapy for specific poisonings.