Post Your Cases > LIPID RESCUE THERAPY in an Intoxication with Diltiazem, Ethanol and Diazepam
Objective: to report a case of abandoning lipid rescue therapy (LRT) in an intoxication involving diltiazem, ethanol and diazepam due to significant arrhythmia.
Case report: Pat. B.S., 52yr female BW 70kg. Patient arrived at EMD after ingesting approximately 4500mg diltiazem (retarded preparation) and 19.000mg diazepam in an attempted suicide. The emergency team recorded a GCS of 7 and administered flumazenil, followed by an arousal reaction. The delay from ingestion to arrival in hospital was estimated with 2 to 4 hours. transferred to our ICU. Medical history showed no significant somatic disease but was positive for major depression.
On arrival, the patient showed somnolence, reacted rapidly to painfull stimuli and was orientated with slurred speech afterwards. physical examination showed signs of hypoperfusion of the peripheral arteries, hypotonia with 60/30 mmHg measured by cuff, bradycardia with 45 bpm (junctional rhythm in ECG), BGA: metabolic acidosis (partly respiratory compensated) with pH 7,28, pCO2 35, pO2 98 (mmHg resp.), BE -9,7, lactate 9,2 (mmol/l resp.) Lab values within limits of normal. Toxicological screening: levels of ethanol elevated with 2,72 g/l as were the ones for benzodiazepines with 3956 ng/ml ,carbamazepine, valproic acid, acetaminophen and tricyclic antidepressants negative. No direct measurement for diltiazem available. No echocardiography was performed for technical reasons, normal chest- X-ray .
CVA, oxygen, infusion, dobutamine (6 mcg/kh/min) and noradrenaline, the latter in rapid increasing doses ( up to 0,8 mcg/kh/min) to achieve an adequate perfusion pressure. BE increasing negative heralding the failure of this strategy, therefore fulfilling our institutional criteria for LRT (life-threatening intoxication present). LRT started app. 1 hour after admission at the ICU, that is app. 3-5 h after ingestion. During the injection of the bolus part of INTRALIPID ® 20%, the heart rate of the patient dropped to 15 bpm (ventricular rhythm with broad QRS complexes) after approximately 50 ml of the drug. Patient lost conciousness immediately and lipid infusion was stopped. The rhythm recovered within app. 2 minutes to junctional rhythm after cessation of lipid rescue as the patient regained normal brain functions, no further attempt of LRT was made (50ml of INTRALIPID 20% ® given totally). Values for blood pressure were about 65 mmHg MAP after that event with noradrenaline and dobutrex in the range mentioned before. In the next 12 hours the vasoplegic state recovered rapidly as the heart rate recovered to normal values after reoccurence of sinus nodal activity. After 40 hours the patient was stable without intervention and was transferred to a medical ward for rehabilitation. No signs of permanent organ damage remained and she left hospital within a couple of days
Discussion: A negative effect probably related to the administration of LRT was observed. The correlation between administration of the bolus part of LRT and the described symptomatic bradycardia was obvious, as was the recovery after cessation of lipid infusion. The bolus was applied manually by the treating physician according to our protocol, with a planned bolus administration of 105ml INTRALIPID 20% ® over 2-3 minutes. After 50 ml, the half of the planned amount, the incident occured and the infusion was halted. Complete atrioventricular block with ventricular rescue beats was detetcted on the monitor, accompanied by symptomatical hypotension, shifting to junctional rhythm after app.2 minutes. An explanation to this event is the intoxication itself, as diltiazem, a calcium channel blocking drug, is a potent antitachycardic agent, producing AV-block of any degree in doses quite below the ones mentioned before in this case. Another explanation would be LRT, as a bolus of highly concentrated fat might produce transient hypoxemia as it travelles through the coronary system.
The patient recovered after standard, symptomatic therapy, without sequelae, neither from intoxication nor LRT. The underlying pathomechanisms remain unclear.
Case report:
Pat. B.S., 52yr female BW 70kg.
Patient arrived at EMD after ingesting approximately 4500mg diltiazem (retarded preparation) and 19.000mg diazepam in an attempted suicide. The emergency team recorded a GCS of 7 and administered flumazenil, followed by an arousal reaction. The delay from ingestion to arrival in hospital was estimated with 2 to 4 hours. transferred to our ICU.
Medical history showed no significant somatic disease but was positive for major depression.
On arrival, the patient showed somnolence, reacted rapidly to painfull stimuli and was orientated with slurred speech afterwards. physical examination showed signs of hypoperfusion of the peripheral arteries, hypotonia with 60/30 mmHg measured by cuff, bradycardia with 45 bpm (junctional rhythm in ECG),
BGA: metabolic acidosis (partly respiratory compensated) with pH 7,28, pCO2 35, pO2 98 (mmHg resp.), BE -9,7, lactate 9,2 (mmol/l resp.)
Lab values within limits of normal.
Toxicological screening: levels of ethanol elevated with 2,72 g/l as were the ones for benzodiazepines with 3956 ng/ml ,carbamazepine, valproic acid, acetaminophen and tricyclic antidepressants negative. No direct measurement for diltiazem available. No echocardiography was performed for technical reasons, normal chest- X-ray .
CVA, oxygen, infusion, dobutamine (6 mcg/kh/min) and noradrenaline, the latter in rapid increasing doses ( up to 0,8 mcg/kh/min) to achieve an adequate perfusion pressure. BE increasing negative heralding the failure of this strategy, therefore fulfilling our institutional criteria for LRT (life-threatening intoxication present).
LRT started app. 1 hour after admission at the ICU, that is app. 3-5 h after ingestion.
During the injection of the bolus part of INTRALIPID ® 20%, the heart rate of the patient dropped to 15 bpm (ventricular rhythm with broad QRS complexes) after approximately 50 ml of the drug. Patient lost conciousness immediately and lipid infusion was stopped. The rhythm recovered within app. 2 minutes to junctional rhythm after cessation of lipid rescue as the patient regained normal brain functions, no further attempt of LRT was made (50ml of INTRALIPID 20% ® given totally). Values for blood pressure were about 65 mmHg MAP after that event with noradrenaline and dobutrex in the range mentioned before.
In the next 12 hours the vasoplegic state recovered rapidly as the heart rate recovered to normal values after reoccurence of sinus nodal activity. After 40 hours the patient was stable without intervention and was transferred to a medical ward for rehabilitation. No signs of permanent organ damage remained and she left hospital within a couple of days
Discussion:
A negative effect probably related to the administration of LRT was observed. The correlation between administration of the bolus part of LRT and the described symptomatic bradycardia was obvious, as was the recovery after cessation of lipid infusion. The bolus was applied manually by the treating physician according to our protocol, with a planned bolus administration of 105ml INTRALIPID 20% ® over 2-3 minutes. After 50 ml, the half of the planned amount, the incident occured and the infusion was halted. Complete atrioventricular block with ventricular rescue beats was detetcted on the monitor, accompanied by symptomatical hypotension, shifting to junctional rhythm after app.2 minutes.
An explanation to this event is the intoxication itself, as diltiazem, a calcium channel blocking drug, is a potent antitachycardic agent, producing AV-block of any degree in doses quite below the ones mentioned before in this case.
Another explanation would be LRT, as a bolus of highly concentrated fat might produce transient hypoxemia as it travelles through the coronary system.
The patient recovered after standard, symptomatic therapy, without sequelae, neither from intoxication nor LRT. The underlying pathomechanisms remain unclear.