CASE REPORT

Treatment of Quetiapine Overdose with Intravenous
Lipid Emulsion

Engin Deniz Arslan, Ali Demir, Fevzi Yilmaz, Cemil Kavalci, Evvah Karakilic and Elif ÇelikelEmergency Department, Ankara Numune Training and Research Hospital, Samanpazarı, Ankara, Turkey(Received for publication on July 9, 2012)(Revised for publication on August 29, 2012)(Accepted for publication on September 25, 2012)(Published online in advance on May 27, 2013)

We report the case of a 29-year-old woman who attempted suicide by oral ingestion of potentially fatal
doses of multiple drugs including quetiapine. Intravenous lipid emulsion (ILE) was administered at adose higher than that used in the standard management of toxicity. Rapid improvement was observedin the patient’s status, and no additional treatment was required during the period of observation. No
adverse effect of lipid administration was observed. ILE treatment seems to have great potential in themanagement of lipophilic drug toxicity in the future. (doi: 10.2302/kjm.2012-0010-CR) ; Keio J Med
62 (2) : 53–57, June 2013)

Key words: intravenous lipid emulsion, quetiapine, toxicity

Introduction
Quetiapine is an atypical antipsychotic drug that, in
toxic doses, has severe adverse effects such as coma, respiratory depression, and hypotension. Toxic ingestionsof quetiapine primarily are managed with gastric lavage
and active charcoal administration to prevent or reduce
absorption; the management of toxic effects is achievedby supportive therapy.
Intravenous lipid emulsions (ILEs) are used as a sourceof calories and essential fatty acids in patients who require parenteral nutrition. In addition, ILEs have reportedly been successful in the treatment of local anesthetic
systemic toxicity; their successful use in case reports andanimal studies of drug toxicity other than local anesthetics has been reported.
Case
A 29-year-old woman presented to our emergency department because she was suspected of having ingested
toxic levels of multiple drugs. She had been found comatose at home by family members. Empty blister packsof quetiapine, escitalopram, ibuprofen, and amoxicillin were found at the scene, and the estimated ingested
amounts of the drugs were 9 g quetiapine, 4 g ibuprofen,
280 mg escitalopram, and 5 g amoxicillin. On arrival,
the patient’s blood pressure (BP) was 90/55 mmHg, herheart rate (HR) was 110 /min, and her oxygen saturation
was 91%. She was non-cooperative and disorientated, andon painful stimulation she flexed her arms, opened hereyes, and moaned [E2M4V2 on the Glasgow Coma Scale(GCS)]. The patient’s pupils were midpoint and reactive,
and her blood glucose level was 114 mg/dl according toa strip test. She was intubated to ensure airway patency
and ventilation. Gastric decompression was performed
and 50 g of active charcoal was administered via a gastric tube. An electrocardiogram (ECG) revealed sinus
tachycardia with a QRS duration of 110 ms (Fig. 1). The
patient’s symptoms attributed to quetiapine toxicity weredepressed consciousness, tachycardia, and hypotension.
Two liters of isotonic fluid was administered intravenously within 1 h of the patient’s admission without any
clinical improvement. Because of the lipophilic nature ofquetiapine, ILE therapy was considered to prevent further complications. One hour after admission, when theReprint requests to: Engin Deniz Arslan, MD, Emergency Department, Ankara Numune Training and Research Hospital, Samanpazarı, 06230,Ankara, Turkey, E-mail: mdengindeniz@yahoo.com
Copyright © 2013 by The Keio Journal of Medicine
53Arslan ED, et al: Quetiapine Overdose and Lipid Emulsion

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Fig. 1 ECG of the patient before ILE administration.

patient’s vital signs were BP 95/55 mmHg, HR 120 /min,
GCS E1M1VT, a 20% lipid emulsion bolus dose was administered intravenously at 1.5 mL/kg. Fifteen minutes
later, an additional bolus dose of 1.5 mL/kg was given togive a total dose of 3 mg/kg. Thirty minutes after the second dose, the patient’s vital signs improved to BP 115/70
mmHg and HR 95/min and she opened her eyes andbegan to move her upper extremities to painful stimuli(E2M4VIntubated). An ECG was obtained 30 minutes after
ILE administration illustrating QRS duration had fallen
to 99 ms (Fig. 2). The patient was extubated 3 h after thesecond dose and her vital signs improved to BP 125/81
mmHg and HR 93 /min. At this time, the QRS duration
was 85 ms, and the patient was localizing pains, opening
her eyes to pain, and was speaking in a disoriented manner (E2M5V4). The patient’s vital signs and GCS score
are illustrated in Figure 3-4. Her physical and mental
status progressively improved to a normal state and wassustained, so she did not need any other medication orintervention during the observation period. The patient
confirmed that she had taken large amounts of quetiapine
pills. The patient was discharged the next day and underwent psychiatric follow up.

Discussion
Quetiapine is an atypical antipsychotic drug thatprovides efficacy with a lower risk of extrapyramidal
symptoms compared to typical antipsychotics. Quetiapine affects multiple neurotransmitter receptors, including serotonergic, dopaminergic, alpha adrenergic,
and histaminergic receptors. Its antipsychotic efficacy
is attributed to antagonistic effects on D2-receptors and5-HT2A-receptors. However; atypical antipsychotics areassociated with a variety of metabolic and cardiovascularadverse effects. Sedation and somnolence are explainedby antagonism of histamine H1-receptors, whereas hypotension is associated with an antagonistic effect on α1adrenergic receptors. Quetiapine also reportedly has anantagonistic effect on M1-muscarinic receptors, resulting
in tachycardia. Currently, there are no specific therapeutic recommendations for quetiapine overdose, and highly
supportive conventional therapeutic measures are applied
according to the patient’s clinical status.
Escitalopram is a selective serotonin reuptake inhibitor
antidepressant that has the advantage of low toxicity inoverdose. In a review of escitalopram overdoses, hyperreflexia and clonus were the most common features andcentral depression was rare. ECG changes involved bothbradycardia and tachycardia, and observed QT prolonga-Keio J Med 2013; 62 (2): 53–57

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Fig. 2 ECG of the patient 30 min after ILE administration.

Fig. 3 Patient’s blood pressure and HR over the course of treatment.
SBP, systolic blood pressure; DBP, diastolic blood pressure.

tion was associated with bradycardia.1 In our patient, theobserved hypotension tachycardia and depressed consciousness can be attributed to the antagonistic effects ofquetiapine on H1, α1-adrenergic, and muscarinic receptors.
Weinberg and colleagues demonstrated that lipid infusion shifts the dose­­‑response to bupivacaine-induced
asystole in rats2. This observation leads to the suggestionof ILE use in patients with highly lipophilic drug toxicity,including that caused by bupropion/lamotrigine, sertraline/quetiapine, verapamil, and atenolol.3–6 Animal studies have also indicated the efficacy of ILE in drug toxicity.7 Highly lipid soluble agents demonstrably respondto lipid infusion, and this fact supports the theory of thelipid sink, with lipid infusions resulting in an expanded
plasma lipid phase that reduces tissue drug levels.

Arslan ED, et al: Quetiapine Overdose and Lipid Emulsion

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Fig. 4 Patient’s Glasgow coma scale over the course of treatment.

Harmon and colleagues reported a patient who ingested
more than 10 g quetiapine who became comatose and recovered 16 h later with supportive therapy.8 In a 5-yearcase series, the largest amount of ingested quetiapine
was 24 grams, and the patient deteriorated into a comaand required intubation; the patient was extubated 4 days
later with supportive therapy.9 Although the ingested
amount of quetiapine was not known exactly in our case,the patient regained consciousness earlier than might be
expected with supportive management of quetiapine toxicity. ILE also improved the cardiovascular side effects ofquetiapine overdose. Finn and colleagues reported that apatient treated with ILE for a quetiapine plus sertraline
overdose underwent rapid recovery consistent with ourpatient.4
Early reports on ILE treatment considered its use as arescue therapy, whereas Finn and colleagues recommendthe earlier use of ILE to prevent adverse events.4 The recommended dose as a rescue treatment in arrest patientsis 1.5 mL/kg 20% lipid followed by 0.25–0.5 mL/kg/min
to a total dose 8 mL/kg, with the bolus dose applied amaximum of twice to restore circulation. However, there
is no dose recommendation for critically ill patients who
have not arrested. We applied two 1.5-mL/kg bolus doses
15 min apart with no infusion drip and the patient did
not need any additional treatment during the observation
period. No adverse effect of lipid administration was observed. Although no adverse effects have been reported

in trials and case reports, the theoretical adverse effects
of ILE treatment are pancreatitis, acute lung injury, allergy, hypercoagulability, and fat embolism.
Conclusion
ILE treatment has the potential to play an importantrole in the management of lipid-soluble-drug toxicity inthe future. Its use should be considered earlier in patients
who have a potential risk of a poor outcome due to lipophilic drug toxidrome. Trials are needed to evaluate theefficacy and potential side effects of ILE therapy.
References
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