© Georg Thieme Verlag KG Stuttgart · New York

A 16-Year-Old Boy with Severe Gamma-Butyrolactone (GBL)

Withdrawal Delirium
F. D. Zepf1 , 2 , 3 , M. Holtmann3 , 4 , E. Duketis3 , J. Maier3 , D. Radeloff3 , A. Wagner3 , F. Poustka3 ,
L. Wöckel1 , 3

Inhaltsübersicht
• Case Report
• Discussion and Conclusion
• Conflict of interest/Disclosure
• References
Here we describe a 16-year-old patient suffering from an acute withdrawal syndrome with gamma-
butyrolactone (GBL), a designer drug with increasing case numbers describing acute abuse, life threatening
withdrawal or overdose complications. Acute management along with complications as regards vegetative
adverse reactions to treatment are presented and briefly discussed. To the best of our knowledge this is the
youngest case of severe GBL withdrawal syndrome reported so far in the available literature.
Because clinicians in psychiatric units are increasingly confronted with cases of severe withdrawal conditions
related to the abuse of gamma-hydroxybutyrate (GHB), gamma-butyrolactone (GBL) and 1,4-butanediol (1,4-
BD) [2] [3] [4] [6] [9] [10] [11], the authors want to present this case of a 16-year-old male adolescent suffering
from acute withdrawal of GBL, a physiological precursor of GHB, and from which the body can produce GHB.
Dyer et al. [2] reported one deadly case after cardiac arrhythmia. Acute withdrawal of GHB often presents with
psychotic symptoms or those of acute alcohol withdrawal [1] [4] [7] [9] [12] [13], and following this these
patients suffering from acute GHB/GBL or 1,4-BD withdrawal are likely to present in psychiatric inpatient units,
making this possibly deadly syndrome highly relevant to child and adolescent psychiatrists and other mental
health professionals. Therefore, we consider the presentation of the youngest case of severe GBL withdrawal
delirium in the existing literature to the scientific public of particular relevance.

Case Report

A 16-year-old male adolescent was transferred from a paediatric hospital because of psychotic symptoms
related to reported withdrawal of GBL. Before admission, the patient had reported to his parents that he had
been consuming GBL since approximately 3 months. For the last two weeks before admission he had been
continuously consuming GBL in intervals of 4 h or even less. He presented with a severe delirium with paranoid
delusions, hallucinations, disorganised behaviour, deficits in memory, increased activity and aggressive
behaviour along with tachycardia, hypertension, sweating and tremor as combined vegetative symptoms. A
drug screen indicated no positive findings for other drugs. At the paediatric hospital the patient had been
receiving an initial intravenous dose of 5 mg of diazepam followed by 2.5 mg of lorazepam, which both however
did not lead to any significant improvements. Upon admission the boy seemed restless and kept talking without
any particular topic.
After admission the patient displayed ataxia and increased activity. The patient first received oral add-on
treatment with 10 mg/d haloperidol (for 1 day). Chlorpothixene had been administered once as a single on-
demand dosage (30 mg, day 2). From day 1 to day 5, the boy received 5−20 mg/d diazepam with lorazepam as
an on-demand treatment. Because of worsened vegetative symptoms he was transferred to an intensive care
unit until his vital parameters had been stabilized under continuous monitoring. While being under intensive
care he had received oral treatment with 15 mg/d of diazepam and 2 mg/d of lorazepam over 2 d along with
5 mg haloperidol and 25 mg of levomepromazin (haloperidol and levomepromazin administered as a single
dose). Until this stage the patient had received a total dose of 105 mg diazepam and 11 mg lorazepam. After re-
admission to the psychiatric ward, the boy still presented with the outlined psychotic symptoms. Under
neuroleptic medication with haloperidol he developed severe neck dystonia, which was why treatment with
haloperidol was discontinued. He continuously received 500−2 000 ml/d of intravenous fluids over 6 d in order
to protect him from acute renal failure. An acute neurological condition was ruled out by using imaging.
In the following period treatment with benzodiazepines was continued (20 mg/d diazepam for 3 d, 10 mg/d for 1
day) in combination with thiamin-nitrate and phenobarbital. Under an oral dose of 20 mg/d diazepam his
restlessness first did not improve, and treatment was changed to lorazepam (first 2 mg/d for 1 day, then 3 mg/d
for 1 day). Because of an unclear rise in temperature and discrete blood parameters marking an unspecific
infection, the boy was again re-transferred to the acute intensive care unit. The infectious signs turned out to be
related to a thrombophlebitis, and were treated with 400 mg/d doxycycline. After normalisation of temperature
and no further signs of infection, the boy was again re-transferred to the acute child and adolescent psychiatric
inpatient unit. Treatment with lorazepam was continued with 3 mg/d for 7 d. Enoxaparin-Na (40 mg s. c.) was
administered for prophylaxis of thrombosis. After about a weak of constant treatment with diazepam the boy
became more settled and was able to sleep. The psychotic and restless symptoms disappeared under constant
treatment with benzodiazepines, and he was fully orientated. The boy's condition improved continuously so
that he could be discharged about 2 weeks after admission. In summary, the patient had received 115 mg of
diazepam and 41.5 mg lorazepam.

Discussion and Conclusion

Along with existing findings the present case underlines that severe GBL withdrawal delirium requires intensive
care with continuous monitoring of vital parameters, in particular to prevent patients from acute renal failure
and cardiac arrhythmia. As regards the clinical management benzodiazepines were effective, but one has to
note that in adults much higher dosages of benzodiazepines were used [8]. Neuroleptic treatment with
haloperidol led to significant dystonia, which had been reported previously [10]. Clinicians should consider acute
GHB withdrawal in adolescents while trying to find a diagnosis when facing unclear psychotic symptoms which
do not respond to neuroleptic treatment.

Conflict of interest/Disclosure

The first author was the recipient of an unrestricted award donated by the American Psychiatric Association
(APA), the American Psychiatric Institute for Research and Education (APIRE), and Astra Zeneca (“Young Minds
in Psychiatry Award”). He has also received research support from the German Society for Social Pediatrics and
Adolescent Medicine (Deutsche Gesellschaft für Sozialpädiatrie und Jugendmedizin, DGSPJ) and from the Paul
and Ursula Klein Foundation, and a travel-stipend donated by the GlaxoSmithKline Foundation. Previous
research has also been funded by the Dr. August Scheidel Foundation. MH is member of Advisory Boards of Lilly
and Novartis and serves on the speaker bureaus of Lilly and Astra Zeneca. FP is member of Advisory Boards of
Lilly, Janssen Cilag, Astra Zeneca, and Novartis. The other authors have nothing to disclose.

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Correspondence

Prof. Dr. med. F. D. Zepf

Juniorprofessor for Translational Neuroscience in Psychiatry and Neurology
Department of Child and Adolescent Psychiatry and Psychotherapy

RWTH Aachen University

Neuenhofer Weg 21
52074 Aachen
Germany

Telefon: +49/241/8085 504

Fax: +49/241/8082 544

eMail: fzepf@ukaachen.de