Article Text
PDF
Statistics from Altmetric.com
The aim of this article is to discuss chloral hydrate and its place in current therapy in various paediatric settings following the 2021 safety update from the Medicines and Healthcare products Regulatory Agency (MHRA). There are two case studies presented to apply learning relating to the place of chloral hydrate in both paediatric sedation and neurology.
2021 MHRA update
When the MHRA issued a drug safety update in October 2021 relating to the use of chloral hydrate and its prodrug cloral betaine in paediatric patients, it sparked concern for families and the paediatric medical community.1 While no new safety concerns were identified, previously known carcinogenicity data in animals, and lack of long-term studies in humans (particularly in infants and neonates), led to the MHRA issuing new prescribing restrictions and advice for healthcare professionals and parents/carers.
MHRA advice to prescribers can be summarised as follows:
Use in children and adolescents is not routinely recommended, and should be under the supervision of a specialist
Indicated in severe insomnia for those with a suspected or definite neurodevelopmental disorder where other treatments have failed
Short-term use only (maximum of 2 weeks) with repeated courses not recommended (only if it has undergone specialist reassessment)
Following prolonged treatment of 2 weeks or more, slowly taper the dose down before discontinuing to avoid withdrawal symptoms, including delirium
What is chloral hydrate?
Chloral hydrate is one of the oldest known synthetic agents and has been used as a hypnotic and sedative agent since the 1800s. It is metabolised to an active metabolite, trichloroethanol, which is responsible for its pharmacological effects.2 The proposed mechanisms for depression of the central nervous system include potentiating γ- Aminobutyric acid type A (GABA-A) receptors, inhibition of excitatory amino acid-activated currents mediated by N-methyl-D-aspartate, and allosteric modulation of the 5- hydroxytryptamine three receptor-mediated depolarisation of the vagus nerve.3 …
Footnotes
BW and JC are joint senior authors.
Twitter @joeyjocrook
Contributors BW and JC led the writing for this review including case studies and referencing. PD and DM coauthored respective sections relating to their specialties.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Provenance and peer review Commissioned; externally peer reviewed.
Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.