Unplanned admissions to two Sydney public hospitals after naltrexone implants

To the Editor: The study by Lintzeris and colleagues1 and the associated editorial2 criticise naltrexone implants. However, the study is replete with errors regarding the 12 cases reported.

A key to successful rapid opioid detoxification (ROD) is octreotide. An agonist of non-μ gut receptors, it prevents gastrointestinal symptoms of withdrawal.3,4 Earlier aggressive dosing is more effective. Only two of the six patients reported as having precipitate opiate withdrawal received octreotide, administered in both cases by their local doctor. Presumably this doctor performed the ROD. Why was the octreotide administration not repeated?

Patient 7 was reported as having a localised abscess at the implant site. These may arise a variable period after implant insertion. Magnesium-monostearate, used as a binder in naltrexone and many other implants, may liquefy, resembling pus. Results of repeated microbiological examination are always negative. An actual infection at the implant site is rare.

Patient 8 demonstrates that many patients use opiates and other drugs as self-medication for their psychiatric symptoms. It is regrettable that this patient’s psychiatrist was not involved in the decision making. Was the doctor doing the ROD aware that there was a psychiatrist involved? Transient psychosis may occur following ROD; use of antipsychotics is appropriate.

Arrhythmias (as diagnosed in Patient 9) are a textbook in themselves. Pre-ROD preparation requires assessment for comorbidities including bacterial endocarditis and arrhythmia syndromes. Substance-misusing patients often use arrhythmogenic agents such as amphetamine. No mention was made of precipitate withdrawal symptoms in this patient, so an electrolyte abnormality is unlikely.

Patients 10–12 had problems that were unrelated to the naltrexone implants and poorly managed by the receiving hospital. Naltrexone has 2 log the affinity for opiate receptors to that of morphine and most other opiates.5 This means that 1 mg of naltrexone will block 1 g of another opiate. Using opiates to treat patients in these circumstances therefore makes no sense. Ketamine, local anaesthetic blocks, paracetamol and non-steroidal anti-inflammatory drugs are alternative options for treatment.

To compare naltrexone implants with thalidomide2 is emotive; all the components of the implants are approved agents. Similarly, to say they have not been fully tested is to condemn all products supplied by compounding pharmacists.

Testing of serum naltrexone levels (to assess whether an implant is still working) is not rebatable under Medicare, so is expensive to perform. Research is a necessary component of naltrexone implants, and I would happily cooperate with any of the study authors in coordinating and performing such research.