Volume 189 - Issue 8

Unplanned admissions to two Sydney public hospitals after naltrexone implants

Author:  Colin L Brewer

Med J Aust 2008; 189 (8): 468-471. || doi: 10.5694/j.1326-5377.2008.tb02130.x
Published online: 20 October 2008

To the Editor: A recent article by Lintzeris and colleagues,1 ostensibly about naltrexone implants, actually has little to do with implant treatment. Only one of the 12 reported cases involved problems linked specifically to naltrexone (antagonist) treatment being administered in implanted rather than oral form. This case involved infection at the implant site — undesirable, certainly, but about as noteworthy as the occasional infections that occur after abdominal surgery or breast implantation, despite antibiotic prophylaxis and careful technique. The remaining 11 admissions reflected not implant use but either the procedure of rapid antagonist induction (RAI) or the desired pharmacological effects for which naltrexone was prescribed in the first place (and one admission for unrelated pneumonia).

RAI is needed because conventional antagonist induction requires complete opiate withdrawal before starting naltrexone. As true conventional withdrawal completion rates, even with inpatients, are typically below 30%,2 conventional techniques will typically achieve only derisory naltrexone induction rates. Various forms of RAI or accelerated induction, with induction rates typically around 100%, are more effective and more cost-effective.3,4 Similarly, complaining that pain management is difficult in naltrexone patients is like complaining that patients being treated with anticoagulants bleed or bruise more after surgery or injury. Fortunately, effective non-opiates (notably subanaesthetic ketamine) exist.

The acute post-RAI problems seen in this case series would have been identical had every patient undergone RAI to oral rather than implanted naltrexone. Indeed, while 150 mg orally could block opiate analgesia for up to 72 hours, implants produce low but consistently effective naltrexone levels, disappearing within hours of implant removal, should that be unavoidable. I agree, however, that RAI clinics should optimise immediate post-RAI management.

A recent conference featured the first presentations of the first four randomised controlled trials of implanted naltrexone. Three showed statistically and (more importantly) clinically significant advantages over “as usual” post-withdrawal treatment,5 or over oral naltrexone and placebo implants.6,7 The fourth,8 comparing implants with methadone maintenance in pre-release prisoners, had only modest statistical power (n = 21), but implant patients had less dropout and used about 50% less heroin. We already know that long-acting implants can largely prevent the opioid overdoses that are otherwise an intrinsic and sometimes lethal hazard of all abstinence-based programs;9 and that all implants prevent the otherwise high relapse rates typical of the first 4–6 weeks after detoxification.10

Surgeons, I am shocked to discover, have been using anaesthesia for 162 years without a comparable placebo-controlled evidence base.


Author


Competing interests


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