A 26-year-old woman presented requesting assistance with polydrug misuse and wanting to detoxify from methadone treatment at a dosing level of 20 mg daily. Her substance misuse history included smoking a packet of 20 cigarettes daily, drinking 1–2 750 ml bottles of wine daily and varying amounts of spirits, smoking 2 g daily of cannabis, injecting 2 g of heroin daily and the use of various stimulants including ecstasy, amphetamines and cocaine. Her cannabis use had begun at age 12 years, and heroin use the following year. She had therefore been opiate dependent for 14 years at the time of presentation, and had spent 8 years on methadone maintenance treatment.
She also had an extensive history of psychosocial trauma and grief and loss, having been sexually abused from 5 years old, lost her 37-year-old boyfriend the year prior who had died from pancreatic cancer after a long history of tobacco, alcohol and cannabis use; and her baby had died at 8 months of age 6 weeks after its third open heart operation for congenital ventricular septal defect after a pregnancy in which she had used large amounts of cannabis and methadone. Both losses had occurred in the preceding year and both were still felt very acutely. Her drug use was financed by prostitution and drug dealing. She lived in motels. She had been raped many times. Her father, a policeman, had been violent towards her mother and herself. Her arm had been twisted behind her back until it broke. Her parents were presently divorced. She had left home at 13 years of age. She had been in the state sprinting team from ages 10 to 13 years. Her boyfriend had run over her in a car, fracturing her ribs, one arm and one leg. She had taken many overdoses, many of them in order to die to be with her deceased children and boyfriend. Her current boyfriend was imprisoned on drug trafficking charges.
Her medical history included anorexia nervosa, genital herpes, a termination of pregnancy and four spontaneous abortions. She worked as a youth worker part time. After appropriate liaison with her previous methadone clinic prescribers, relevant government authorities and the dispensing chemist, and 1 day without methadone, the patient was given a low dose of buprenorphine (2/0.5 mg, as the combined buprenorphine/naloxone sublingual tablet ‘Suboxone’) to introduce this partial agonist into her system 1 December 2008, together with symptomatic support including 30 diazepam daily. By 9 December 2008 the dose was increased up to 10 mg buprenorphine. Acamprosate was added on 11 December 2008 to assist her with reduction of her alcohol misuse and varenicline on 12 December 2008 to assist with cessation of tobacco consumption.
She also made approaches to an inpatient detoxification unit for assistance, but was not successful in gaining admission. Similarly she applied to several rehab centres of inpatient accommodation, but was also unsuccessful. She did experience significant support through a community recovery programme called the Hope Foundation, which specialises in assisting women who have been victims of sexual abuse, drug addiction or the sex industry to find more constructive pathways to rehabilitate their lives. In particular this group was able to offer her a supportive accommodation environment in which to facilitate her recovery. She maintained and used a useful therapeutic relationship with a community counsellor with whom she had been in contact over a long period. She also had some links, albeit tenuous, with various community faith-based organisations, with usually positive interactions.
Over the following year, and at the patient's vehement request, her dose of buprenorphine was reduced three times in an attempt to reduce her gradually to become completely opiate free. However whenever she got below 2–4 mg she became unstable and relapsed into dependent drug use. At one point her dose of buprenorphine had to be increased to 24 mg.
Eventually the patient decided to opt for a different mode of treatment and chose the naltrexone implant as a putative way to control her opiate and alcohol use. Her buprenorphine dose was therefore gradually reduced again, with the support of extra benzodiazepine sedation and some caring friends from the Hope Foundation with whom she was able to live. On 3 November 2009 a single 3.1 g Perth ‘Go Medical’ naltrexone implant was inserted in the subcutaneous tissue of the patient's left iliac fossa by techniques previously described.11
Her main difficulty after naltrexone implant insertion was insomnia. This required alprazolam (4 mg daily, dispensed from the pharmacy as single daily doses) and quetiapine (200 mg daily from sample stocks) for control.
Some local irritation at the implant site manifesting as pain and swelling and local discomfort with movement was noted, which required the injection of local steroids (as celestone chronodose 1 ml on three occasions) or short courses of oral prednisone treatment (on two occasions from 4 to 16 weeks after the implant), and temporally associated with drinking binges. Interestingly after one of these doses of oral steroids she became very ill with a severe vomiting attack over 4 days, which responded only temporarily to treatment in the local Emergency Department with parenteral metoclopramide and intravenous fluids. On a plain abdominal film gross distension of her stomach was evident. Acute gastritis was therefore diagnosed, and the patient responded promptly and definitively to oral treatment with pantoprozole (‘Somac’) and antacids (‘Mylanta’). Oral steroid administration on both occasions was also complicated by recurrence of genital herpes outbreaks, which were managed in the usual manner with valaciclovir.
The Christmas/New Year holiday period was difficult for this patient in view of the social isolation she experienced, including some significant painful anniversaries of various losses. The usual support structures she used were not available at this period. Some binge drinking occurred over this time. The craving for drugs and alcohol had increased to the point where on 27 January 2010 oral naltrexone was given in addition to the implant naltrexone she already had placed. In view of the local difficulties she had experienced at the implant site it was felt that this route of administration was safer in terms of less local tissue irritation, and would also achieve higher levels of naltrexone in her serum to challenge the alcohol craving. Unfortunately no carer was available to supervise her dosing in this way as she had become increasingly socially isolated.
On 15 March 2010 the patient again reported intense opiate craving after another alcoholic binge. She also had a stinging sensation locally in the implant site, although there was almost imperceptible local swelling to see on inspection and palpation. As treatment for her implant site irritation she was prescribed 50 mg oral prednisone. As she was being non-compliant with her oral naltrexone, she was encouraged to take this medication again. The next day she presented and described that in her frustration and torment at the continued drug and alcohol craving, she had in fact taken a whole bottle of oral naltrexone (=1500 mg). She had been vomiting all night. An ambulance and police had attended her, but she had declined hospital admission. On examination she was hypertensive (blood pressure (BP) 165/90) and tachycardic P 116 with no change in BP with posture. Abdominal examination was unremarkable. Upon discussion with the local poisons centre, little information was available on such large overdoses. Pathology tests were taken including blood count (white cell count (WCC)=11.9 × 109/l, neutrophils=10.5 × 109/l), biochemical profile (alanine transaminase (ALT)=13 u/l, bilirubin=6 mcmol/l , albumin=49g/l) and prothrombin time (international normalised ratio (INR)=1.2 (1.0 to 1.5)) and inflammatory markers (erythrocyte sedimentation rate=8 mm/hr, high sensitivity C reactive protein (CRP)=0.1 mg/l), which were all essentially normal excepting her low-level neutrophilia. Semiquantitative mass spectrometry analysis of her urine drug screen confirmed that massive amounts of naltrexone were present requiring dilution for meaningful analysis (urinary creatinine 12.7 mmol/l consistent with a moderately concentrated sample).
When seen the following day she was clinically normal and able to eat and drink well. On the next day she was not well and stated that she was only able to eat and drink a little. As her implant was again uncomfortable, another dose of prednisone (50 mg) was again prescribed, together with Mylanta to protect her stomach. On 19 March 2010 she phoned in again after experiencing vomiting and was sent to the local emergency department for treatment and rehydration. As they refused to see her, she re-presented to this clinic. Abdominal examination in the clinic revealed a hyper-resonant, greatly distended stomach. Parenteral octreotide (0.1 mg subcutaneous injection) and ondansetron (4 mg intramuscular injection) were administered, and the patient quickly began to feel a little better. The following day she was back to normal. Laboratory studies and urine drug screen were again performed on 22 March 2010, and were normal. In particular the urine drug screen showed only nicotine and quetiapine, ALT=15 u/l, bilirubin=5 mcmol/l, albumin=46g/l, WCC=9.8 × 109/l, neutrophils=6.4 × 109/l, INR=1.1(1.0 to 1.5) and high sensitivity CRP <0.1 mg/l.
The patient's drug craving remained controlled for 2 weeks, after which time it returned once again. It is now controlled with oral naltrexone dispensed on a weekly basis from the chemist. The patient reports that she has no intention of ever repeating this overdose episode again. She is now working about 30 h weekly, is becoming ever better integrated into the community and her social isolation is gradually reducing. She is very much enjoying being drug free. She is abstinent from alcohol and is planning to work on her tobacco addiction in the near future.