Departments of Pain Management and
1 Rheumatology, Dudley Group of Hospitals NHS Trust, West Midlands, UK
SIR, Fibromyalgia is poorly understood in neurobiological terms, with no general agreement about its aetiology and pathogenesis. The symmetry of the condition leads to the hypothesis of a central nervous system disturbance [1]. In neuropathic pain states, it has been shown that inhibition of the pain pathway can be achieved by systemic administration of local anaesthetics such as intravenous lignocaine [2, 3].
On this basis, intravenous lignocaine is also used for the management of the pain of fibomyalgia [4, 5], particularly in patients who have not responded to more traditional therapeutic measures, such as physical therapy, analgesics and/or tricyclic antidepressants. The doses of lignocaine used range from 5 to 7 mg/kg by infusion over a period from 2 to 6 h. Such doses may be associated with adverse effects, particularly those of cardiac and neurological origin. Such side-effects have been described but not quantified in a group of patients with neuropathic pain [6]. No study has addressed the safety of intravenous lignocaine therapy in patients with fibromyalgia.
We have conducted a prospective study of the nature and incidence of adverse effects of intravenous lignocaine therapy in a group of 110 patients with fibromyalgia having this therapy at our unit over a 6-month period. All patients fulfilled classification criteria for fibromyalgia [7] and had not achieved sufficient symptom relief using the more traditional modes of treatment, either in the rheumatology or pain relief departments. The patients' nurses completed a questionnaire addressing any side-effects noted at the time of treatment. One hundred and six usable questionnaires were returned (96%) and adverse events were computed by a third party, not working on the ward. No patient was treated more than once in the study period. The mean (range) age of this sample was 51.4 (2974) yr; 88 of the 106 patients were female (83%); 72 had primary fibromyalgia (68%) and the remainder had fibromyalgia secondary to osteoarthritis.
The intravenous infusion of lignocaine was given only to patients with normal electrocardiographic conduction and normal serum electrolyte concentrations, to minimize the risk of cardiac dysrhythmias. Patients had continuous electrocardiographic monitoring and measurements of pulse and blood pressure every 15 min by an automated device during infusion. They were kept under close observation by nursing staff taught to detect symptoms and signs of neurological side-effects, such as tinnitus and tunnel vision. Serial infusions of intravenous lignocaine were given for six consecutive days. They were started at 5 mg/kg minus 100 mg and increased by 50 mg per day to 5 mg/kg plus 150 mg provided the maximum was no greater than 550 mg. The lignocaine was infused in 500 ml Hartman solution over 6 h. The infusion rate was reduced if there was bradycardia, tachycardia, hypotension, headaches, dizziness, arrythmias or tunnel vision. If slowing the infusion failed to correct these, the infusion was stopped.
There were 44 incidences of side-effects (42%), of which two were serious (Table 1). The commonest side-effect was hypotension, which required slowing or stopping of infusion; no incidence of hypotension required any other active measures. The most serious side-effects were supraventricular tachycardia requiring pharmacological treatment and a case of pulmonary oedema requiring diuresis. The miscellaneous group included an infected cannula site, tissue infusion and reaction to ECG electrode pads. None had long-term sequelae.
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Notes
Correspondence to: J. H. Raphael, Department of Pain Management, Guest Hospital, Tipton Road, Dudley DY1 4SE, West Midlands, UK. E-mail: JonRaph{at}aol.com
References
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