Respiratory decompensation: An unrecognized potential complication of Botulinum toxin in at risk patients
Background: Botulinum toxin is widely used for the treatment of dystonia and spasticity. Although relatively safe, transient local weakness and rarely generalized weakness related to systemic spread can be seen. Pulmonary decompensation following botulinum toxin has not previously been described. We report a patient developing type 2 respiratory failure following treatment with Botulinum toxin.
Case Report: A 45 year old man with long standing complete T5 paraplegia was treated with increasing doses of botulinum toxin for severe lower limb adductor spasticity. He had no previous history of any other neuromuscular disease. Initial tratment with 1500 mouse units (mu) of Botulinum toxin (Dysport), divided equally into each adductor group, resulted in no improvement. Four months later the dose was increased to 2500 mu with improvement but a still suboptimal response. After a further 4 months he received a third series of adductor injections totaling 3000 mu. Eight days later he developed gradually increasing upper limb weakness, dyspnoea associated with early morning headache and anxiety, mild dysphagia and some difficulty with cough. His neurological examination revealed new mild diffuse upper limb weakness (4/5). There was no objective facial or bulbar muscle weakness. Pulmonary evaluation showed markedly reduced FEV1 (1.4L) and Vital Capacity (1.5L) consistent with a severe restrictive ventilatory defect. Maximal inspiratory and expiratory pressures were severely reduced. Arterial gases showed pCO2 52mmHg, pO2 118mmHg, pH 7.39, and bicarb 31 mmol/l with Base Excess +5 mmol/l, consistent with compensated Type 2 respiratory failure. Upper limb NCS and routine EMG were normal. Single fiber EMG showed abnormal jitter and blocking. Repetitive stimulation was normal. The patient was managed conservatively and made a full recovery over 4 weeks.
Conclusions: Localized lower limb weakness from Botulinum toxin in paraplegic patients may not always be of functional concern and may encourage the use of larger doses to treat severe spasticity. Our case demonstrates that generalised mild weakness in patients with reduced respiratory reserve can result in respiratory compromise