Aftermath

Prevention of death from respiratory failure is merely the first stage in treatment of an illness such as GBS. Maintenance of morale and recognition and treatment of depression are important and difficult tasks that call on all the resources of the intensive care team. For some conditions, patient support groups exist which offer counselling services (for example,

Guillain-Barre Syndrome Support Group International, PO Box 262, Wynnewood, PA 19096, United States, www.guillain-barre.com; Guillain-Barre Syndrome Support Group, Foxley, Holdingham, Sleaford, Lines NG34 8NR, United Kingdom, www.gbs.org.uk). There are no easy guidelines. The patient and the family need clear information about what is happening and what may be expected. Overoptimistic prognoses may be greeted eagerly at first but reap a grim harvest of dashed hopes later. Above all, a conscious patient festooned with monitoring equipment in a modern intensive care unit needs a sympathetic caring approach tailored to his or her own needs.

Management of acute neuromuscular paralysis

• Respiratory paralysis occurs in a small percentage of patients with acute neuromuscular disease and accounts for less than 1% of admissions to general intensive care units. Its development may be insidious so that patients with acute neuromuscular disease should have their vital capacity monitored. Orotracheal intubation and ventilatory support should be instituted prophylactically when the vital capacity is falling towards 15 ml/kg. Earlier intervention is necessar y in the presence of bulbar palsy.

• The cause of the respiratory paralysis can usually be deduced from the clinical history and examination. It is necessary to distinguish disease affecting the respiratory centre and its CNS connections to the cervical and thoracic spinal cord (Box 11.1), peripheral neuropathy, disorders of neuromuscular conduction, and muscle disease. In practice the commonest cause is Guillain—Barré syndrome, but the possibility of metabolic, vasculitic, and toxic neuropathies should not be ignored (Table 11.1). If the reflexes are preserved and there is no sensory deficit, the possibility of myasthenia, botulism, other rare causes of neuromuscular conduction block (Table 11.2), and muscle disease (Table 11.3) should be considered.

• If artificial ventilation is likely to be required for more than about seven days, a tracheostomy should be created and is more comfortable for the patient than continued orotracheal intubation. Nutrition should be provided early via a nasogastric tube. Strenuous efforts should be made to reduce the incidence of nosocomial infection. Patients with neuropathy should be monitored for autonomic dysfunction causing cardiac arrhythmia or fluctuating blood pressure. Deep vein thrombosis should be avoided by regular passive limb movements and low dose subcutaneous heparin (for example enoxaparin 40 mg daily).

• Specific interventions to shorten the duration of artificial ventilation should be applied appropriate to the nature of the underlying condition. Metabolic disturbances such as hypokalaemia or hypermagnesaemia should always be sought and corrected first. In Guillain—Barre syndrome we recommend intravenous immunoglobulin as being equally effective to plasma exchange, safer, and more convenient. We do not recommend steroids but will review this advice when the results of the latest trial have been published and included in the Cochrane review. In myasthenia gravis we recommend intravenous immunoglobulin followed by thymectomy or, where thymectomy is inappropriate or has been unsuccessful, intravenous immunoglobulin combined with steroids and azathioprine. In polymyositis and dermatomyositis steroids are the mainstay of treatment but intravenous immunoglobulin is also effective.

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