Complications
Neuromuscular respiratory function is compromised in some patients with GBS.[108][94] Bulbar dysfunction may cause difficulty with clearing secretions, adversely affecting gas exchange and increasing the risk of aspiration.
Tachypnoea, sweating, tachycardia, asynchronous movements of the chest and abdomen, and episodic use of accessory muscles of respiration indicate fatigue of respiratory muscles.[151]
In the case of worsening respiratory failure, the patient should be started on invasive or non-invasive mechanical ventilation.
Bladder areflexia and disturbed bladder sensation occurs secondary to dysfunction of peripheral types of parasympathetic and somatic nerve.[93]
Voiding is more frequently compromised with axonal type GBS. Patients exhibit evacuation and storage disorders, bladder areflexia, and disturbed bladder sensation indicative of peripheral types of parasympathetic and somatic nerve dysfunction.[93]
Maintaining an indwelling urethral catheter during the acute phase is helpful.[151]
Adynamic ileus occurs secondary to dysfunction of the autonomic nervous system. Daily abdominal examination and auscultation should be performed to facilitate early detection.[151]
Feeding should be suspended and nasogastric tube placed. Nasogastric feeds can be given at 10 mL/hour if the ileus is not severe.
Opioids should be avoided and promotility agents are contraindicated with dysautonomia.
Up to 80% of patients are able to walk independently 6 months after disease onset, with or without treatment.[11]
Treatment in the acute phase should include an individual programme of gentle strengthening involving isometric, isotonic, isokinetic, and manual resistive and progressive resistive exercises.
Rehabilitation should be focused on proper limb positioning, posture, orthotics and nutrition.[151][11]
The cause and contributing factors are not fully known, but fatigue appears in part to be a sequel of forced inactivity and general muscle deconditioning.
Supervised exercise programmes are recommended for both fatigue and functional abilities, which were measurably improved in studies.[151]
Immobilisation is a risk factor for the development of DVT.[185] Anticoagulation is the mainstay of therapy for the treatment of DVT. The choice of agent depends on patient factors such as hepatic function, renal function, pregnancy, presence of cancer, obesity, concomitant medications and the ability to monitor drug-drug interactions, and the risk of bleeding. Choice may also depend on individual physician or patient preference or recommendations in local guidelines.
Appropriate prophylactic anticoagulation (e.g., a direct oral anticoagulant, subcutaneous unfractionated heparin, or a low molecular weight heparin) and support stockings are recommended for non-ambulatory patients until they are able to walk independently.[151]
Use of this content is subject to our disclaimer