Complications
Neuromuscular respiratory function is compromised in some patients with Guillain-Barre syndrome.[100][113] 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.[165]
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.[99]
Voiding is more frequently compromised with axonal type Guillain-Barre syndrome. Patients exhibit evacuation and storage disorders, bladder areflexia, and disturbed bladder sensation indicative of peripheral types of parasympathetic and somatic nerve dysfunction.[99]
Maintaining an indwelling urethral catheter during the acute phase is helpful.[165]
Guidance on assessment and management of urinary incontinence in patients with neurological disease is available from the UK National Institute for Health and Care Excellence.[196]
Adynamic ileus occurs secondary to dysfunction of the autonomic nervous system. Daily abdominal examination and auscultation should be performed to facilitate early detection.[165]
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.[21]
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.[21][165]
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.[165]
This may become evident approximately 4 months after the onset of paralysis, as in other states of immobilisation that favour resorption of the calcium.[193][194]
Treatment of immobilisation hypercalcaemia includes conventional calcium-lowering therapies such as hydration, furosemide, and calcitonin. Bisphosphonates may be useful when conventional therapies fail.[195]
Immobilisation is a risk factor for the development of DVT.[21] 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 drugs 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.
Pharmacological thromboprophylaxis (e.g., a direct oral anticoagulant, subcutaneous unfractionated heparin, or a low molecular weight heparin) and anti-embolism stockings are recommended for non-ambulatory patients until they are able to walk independently.[165]
Distress, anxiety and depression have been reported following Guillain-Barre syndrome. Early recognition and management of psychological problems is important.[21] Referral to a psychologist or psychiatrist may benefit some patients. Psychological problems may persist after physical recovery is complete.[165]
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