Dysautonomia and related outcomes in Guillain-Barre syndrome

Predictors of respiratory failure in Guillain−Barré syndrome: a 22 year cohort study from a single Italian centre

“…The latter finding provides insights into the pathology of GBS, where inflammatory endoneurial oedema, from early stages, predominates in proximal nerves, where spinal roots unite to form spinal nerves, suggesting that root involvement is highly threatening for breathing [45]. Patients with bulbar palsy are at high risk of aspiration and airway occlusion [15, 23, 37, 38]; therefore, in the presence of relevant dysphagia, early hospitalization is necessary to protect airways from aspiration pneumonia. In this subset of patients, endotracheal intubation is recommended to protect the airways [15]; however, in a recent trial, early MV was unable to prevent pneumonia in patients with increased risk of respiratory failure [46].…”

“…In our study, all patients requiring ventilation underwent endotracheal intubation; thus our population was probably more severely affected. NIV is an unsafe therapeutic option in GBS for several reasons: first, a persisting decline of respiratory muscle weakness, followed by prolonged nadir, makes NIV temporization meaningless; secondly, patients with dysautonomia have high risks of emergency intubation, due to labile blood pressure and arrhythmias; thirdly, patients may need ventilation for long periods and respiratory failure worsens dysautonomia [15,23,25,[35][36][37].…”

“…Patients with resting blood pressure level above 140/90 mmHg were considered hypertensive. Parameters of cardiac dysautonomia were fluctuations on maximum systolic blood pressure >180 or >160 mmHg on antihypertensive medications, minimum diastolic blood pressure >90 mmHg, hypotension with systolic blood pressure <90 mmHg, tachycardia >120 beats per minute or tachycardia >100 beats per minute with beta-blocker use, or bradycardia <50 beats per minute for over 2 h [35][36][37].…”

“…Involvement of the autonomic nervous system occurs in about twothirds of GBS patients and increases mortality, due to several factors including fatal arrhythmias and stress-induced cardiomyopathy [15,17,[35][36][37]; interestingly, dysautonomia may resolve in the recovery phase, preceding the motor improvement [35,36]. The mechanism of dysautonomia is thought to be due to an imbalance in sympathovagal transmission, shifted toward a sympathetic predominance, mediated by afferent fibres from arterial baroreceptors, efferent parasympathetic fibres innervating the heart and in preganglionic sympathetic fibres controlling sudomotor and vasomotor functions [36][37][38].…”

“…Involvement of the autonomic nervous system occurs in about twothirds of GBS patients and increases mortality, due to several factors including fatal arrhythmias and stress-induced cardiomyopathy [15,17,[35][36][37]; interestingly, dysautonomia may resolve in the recovery phase, preceding the motor improvement [35,36]. The mechanism of dysautonomia is thought to be due to an imbalance in sympathovagal transmission, shifted toward a sympathetic predominance, mediated by afferent fibres from arterial baroreceptors, efferent parasympathetic fibres innervating the heart and in preganglionic sympathetic fibres controlling sudomotor and vasomotor functions [36][37][38]. Previous studies interestingly suggested that dysautonomia might cause respiratory deterioration also through a different mechanism: the inflammatory demyelination of vagal afferent fibres results in an excessive sympathetic outflow, leading to hyperdynamic pulmonary circulation, which in turn causes worsening of hypoxaemia through an increase in intrapulmonary shunt [47].…”