Critical illness polyneuropathy (CIP) is a recognized cause of muscle weakness and failure of weaning from a ventilator. In order to characterize the features of CIP, we have examined 28 consecutive surgical patients with severe sepsis using bedside electrophysiology. Of the 28 patients (median APACHE II score 31), 20 developed moderate to severe CIP, as shown by the presence of moderate to severe denervation activity on resting EMG. The median nerve compound muscle action potential (CMAP) amplitudes were reduced to 3.24 (SEM 0.48) mV, while sensory nerve action potential (SNAP) amplitudes obtained from the same nerve were normal (13.1 (1.9) microV). In approximately 50% of these patients, the reduction in CMAP exceeded 50% of the lower limit of normal. Similar results were obtained from stimulation of the ulnar nerve. We conclude that CIP is a major complication in patients with severe sepsis and prolonged artificial ventilation. It predominantly involves motor fibres and thus markedly interferes with weaning from the ventilator.

Although biventricular repair for pulmonary atresia and intact ventricular septum proved to attain a satisfactory long-term result, it failed to resolve right heart dysfunction. Postoperative arrhythmia was prone to precipitate progressive dilatation of the right atrium.

CIP, despite it's benign nature due to it's spontaneous remission in patients who survive, is a disturbing complication following cardiac surgery which is associated with high mortality, a prolonged stay in the ICU, as well as an extended time on ventilator support. Interventions like chronic hemodiafiltration, the application of corticosteroids and the administration of high doses of catecholamines are more frequent in patients with CIP. Whether this indicates a causal relationship remains to be elucidated.

The persistence of a very low peribronchial tissue oxygen tension in the early phase after lung transplantation cannot be influenced by improved pulmonary artery flow and solely relates to the central venous pO2, which cannot be augmented by the addition of NO. This mechanism might be a trigger for anastomotic healing problems, infectious complications and later development of obliterative bronchiolitis (OB).

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