Epidural anesthesia and analgesia. Their role in postoperative outcome.

THE Confederate General “Stonewall” Jackson was one of the earliest known victims of a respiratory complication after surgery, dying of pneumonia 10 days after an otherwise successful ether anesthetic in 1863. Despite subsequent advances in anesthesia and surgical care, postoperative pulmonary complications (PPCs) still are a significant problem in modern practice. This commentary examines why PPCs occur and how the anesthesiologist can help prevent them.

Preventing postoperative pulmonary complications: the role of the anesthesiologist.

Diaphragm weakness is highly prevalent in critically ill patients. It may exist prior to ICU admission and may precipitate the need for mechanical ventilation but it also frequently develops during the ICU stay. Several risk factors for diaphragm weakness have been identified; among them sepsis and mechanical ventilation play central roles. We employ the term critical illness-associated diaphragm weakness to refer to the collective effects of all mechanisms of diaphragm injury and weakness occurring in critically ill patients. Critical illness-associated diaphragm weakness is consistently associated with poor outcomes including increased ICU mortality, difficult weaning, and prolonged duration of mechanical ventilation. Bedside techniques for assessing the respiratory muscles promise to improve detection of diaphragm weakness and enable preventive or curative strategies. Inspiratory muscle training and pharmacological interventions may improve respiratory muscle function but data on clinical outcomes remain limited.

/pdf/critical-illness-associated-diaphragm-weakness-3yr7v9j472.pdf

Critical illness-associated diaphragm weakness

Control of abdominal muscles

The lobar and cephalocaudal distribution of aerated and nonaerated lung and of PEEP-induced alveolar recruitment is unknown in acute lung injury (ALI). Dimensions of the lungs and volumes of aerated and nonaerated parts of each pulmonary lobe were measured using a computerized tomographic quantitative analysis and compared between 21 patients with ALI and 10 healthy volunteers. Distribution of PEEP-induced alveolar recruitment along the anteroposterior and cephalocaudal axis and influence of the resting volume of nonaerated lower lobes were also assessed. Anteroposterior and transverse dimensions of the lungs of the patients were similar to those of healthy volunteers, whereas cephalocaudal dimensions were reduced by more than 15%. Total lung volume (aerated plus nonaerated lung) was reduced by 27%. Volumes of upper and lower lobes were 99 and 48% of normal values. In addition to an anteroposterior gradient in the distribution of aerated and nonaerated areas, a cephalocaudal gradient was also observed. Nonaerated areas were predominantly found in juxtadiaphragmatic regions. PEEP-induced alveolar recruitment was more pronounced in nondependent than in dependent regions and in cephalad than in caudal regions. A significant correlation between resting volume of nonaerated lower lobes and regional PEEP-induced alveolar recruitment was observed. In ALI, loss of lung volume involves predominantly lower lobes. The thorax shortens along its cephalocaudal axis. PEEP-induced alveolar recruitment predominates in nondependent and cephalad lung regions and is inversely correlated with the resting volume of nonaerated lung.

/pdf/a-computed-tomography-scan-assessment-of-regional-lung-dv2cxw3i6c.pdf

A Computed Tomography Scan Assessment of Regional Lung Volume in Acute Lung Injury

The effects of upper abdominal surgery on diaphragmatic function were studied in 5 patients. During quiet tidal breathing, the volume displacement of the abdomen within the tidal volume (Vab/Vt) and the ratio of abdominal and transdiaphragmatic pressure changes (delta Pab/delta Pdi), taken as an index of the diaphragmatic contribution to the breathing process, decreased significantly on the first postoperative day (p less than 0.001); in 2 patients, a cephalad paradoxical motion of the diaphragm during inspiration was observed. Diaphragmatic dysfunction also occurred during maximal inspiratory efforts as shown by the significant fall in maximal static transdiaphragmatic pressure (Pdimax) and cephalocaudal diaphragmatic displacement on the first (p less than 0.001) and third (p less than 0.001) postoperative days. On the first postoperative day, opiate epidural analgesia did not modify Vab/VT, delta Pab/delta Pdi, and Pdimax. These parameters spontaneously returned towards control values on the seventh postoperative day. We conclude that upper abdominal surgery induces a marked diaphragmatic dysfunction lasting about 1 wk and that it is not suppressed by postoperative pain relief. The mechanism of this dysfunction remains to be determined. It may be the main cause of the postoperative pulmonary restrictive pattern.

Diaphragm Dysfunction Induced by Upper Abdominal Surgery. Role of Postoperative Pain

The effects of upper abdominal surgery on diaphragmatic function were studied in 5 patients During quiet tidal breathing, the volume displacement of the abdomen within the tidal volume (Vab/Vt) and the ratio of abdominal and transdiaphragmatic pressure changes (delta Pab/delta Pdi), taken as an index of the diaphragmatic contribution to the breathing process, decreased significantly on the first postoperative day (p less than 0001); in 2 patients, a cephalad paradoxical motion of the diaphragm during inspiration was observed Diaphragmatic dysfunction also occurred during maximal inspiratory efforts as shown by the significant fall in maximal static transdiaphragmatic pressure (Pdimax) and cephalocaudal diaphragmatic displacement on the first (p less than 0001) and third (p less than 0001) postoperative days On the first postoperative day, opiate epidural analgesia did not modify Vab/VT, delta Pab/delta Pdi, and Pdimax These parameters spontaneously returned towards control values on the seventh postoperative day We conclude that upper abdominal surgery induces a marked diaphragmatic dysfunction lasting about 1 wk and that it is not suppressed by postoperative pain relief The mechanism of this dysfunction remains to be determined It may be the main cause of the postoperative pulmonary restrictive pattern

Diaphragm dysfunction induced by upper abdominal surgery. Role of postoperative pain.

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Diaphragm Dysfunction Induced by Upper Abdominal Surgery. Role of Postoperative Pain

Diaphragm dysfunction induced by upper abdominal surgery. Role of postoperative pain.