Chest closure after cardiac surgery occasionally results in cardiac compression leading to circulatory failure. In shunt-dependent circulation, the arterial oxygen saturation may decrease significantly due to the increase in pulmonary vascular resistance caused by chest closure. Temporary patch implantation with delayed sternal closure facilitates circulatory and/or pulmonary stabilization (temporary chest wall patch plasty, TCWPP). Between July 1986 and June 1991, 42 patients underwent staged chest closure (TCWPP) after open heart surgery for congenital lesions (4.9% of 854 patients). TCWPP was performed when either primary hemodynamic deterioration or an increase in cyanosis (palliative procedures only) followed by hemodynamic deterioration occurred during attempted or shortly after sternal closure. Overall mortality was 40.4% (17/42). It was 32.3% (11/34) when the patch was inserted primarily at the end of the operation. If the patch was inserted emergently 4-24 h postoperatively, mortality was 75% (6/8). Definite chest closure was performed from 4 h to 6 days (mean 72 h) postoperatively. In 2 patients closure had to be performed emergently (single ventricles); 7 patients died before chest closure. One mediastinal microbiology examination was positive. Deep sternal infection necessitating operative revision occurred in one other patient. In conclusion, TCWPP may considerably lower mortality of the illest patients after surgery for complex congenital heart disease. A timely decision as to the performance of staged chest closure is mandatory. This procedure rarely causes infection. We now apply this technique liberally, by cardio-mediastinal size judgement in over 30% of our TCWPP candidates even without a prior trial of primary closure.

In the seventies and eighties spinal mechanisms inhibiting pain processing were discovered in animal studies leading to new therapeutic regimens such the use of spinal opioids. During the last decade additional studies revealed an increased sensibility of the spinal cord upon severe, long lasting pain perception, a mechanism called wind-up. Hyperalgesia is accompanied by persisting genetic changes of spinal cord cells, which may contribute to the chronification of pain. The severity and duration of acute pain apparently contributes to the possibility of chronic pain development. Although not all the consequences of these findings are clear, they may influence our way of performing anaesthesia and treating postoperative or acute pain situations, e.g. pain during herpes zoster or pain after trauma and amputation. In general, analgetic measures should be potent enough to prevent spinal sensiblisation, which can be best achieved with spinal blockade by local anesthetics. Another way of counteracting pain-induced spinal plasticity is by blocking or antagonizing its pathways with specific transmitters or their equivalents. All these spinally mediated regimens should be performed prior to later predominating mechanisms of supraspinal plasticity involving psychic changes due to persisting pain, which seem to evolve with delay to spinal processes.

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