Has XXXX been eradicated?

@entity1 @entity6220 @entity1337 @entity149 @entity616 @entity701 @entity158 @entity282 @entity1118 @entity413 @entity130
Recent evidence suggests that surgical @entity130 induces a @entity149 that contributes to and enhances @entity282 . These changes are also thought to be the underlying cause of much @entity1118 . @entity6220 is generated not only during surgery, but also postoperatively as a result of the inflammatory response to the damaged tissue. This knowledge provides a rational basis for pro-active, pre-emptive and postoperative analgesic strategies to reduce the neuronal barrage associated with tissue damage. Reduction or elimination of @entity282 is therefore possible. We advocate the use of continuous @entity616 for postoperative @entity1337 in @entity1 undergoing thoracotomy. When this is begun pre-emptively (by precutaneous, pre-incisional @entity616 ) it is combined with an opiate and a non-steroidal anti-inflammatory drug premedication. In a randomised study of 56 @entity1 , @entity158 scores of less than 0.5 cm on a 10 cm scale were produced, postoperative lung function was preserved and @entity413 and @entity701 responses were significantly unchanged from preoperative values. Evidence that effective perioperative @entity1337 reduces the incidence of chronic post-thoracotomy chest wall @entity158 was found in a retrospective study of 1000 consecutive thoracotomies. The endpoints of a zero @entity158 score, complete preservation of preoperative lung function and prevention of the stress response to @entity130 are currently achievable and should be provided for virtually all @entity1 undergoing chest surgery. Pre-empting @entity158 must be the goal for all those involved in the postoperative care of @entity1 .
