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Excerpt
The function of maintaining homeostasis during stress makes the endocrine and sympathetic nervous systems important candidates as markers of injury severity and potential indicators of patient outcome. Plasma catecholamines and cortisol concentrations correlate with severity of brain injury, and high concentrations predict poor outcomes in brain-injured patients [1,2]. Hormonal responses are greater in patients undergoing more difficult surgical procedures than in those patients having inguinal hernia repairs [3]. Patients in a medical intensive care unit with thyroxine concentrations of less than 3 micro gram/dL have mortality rates of 67% [4] and head-injured patients who die or remain in a vegetative state have 3,5,3 prime-triiodothyronine and thyroxine concentrations that are 30% to 50% lower than patients with better outcomes [5]. The relevant question, however, is whether these humoral changes are adaptive or maladaptive.
More recently, there has been increasing interest in the humoral changes that occur during and after surgery in patients given regional anesthesia, together with continuous postoperative pain relief [6-8]. Compared with patients receiving general anesthesia, patients receiving regional anesthesia have lower sympathoadrenal responses [6-8], but not necessarily lower adrenocortical [7] responses. The data also seem clear in showing that patients treated with epidural blockade have lower blood pressures [6,7] and a lower frequency of thrombotic phenomena [7,9]. Given these observations, it has been speculated that changes in norepinephrine and cortisol concentrations and postoperative complications are related.
The study by Dr. Parker and colleagues [10] in this issue of Critical Care Medicine attempts to develop a causal relationship between activation of the sympathetic nervous system or adrenocortical systems, hypercoagulability, and morbid events in a cohort of 60 patients that was drawn from a larger study of 100 patients undergoing lower extremity vascular surgery. The patients were randomized to receive either epidural anesthesia/epidural opiate analgesia or general anesthesia/intravenous patientcontrolled analgesia. An earlier study [7] by the same group demonstrated that patients receiving epidural anesthesia/epidural opiate analgesia had lower occurrence rates of hypertension, repeat surgery for graft revision, thrombectomy, or amputation; they also had lower catecholamine concentrations, which started from the time of skin closure and continued for 18 hrs [11]. What separates the current study from others of the genre is the attempt to find a cause and effect relationship between the two observations. While the authors repeated their earlier observations that patients receiving epidural anesthesia/epidural opiate analgesia had lower graft complications, one of their new findings is that irrespective of the anesthesia regimen, complications correlated only with higher norepinephrine concentrations. Greater levels of pain did not appear to be responsible for the catecholamine concentration differences, as these values were similar at the time of emergence from anesthesia. Although at 6 and 12 hrs, postoperative pain as well as norepinephrine concentrations were higher in patients with complications, the fascinating point is that norepinephrine concentrations were higher in patients with complications very early in their postoperative course.
Dr. Parker and colleagues [11] also reported potential problems with fibrinolysis. Increasing plasminogen activator inhibitor-1 concentrations were present in patients with higher norepinephrine concentrations. A previous study [12] by this group demonstrated a relationship between plasminogen activator inhibitor-1 concentrations and graft failure.
Although the authors have woven an increasingly tight (but as yet, still circumstantial) web of evidence incriminating excessive sympathetic nervous system responses in morbid postoperative complications following lower extremity vascular surgery, it remains to be proven that humoral markers of the stress response contribute to postoperative complications. Given the known effects of catecholamines on myocardial function, one is unlikely to quibble about the association between hypertension and excessive sympathetic nervous system discharge.
