Cancer patients commonly undergo surgical procedures. The perioperative period is characterized by immunosuppression and may predispose already immunosupressed cancer patients to tumor spread. Cancer patients typically show depression of both cellular and humoral immune functions. Possible mediating factors for immunosuppression during the perioperative period include anesthetic agents, opioids, surgery, blood transfusions, temperature changes, pain, and psychological stress. A surgically mediated decrease in natural killer (NK) cell activity has been implicated as the major contributing factor associated with an increase in metastasis. The decreased NK cell activity during the perioperative period is associated with increased risk of mortality and cancer. Commonly used anesthetic agents and opioids are known to inhibit NK cell activity. Despite the in vivo evidence of anesthetic- and analgesic-agent-mediated immunosupression, surgery by itself results in a three- to four-fold increase in retention of metastasis when compared to the groups in which anesthesia and analgesia were combined. The negative consequences associated with perioperative immunosuppression may be decreased by several strategies, including aggressive pain control, selection of specific anesthetic and analgesic agents, avoidance of unnecessary transfusions, and delay of elective surgeries until the patient's nutritional and immune status is optimized. Recognizing and neutralizing its mediating factors, perioperative immunosuppression in cancer patients may be reduced.

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Complex regional pain syndrome consists of pain and other symptoms that are unexpectedly severe or protracted after an injury. In type II complex regional pain syndrome, major nerve injury, often with motor involvement, is the cause; in complex regional pain syndrome I, the culprit is a more occult lesion, often a lesser injury that predominantly affects unmyelinated axons. In florid form, disturbances of vasoregulation (eg, edema) and abnormalities of other innervated tissues (skin, muscle, bone) can appear. Because of these various symptoms and the difficulty in identifying causative lesions, complex regional pain syndrome is difficult to treat or cure. Complex regional pain syndrome has not been systematically investigated; there are few controlled treatment trials for established complex regional pain syndrome. This article reviews the existing studies (even if preliminary) to direct clinicians toward the best options. Treatments for other neuropathic pain syndromes that may be efficacious for complex regional pain syndrome also are discussed. Some common treatments (eg, local anesthetic blockade of sympathetic ganglia) are not supported by the aggregate of published studies and should be used less frequently. Other treatments with encouraging published results (eg, neural stimulators) are not used often enough. We hope to encourage clinicians to rely more on evidence-supported treatments for complex regional pain syndrome.