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Ketoprofen is a NSAIDs of the 2-aryl propionic acid class commonly used in the treatment of inflammatory rheumatic disease, acute pain and fever. Clinically, ketoprofen seems to reduce morphine requirements by 33 to 40% with ketoprofen's supposed central mechanism of analgesia. We evaluated the efficacy and safety of intravenous (IV) ketoprofen as an adjuvant to IV PCA (patient controlled analgesia) with tramadol after major gynecological cancer surgery for postoperative analgesia. Fifty patients were enrolled in this double-blinded, randomized, placebo-controlled study. Patients were allocated randomly to two groups: group I (25 patients) served as a control group, with patients receiving saline; group II (25 patients) received ketoprofen. Patients received an intravenous bolus of saline or 100 mg ketoprofen at the end of surgery. Then, PCA was given as a 20 mg tramadol bolus and 10 min lockout time. Pain relief was regularly assessed using a visual analog scale. Tramadol consumption, side-effects, and patient satisfaction were noted during the 24 hours after the surgery. No significant difference was observed in pain score, side-effects and patient satisfaction between the groups (p > 0.05). The cumulative PCA-tramadol consumption was lower in the ketoprofen-treated patients than placebo-treated patients (p < 0.05). Our results demonstrate that a single dose of 100 mg ketoprofen reduced tramadol consumption for treatment of postoperative pain after major gynecological cancer surgery.

Infection is a potentially serious complication of long-term epidural (EP) catheterization in cancer patients. Although the use of epidural opioid analgesia is an effective and safe means for pain relief in terminally ill patients, these patients are in need of monitorization for possible infection. This is the first report in which EP catheter cultivation has been assessed in an immunocompromised and febrile neutropenic endometrial cancer patient.

In this study the pathophysiology and characteristics of cancer pain together with cancer pain syndromes and guidelines of management are reviewed. Tumour-associated pain may be nociceptive (somatic or visceral) if the sustaining mechanisms are related to ongoing tissue pathology, or neuropathic when pain is associated with injury to neural tissues. The mechanism by which tumours produce pain include obstruction of lymphatic and vascular channels, distension of a hollow viscous, oedema and tissue inflammation or necrosis. Injury to tissues results in the local release of numerous chemicals that mediate transmission of pain stimulus. Cancer pain syndromes result from one or more of three fundamental causes; direct tumour involvement of tissues, cancer-directed therapy, and mechanisms unrelated to cancer or its treatment. Cancer pain syndromes are also classified as acute or chronic. Cancer pain characteristics provide some of the data essential for syndrome identification. These characteristics include intensity, quality, distribution and temporal relationships. The principles of tumour-directed pain control include modifying the source of pain by treating the cancer and the inflammatory response to cancer, altering the central perception of pain and interfering with nociceptive transmission within the central nervous system.