Stercoral Perforation in the Setting of Chronic Antipsychotic Use: A Case Report.

Stercoral perforation is a rare form of colonic perforation with limited reports in the literature, accounting for less than 140 documented cases. This complication occurs due to increased intraluminal pressure created by fecal impaction, ultimately causing colonic ulceration and necrosis. It is most often seen in elderly or debilitated patients with chronic constipation. The long-term use of drugs or medications with side effects of chronic constipation such as opioids, antispasmodics, tricyclic antidepressants, and calcium channel blockers have been implicated in these cases. Here we present a case of stercoral perforation in a patient with short-term opioid use following an orthopedic procedure, but more likely complicated by long-term use of antipsychotics and antidepressants.

Management of Warfarin-Induced Adrenal Adenoma Hemorrhage in the Setting of a History of Pulmonary Embolism.

Adrenal hemorrhage (AH) is associated with trauma, acute stress, sepsis, coagulopathy, pregnancy, neonatal stress, and underlying adrenal masses, which can include metastases, pheochromocytomas, adrenocortical cancers, or hematomas. However, the literature on nontraumatic AH secondary to an adenoma in the setting of chronic anticoagulation is limited. We present a case report of a patient found to have AH from an incidental adrenal adenoma associated with the use of warfarin in the setting of a recent history of pulmonary embolism requiring anticoagulation. In a patient who presents with AH while on anticoagulation, initial management should include reversal of coagulopathy, supportive care with serial hematocrits and blood transfusions as necessary, and biochemical workup to assess for functional tumors. However, aggressive surgical management with adrenalectomy should ideally follow for those patients who will require long-term anticoagulation to minimize future risk for rebleeding.

Role of lymphadenectomy in surgical treatment of solid tumors: an update on the clinical data.

BACKGROUND: The role of lymphadenectomy as an adjunct of standard excision for treatment of cancer is highly debated and controversial. Standard practice for treatment of solid tumors is resection with regional lymphadenectomy. This surgical concept assumes that cancers grow and spread in an orderly manner, from primary cancer to regional lymph nodes and finally to vital organs. We reviewed randomized trials, published a description of lymphatic anatomy and physiology, and presented data that disputed the role of lymphadenectomy as standard practice. The present review updates the literature and reiterates the concept that lymphadenectomy does not increase survival in the surgical treatment of solid tumors. METHODS: We reviewed the English-language literature (Medline) for prospective randomized trials and nonrandomized reports, as well as retrospective studies addressing the role of lymphadenectomy in cancers of the esophagus, lung, stomach, pancreas, breast, and skin (melanoma) reported between 2000 and 2006. RESULTS: This extensive review demonstrates that there are few prospective randomized trials assessing patient survival with solid tumors that contrast resection with or without lymphadenectomy. However, there was at least one, and for some cancers more than one, prospective randomized trial for each organ site studied, and the data demonstrate no statistically significant difference in overall survival of patients treated with or without lymphadenectomy. Most nonrandomized and retrospective studies, with a few exceptions, support the conclusions of randomized trials; lymphadenectomy does not improve overall survival in solid tumors. Overall survival is primarily a function of the biological nature of the primary tumor, as evidenced by lymphovascular invasion, lymph node involvement, and other prognostic features. CONCLUSIONS: This extensive literature review of recent reports indicates that lymphadenectomy does not improve overall survival. Lymph node resection should be conceived in terms of staging, prognosis, and regional control only.

An effective in vitro antitumor response against human pancreatic carcinoma with paclitaxel and daunorubicin by induction of both necrosis and apoptosis.

The highly metastatic human pancreatic cell line L3.6 was used to study mechanisms for antitumor activity with various chemotherapeutic drug combinations. The most effective drugs were daunorubicin (IC50 0.4 microM), doxorubicin (IC50 22 microM), paclitaxel (IC50 5.3 microM) and 5-fluorouracil (IC50 5.4 microM). The most effective drug combination was equitoxic concentrations of paclitaxel and daunorubicin. Kinetic analysis demonstrated that both paclitaxel and daunorubicin had to be added simultaneously for maximum cytotoxicity. Daunorubicin treatment alone demonstrated ROS (reactive oxygen species) induction and cellular morphological changes more consistent with chemical damage in a total of 93% of the cells and apoptotic changes in 20% of the cell population. The apoptosis induced by daunorubicin does not appear to be caspase-dependent, as demonstrated by the lack of conversion of the procaspases 8 and 3. Within 24 h of treatment with paclitaxel, Bcl-2 formed a doublet at 26 kilodaltons and the expression was abrogated with daunorubicin and the combination of the two drugs as determined by Western blots. These data suggest that the human pancreatic cell line L3.6 is more effectively killed following treatment with chemotherapeutic agents that cause death through at least two pathways, a caspase-dependent and caspase-independent apoptosis and necrosis.