No abstract

Postoperative ileus (POI) is a predictable delay in gastrointestinal (GI) motility that occurs after abdominal surgery. Probable mechanisms include disruption of the sympathetic/parasympathetic pathways to the GI tract, inflammatory changes mediated over multiple pathways, and the use of opioids for the management of postoperative pain. Pharmacologic treatment of postoperative ileus continues to be problematic as most agents are unreliable and unsubstantiated with robust clinical trials. The selective opioid antagonist alvimopan has shown promise in reducing POI, but needs more rigorous investigation. Clinician interventions proven to be of benefit include laparoscopy, thoracic epidural anesthesia, avoidance of opioids, and early feeding. Early ambulation may also contribute to early resolution of POI; however, routine nasogastric decompression plays no role and may increase complications. Multimodal care plans remain the mainstay of treatment for POI. Defined as a temporary delay in gastrointestinal (GI) motility after surgery, postoperative ileus (POI) is a well-described surgical complication perceived as inevitable by some authors.1 The symptoms of POI include nausea, vomiting, abdominal distention, abdominal tenderness, and delayed passage of flatus and stool. Prevention of POI may improve patient comfort, decrease length of hospital stay, and limit costs associated with postoperative recovery. 2 POI was first described by Cannon and Murphy in 1906, and is now commonly described as a transient postoperative period of gut motility dysfunction.3,4 Long considered a routine event in the postoperative course, POI has emerged as an important facet of patient care and hospital stay, and its obscure pathogenesis merits considerable attention.3,5 PATHOPHYSIOLOGYThe pathophysiology of POI is not fully understood despite an increased understanding of mechanisms that contribute to altered GI motility following surgery, which include spinal-intestinal neural reflexes, sympathetic hyperactivity, opiate use, and electrolyte abnormalities. 3 Autonomic nervous dysfunction appears to be

The purpose of this study is to provide more definite evidence regarding the role of dose modification of chemotherapy in obese women with breast cancer by systematically reviewing current literature regarding chemotherapy-induced toxicity rates in obese and non-obese women with early-stage breast cancer. A systematic search of Pubmed and EMBASE was conducted to identify original studies investigating chemotherapy-induced toxicity in obese women receiving adjuvant chemotherapy treatment for breast cancer. Ten studies were identified. We noted low rates of adjustment for confounders such as prophylactic hematopoietic growth factor use and empirical dose reductions. Seven studies found reduced toxicity in obese compared to non-obese women. Of four studies, where dose capping was precluded or statistically adjusted for, three found reduced toxicity in obese women. These outcomes include less febrile neutropenia (body mass index (BMI) >23.6; odds ratio (OR) 4.4; 95 % confidence interval (CI) 1.65-12.01), fewer hospital admissions (BMI >35; OR 0.61, 95 % CI 0.38-0.97), and fewer neutropenic events (BMI >25; OR 0.49; 95 % CI 0.37-0.66). Only a single study reported higher rates of toxicity in obese women, but this study had significant methodological issues. As a conclusion, we observed that obese patients tolerate chemotherapy better than lean patients. However, this may be confounded by poorly specified dose capping practices and the use of hematopoietic growth factors. Further research should focus on improved documentation of body size, of dose, and of use of growth factors, and analysis of how these affect recurrence rates, toxicity, and survival.

Hypothermia is a significant contributor to mortality in severely injured patients. Rewarming is an enormous challenge, especially in those who require operative or angiographic intervention. In this patient population, external warming methods are only capable of reducing further heat loss, whereas active rewarming adds heat to the body's core but is invasive. This article analyzes our initial experience with a minimally invasive, continuous, automated, and easily portable intravascular rewarming technique using the Alsius Corporation's CoolGard system. The records of 11 hypothermic critically injured patients presenting to our level 1 trauma center over a 6-month period were reviewed. The patients' mean age was 39 +/- 22 years, 7 (64%) were male, and 7 (64%) had blunt mechanisms of injury. The mean injury severity score was 40 +/- 16, and the mean initial systolic blood pressure was 91 +/- 60 mm Hg. The mean core temperature at the initiation of rewarming was 33.6 +/- 1.0 degrees C, and the mean rewarming rate was 1.5 +/- 1.0 degrees C/h. Six patients died (55%), two of acute exsanguination and four of unsurvivable traumatic brain injuries. One patient developed a deep vein thrombosis at the femoral catheter site and experienced a nonfatal pulmonary embolus. Our experience demonstrates that active intravascular balloon-catheter rewarming represents a practical, automated technique for the immediate and continuous treatment of hypothermia in all phases of the acute care of trauma patients.