Advances in Surgery 2011

John L. Cameron

Description

Each year, Elsevier’s Advances in Surgery reviews the latest techniques, data, and evidence in general surgery. A distinguished editorial board, led by Dr. John L. Cameron of Johns Hopkins, identifies current areas of major progress and controversy, and invites specialists from around the world to contribute comprehensive, detailed reviews on these topics.

Sujets

• Medical
• Médecine
• Surgery

Informations

• Publié par: Mosby
• Date de parution: 01 septembre 2011
• Nombre de lectures: 0
• EAN13: 9780323087278
• Langue: English
• Poids de l'ouvrage: 2 Mo

Extrait

Advances in Surgery , Vol. 45, No. 1, September 2011
ISSN: 0065-3411
doi: 10.1016/S0065-3411(11)00032-7

Contributors
Advances in Surgery
John L. Cameron
B. Mark Evers
Yuman Fong
David Herndon
Keith Lillemoe
John A. Mannick
Charles J. Yeo
ISSN  0065-3411
Volume 45 • Number 1 • September 2011

Contents
Cover
Contributors
Current Management of Small Bowel Obstruction
Screening for Colorectal Cancer
Varicose Vein: Current Management
Geographic Variation in Health Care and the Affluence-Poverty Nexus
Endovascular Approaches to Arteriovenous Fistula
Local and Regional Control in Breast Cancer: Role of Sentinel Node Biopsy
Stem Cells in Acute Liver Failure
Is There a Role for Bowel Preparation and Oral or Parenteral Antibiotics In Infection Control in Contemporary Colon Surgery?
Oral Antibiotics to Prevent Surgical Site Infections Following Colon Surgery
Pancreatic Necrosectomy
The Impact of Health Care Reform on Surgery
Glucose Elevations and Outcome in Critically Injured Trauma Patients
Advances in the Surgical Management of Gastrointestinal Stromal Tumor
Choledochoceles: Are They Choledochal Cysts?
What Does Ulceration of a Melanoma Mean for Prognosis?
Influence of Surgical Volume on Operative Failures for Hyperparathyroidism
Perioperative Normothermia During Major Surgery: Is It Important?
Surgical Management of Hereditary Nonpolyposis Colorectal Cancer
How to Change General Surgery Residency Training
Recent Advances in the Diagnosis and Treatment of Gastrointestinal Carcinoids
The Past, Present, and Future of Biomarkers: A Need for Molecular Beacons for the Clinical Management of Pancreatic Cancer
Robotic-Assisted Major Pancreatic Resection
Immunotherapy for Metastatic Solid Cancers
Prophylaxis for Deep Vein Thrombosis and Pulmonary Embolism in the Surgical Patient
Index
Advances in Surgery , Vol. 45, No. 1, September 2011
ISSN: 0065-3411
doi: 10.1016/j.yasu.2011.03.017

Current Management of Small Bowel Obstruction

Martin Donald Zielinski, MD * , Michael Patrick Bannon, MD.
Department of Surgery, Mayo Clinic, 200 1st Street SW, Rochester, MN 55905, USA
* Corresponding author.
E-mail address: [e-mail]
Although common, small bowel obstruction (SBO) remains one of the most challenging clinical problems treated by surgeons. Responsible for up to 300,000 hospital admissions every year in North America, SBO arises from multiple etiologies and manifests as a diverse panoply of clinical presentations [1] . Initial evaluation should center on differentiating those patients who need urgent exploration from those who may undergo a safe, nonoperative trial. The wide range of etiologies, however, combined with specific, and often unique, patient parameters, renders this decision difficult. Traditionally, the decision between urgent operative intervention and initial nonoperative management has hinged on the distinction between complete and partial obstruction. However, the clinical diagnosis of complete obstruction is imprecise, and the complete/partial dichotomy has not eliminated avoidable obstruction-associated ischemia and necrosis. Rather than trying to predict those patients at risk for ischemic complications, we may do better to define clinical parameters that predict failure of nonoperative management and offer prompt operation to patients demonstrating these parameters. Hopefully, such an approach, codified into practice management guidelines, will minimize both ischemia and hospital length of stay associated with SBO. After reviewing the pathogenesis and pathophysiology of SBO, this article outlines newly developed and refined management and surgical techniques to reach these goals.

Pathogenesis
SBO implies compromised luminal patency and as such is differentiated from the functional abnormalities of ileus and dysmotility disorders. Adhesive disease, neoplasia, and hernias are the 3 most common causes in the western world, collectively accounting for 80% of all obstructions [2 , 3] . In developing countries, hernias, intussusceptions, and volvulae predominate [4] .
SBO most frequently arises from adhesive disease (49%), which in turn is almost always related to prior operation ( Fig. 1 ) [2] . Only a minority of patients with adhesions will experience SBO. Although 93.0% of patients with more than one abdominal operation will have adhesions at autopsy, only 4.6% of patients with a prior abdominal procedure will have an adhesive SBO [5 , 6] . Adhesive SBO is frequently a relapsing disease: up to 30% of patients who undergo celiotomy for obstruction will require reexploration for recurrence [2 , 7] .

Fig. 1 Adhesive small bowel obstruction.
Barmparas and colleagues [5] reviewed the English literature and collected more than 440,000 reported patients with postceliotomy adhesive SBO to examine risk factors. The likelihood of subsequent SBO varied among different index operative procedures, and was greatest after open adnexal operations (23.9%), followed by ileal pouch anal-anastomosis (19.3%), and open total abdominal hysterectomy (9.5%). Laparoscopic cholecystectomy (0.2% vs 7.1%), laparoscopic total abdominal hysterectomy (0.0% vs 15.6%), and laparoscopic adnexal operations (0.0% vs 23.9%), but not laparoscopic appendectomies (1.3% vs 1.4%), all resulted in fewer adhesive obstructions than their open counterparts. Overall, open procedures were associated with twice as many adhesive obstructions as was laparoscopy, but the investigators cautioned that interpretation of this collective comparison was hampered by limited follow-up, heterogeneity between the primary studies, and selection biases. Indeed, early review of the Conventional versus Laparoscopic-Assisted Surgery In Colorectal Cancer CLASICC (CLASICC) trial data demonstrated no statistical difference between adhesive obstructions after laparoscopic (2.5%) versus open resections (3.1%) for colorectal cancer at 3-year follow-up [8] .
Neoplasia, the second leading cause of SBO, is responsible for 16% of SBO admissions ( Fig. 2 ) [2] . Although primary small bowel tumors do cause obstruction, colorectal and ovarian metastases are the most common malignant etiologies (41% and 28%, respectively) [9] . Breast cancer and malignant melanoma are the 2 most common nonabdominal tumors that can cause obstruction [10] . Neoplastic masses causing obstruction may be a result of the primary tumor, peritoneal metastases, or bulky lymph node metastases. The mechanism of obstruction may be direct compression, malignant adhesion with consequent torsion, knuckling, or internal herniation. The median time from the diagnosis of cancer to the first episode of obstruction is about 1 year, but decades can pass from the time of initial diagnosis to obstruction. Median survival is on the order of 3 to 6 months after onset of initial obstructive symptoms and is almost universally fatal [9 , 10] .

Fig. 2 Malignant small bowel obstruction.
Hernias cause 15% of SBOs [2] . There are 2 main categories of hernia: external and internal. Among external hernias, incarceration is encountered most frequently from inguinal and incisional hernias, but is also seen with femoral, umbilical, traumatic, and peristomal hernias ( Fig. 3 ). Whereas external hernias are diagnosed on physical examination, internal hernias are generally diagnosed in the operating room, and on occasion, by preoperative computed tomography (CT). Internal hernias can be further classified into congenital or acquired types. For example, an obturator hernia, resulting from protrusion of intra-abdominal contents through the obturator foramen created by the pubic bones and ischium, is considered a congenital internal hernia ( Fig. 4 ) [11] . Obturator hernias, generally present in elderly women after significant weight loss, are associated with a 25% mortality owing to the difficulty in diagnosis and the comorbidities of the patient population [12] . Omental and paraduodenal defects, as well as the foramen of Winslow are additional, but uncommon, sites of congenital herniation [13] .

Fig. 3 Incarcerated inguinal hernia.

Fig. 4 Incarcerated left obturator hernia.
Acquired internal hernias arise after surgical manipulation. With the rapid increase in the rate of laparoscopic bariatric procedures, the rate of internal hernia is rising [14] . Surgeons must be knowledgeable in the diagnosis and treatment of the specific hernias that can result from Roux-En-Y Gastric Bypass including those through mesocolic, Petersen, and mesomesenteric defects ( Fig. 5 ) [13 , 14] . The incidence has been reported to be as high as 3.1%, but this is likely declining with greater awareness of the need to close the defects at the primary operation [15] . The mesocolic defect is created for the retrocolic passage of the Roux limb. Petersen defect is bordered by the transverse mesocolon superiorly, the Roux limb and its mesentery anteriorly, and the proximal-most jejunum and its mesentery posteriorly [16] . Mesomesenteric defects are created by inadequate apposition of mesentery after bowel resection with anastomosis; after gastric bypass, a large such defect exists between the mesentery of the biliopancreatic limb anteriorly and the mesentery of the alimentary limb/common channel posteriorly. Symptomatic hernias can occur at any time after bypass, especially as the patients lose weight, allowing for widening of defects not closed properly during the initial procedure. As an additional consideration in patients with gastr