Sengstaken-Blakemore Tube

Balloon tamponade of bleeding esophageal varices was described as early as the 1930s. A double-balloon tamponade system originally developed by Sengstaken and Blakemore in 1950 has undergone relatively few changes to the current day.^{[1, 2, 3]} The 3 major components of a Sengstaken-Blakemore tube are a gastric balloon, an esophageal balloon, and a gastric suction port. The addition of an esophageal suction port to help prevent aspiration of esophageal contents resulted in what is called the Minnesota tube. Another nasogastric (NG) device with a single gastric balloon is most effective at terminating bleeding from gastric varices and is known as the Linton-Nachlas tube.^[4] The advent of endoscopy has reduced the use of balloon tamponade, but the use of such devices can still be temporizing or lifesaving, despite their potential for serious complications.^{[5, 6, 7, 8]}
See the images below.
Sengstaken-Blakemore tube. Image courtesy of Richard Treger, MD. Linton-Nachlas tube. Image courtesy of Richard Treger, MD.

Cytomegalovirus Colitis

Cytomegalovirus (CMV) is a member of the Herpesviridae family, along with herpes simplex viruses 1 and 2, Epstein-Barr virus, and varicella-zoster virus. It is a double-stranded DNA virus with a protein coat and lipoprotein envelope. Similar to other herpesviruses, CMV is icosahedral and replicates in the host's nucleus. Replication in the host cell typically manifests pathologically with large intranuclear inclusion bodies and smaller cytoplasmic inclusions, and is accompanied by presence of CMV viral particles in the plasma.

Gross specimen of bowel showing ulceration secondary to cytomegalovirus colitis. Giant cell with inclusion body characteristic of cytomegalovirus colitis.

Between 50% and 80% of the world's population is seropositive for CMV. Initial CMV infection in the immunocompetent host typically is mild and goes undetected clinically. This is followed by a chronic latent state, during which the virus remains present within host cells, but viral proliferation is prevented by host cell-mediated immunity. Failure of immune containment may lead to reactivation with viral proliferation and severe systemic illness. Systemic CMV disease is characterized by fever, pancytopenia, and inflammatory changes in multiple organs including the liver and lungs, and in the retina. Colitis is a frequent manifestation of this acute systemic illness.

Patients are rendered susceptible to systemic CMV disease by treatment with immunosuppressive medications, or by illnesses that reduce cellular immunity, such as human immunodeficiency virus (HIV) infection. Acute systemic illness caused by CMV is particularly common following initial exposure in an immune compromised individual (in particular, in a CMV-negative transplant recipient who receives an organ from a CMV-positive donor).

Hirschsprung Disease

Hirschsprung disease is a developmental disorder of the enteric nervous system and is characterized by an absence of ganglion cells in the distal colon resulting in a functional obstruction.^[1] See the image below.
Hirschsprung disease. Contrast enema demonstrating transition zone in the rectosigmoid region.
Although this condition was described by Ruysch in 1691 and popularized by Hirschsprung in 1886, the pathophysiology was not clearly determined until the middle of the 20th century, when Whitehouse and Kernohan described the aganglionosis of the distal intestine as the cause of obstruction in their series of patients.^[2]
In 1949, Swenson described the first consistent definitive procedure for Hirschsprung disease, rectosigmoidectomy with coloanal anastomosis. Since then, other operations have been described, including the Duhamel and Soave techniques. More recently, advances in surgical technique, including minimally invasive procedures, and earlier diagnosis have resulted in decreased morbidity and mortality for patients with Hirschsprung disease.
Most cases of Hirschsprung disease are now diagnosed in the newborn period. Hirschsprung disease should be considered in any newborn who fails to pass meconium within 24-48 hours after birth. Although contrast enema is useful in establishing the diagnosis, full-thickness rectal biopsy remains the criterion standard. Once the diagnosis is confirmed, the basic treatment is to remove the poorly functioning aganglionic bowel and to create an anastomosis to the distal rectum with the healthy innervated bowel (with or without an initial diversion).

Pseudomembranous Colitis Surgery

Pseudomembranous colitis is an inflammatory disease of the colon (see image below). It has changed in the last 100 years from a fatal disease caused by a postoperative event to, in the era of antibiotics, a commonly occurring complication of antibiotic use that may lead to serious morbidity but that usually is treated easily.
Colonic pseudomembranes of pseudomembranous colitis. Photographs courtesy of Eric M. Osgard, MD.

• In the late 1800s, prior to the availability of antibiotics, Finney reported the first case of pseudomembranous colitis, calling it "diphtheritic colitis."^[1]
• Hall and O'Toole first described Clostridium difficile in 1935.^[2]
• C difficile was first implicated as a causative factor in pseudomembranous colitis in the 1970s

Toxic Megacolon

Toxic megacolon is the clinical term for an acute toxic colitis with dilatation of the colon. The dilatation can be either total or segmental. A more contemporary term for toxic megacolon is simply toxic colitis, because patients may develop toxicity without megacolon. For the purposes of this article, the term toxic megacolon (toxic colitis) is used, but either toxicity or megacolon can occur exclusively of each other.^[1]
The hallmarks of toxic megacolon (toxic colitis), a potentially lethal condition, are nonobstructive colonic dilatation larger than 6 cm and signs of systemic toxicity. Toxic megacolon (toxic colitis)was recognized by Marshak and Lester in 1950.^[2] Jalan et al described the diagnostic criteria.^[3] The first criterion is radiographic evidence of colonic dilatation. The second criterion is any 3 of the following: fever (>101.5°F), tachycardia (>120 beats/min), leukocytosis (>10.5 10³/µL), or anemia. The third criterion is any 1 of the following: dehydration, altered mental status, electrolyte abnormality, or hypotension.
Toxic megacolon (toxic colitis) was first thought to be a complication of ulcerative colitis. In fact, toxic megacolon (toxic colitis) may complicate any number of colitides, including inflammatory, ischemic, infectious, radiation, and pseudomembranous.^{[4, 5]} See the image below.
A 22-year-old man presented with abdominal pain, passage of blood and mucus per rectum, abdominal distention, fever, and disorientation. Findings from sigmoidoscopy confirmed ulcerative colitis. Abdominal radiographs obtained 2 days apart show mucosal edema and worsening of the distention in the transverse colon. The patient's clinical condition deteriorated over the next 36 hours despite steroid and antibiotic therapy, and the patient had to undergo a total colectomy and ileostomy.
The incidence of toxic megacolon (toxic colitis) is expected to increase due to the rising prevalence of pseudomembranous colitis. Colonic dilatation may be present in other conditions, such as Hirschsprung disease, idiopathic megacolon/chronic constipation, and intestinal pseudo-obstruction (Ogilvie syndrome). However, these patients do not develop signs of systemic toxicity and, therefore, do not fall into the category of having toxic megacolon (toxic colitis). See the images below.
Gross pathology specimen from a case of pseudomembranous colitis demonstrating characteristic yellowish plaques. Computed tomography scan from a patient with pseudomembranous colitis demonstrating the classic accordion sign.

Villous Adenoma

Adenomatous polyps are, by definition, neoplastic. Although benign, they are the direct precursors of adenocarcinomas and follow a predictable cancerous temporal course unless interrupted by treatment. They can be either pedunculated or sessile. Polyps are generally asymptomatic but may occasionally ulcerate and bleed; uncommonly, they may result in obstruction if very large. Adenomas are divided into 3 subtypes based on histologic criteria, as follows: (1) tubular, (2) tubulovillous, and (3) villous. According to World Health Organization (WHO) criteria, villous adenomas are composed of greater than 80% villous architecture. Tubular adenomas are encountered most frequently (80-86%). Tubulovillous adenomas are encountered less frequently (8-16%), and villous adenomas are encountered least frequently (5%).
See the images below.
Endoscopic view of a sessile polyp, which histology studies revealed to be a villous adenoma. Courtesy of H. Chaun, MD. Endoscopic view of a sessile polyp histologically determined to be a villous adenoma. Courtesy of R. Enns, MD. Histology of villous adenoma. Fingerlike projections stretching from the surface of a polyp downward with minimal branching. Courtesy of D. Owen, MD. Histology of villous adenoma. Low-grade dysplasia with loss of mucin, prominent nucleoli, and hyperchromatic and elongated cells. Courtesy of D. Owen, MD.
Villous adenomas are associated more often with larger adenomas and more severe degrees of dysplasia. These adenomas occur more frequently in the rectum and rectosigmoid, although they may occur anywhere in the colon. They generally are sessile structures that appear as velvety or cauliflowerlike projections. Although rare, villous adenomas of the duodenum and the small bowel, particularly at the ampulla, can occur. Villous adenomas are of concern primarily because of the risk of malignant transformation (approximately 15-25% overall but higher once >2 cm).
The primary focus of this article is colonic villous adenomas. Where appropriate, certain aspects of small bowel villous adenomas are addressed

Bile Duct Strictures

Bile duct stricture (biliary stricture) is an uncommon but challenging clinical condition that requires a coordinated multidisciplinary approach involving gastroenterologists, radiologists, and surgical specialists. Unfortunately, most benign bile duct strictures (biliary strictures) are iatrogenic, resulting from operative trauma (see images below).^[1] Bile duct strictures (biliary strictures) may be asymptomatic but, if ignored, can cause life-threatening complications, such as ascending cholangitis,^{[2, 3]} liver abscess, and secondary biliary cirrhosis.
Focal intrahepatic benign bile duct stricture after cholecystectomy. Percutaneous transhepatic cholangiogram with balloon dilation of a postoperative bile duct stricture.
However, not all bile duct strictures (biliary strictures) are benign. Pancreatic cancer is the most common cause of malignant biliary strictures (see images below).^{[4, 5]} Most of these patients die of complications of tumor invasion and metastasis rather than from the bile duct stricture (biliary stricture) per se. Nonetheless, both benign and malignant bile duct strictures can be associated with distressing symptoms and excessive morbidity.^[6]
Endoscopic retrograde cholangiopancreatographic cholangiogram demonstrating an isolated mid-hepatic duct stricture as a result of pancreatic cancer. Focal bile duct stricture as a result of pancreatic cancer in the head of the pancreas.
For excellent patient education resources, visit eMedicine's Liver, Gallbladder, and Pancreas Center and Hepatitis Center. Also, see eMedicine's patient education articles Cirrhosis and Gallstones.