Paciente masculino de 49 años, quien había sufrido de vómitos incoercibles desde hace 7 años, había sido estudiado en múltiples ocasiones en otras clínicas tanto en El Salvador como los Estados Unidos pero no se había establecido el diagnostico. Fue referido a nuestra unidad, tenia antecedente de cirugía en sus primeros meses de edad posiblemente era una hipertrofia pilórica inmediatamente sospechamos que el paciente podría tener bridas y adherencia y en el mismo día fue intervenido quirúrgicamente vía laparoscópica.
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Video Endoscopic Sequence 2 of 6.
Otra imagen y video de la liberación de adherencias
Intraabdominal adhesions develop after abdominal surgery as part of the normal healing processes that occur after damage to the peritoneum. Over the last 2 decades, much research has gone into understanding the biochemical and cellular processes that lead to adhesion formation. The early balance between fibrin deposition and degradation seems to be the critical factor in adhesion formation. Although adhesions do have some beneficial effects, they also cause significant morbidity, including adhesive small bowel obstruction, infertility and increased difficulty with reoperative surgery. Several strategies have been employed over the years to prevent adhesion formation while not interfering with wound healing.
Video Endoscopic Sequence 3 of 6.
Postoperative adhesions form after trauma to the peritoneal cavity and are a result of the biochemical and cellular response that occurs in an attempt to repair the peritoneum. Although there are beneficial effects to adhesions, they are the leading cause of small intestinal obstruction after abdominal surgery and can be the source of significant morbidity, in some cases leading to mortality. This review aims to provide general surgeons with a broad overview of what is currently known about adhesions, the cellular and molecular events that are involved in their formation, the latest re-search developments in this area and the current available methods of prevention.
Peritoneal adhesions can be defined as abnormal fibrous bands between organs or tissues or both in the abdominal cavity that are normally separated. Adhesions may be acquired or congenital; however, most are acquired as a result of peritoneal injury, the most common cause of which is abdomino-pelvic surgery.4Less commonly, adhesions may form as the result of inflammatory conditions, intraperitoneal infection or abdominal traum
Video Endoscopic Sequence 4 of 6.
It is estimated that 93% to 100% of patients who undergo transperitoneal surgery will develop postoperative adhesions.5 The extent of adhesion formation varies from one patient to another and is most dependent on the type and magnitude of surgery performed, as well as whether any postoperative complications develop.6Another surgical factor that has been shown to contribute to adhesion formation is intraperitoneal foreign bodies, including mesh, glove powder, suture material and spilled gallstones.7 Fortunately, most patients with adhesions do not experience any overt clinical symptoms. For others, adhesions may lead to any one of a host of problems and can be the cause of significant morbidity and mortality
Video Endoscopic Sequence 5 of 6.
It has been suggested that the inability to discover effective ways to reduce or abolish adhesion formation over the years has been due to a lack of insight into the basic tenets of peritoneal tissue repair. Only in the last 15 to 20 years have researchers started to unravel the complexities of this process, which involves several different cell types, cytokines, coagulation factors and proteases, all acting together to restore tissue integrity.25 Although our understanding is far from complete, studies of adhesion formation thus far have determined what is believed to be the central pathophysiological mechanism leading to ad-hesion development.24,26 This is discussed below. If effective preventative and treatment strategies are to be developed, a more comprehensive understanding of this process at both the cellular and the molecular level, as well as the identification of inflammatory mediators involved, is essential. The key to preventing post-operative adhesions will most likely be based on selective inhibition of one or more of the critical factors required for their formation.
Video Endoscopic Sequence 6 of 6.
Peritoneal wound healing differs from skin in both the mode of epithelialization and the consequences of fibrin deposition. To understand how the peritoneum responds to injury, some basic knowledge about its structure is required. The peritoneum consists of a single outer layer of mesothelial cells that are loosely anchored to a basement membrane and that detach readily with even the slightest trauma.
Video Endoscopic Sequence 1 of 7.
The Black Esophagus: JG
Acute Esophageal Necrosis Syndrome
A 70 – year old man, with cholangiocarcinoma was admitted to our ward because septicemia and medically compromised patient.
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The "black esophagus" is an extremely rare endoscopic
Acute esophageal necrosis (AEN), commonly referred to
as “black esophagus”, is a rare clinical entity arising from
a combination of ischemic insult seen in hemodynamic
compromise and low-flow states, corrosive injury from
gastric contents in the setting of esophago-gastroparesis
and gastric outlet obstruction, and decreased function of
mucosal barrier systems and reparative mechanisms
present in malnourished and debilitated physical states.
AEN may arise in the setting of multiorgan dysfunction,
hypoperfusion, vasculopathy, sepsis, diabetic ketoacidosis,
alcohol intoxication, gastric volvulus, traumatic transection
of the thoracic aorta, thromboembolic phenomena, and
A typical patient with AEN is an elderly male with multiple
medical comorbidities, who manifests with signs of upper
gastrointestinal bleeding. Clinical presentation of AEN
ranges from hematemesis, coffee ground emesis, and
melena (overall, accounting for nearly 90% of the cases) to
asymptomatic black esophagus that was noted during a
percutaneous gastrostomy tube placement Generally,
uncomplicated AEN follows an indolent clinical course and
has a predictable endoscopic and histopathological
Video Endoscopic Sequence 3 of 7.
Clinical presentation is remarkable for upper
gastrointestinal bleeding. Notable symptoms may include
epigastric/abdominal pain, vomiting, dysphagia, fever,
nausea, and syncope. Associated laboratory findings may
reflect anemia and leukocytosis. The hallmark of this
syndrome is the development of diffuse circumferential
black mucosal discoloration in the distal esophagus that
may extend proximally to involve variable length of the
organ. Classic “black esophagus” abruptly stops at the
gastroesophageal junction. Biopsy is recommended but not
required for the diagnosis. Histologically, necrotic debris,
absence of viable squamous epithelium, and necrosis of
esophageal mucosa, with possible involvement of
submucosa and muscularis propria, are present.
Classification of the disease spectrum is best described by
a staging system.
Video Endoscopic Sequence 4 of 7.
Treatment is directed at correcting coexisting clinical
conditions, restoring hemodynamic stability, nil-per-os
restriction, supportive red blood cell transfusion, and
intravenous acid suppression with proton pump inhibitors.
Complications include perforation with mediastinal
infection/abscess, esophageal stricture and stenosis,
superinfection, and death. A high mortality of 32% seen in
the setting of AEN syndrome is usually related to the
underlying medical co-morbidities and diseases.
Video Endoscopic Sequence 5 of 7.
Proximal esophageal extension is common. Biopsy is
recommended although not required to make the diagnosis.
First described in 1990 by Goldenberg et al
Male sex, older age, chronic medical conditions, including
diabetes mellitus, hematologic and solid organ malignancy,
malnutrition, renal insufficiency, cardiovascular
compromise, trauma, and thromboembolic phenomena
place a patient at a higher risk for developing AEN.
Clinical presentation is almost universally related to upper
gastrointestinal bleeding. Complications may include
stenosis or stricture formation in the distal esophagus,
perforation, mediastinitis, and death. Overall mortality is
largely related to the underlying medical condition and
Video Endoscopic Sequence 6 of 7.
Biliary Plastic Stent
Our patient has the diagnosis of a cholangiocarcinoma
Classic AEN presents as a circumferential,
black-appearing, diffusely necrotic esophageal mucosa,
preferentially affecting the distal esophagus, of variable
length, that stops abruptly at the GEJ. Proximal extension
of the mucosal injury is common and the entire esophagus
can appear black. Differential diagnosis includes malignant
melanoma, acanthosis nigricans, coal dust deposition,
pseudomelanosis, and melanocytosis of the esophagus.
Detailed history and physical examination provide essential
clues to the diagnosis. Classic endoscopic appearance may
be supported by brush cytology or biopsy specimen that
will confirm the diagnosis. This is especially important in
rare cases of isolated involvement of proximal and middle
esophagus. Additionally, a history of corrosive ingestion
should be sought for and diligently excluded.
Video Endoscopic Sequence 7 of 7.
Cholangiocarcinoma is a slow-growing malignancy of the
bile duct. It is the second most common primary hepatic
tumor after hepatoma. The cause of bile duct cancer is
unclear. Results of some epidemiologic studies have
implicated bacteria-induced carcinogens derived from bile
salts (eg, lithocholate) as a causative factor in the
pathogenesis of cholangiocarcinomas. Biliary ductal calculi
occur in 20-50% of patients with cholangiocarcinoma;
however, the association of gallstones with
cholangiocarcinoma is less marked than it is with
carcinoma of the gallbladder. The most common cause of
malignant biliary obstruction is pancreatic adenocarcinoma.
Gallbladder carcinoma is 9 times more common than bile