ВУЗ: Не указан
Категория: Не указан
Дисциплина: Не указана
Добавлен: 09.04.2024
Просмотров: 184
Скачиваний: 0
Endoscopy (see III E 1) is therefore required to rule out upper GI bleeding with absolute certainty. Most physicians will withhold endoscopy when a highly probable source of the bleeding is found in the lower GI tract. However, if surgery is anticipated, particularly when one is not sure of the diagnosis, endoscopy of the upper GI tract should be performed to exclude any bleeding site there.
A bleeding site in the lower GI tract must be located. Once the upper tract has been eliminated as a source of bleeding, the lower tract should be investigated, including the distal small bowel, colon, and anorectal area (Table 9-3).
Colonoscopy should be performed.
The presence of a mass lesion, such as rectal carcinoma, is visualized in about 3% of patients with massive lower GI bleeding.
Discrete bleeding sites from ulcers or hemorrhoids may be seen.
A diffusely hemorrhagic mucosa suggests colitis, a platelet deficiency, or a hematologic disorder.
Even if no lesion is visualized, it is important to make certain that the lower 15 cm of the rectum is normal because this region is inaccessible intraperitoneally if laparotomy is necessary. Additionally, if it is normal, it gives presumptive evidence that the bleeding is coming from a more proximal site.
Anoscopy is frequently overlooked but should be routinely performed because bleeding lesions in the anal canal may be missed on sigmoidoscopy.
C
Subsequent diagnostic tests will depend on whether the bleeding stops or continues. About 75% of the patients will spontaneously stop bleeding without further intervention.
If bleeding stops , the following steps are taken.
A barium enema , a colonoscopy , or both procedures should be performed:
To identify or rule out diverticulosis or colon carcinoma
To provide indirect evidence for colonic mucosal ischemia
The patient should be monitored thereafter.
If bleeding continues, further diagnostic studies should be done to identify the source more precisely in preparation for surgery, if it becomes necessary.
TABLE 9-3 Causes of Lower Gastrointestinal Bleeding
Adults |
Children |
Anorectal disease |
Meckel's diverticulum |
|
|
Diverticular disease |
Intussusception |
|
|
Angiodysplasia |
|
|
|
Polyps
Malignancy
Inflammatory bowel disease
Ischemic colitis
P.191
If bleeding continues, a barium enema should not be performed. The residual barium in the colon may make subsequent angiography difficult or impossible.
Angiography and radionuclide scanning are useful.
Selective mesenteric angiogram will identify the bleeding site (or sites) in up to 80% of patients when the rate of bleeding exceeds 0.5 mL/minute. Angiography is also highly useful for identifying angiodysplastic lesions of the colon.
Radionuclide scan , which uses red blood cells labeled with technetium-99m (99m Tc), is sensitive enough to detect a bleeding site when the rate is as low as 0.10 mL/minute.
Colonoscopy is unsatisfactory and may be dangerous when lower GI bleeding is rapid: Visualization is poor, and there is a risk of colon perforation.
D
Indication for surgery is persistent bleeding.
The patient's cardiovascular status and amount and duration of bleeding are taken into consideration, as for upper GI hemorrhage (see III F 1, 2).
The surgical procedure is aimed at removing the underlying cause of the bleeding.
On occasion, the precise point of bleeding cannot be established.
In these instances, the stomach, duodenum, and small intestine should be carefully examined. Meckel's diverticulum, Crohn's disease, and other inflammatory or malignant lesions should not be overlooked.
A “blind” total colectomy may be necessary if no other source of the bleeding is found.
Intraoperative endoscopy of the colon, upper GI tract, and small bowel may be very useful in this setting.
The mortality rate for lower GI bleeding is currently about 10%.
Chapter 10
Esophagus
William R. Alex
D. Bruce Panasuk
Richard N. Edie
I Introduction
A Anatomy
Location. The esophagus is approximately 24 cm in length. It extends from the C6 vertebral level to the T11 level.
It originates at the upper esophageal sphincter , which is essentially made up of the cricopharyngeal muscle, then courses behind the arch of the aorta, and descends into the thorax on the right.
It deviates anteriorly and enters the abdomen via the esophageal hiatus , which is formed by the right crus of the diaphragm.
The tubular esophagus meets the saccular stomach at the gastroesophageal junction, where the esophagus is anchored by the phrenoesophageal ligament. The gastroesophageal junction is approximately 40 cm from the incisors.
Histology
The esophageal mucosa consists of squamous cell epithelium except for the distal 1–2 cm, which is columnar epithelium.
There are two layers of muscle throughout the esophagus, an inner circular and outer longitudinal layer. The upper one third is striated muscle, whereas smooth muscle predominates in the lower two thirds.
The esophagus, unlike the rest of the gastrointestinal tract, lacks a serosal covering.
B Vasculature
Arterial supply to the esophagus is from branches of the inferior thyroid; the bronchial, intercostal, inferior phrenic, left gastric arteries; and direct esophageal branches from the aorta.
Venous return is more complicated.
An extensive subepithelial venous plexus empties superiorly into the hypopharyngeal veins and inferiorly into the gastric veins. The left gastric vein is also known as the coronary vein. Segmental drainage occurs also via the azygous and hemiazygous systems.
Lymphatic drainage is to the nearest lymph nodes. Lymphatics of the upper esophagus drain into the cervical or mediastinal nodes, whereas drainage of the distal lymphatics is more often to the celiac nodes.
C Innervation
The esophagus is supplied by the sympathetic and parasympathetic system via the pharyngeal plexus, the vagus, upper and lower cervical sympathetic, and splanchnic nerves. Meissner and Auerbach's plexuses are present in the normal esophagus.
D Physiology
The upper esophageal sphincter is a high-pressure zone at the upper border of the esophagus. It is 3–5 cm in length, and it relaxes during swallowing and contracts thereafter.
Peristalsis in the central portion of the esophagus consists of wavelike movements that pass down the body of the esophagus and become stronger toward the lower portion. Esophageal peristaltic pressures range from 25–80 mm Hg.
P.193
The lower esophageal sphincter (LES) is a high-pressure zone at the lower portion of the esophagus. It is 3–5 cm in length and functions to prevent gastroesophageal reflux. LES pressure is influenced by several factors and substances.
LES pressure is increased by a protein meal, alkalinization of the stomach, gastrin, vasopressin, and cholinergic drugs.
LES pressure is decreased by secretin, nitroglycerine, glucagon, chocolate, fatty meals, and gastric acidification.
II Disorders of Esophageal Motility
A Cricopharyngeal dysfunction and Zenker's diverticulum
Pathophysiology
Cricopharyngeal dysfunction is caused by a failure of the upper esophageal sphincter to relax properly.
The problem may be an incoordination between relaxation in the upper esophageal sphincter and simultaneous contraction of the pharynx, which results in a pharyngoesophageal (Zenker's) diverticulum . This is a false diverticulum that consists only of mucosa that herniate posteriorly between the fibers of the cricopharyngeal muscle.
Cricopharyngeal dysfunction and Zenker's diverticulum is often associated with hiatal hernia and gastroesophageal reflux.
Symptoms of Zenker's diverticulum include dysphagia, halitosis, regurgitation of undigested food, nocturnal aspiration, and recurrent aspiration pneumonia.
Diagnosis
The history and physical examination are usually adequate to diagnose cricopharyngeal dysfunction.
Radiographs , which include a barium swallow, are helpful in delineating a diverticulum.
Endoscopy is contraindicated when Zenker's diverticulum has been documented by barium swallow because the risk of perforation is high. If a diverticulum is not seen on contrast studies, then endoscopy is indicated to rule out other esophageal disorders, including gastroesophageal reflux or neoplasm.
Treatment
Cricopharyngeal myotomy is the treatment of choice for cricopharyngeal dysfunction.
Resection or suspension of the diverticulum is combined with the myotomy.
B Achalasia
Pathophysiology
Achalasia is an esophageal disease of unknown etiology, although it may be secondary to ganglionic dysfunction, which causes:
High resting LES pressure
Failure of the LES to relax during swallowing
Absence of coordinated peristalsis in the body of the esophagus
The body of the esophagus becomes dilated, and the muscle hypertrophies in an attempt to force material through the dysfunctional LES. A similar symptom complex can be caused by Chagas disease , which is caused by the organism Trypanosoma cruzi.
Carcinoma of the esophagus is 10 times more common in patients with achalasia than in the general population.
Symptoms of achalasia include dysphagia, followed by regurgitation and weight loss. Frequently, respiratory symptoms caused by aspiration are present.
Diagnosis
Radiographic studies reveal a dilated esophagus with a bird's beaklike extension into the lower narrowed segment at the LES.
Esophageal manometry reveals the high resting LES pressure, failure of relaxation during swallowing, higher than normal resting pressure in the body of the esophagus, and absence of peristalsis.
P.194
Esophagoscopy is required to rule out neoplasia and to document the extent of esophagitis.
Treatment for achalasia is palliative because LES function can never be restored to normal.
Nonsurgical treatment consists of forced pneumatic dilatation of the spastic lower esophageal sphincter, which is just above the gastroesophageal junction.
Surgical treatment is esophagomyotomy by the modified Heller procedure, via laparotomy/laparoscopy, or occasionally left thoracotomy. Care is taken not to disturb the vagus nerve attachments to the esophagus to prevent reflux. The myotomy is confined to the lower portion of the esophagus, usually 6–8 cm in length.
Surgical results with the Heller procedure are generally better than with pneumatic dilatation for relief of dysphagia.
Esophagomyotomy can be combined with an antireflux procedure if indicated.
C Diffuse esophageal spasm
Pathophysiology
Diffuse esophageal spasm is a disorder of esophageal motility that consists of strong nonperistaltic contractions.
Unlike achalasia, this condition has normal sphincteric relaxation and may be associated with gastroesophageal reflux.
Symptoms consist of chest pain, which can radiate to the back, neck, ears, jaw, or arms and may be confused with typical angina pectoris. The pain usually occurs spontaneously, and many patients are considered to have a psychoneurosis.
Diagnosis
Manometry reveals high-amplitude repetitive contractions with a normal sphincteric response to swallowing.
Radiographs are normal in one half of the cases but may reveal diverticula, segmental spasm, and a corkscrew appearance of the esophagus.
Treatment
Surgery is moderately effective with good results obtained in over two thirds of the patients. The best results are obtained in emotionally stable patients with severe disease and without associated lower gastrointestinal problems.
Surgery consists of a long esophagomyotomy that extends from the arch of the aorta to just above the LES.
Care is taken to preserve LES function, which is usually normal in these patients.
If significant gastroesophageal reflux is present, an antireflux procedure is performed.
Medical treatment. Calcium channel blockers and smooth muscle relaxants, such as nitrates, may ameliorate symptoms.
D Esophageal reflux
Etiology. Esophageal reflux is a common condition that may affect up to 80% of the population in varying degrees. Gastroesophageal reflux disease remains a multifactorial disease.
LES is a physiologic sphincter that is normally in an intra -abdominal position. Loss of LES pressure results in gastric reflux.
Esophageal motility, in the normal esophagus, causes refluxed secretions to be cleared by esophageal peristalsis.
Gastric secretions, gastric acid, pepsin, and bile reflux have been shown to produce severe esophagitis.
Symptoms of esophageal reflux are substernal pain, heartburn, and regurgitation, all of which may increase with bending and lying down.
Diagnosis is made by:
Manometry , which reveals decreased LES pressure
Esophagoscopy, which reveals varying degrees of esophagitis
Twenty -four hour pH measurements in the lower esophageal area, which demonstrate increased acidity
P.195
Treatment
Medical treatment
Proton pump inhibitors and H2 -receptor antagonists to reduce acidity
Cisapride and metoclopramide, which increase both LES pressure and gastric motility, thus increasing the rate of gastric emptying
Antacids
Weight reduction
Abstinence from smoking and alcohol
Elevation of the head of the bed at night
Surgical treatment
Indications for surgery include:
Symptoms refractory to medical treatment
Additional problems, such as esophageal webs (see VII B ) or severe esophagitis, stricture formation, or Barrett's esophagus with severe dysplasia (i.e., replacement of the normal epithelial lining with columnar epithelium in the lower esophagus secondary to esophagitis)
Antireflux operations are designed to increase LES tone. All of the operations involve wrapping the lower esophagus with gastric fundus and restoring the distal esophagus to its original intra -abdominal position with the gastroesophageal junction below the diaphragm. The three most commonly used operations are:
The Nissen fundoplication, which is a 360 -degree wrap of the stomach around the esophagus performed through the abdomen. The procedure may now be successfully performed laparoscopically with minimal pain and a shorter recovery time.
Belsey Mark IV operation, which is a 270 -degree wrap performed through a left thoracotomy
The Hill repair , or posterior gastropexy, which uses the arcuate ligament to re-establish the intra -abdominal position of the distal esophagus.
III Esophageal Strictures
A Caustic stricture
Etiology. Caustic stricture is caused by the ingestion of caustic agents, such as lye, drain openers, and oven cleaners.
Diagnosis
The diagnosis may be made by the history of caustic ingestion and the presenting symptoms , which may be mild or very severe. Shock may ensue from severe burning or perforation of the esophagus. It is important to identify airway compromise early.
Endoscopy is indicated within 24 hours to determine the extent of damage.
Treatment
Broad -spectrum antibiotics are administered.
Corticosteroids are no longer indicated.
Radiographs of the esophagus are performed at 10–14 days to determine if strictures are developing.
Strictures occur in 5%–10% of patients who have ingested lye.
If strictures have formed, a program of dilatation, using esophageal dilators, is begun 3–4 weeks after ingestion.
Esophageal replacement with stomach or colon may be necessary.
B Strictures secondary to esophagitis and reflux
Pathophysiology. These strictures are caused by a recurrent alternating pattern of mucosal destruction secondary to gastric acid reflux and subsequent healing.
The strictures most often occur at the gastroesophageal junction.
In severe cases, a long stricture may result.
Diagnosis
A history of reflux symptoms and dysphagia is suggestive of strictures.
P.196
Radiograph of the esophagus confirms the diagnosis.
Esophagoscopy is important to determine the extent of the disease and to rule out malignancy.
Treatment
Dilatation of the esophagus is attempted first, then an antireflux operation is performed.
