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DISORDERS OF THE ESOPHAGUS HIATAL HERNIA The distal esophagus normally is held in position by a fusion of the endothoracic and endoabdominal fascias at the diaphragmatic hiatus called the phrenoesophageal ligament. A hiatal hernia is the most commonly reported abnormality seen on upper gastro-intestinal X- ray contrast study. It occurs most commonly in women in their 5th and 6th decades. Most hiatal hernias are asymptomatic. 5-10% of patients with herniation of the stomach through the diaphragmatic hiatus will develop reflux esophagitis. Rare instances of posttraumatic herniation of the stomach through the hiatus must be differentiated from traumatic rupture of the diaphragm. In the vast majority of cases, the development of a hiatal hernia is spontaneous and there is a strong association with obesity. Gallstones and colonic diverticular disease are commonly present in these patients (Saint’s triad) and difficulty may be encountered in establishing which of the three disorders accounts for the patient’s symptoms. Pathology Three types of hiatal hernia (HH) are recognized. The type of HH is defined by the location of the gastroesophageal junction. 1. Type I or sliding HH. In this type, the phrenoesophageal ligament is intact but lax, thereby allowing the distal esophagus and gastric cardia to herniate through the esophageal hiatus. The gastroesophageal junction is, therefore, located above the diaphragm. This is the most common type and usually is asymptomatic. 2. Type II or paraesophageal HH. This occurs when there is a focal defect in the phrenoesophageal ligament, anterior and lateral to the esophagus, which allows a protrusion of peritoneum to herniate upward alongside the esophagus through the esophageal hiatus. The gastroesophageal junction remains anchored within the abdomen, whereas the greater curvature of the stomach rolls up into the chest. Eventually most of the stomach can herniate. However, because the stomach is anchored at the pylorus and cardia, the body of the stomach undergoes a 180 degree organoaxial rotation and ends up as an upside-down, intrathoracic stomach when it is herniated.

2 3. Type III represents a combination of type I and II. This is characterized by herniation of both the greater curvature of the stomach and the gastroesophageal junction into the chest. Patients thus affected are exposed to the problems and risks of both types of hernias. Symptoms and complications in patients with sliding HH are related to associate gastroesophageal reflux. Paraesophageal and type III HH frequently produce postprandial pain or bloating, breathlessness with meals and mild dysphagia related to compression of the distal esophagus by the adjacent gastric hernia. The herniated gastric pouch is susceptible to volvulus, obstruction and infarction and can develop ischemic ulcers with frank or occult bleeding, perforation or gangrene. Diagnostic and evaluation 1. CXR. The finding of an air-fluid level in the posterior mediastinum on the lateral X-ray suggests the presence of a type II or III HH. Differential diagnosis includes mediastinal cyst or abscess or a dilated, obstructed esophagus. 2. A barium swallow will confirm the diagnosis and define any coexisting esophageal abnormalities, including strictures or ulcers and is the diagnostic study of choice. The position of the gastro-esophageal junction will define the type of HH. 3. Esophagoscopy is indicated in patients with symptoms of reflux or dysphagia to determine the degree of esophagitis, presence of a stricture, Barrett’s esophagus or a coexisting abnormality. 4. Symptoms of reflux warrant investigation with esophageal manometry and pH testing. Management - asymptomatic sliding hernias require no treatment. - patients with sliding hernias and reflux with mild esophagitis should undergo a trial of medical management. - patients who fail to obtain symptomatic relief with medical therapy or who have severe esophagitis, should undergo esophageal Ph testing to determine their suitability for an antireflux procedure and HH repair. - patients who do not expierence reflux but have symptoms related to their hernia (chest pain, intermittent dysphagia or esophageal obstruction) should undergo HH repair. - all patients who are found to have a type II, III HH and who are operative candidates with a paraesophageal hernia; there is nearly a 30% incidence of death from the development of a catastrophic complication.

3 Operative repair can be done through either an abdominal or thoracic approach and consists of reduction of the hernia, resection of the sac and closure of the hiatal defect. - people with a paraesophageal HH are known to have a 60% incidence of associated gastroesophageal reflux. Therefore, in patients undergoing an emergency operation for complications of a paraesophageal HH, consideration should be given to performing an antireflux procedure in addition to repair of the hernia. When operating electively on a patient with documented reflux and a paraesophageal HH, a concomitant antireflux procedure is indicated. Esophageal Strictures Caustic strictures Etiology Caustic stricture is caused by the ingestion of caustic agents such as lye, soda or acids. Diagnostic A history of caustic ingestion and the presenting symptoms (retrosternal burning pain, dysphagia, shock) are sufficient to make the diagnosis. Endoscopy is indicated as soon as possible to determine the extent of damage. Treatment A neutralizing agent is given as soon as possible to counteract the effects of the caustic agent (debatable). Steroids and broad spectrum antibiotics are administered for 2-3 weeks. X-ray of the esophagus is performed at 10-14 days to determine if strictures are developing. If strictures have formed a program of dilatation using esophageal dilators is begun 3-4 weeks after ingestion. Esophageal replacement with stomach, iliocolon or left colon may be necessary. Strictures Secondary to Reflux Esophagitis 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. X-ray of the esophagus confirms the diagnosis. Esophagoscopy is important to determine the extent of the disease and to rule out malignancy.

4 Treatment Dilatation of the esophagus is attempted first and then an antireflux operation is performed. If dilatation and an antireflux operation do not relieve the esophageal obstruction, a reconstructive procedure, using either the stomach or colon for esophageal replacement may be necessary to restore adequate swallowing function. TUMOURS OF THE ESOPHAGUS Tumours of the esophagus are predominantly malignant. Symptomatic benign lesions are rarely encountered in clinical practice and account for less than 1% of all esophageal neoplasms. Benign tumours The commonest benign tumour of the esophagus is leiomyoma (smooth muscle tumour). They occur most commonly in the lower esophagus as uniform oval swelling which project into the lumen of the esophagus and are covered by an intact mucosa. The most common presentation is with dysphagia. Bleeding, due to ulceration is less common. As the tumours are well encapsulated, they can be removed by enucleation without esophageal resection. However, differentiation between benign and smooth muscle tumours can be difficult even histologically and these patients require careful follow-up. Other benign tumours include papillomas (caused by the human pappiloma virus) which may occur anywhere in the esophagus, granular-cell tumours, inflammatory polyps at the gastro-esophageal junction, pseudotumours resulting from sclerotherapy and adenomatous polyps which are usually encountered at the lower end of the gullet and may be sessile or pedunculated. Some adenomatous esophageal polyps arise as a consequence of reflux esophagitis. The inflammatory polyps are associated with chronic esophagitis. Malignant Esophageal Neoplasms Compared with carcinoma of the colon and stomach, the incidence of esophageal carcinoma is relatively low. Because the disease is usually advanced by the time of presentation, the mortality rate is appaling; 75% die within 1 year of presentation and only 6% survive five year. Malignant esophageal neoplasms are mostly carcinomas and carry a poor prognosis.

5 Etiology The etiology of esophageal carcinoma remains unknown but is currently thought to be multifactorial. The important factors appear to be the following: - excess alcohol intake; is associated with a 20 times greater risk - smoking; smokers have 5 times the risk of non-smokers. - absence of protective substances in fruits and green vegetables - ingestion of exogenous carcinogens and promoting factors - infection with the human pappiloma virus Certain preexisting conditions also increase the likelihood of developing esophageal cancer, including achalasia, esophagitis and Barret’s esophagus (esophageal epithelium is replaced by gastric glandular epithelium) Pathology The vast majority of malignant neoplasms of the esophagus are carcinomas. The predominant histological type is squamous. Confusion has been generated by the inclusion of carcinomas of the cardia with esophageal neoplasms. These are gastric neoplasms which invade the lower or abdominal end of the esophagus. Macroscopically, the disease assumes one of three forms: - polypoid (fungating) - stenosing (scirrhous) - ulcerative Early cancer of the esophagus (confined to mucosa/submucosa ) is rarely encountered because of the absence of screening programmes. The transition between severe dysplasia to carcinoma –in-situ and invasive esophageal cancer is well documented. The results of surgical treatment for early esophageal cancer are extremely good with a very low operative mortality and a 5-year survival of 80-85%. There is therefore, a strong argument for screening programmes, particularly in areas of high incidence and in patients with known predisposing conditions. Histology of malignant esophageal neoplasms Carcinoma Sarcoma - squamous (95%) -leiomyosarcoma - adenocarcinoma (1-2%) - rhabdomyosarcoma - melanoma - fibrosarcoma, lymphoma Squamous-cell Carcinoma Dysphagia in a middle-aged or elderly patient demands investigation in order to exclude carcinoma.

6 Physical examination is usually unrewarding except in advanced disease where there may be signs of wasting, hepatomegaly due to secondaries or hoarseness due to involvement of the recurrent laryngeal nerve. Barium swallow examination is the investigation of first choice. The typical appearance of carcinoma is an irregular narrowing of the esophageal lumen. Esophagoscopy with biopsy from suspicious lesions is a useful diagnostic investigation. Once carcinoma of the esophagus is diagnosed, it is desirable to establish the extent of local invasion and discover whether metastasis to thoracic lymph nodes or liver has occurred. Thoracic CT is the investigation of choice for that. The tumour infiltrates the submucosal plane quite extensively and tends to grow longitudinally as well as circumferentially. Squamous-cell carcinomas occur throughout the length of the esophagus and are equally common in the middle and lower thirds though they are less frequent at the upper end. The carcinoma invades the muscle walls of the esophagus and then adjacent mediastinal structures, particularly nerves (recurrent laryngeal and frenic) and/or the major bronchi and trachea and pericardium. Lymph node spread from tumours of the upper third is predominantly to the supraclavicular, cervical and upper mediastinal nodes; middle third neoplasms may involve all the mediastinal nodes and those along the left gastric and celiac artery whereas growths in the lower third usually tend to spread preferentially to the lower mediastinal and subdiaphragmatic nodes. Metastatic spread is preferentially to the liver and bones. Squamous-cell carcinoma of the esophagus is sensitive to radiotherapy. Adenocarcinoma True adenocarcinomas of the esophagus usually originate from Barrett’s epithelium following longstanding reflux esophagitis. Less commonly, they may arise from ectopic gastric epithelium or from the esophageal submucous glands. The vast majority are found at the lower end of the esophagus. The development of metaplasia and dedifferentiation of cells and severe dysplasia precedes the onset of in situ and invasive carcinoma. The prognosis of esophageal adenocarcinoma is poor and these tumours are relatively insensitive to radiotherapy. The mode of spread is similar to that of squamous tumours. Symptoms of esophageal cancer are progressive dysphagia, weight loss and pain.

7 Late symptoms suggestive of unresectability include hoarseness, abdominal pain, persistent back pain, cough, aspiration pneumonia suggesting possible esophago-respiratory fistula formation. Diagnosis The key investigations for establishing the diagnosis are barium swallow and endoscopy with biopsy and cytology. Both are necessary as they complement each other. Endoscopy gives precise information of the site and extent of circumferential involvement of the esophagus by tumour. Contrast radiology gives a good assessment of the length of the lesions. Resectability and intent for cure, decline sharply for lesions longer than 5 cm. Both techniques are also used for screening in high risk areas and in individuals with known predisposing conditions. Balloon cytology whereby a rubber balloon is swallowed attached to a string and then retrieved to collect esophageal cells, has been found to be a very effective and simple screening technique in high incidence areas. Serum markers have not been shown to be useful in the detection to esophageal tumours. Staging Once a diagnosis of esophageal carcinoma is made, staging of the disease is necessary to establish the appropriate method of treatment in the individual patient. The most common clinical staging system used is the TNM. Staging is the process of finding out how far a cancer has spread. The treatment and outlook for people with esophageal cancer depend, to a great extent, on the cancer's stage. Esophageal cancer is staged with the imaging tests described above, combined with endoscopy and biopsy. The most common system used to stage esophageal cancer is the TNM system of the American Joint Committee on Cancer (AJCC). The TNM system describes 3 key pieces of information. T refers to the size of the primary tumor and how far it has spread within the esophagus and to nearby organs. N refers to cancer spread to nearby lymph nodes. M indicates whether the cancer has metastasized (spread to distant organs). T stages Tis-The cancer is only in the epithelium (the top layer of cells lining the esophagus). It has not started growing into the deeper layers. This stage is also known as carcinoma in situ.

8 T1-The cancer is growing into the tissue under the epithelium, such as the lamina propria or submucosa. T2-The cancer is growing into the muscle layer (muscularis propria). T3-The cancer is growing into the outer layer of tissue covering the esophagus (the adventitia). T4-The cancer is growing into nearby structures, such as the trachea, the pleura or the the pericardium. N stages N0-The cancer has not spread to nearby lymph nodes. N1-The cancer has spread to nearby lymph nodes. M stages M0-The cancer has not spread to distant organs or lymph nodes. M1a-The cancer has spread to distant lymph nodes but not to other organs. M1b-The cancer has spread to distant organs. Stages Stage 0 (Tis, N0, M0) This is the earliest stage of esophageal cancer. The cancer cells are only found in the epithelium (the layer of cells lining of the esophagus). The cancer has not grown into the connective tissue beneath these cells. The cancer has not spread to lymph nodes or other organs. This stage is also called carcinoma in situ. Stage I (T1, N0, M0) The cancer has grown from the epithelium into the connective tissue underneath (the lamina propria). It may also have grown through that tissue into the layer below (the submucosa), but it has not grown any deeper. It has not spread to lymph nodes or to distant sites. Stage II This stage is split into 2 substages, stage IIA and stage IIB.

9 Stage IIA (T2 or 3, N0, M0): The cancer has grown into the muscle layer called the muscularis propria (T2). It may also have grown through the muscle layer into the adventitia, the connective tissue covering the outside of the esophagus (T3). The cancer has not spread to lymph nodes or to distant sites. Stage IIB (T1 or 2, N1, M0): The cancer has grown into the lamina propria (T1). It may also have grown into layers below: the submucosa (T1) and the muscularis propria (T2). It has not grown through to the outer layer of tissue covering the esophagus. It has spread to lymph nodes near the esophagus (N1) but has not spread to lymph nodes farther away from the esophagus or to distant sites. Stage III (T3, N1, M0; or T4, N0 or 1, M0) Stage IV This is split into 2 substages, stage IVA and stage IVB Stage IVA (any T, any N, M1a) Stage IVB (any T, any N, M1b)

Survival rates by stage 5-Year Relative Survival Rate >95% 50 to 80% 30 to 40% 10 to 30% 10 to 15% less than 5%

Stage 0 I IIA IIB III IV

The staging tests in patients with esophageal cancer are designed to establish the presence of inoperable mediastinal disease or subdiaphragmatic involvement (hepatic and nodal). Vocal cord paralysis (ENT examination) and phrenic nerve paralysis (diaphragmatic screening by fluoroscopy or ultrasound) are indications of

10 inoperability as is lung parenchymal involvement demonstrated on the chest radiograph. All middle and upper third neoplasms require a bronchoscopy to exclude involvement of the tracheobronchial tree. Both CT scanning and magnetic resonance imaging (MRI) have been found dissapointing in the assessment of the resectability of esophageal cancers as these techniques are unable to define individual layers of the esophagus and do not detect early mediastinal invasion. The best and most cost-effective technique for the detection of intra-abdominal disease is laparoscopy which has been found to be superior to ultrasonography. Treatment The treatment of patients with esophageal cancer depends on the staging of the disease and the condition of the patients with esophageal cancer, some of whom have resectable lesions but are unfit for surgery by virtue of old age or significant intercurrent cardiorespiratory disease. The nutritional state must also be assessed by both anthropomorphic measurement (skin-fold thickness, triceps girth ), biochemical and hematological tests (albumin, Hb, serum iron, etc.) In malnurished patients, a period of parenteral or enteral nutrition for a few weeks before surgery should be undertaken. The treatment options available are: - surgical excision and bypass operation - radiotherapy - transtumoral intubation - laser coagulation - combined modality treatment Surgical treatment The main objective of surgical therapy is the restoration of the ability to swallow. The procedures available are resection and bypass operations. Surgical resection In general, some 30-40% of esophageal tumours are resectable. At operation a few of these are found to be inoperable and in some there is residual tumour after the resection. Surgical resection is the treatment of choice for tumours of the lower two-thirds of the esophagus provided: - the patient is considered fit for major surgical intervention - preoperative staging tests indicate that the tumour is resectable and there is no metastatic disease. Types of resections: esophagectomy with intrathoracic esophago- gastro anastomosis or esophageal stripping with cervical eso-gastroanastomosis.

11 Controversy exists regarding tumours at the upper end. Some consider that these lesions are best treated by radiotherapy, others by pharyngolaryngectomy. Palliative bypass procedures These are less popular than intubation procedures because they carry a high mortality (30%) and are major operations which do not seem justified in patients with advanced disease or poor general condition with very limited survival. When successful, however, the relief of dysphagia is better than that obtained by intubation and the patient can swallow ordinary meals. The various procedures are: - reversed gastric tube - gastroesophagostomy proximal to the tumour - colon bypass, right or left - jejunal bypass. Intubation. This is still most popular method of palliation of dysphagia for inoperable malignancy. Traction intubation entails surgical intervention to railroad the tube in position and anchor it to the stomach. Pulsion intubation is preferred since this avoids an operation. Pulsion tubes which can be placed through the lesion by means of a flexible introducer inserted over a guidewire, are commonly used nowadays. A preliminary dilatation is usually necessary before insertion of pulsion tubes. Intubation is more effective for distal than proximal lesions. The palliation of the dysphagia is not complete and the patients are able to swallow only liquidized food. Feeding gastrostomy or jejunostomy is the last palliative method for dysphagia in advanced lesion and unfit patient for major surgery Radiotherapy Squamous carcinomas are radiosensitive. Treatment by external beam radiotherapy may relieve the dysphagia in patients with advanced disease. Laser therapy Laser photocoagulation is an effective method of palliation in patients with advanced esophageal carcinoma. It produces good destruction of malignant tissue. Dysphagia is relieved in 70% of patients. Multi-modality treatment There has been considerable interest in the use of radiotherapy as adjuvant treatment to surgical excision either pre- or postoperatively.

12 Chemotherapy has also been used in the adjuvant setting either in combination with surgical excision and radiotherapy. The results with chemotherapy alone for esophageal carcinoma to date have been poor and do not justify their routine use. PERFORATION OF THE ESOPHAGUS Causes Esophageal perforation occurs either intraluminally or extraluminally. 1. Intraluminal causes - Instrumental injuries represent 75% of esophageal perforations and occur during endoscopy, dilatation, sclerosis of esophageal varices or tube passage. The common sites are at the normal anatomic sites of narrowing. Tumours located at the cardia pose a particular risk for perforation during dilatation, owing to fixation and angulation of the esophagus at the GE junction with this condition. - Foreign bodies cause acute perforation, or commonly, there is a more indolent course with late abscess formation in the mediastinum or development of an empyema. - Caustic substance ingestion can produce necrosis of the esophagus and perforation. - Cancer of the esophagus may lead to perforation. - Barotrauma from exposure to external compressed air or during large internal pressure changes accompanying forceful vomiting (Boerhaave’s syndromepostemetic rupture of the esophagus)) seizures or lifting can produce esophageal perforation. Almost all of these perforations occur in the distal esophagus on the left side. 2. Extraluminal causes - Penetrating injuries can occur from stab wounds or gunshot wounds. - Blunt trauma may produce an esophageal perforation related to a rapid increase in intraluminal pressure or may produce compression of the esophagus between the sternum and the spine. - Operative injury to the esophagus during an unrelated procedure occurs infrequently but has been reported in association with thyroid resection, anterior cervical spine operations, proximal gastric vagotomy, pneumonectomy and laparoscopic fundoplication procedures. Signs and symptoms of esophageal perforation typically begin with dysphagia, pain, fever and progress to leukocytosis, tachycardia, respiratory distress and shock if left untreated. Cervical perforations may present with neck stiffness and subcutaneous emphysema. An intrathoracic perforation should be suspected in patients with chest pain, subcutaneous emphysema, dyspnea and a pleural effusion.

13 Diagnosis History Patients give a recent history of instrumentation of the esophagus or severe vomiting. All patients complain of severe chest pain, which usually is most prominent in the area of the rupture. Physical examination Crepitation in the neck results from mediastinal air. Occasionally a crunching sound can be heard over the heart (Hamman’s sign) due to air in the mediastinum behind the heart. Septic shock also can occur. Investigations CXR reveals air in the mediastinum and possibly a widened mediastinum. If the perforation is in the lower esophagus, air may be present under the diaphragm within the abdomen. If the pleura has been violated a pneumothorax may be present. A water-soluble or dilute barium swallow (esophagography) should be performed if perforation is suspected. This study is better than esophagoscopy. Treatment The controversy is between non-operative and operative management. Everyone would agree on a policy of: nil by mouth for at least 5 days, broad spectrum antibiotics, H2 blockers to suppress gastric acidity, pleural drainage where indicated by the development of an effusion. Clearly every case of esophageal perforation differs so that it is difficult to have hard and fast rules. The small contained perforation should be managed conservatively with a contrast study at 5 days to confirm healing. The delayed presentation at 2 days or thereafter should also be managed conservatively. It would be impossible to suture the perforation as the esophagus tissues will be friable. When there is obvious mediastinal contamination, surgery is advised. Surgical treatment is primarily an attempt to provide wide drainage of the mediastinum and is best approached by a thoracotomy. If diagnosed early (6 hours) perforation can be treated with simple drainage, esophageal repair and appropriate antibiotic coverage. If the diagnosis is delayed, the esophagus is impossible to repair because of the massive inflammation and tissue edema in the area. In this case, drainage and esophageal diversion must be considered. MALLORY-WEISS SYNDROME This condition presents as acute massive upper GI hemorrhage. The bleeding occurs in the lower esophagus, usually near the GE junction and is secondary to

14 a partial thickness tear in the lower esophagus which follows a prolonged period of severe vomiting and retching. The tear usually extends into the stomach and may involve the greater curvature of the cardia. Diagnosis is made by endoscopy which is performed to locate the tear and rule out other causes of bleeding. Treatment is by supportive measures as blood volume replacement, antacids and gastric lavage. In most cases the bleeding subsides spontaneously. Exploratory laparotomy is performed with gastrotomy and suture of the tear of the esophagus from within the stomach if the bleeding persists. The lacerations are closed using continous nonabsorbable sutures. ESOPHAGEAL VARICES Esophageal varices result from portal venous hypertension. The most common cause is cirrhosis of the liver, usually associated with alcohol abuse. Less common causes include portal vein thrombosis, hepatic vein thrombosis and schistosomiasis. As resistance to flow and pressure in the portal venous system rises, abnormal venous communications develop between the peripheral part of the portal system and the systemic circulation. This is known as portal-systemic shunting. Multiple large veins also appear at the lower end of the esophagus and gastric fundus and these are known as esophageal varices. These varices are easily traumatised by food and produce massive gastrointestinal hemorrhage. Up to 40% of cirrhotic patients suffer variceal hemorrhage at some stage. A further result of portal hypertension is splenic enlargement. This may result in hypersplenism, causing anemia, thrombocytopenia and leucopenia. Patients in late stages of cirrhosis also develop ascites. If there is massive portal-systemic shunting, either spontaneous or resulting from a surgically created shunt, portal-systemic encephalopathy may occur. This is due to toxins such as ammonia passing directly into the systemic circulation without traversing the liver, where they would normally be detoxified. Management of esophageal varices Esophageal varices do not usually require treatment unless hemorrhage has occurred. However, elective injection sclerotherapy may be carried out if prophylactic treatment is considered desirable. Acute variceal hemorrhage When a patient is known with cirrhosis or varices presents with massive upper GI hemorrhage, the first priority is resuscitation.

15 Following this, the sourse of hemorrhage is sought. It must be remembered, however, that cirrhotic patients often have defective clotting. Clotting studies should be performed and specific corrective factors given. Balloon tamponade If bleeding is from varices, an attempt is made to apply tamponade. A special tube is passed through the mouth into the stomach and a balloon inflated. Traction is exerted on the upper end for up to four hours in the hope that hemorrhage will stop. The Blackmore tube has separate intragastric and esophageal balloons. Surgical treatment is less commonly performed nowadays. Operations include transgastric esophageal stapling. A circular stapler is passed into the esophagus via a gastrostomy and the gun fired. This places two rows of staples through the full thickness of the esophageal wall, disconecting the longitudinal veins. Emergency portal-systemic shunting is hardly used because of the risk of portalsystemic encephalopathy and the unpredictable outcome with regard to hemorrhage. These operations are still used following recovery from the acute hemorrhage to prevent further hemorrhage, although many doctors believe that repeated injection sclerotherapy via a flexible endoscope is the best treatment. These operations include porta-caval shunting in which the main portal vein is anastomosed to the inferior vena cava, meso-caval shunting in which the superior mesenteric vein is connected to the inferior vena cava via an interposition graft, and lieno-renal shunting (Warren shunt) in which the splenic vein is anastomosed to the left renal vein. The last is said to cause the lowest incidence of encephalopathy, but is also the least effective at decompressing the portal venous pressure. Child’s criteria for assessing operative risk in portal hypertension Score points 1 Encephalopathy 0 Ascites 0 Bilirubin less than35mmol/l, Albumin more than35g/l Prothrombin ratio less than1,4 2 minimal slight 36-50 28-35 1,4-2 3 marked moderate greater than 50 less than 28g/l greater than 2.

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Each criterion is scored and the total added: Child’s A=5-6 ( good risk), Child’s B=7-9 ( moderate risk), Child’s C=10-15 (bad risk). Study questions 1. What are the best investigations for the diagnosis of squamous cell carcinoma of the esophagus? 2. A 32 years old man came in Casualty complaining of chest pain, fever and general malaise. The onset of these symptoms was 3 days ago following heavy drinking and repeated vomiting. On examination he looks ill with neck subcutaneous emphysema, respiratory rate of 30/min, chest auscultation unremarkable. What diagnosis would you suspect and what investigations would you ask to document your clinical diagnosis? 3. What are the palliative treatment options in advanced, unresectable esophageal cancer? 4. What type of hiatal hernia is prone to serious complications and what are these?

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