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DISEASES OF DIAPHRAGMA
With the advent of clinical radiology, it became evident that a diaphragmatic hernia was a relatively common abnormality and was not always accompanied by symptoms. Three types of esophageal hiatal hernia were identified: (1) the sliding hernia, type I, characterized by an upward dislocation of the cardia in the posterior mediastinum; (2) the rolling or paraesophageal hernia, type II, characterized by an upward dislocation of the gastric fundus alongside a normally positioned cardia; and (3) the combined sliding-rolling or mixed hernia, type III, characterized by an upward dislocation of both the cardia and the gastric fundus. The end stage of type I and type II hernias occurs when the whole stomach migrates up into the chest by rotating 180 degrees around its longitudinal axis, with the cardia and pylorus as fixed points. In this situation the abnormality is usually referred to as an intrathoracic stomach.
The clinical presentation of a paraesophageal hiatal hernia differs from that of a sliding hernia. There is usually a higher prevalence of symptoms of dysphagia and postprandial fullness with paraesophageal hernias, but the typical symptoms of heartburn and regurgitation present in sliding hiatal hernias can also occur. Both are caused by gastroesophageal reflux secondary to an underlying mechanical deficiency of the cardia. The symptoms of dysphagia and postprandial fullness in patients with a paraesophageal hernia are explained by the compression of the adjacent esophagus by a distended cardia, or twisting of the gastroesophageal junction by the torsion of the stomach that occurs as it becomes progressively displaced in the chest. Approximately one-third of patients with a paraesophageal hernia are found to be anemic, which is because of recurrent bleeding from ulceration of the gastric mucosa in the herniated portion of the stomach. Respiratory complications are frequently associated with a paraesophageal hernia, and consist of dyspnea from mechanical compression and recurrent pneumonia from aspiration. With time the stomach migrates into the chest and can cause intermittent obstruction because of the rotation that has occurred. In contrast, many patients with paraesophageal hiatal hernia are asymptomatic or complain of minor symptoms. However, the presence of a paraesophageal hernia can be life-threatening in that the hernia can lead to sudden catastrophic events, such as excessive bleeding or volvulus with acute gastric obstruction or infarction. With mild dilatation of the stomach, the gastric blood supply can be markedly reduced, causing gastric ischemia, ulceration, perforation, and sepsis. The probability of incarceration is not well known, although recent analysis using mathematical modelling suggests the risk is small. The symptoms of sliding hiatal hernias are usually because of functional abnormalities associated with gastroesophageal reflux and include heartburn, regurgitation, and dysphagia. These patients have a mechanically defective LES, giving rise to the reflux of gastric juice into the esophagus and the symptoms of heartburn and regurgitation. The symptom of dysphagia occurs from the presence of mucosal edema, Schatzki ring, stricture, or the inability to organize peristaltic activity in the body of the esophagus as a consequence of the disease.
A radiogram of the chest with the patient in the upright position can diagnose a hiatal hernia if it shows an air-fluid level behind the cardiac shadow. This is usually caused by a paraesophageal hernia or an intrathoracic stomach. The accuracy of the upper GI barium study in detecting a paraesophageal hiatal hernia is greater than for a sliding hernia, because the latter can often spontaneously reduce. The paraesophageal hiatal hernia is a permanent herniation of the stomach into the thoracic cavity, so a barium swallow provides the diagnosis in virtually every case. Attention should be focused on the position of the gastroesophageal junction, when seen, to differentiate it from a type II hernia. Fiberoptic esophagoscopy is useful in the diagnosis and classification of a hiatal hernia because the scope can be retroflexed. In this position, a sliding hiatal hernia can be identified by noting a gastric pouch lined with rugal folds extending above the impression caused by the crura of the diaphragm, or measuring at least 2 cm between the crura, identified by having the patient sniff, and the squamocolumnar junction on withdrawal of the scope. A paraesophageal hernia is identified on retroversion of the scope by noting a separate orifice adjacent to the gastroesophageal junction into that which gastric rugal folds ascend. A sliding-rolling or mixed hernia can be identified by noting a gastric pouch lined with rugal folds above the diaphragm, with the gastroesophageal junction entering about midway up the side of the pouch.
The treatment of paraesophageal hiatal hernia is largely surgical. Controversial aspects include (1) indications for repair, (2) surgical approach, and (3) role of fundoplication.
The presence of a paraesophageal hiatus hernia has traditionally been considered an indication for surgical repair. This recommendation is largely based on two clinical observations. First, retrospective studies have shown a significant incidence of catastrophic, life-threatening complications of bleeding, infarction, and perforation in patients being followed with known paraesophageal herniation. Second, emergency repair carries a high mortality. In the classic report of Skinner and Belsey, 6 of 21 patients with a paraesophageal hernia, treated medically because of minimal symptoms, died from the complications of strangulation, perforation, exsanguinating hemorrhage, or acute dilatation of the herniated intrathoracic stomach. These catastrophes occurred for the most part without warning. Others have reported similar findings. Recent studies suggest that catastrophic complications may be somewhat less common. Allen and colleagues followed 23 patients for a median of 78 months with only four patients progressively worsening. There was a single mortality secondary to aspiration that occurred during a barium swallow examination to investigate progressive symptoms. Although emergency repairs had a median hospital stay of 48 days compared to a stay of 9 days in those having elective repair, there were only three cases of gastric strangulation in 735 patient-years of follow-up. If surgery is delayed and repair is done on an emergency basis, operative mortality is high, compared to less than 1 percent for an elective repair. With this in mind, patients with a paraesophageal hernia are generally counseled to have elective repair of their hernia, particularly if they are symptomatic. Watchful waiting of asymptomatic paraesophageal hernias may be an acceptable option.
The surgical approach to repair of a paraesophageal hiatal hernia may be either transabdominal (laparoscopic or open) or transthoracic. Each has its advantages and disadvantages. A transthoracic approach facilitates complete esophageal mobilization and removal of the hernia sac. Thoracotomy also allows for the occasional gastroplasty, which may be required for esophageal lengthening to achieve a tension-free repair. The transabdominal approach facilitates reduction of the volvulus that is often associated with paraesophageal hernias. Although some degree of esophageal mobilization can be accomplished transhiatally, complete mobilization to the aortic arch is difficult or impossible without risk of injury to the vagal nerves. Several authors have reported the successful repair of paraesophageal hernias using a laparoscopic approach. Laparoscopic repair of a pure type II, or mixed type III paraesophageal hernia is an order of magnitude more difficult than a standard laparoscopic Nissen fundoplication. Most would recommend that these procedures are best avoided until the surgeon has accumulated considerable experience with laparoscopic antireflux surgery. There are several reasons for this. First, the vertical and horizontal volvulus of the stomach often associated with paraesophageal hernias makes identification of the anatomy, in particular the location of the esophagus, difficult. Second, dissection of a large paraesophageal hernia sac usually results in significant bleeding, obscuring the operative field. Finally, redundant tissue present at the gastroesophageal junction following dissection of the sac frustrates the creation of a fundoplication, which these authors believe should accompany the repair of all paraesophageal hernias. Mindful of these difficulties, and given appropriate experience, patients with paraesophageal hernia may be approached laparoscopically, with expectation of success in the majority.
Most outcome studies report relief of symptoms following surgical repair of paraesophageal hernias in over 90 percent of patients. The current literature suggests that laparoscopic repair of a paraesophageal hiatal hernia can be successful. Most authors report symptomatic improvement in 80–90 percent of patients, and less than 10–15 percent prevalence of recurrent hernia. However, the problem of recurrent hernia following laparoscopic repair of any hiatal hernia is becoming increasingly appreciated. Recurrent hernia is now the most common cause of anatomic failure following laparoscopic Nissen fundoplication done for GERD. The problem of recurrent hernia following repair of large type III hiatal hernias has received less attention. Outcome following repair of these hernias is usually based on symptomatic assessment alone. Although recurrence rates of 6–13 percent have been reported, they have largely been based on the need for reoperation or investigations that are performed on a selective basis. Recent reports have shown some degree of anatomic recurrence in up to 45 percent of patients who underwent laparoscopic repair of their
hernia. The principles of laparoscopic repair of a large intrathoracic hernia are analogous to those for an open procedure, namely reduction of the hernia, excision of the peritoneal sac, crural repair, and fundoplication. However, there are several factors that make the laparoscopic repair of these large hernias complex. First, the hiatal opening in a patient with a large hernia is wide, with the right and left muscular crura often separated by 4 cm or more. This can make closure problematic because of the tension required to bring the crura together. Second, the right crus may be devoid of stout tissue and sutures may pull through it easily. Finally, redundant tissue present at the gastroesophageal junction following dissection of the sac retards the creation of the fundoplication. The use of prosthetic mesh as an adjunct to repair has been advocated for both open and laparoscopic repair of large hiatal hernias. Whether its use is beneficial or not remains controversial, but most prefer to avoid prosthetic material if possible. In contrast to groin hernias, the esophageal hiatus is a dynamic area with constant movement of the diaphragm, esophagus, stomach, and pericardium. Erosion of prosthetic material placed in this area into the GI tract will occur, the only question is how often. The short-term follow-up of most studies is insufficient to provide insight into this problem.
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