Hiatal Hernia
Definition and classification
hiatal hernia is an extension of the peritoneal cavity into the chest through the esophageal hiatal of the diaphragm. The hernia consists of a peritoneal sac which usually contains part or all of the stomach but can rarely contain other abdominal viscera such as the colon or spleen. hiatal hernias are classified according to the position of the gastroesophageal junction in relation to the diaphragm. The type I or sliding hiatal hernia is characterized by proximal herniation of the gastroesophageal junction though the esophageal diaphragmatic hiatus into the posterior mediastinum. In a type II hernia, also known as a rolling or pure paraesophageal hernia, the gastroesophageal junction is anchored in its normal subdiaphragmatic position, and the gastric fundus herniates alongside the esophagus into the chest. A type III hernia, also known as a combined sliding/rolling, or mixed hernia, is usually a large hernia and is characterized by proximal herniation of both the gastroesophageal junction and the gastric fundus through a widely open diaphragmatic hiatus. Type III hernias are commonly but inappropriately classified as type II paraesophageal hernias, but a pure type II hernia is a rare finding. The endstage of a type I or II hernia is a large type III hernia, which occurs when the entire stomach migrates up into the chest by rotating 180° around its longitudinal axis, with the gastroesophageal junction and pylorus as fixed points. The greater curvature is thus uppermost in the chest. In this situation, the abnormality is usually referred to as an intrathoracic stomach with organoaxial volvulus. In a type IV hernia, the hiatal defect is very large and has allowed other organs such as the colon, spleen, small intestine, and pancreas to enter the chest. Type IV hernias develop from type III hernias, and are exceedingly uncommon.
Prevalence of hiatal hernia
The majority of hernias, probably more than 95 per cent, are type I sliding hernias. The exact prevalence of hiatal hernia, both in the general population and in patients with foregut symptoms, remains unclear. Reasons for this uncertainty are that most hernias are small sliding hernias which reduce in the upright position, most are asymptomatic, and the detection rate varies with the method used for diagnosis and with the age of the population studied. The reported prevalence of hiatal hernia detected by barium contrast studies in the general population ranges from 10 per cent to more than 70 per cent. It is likely that some of these studies, especially if they are based on static rather than videotaped imaging, classified some physiologic hernias as pathologic hernias. A reasonable estimate of the prevalence of pathologic herniation in the general adult population is 20 per cent, with the prevalence of hernias in patients with gastroesophageal reflux disease being 80 per cent. The mean age of patients with a type I hernia is approximately 50 years and for those with a type III hernia is approximately 60 years. Type III hernias are more common in females, with a female:male ratio of 4:1.
Pathophysiology
A pathologic hiatal hernia is an acquired condition. Anatomic alterations found in patients with hiatal hernia are widening of the hiatus and thinning and lengthening of the phrenoesophageal membrane. The phrenoesophageal membrane consists of an upper fascial layer of loose connective tissue and a lower fascial layer of thicker, stronger, elastic tissue. The upper layer is formed by a supradiaphragmatic continuation of the endothoracic fascia. The more important lower layer is formed by a subdiaphragmatic continuation of the transversalis fascia. The phrenoesophageal membrane functions as an elastic barrier. In comparison with the other diaphragmatic openings, the esophageal hiatal is relatively incompletely filled by the esophagus, and the barrier function of the phrenoesophageal membrane is needed to close the gap between esophagus and diaphragm. The elastic function of the phrenoesophageal membrane allows it to stretch and contract with swallowing and respiration. There are normally more than 1000 swallows per day, and the diaphragm moves up and down between 16 000 and 35 000 times per day. The lengthening and loss of elasticity of the phrenoesophageal membrane that is found in a hiatal hernia is thought to be a gradual age-related wear and tear effect, but obesity, pregnancy, and sudden traumatic elevations in the intra-abdominal pressure may all place additional pressure on the phrenoesophageal membrane.
Mixed or type III hernias are thought to be complications of type I hernias, and are more likely in patients who have an abnormally wide esophageal hiatus. Pure paraesophageal or type II hernias are thought to arise by the same mechanism as sliding hernias, with the difference that the gastroesophageal junction is fixed below the hiatus by firm posterior fixation to the preaortic fascia and the median arcuate ligament. Another difference is that the herniation may occur either through a widened esophageal hiatus or through a defect adjacent to the esophageal hiatus. The fundus of the stomach rolls up alongside the esophagus through the widened hiatus or the adjacent defect, but the gastroesophageal junction remains in its normal intra-abdominal position.
A hiatal hernia predisposes to the development of gastroesophageal reflux by four mechanisms. First, contraction of the crural components of the diaphragm augments the antireflux mechanism by buttressing the lower esophageal sphincter, adding the pressure produced by crural contraction to the underlying pressure in the lower esophageal sphincter. The presence of a hiatal hernia interferes with this buttressing because the normal alignment between the crura and the lower esophageal sphincter is lost. This encourages reflux during periods of increased intra-abdominal pressure. Second, the formation of a hiatal hernia results in loss of the acute angle of His. Third, the clearance of refluxed acid from the esophagus is also impaired in patients with hiatal hernias, especially non-reducing hernias, due to loss of anchoring of the distal esophagus. Fourth, the presence of a hiatal hernia interferes with transhiatal flow of gastric juice. This occurs in particular in patients with a non-reducing hernia, in whom the hernia remains above the diaphragm during inspiration. Fluid trapped within the supradiaphragmatic stomach is prevented from flowing into the subdiaphragmatic stomach by closure of the crura during inspiration, and thus refluxes freely into the negative-pressure thoracic esophagus.
Symptoms
Symptoms in patients with a sliding hernia are mostly those of the associated gastroesophageal reflux. The likelihood of reflux increases with increasing hernia size. Dysphagia and intermittent vomiting can occur in patients with a large sliding hernia, due to diaphragmatic contraction obstructing the passage of a bolus through the herniated stomach. Dysphagia is common in patients with type II hernias, due to compression and angulation of the esophagus by the herniated gastric fundus. In large type III hernias with gastric volvulus, dysphagia can be caused by twisting of the gastroesophageal junction. Recurrent bleeding or anemia may be caused by ulceration or erosive gastritis secondary to ischemia of the herniated gastric mucosa. Crural contractions may also cause ‘riding ulcers' at the level of the diaphragmatic indentations. Respiratory symptoms such as dyspnea may occur from compression of the lungs by a very large hernia, and cough, choking, and pneumonia may result from aspiration of regurgitated gastric juice into the airways.
Type II or III hernias can cause acute life-threatening events in up to 20 per cent of patients due to acute obstruction from gastric torsion or volvulus. Swallowed air causes gastric distention, which compresses the blood supply passing to the intrathoracic stomach along the margins of the diaphragmatic hiatus. This can result in gastric ischemia, perforation, and sepsis. The triad of epigastric pain, inability to vomit, and difficulty in the ability to pass a nasogastric tube is an indication for immediate endoscopic decompression or operative intervention.
Diagnosis
Radiology
Large hernias may be detected on an upright or lateral plain chest radiograph by the presence of a gas-filled viscus behind the heart. Smaller hernias require a barium swallow study for diagnosis. Barium studies are diagnostic in more than 90 per cent of patients. The barium swallow study should include examination in both upright and supine positions, to detect sliding hernias that reduce when upright. Video-esophagram studies demonstrate that most sliding hernias empty during expiration.
Endoscopy
A hiatal hernia is present endoscopically when the anatomic gastroesophageal junction, identified as the proximal extent of the gastric rugal folds, is more than 2 cm above the crura, identified by having the patient sniff. Small hernias are best detected endoscopically if the endoscope is retroflexed within the stomach, allowing inspection of the gastroesophageal junction from below. The geometry of the gastroesophageal junction seen on retroflexed view can be classified using the Hill grading system. This classification system emphasizes that development of a sliding hernia is accompanied by loss of the angle of His, signified by the loss of the normal frenulum over the endoscope on retroflexed viewing. A true paraesophageal hernia is identified on retroflexed view by noting a hernia orifice adjacent to the gastroesophageal junction. A type III hernia appears on retroflexed view as a sliding hernia with the gastroesophageal junction entering on the side of the sac, rather than at the apex of the sac as in a type I hernia.
Manometry
Stationary manometry studies are not used for the diagnosis of hiatal hernia, but an awareness of manometric features of hiatal hernia is helpful since many patients undergoing manometry for the investigation of reflux disease have a hiatal hernia. A ‘double hump' motility pattern is characteristic of a sliding hernia. As the manometry catheter is withdrawn from the stomach into the esophagus, pressurized areas or ‘humps' are recorded, with the distal hump corresponding to the crural compression of the stomach and the proximal hump corresponding to the lower esophageal sphincter. Between the two humps is a plateau region in which the pressure is slightly above the gastric baseline pressure. The plateau region corresponds to the hernia sac. The pressure fluctuations that occur with respiration indicate that the hernia sac may be exposed to both intra-abdominal and intrathoracic pressure conditions, depending upon whether the crura compartmentalize the herniated proximal stomach from the distal stomach and peritoneal cavity.
Treatment
Sliding hernias do not require treatment unless they produce symptoms specific to the presence of the hernia. In patients with gastroesophageal reflux disease, reduction of the hernia and closure of the hiatus is an essential part of operative treatment, and as a consequence the hernia is repaired. Patients with large hernias undergoing antireflux surgery are likely to have a shortened esophagus requiring special operative techniques. The high rate of serious or life-threatening complications in patients with type II or III hernias indicates that operative repair should be performed in all patients with these hernias, regardless of the presence or severity of symptoms or the size of the hernia. Type II or III hernias progressively worsen unless repaired by operation. There is an approximately 20 per cent mortality for emergency repair of an incarcerated paraesophageal hernia, compared with less than 1 per cent mortality for elective repair of a non-incarcerated hernia.
Repair of type II or III hernias by laparoscopic methods can be difficult and is associated with a higher rate of recurrence. We prefer an open approach to these large hernias. An open transthoracic approach allows full esophageal mobilization, resection of the sac, and proper closure of the wide hiatus. An open approach also facilitates performance of a Collis gastroplasty if this is needed to gain adequate esophageal length to reduce tension on the repair. The transabdominal open approach facilitates reduction of a volvulus, but it may be difficult to obtain an adequate view for dissection in the posterior mediastinum, the risk of vagus nerve injury is high, and stout closure of the widened hiatus may be compromised.