Diaphragmatic hernias and gastric volvulus

Bochdalek hernias

Bochdalek hernias, first described by Bochdalek in 1848, are characterised by a congenital defect on the posterolateral region of the diaphragm that does not contain a hernial sac. Closure of the pleuroperitoneal canal occurs around the eighth week of gestation. Failure of closure results in a characteristic defect through the posterior lumbocostal triangle. Since the right canal closes before the left canal, most Bochdalek hernias (85%) are left sided. Although the majority of these will present in early childhood, congenital defects can present in adulthood. The incidence of adults with asymptomatic Bochdalek hernias has been estimated to be between 0.17% and 6%, although some are suggested to have been acquired during adulthood. The diagnosis of a Bochdalek hernia in adults is not easy and it is commonly misdiagnosed. Unlike infants, who present with respiratory distress in early life, the most frequent symptoms in adults are chest and/or abdominal pain (in 66%) or symptoms of ileus (in 38%). 25% of adult patients are asymptomatic. A variety of abdominal organs may be present in the thorax, which may lead to hypoplasia of the left lung. Retroperitoneal structures including pancreas and kidney may also be present. On chest X-ray Bochdalek hernias may be diagnosed by the presence of gas-filled loops of bowel or a soft tissue mass above the level of the diaphragm ( Fig. 15.2 ). Correct interpretation may however be difficult, as the appearance can be similar to other thoracic pathologies or the more common condition of a paraoesophageal hernia. Computed tomography (CT) of the chest and abdomen allows clear visualisation of the location of the diaphragmatic defect and the herniated abdominal organs ( Fig. 15.3 ). In symptomatic patients surgical repair must be considered. In patients with suspected obstruction or strangulation, an abdominal approach allows reduction and inspection of the abdominal viscera. It is the author’s experience that the margins of the defect are usually of good quality and allow approximation with minimal tension using a non-absorbable suture. If mesh is felt to be necessary to reinforce the repair, a composite form should be considered. A transthoracic repair has been proposed if the bowel does not display signs of strangulation or necrosis due to its technical simplicity in comparison to a midline laparotomy.

Foramen of Morgagni hernia

In 1769 Morgagni described the herniation of abdominal contents through a triangular diaphragmatic defect between the muscle fibres of the diaphragm that originate from the xiphisternum and the costal margin and insert on the central tendon of the diaphragm. A natural weakness in this retrosternal area arises due to the passage of the internal mammary artery as it becomes the superior epigastric artery with its associated vein and lymphatics. The majority of Morgagni hernias are right sided, with only rare left-sided occurrences because of the protection provided by the pericardial sac. Herniation of abdominal contents is typically caused by an increase in intra-abdominal pressure secondary to trauma, pregnancy, or obesity. Foramen of Morgagni hernias account for 3% of all surgically treated diaphragmatic hernias. In a study of 50 cases, Comer reported that 70% of the patients were female, 90% of the hernias were right sided, and 92% of the hernias had hernia sacs. The most common contents of the hernia were omentum, with 60% containing transverse colon and 12% containing stomach. Only 28% of patients were symptomatic, with symptoms including upper abdominal discomfort, fullness, bloating, vomiting, and bouts of large-bowel obstruction. Investigation is with CT, which may show contrast-filled bowel in the chest or a solid-appearing mass that can be confused with a lipoma. Fine curvilinear or linear densities within the mass most likely represent vessels within the omentum and confirm the diagnosis. Once confirmed, these hernias should be referred for surgical repair. A laparoscopic abdominal approach is recommended, allowing reduction of the hernia contents, assessment of the abdominal viscera, and repair of the defect ( Fig. 15.4 ). This is achieved with the insertion of non-absorbable sutures and placement of mesh, if required. Resection of the hernia sac is not universally performed.

Hiatus hernia

Classification of hiatal hernias

Hiatal hernias are classified into four types ( Fig. 15.5 ).

• Type I (sliding hiatal hernia)

  • Type I hiatus hernias are the most common type and are often diagnosed in patients undergoing investigation for reflux disease. An increase in the diameter of the oesophageal hiatus and an associated laxity of the phreno-oesophageal membrane allows the upper portion of the gastric cardia to herniate upwards. Although thinned, the phreno-oesophageal membrane remains intact and the herniated gastric cardia is contained within the posterior mediastinum.

• Type II, III, and IV (varieties of paraoesophageal hernias)

  • These less common types are all varieties of paraesophageal hernias and account for 5–15% of all hiatal hernias. In addition to reflux, patients often present with chest pain, dysphagia, intermittent vomiting, and worsening respiratory symptoms. True type II hernias are rare and result from a localised defect in the phreno-oesophageal membrane that allows the gastric fundus to herniate upwards. The oesophagogastric junction (OGJ) remains in its normal position fixed to the preaortic fascia and the median arcuate ligament. Type III hernias have elements of both types I and II hernias. With progressive enlargement of the hernia through the hiatus, the phreno-oesophageal membrane stretches, displacing the OGJ above the diaphragm and thereby adding a sliding element to the type II hernia. Type IV hiatus hernia is associated with a large defect in the phreno-oesophageal membrane, allowing other organs such as the colon, spleen, pancreas, and small intestine, to enter the hernia sac.

  • The natural history of a type II hernia is progressive enlargement so that the entire stomach eventually herniates with the pylorus juxtaposed to the gastric cardia, forming an upside-down intrathoracic stomach. Paraesophageal hernias are associated with abnormal laxity of structures which act to prevent displacement of the stomach; the gastrosplenic and gastrocolic ligaments. As the hernia enlarges, the greater curvature of the stomach rolls up into the thorax. Because the stomach is fixed at the OGJ, the herniated stomach tends to rotate around its longitudinal axis, resulting in an organoaxial volvulus. Gastric volvulus may lead to acute gastric obstruction, strangulation, and perforation.