Hiatal Hernia

Hiatal hernias occur when abdominal contents protrude through the esophageal hiatus of the diaphragm into the thorax. Hiatal hernias are classified into two main types, sliding (or axial) and paraesophageal, according to the position of the gastroesophageal junction [1,2]. In dogs and cats, the most common type is the sliding hernia, in which the esophagus, esophagogastric junction, and part of the stomach move through the esophageal hiatus into the thoracic cavity [3-5]. This is also described as Type 1 (Fig. 27-1). Paraesophageal (Type 2) hiatal hernia has been described infrequently and involves movement of the fundus of the stomach in a rolling fashion through a defect in the esophageal hiatus while the gastroesophageal junction remains fixed in its normal position. Type 2 hernias have been reported only sporadically in dogs, and never in cats [3,6]. In cases where a combination of the above two abnormalities occur, the hernia is classified as Type 3. In extreme cases, other abdominal organs may accompany the stomach in the thorax, in which case the hernia is classified as Type 4 (Fig. 27-2) [7]. Hiatal hernias may be fixed or dynamic, with herniated tissues moving in and out of the thorax according to changes in position and pleural pressure. Hence, clinical or radiographic signs may not always be present, and dynamic studies may be required to confirm a diagnosis.

Figure 27.1a. Lateral and ventrodorsal radiographs of a 14-month-old Burmese cat with lordosis. A type 1 hiatal hernia was diagnosed coincidentally.

Figure 27.1b. Administration of barium paste reveals cranial malpositioning of the stomach through the diaphragmatic hiatus. This cat did show evidence of clinical signs associated with its hiatal hernia.

Figure 27.2. Lateral and ventrodorsal radiographs of a 10-week-old domestic shorthaired kitten with dyspnea. A large hiatal hernia is present, possibly incorporating other abdominal organs in addition to the stomach. A few days after these radiographs were taken, the kitten suffered a sudden deterioration in its respiratory function and died. Postmortem examination was not performed.

Hiatal hernias may be diagnosed at any age. A distinction has been made between congenital and acquired sliding hiatal hernias in dogs, based on age of diagnosis [2]. However, reported case series demonstrate that acquired posttraumatic hiatal hernias can occur in animals as young as a few months.

Anatomy and Physiology of the Diaphragmatic Hiatus and Gastroesophageal Junction

The diaphragm is a musculotendinous partition that separates the abdominal and thoracic organs, assists in ventilation, and has a role in the movement of lymphatic fluid. The diaphragm is composed of a strong central tendinous section and three separate muscles: the costal, sternal, and lumbar parts. The right crus is larger than the left. A tendon attaches each crus to the bodies of the third and fourth lumbar vertebrae, medial to the psoas minor muscles. Motor innervation of the diaphragm is from the phrenic nerves [8].

Gastroesophageal reflux is normally controlled by a zone of increased pressure, the lower esophageal sphincter of the terminal esophagus [9]. At this point, the muscular layer is the thickest of the entire esophageal length. No anatomic or histologic differentiation exists between this zone and the rest of the esophagus. A complex arrangement of transverse, oblique, and longitudinal muscle fibers blends with the muscular layers of the stomach. A section of inner, transverse fibers blends with the inner muscular fibers of the stomach. Dorsal longitudinal fibers of the outer layer continue on the dorsal wall of the stomach. Oblique, inner fibers pass external to the transverse fibers to blend with longitudinal fibers of the stomach wall [10]. The lower esophageal sphincter (esophageal high-pressure zone) is traditionally considered to be part of the intra-abdominal esophagus, situated between the diaphragmatic hiatus and the gastroesophageal junction. It has been contended that the intra-abdominal esophagus is subjected to higher extraluminal pressures, increasing its resistance to gastroesophageal reflux. However, some anatomic studies challenge this concept by suggesting that in many canines there is little or no intra-abdominal esophagus [11]. It has also been proposed that extrinsic influences imposed by diaphragmatic tone and the anatomic arrangement of the esophagus, hiatus, and stomach support the action of the increased pressure zone. Primary incompetence of the lower esophageal sphincter has not been demonstrated in dogs and cats [28]. Pratschke et al. [12] demonstrated significant differences in the barrier pressure at the gastroesophageal junction in anesthetized dogs positioned in ventral versus lateral recumbency. Hence, the intrinsic muscular activity of the lower esophagus, exertion of extraluminal compression by surrounding structures such as the diaphragm, and geometric relationship of the cardia and esophagus seem most likely to work in concert to moderate gastroesophageal reflux.

Clinical Signs

In congenital hiatal hernias, clinical signs may be observed immediately after weaning onto solid food and are usually seen before the animal is 1 year of age. Acquired hiatal hernias can occur at any age and are most often associated with abdominal trauma. In some instances, animals with a congenital predisposition toward hiatal hernia may develop signs following development of an exacerbating problem such as upper respiratory tract obstruction or diaphragmatic dysfunction. In other individuals, such as the cat shown in Fig. 27-1, hiatal hernias may be diagnosed incidentally during investigation for other problems. Clinical signs result from esophagitis, esophageal dysfunction, and the mass effect of herniated organs within the thorax. They include hypersalivation, regurgitation of frothy saliva and/or food, vomiting, dysphagia, dyspnea, and exercise intolerance [2-4]. The severity of disease may range from minor, with discomfort from mild esophagitis, to life-threatening, with cachexia, dehydration, and aspiration pneumonia. It is likely that, in contrast to humans in whom mild reflux esophagitis may be detected as a result of the patient's complaining of heartburn, most animals presenting for management of hiatal hernias will be diagnosed as a result of relatively severe clinical signs, such as hypersalivation, regurgitation, or dyspnea.

Predisposition to Hiatal Hernia

Breed

Multiple case reports and case series indicate that Chinese Shar Peis appear to have a breed predisposition to the disease [6,13,14]. Hiatal hernias have also been described in a range of brachycephalic breeds. No breed predispositions have been reported in cats.

Upper Respiratory Obstruction

Evidence is growing that upper respiratory tract obstruction exacerbates the clinical signs associated with hiatal hernias [15-19]. A case-control study of bulldogs demonstrated that hiatal hernias were associated with the more severe manifestations of brachycephalic syndrome [16]. Single case reports have described complete remission of clinical signs associated with a sliding hiatal hernia in a Labrador-cross after surgical treatment of laryngeal paralysis [15], and resolution of clinical signs and radiographic signs of a hiatal hernia following surgical correction of congenital stenosis of the soft palate in a dachshund [17]. A review of 30 dogs with brachycephalic obstructive airway syndrome revealed evidence of esophagitis in 25 and sliding hiatal hernias in 13 [18]. Marked improvement in esophagitis and herniation followed surgical correction of the upper airway problems. Esophagitis (among other gastrointestinal tract lesions) was found in a substantial proportion of brachycephalic dogs with upper respiratory syndrome in another study [19]. Proposed mechanisms for exacerbation of hiatal hernias and gastroesophageal reflux by respiratory tract disease include increased force of ventilation, exaggerated negative pleural pressures, and aerophagia leading to gastric distention. Conversely, a strong association between gastroesophageal reflux and chronic respiratory and otolaryngeal disease has been identified in people, with speculation that gastroesophageal reflux may exacerbate airway disease by mechanisms including direct stimulation of the respiratory mucosa, aspiration pneumonia, and reflex bronchoconstriction [20,21].

Other Disease Processes

Hiatal hernias may also occur as a result of other diseases that interfere with normal diaphragmatic function. Symptoms of hiatal hernias have been repeatedly observed following surgery for diaphragmatic hernias in cats and dogs [3,4,22,23]. Proposed mechanisms by which diaphragmatic hernia repair might predispose animals to clinical signs of hiatal hernias include physical damage to the diaphragmatic hiatus, abnormal tension on the central tendon of the diaphragm and hence the hiatus, increases in intra-abdominal pressure as a result of loss of abdominal domain following chronic diaphragmatic hernia, and alterations in vagal activity as a result of surgical trauma and organ repositioning.

Four cases of hiatal hernias associated with generalized tetanus have been reported in dogs [24-26]. Proposed mechanisms relate to abnormal neuromuscular function of the diaphragm, distal esophagus, and abdominal musculature, causing diaphragmatic spasm or esophageal dysmotility with a subsequent tendency to herniation.

Regardless of the observations that clinical signs did not appear until after a precipitating event, it has not been possible to rule out the possibility of a preexisting predisposition to hiatal hernias in these patients.

Obesity

Excessive body weight has been reported as a significant factor predisposing both to hiatal hernia and esophagitis as a result of gastroesophageal reflux disease in humans. Obesity is considered to exacerbate the signs of hiatal hernias owing to an increase in intra-abdominal pressure, increasing the likelihood of organ herniation and gastroesophageal reflux [27].

Consequences of Hiatal Hernia

In humans, clinical signs associated with hiatal hernias do not result from the major anatomic abnormality (laxity of the esophageal hiatus of the diaphragm) but secondary to the events that occur as a result of movement of the gastroesophageal junction and axial displacement of the lower esophageal sphincter from the esophageal hiatus [28].

Gastroesophageal Reflux

Gastroesophageal reflux is the major consequence of hiatal hernia [29,30], causing esophagitis, esophageal dysmotility, airway contamination, and pneumonia [3,4]. Gastroesophageal reflux occurs as a normal event in humans when lower esophageal sphincter pressure falls below 4 mm Hg31, but regurgitated material is usually cleared promptly by esophageal peristalsis [32,33]. Increased exposure to gastric acid, increased acidity of gastric contents, reduced passage of saliva through the esophagus, and failure of normal esophageal clearance result in esophagitis. Esophagitis caused by reflux of acidic gastric contents induces vomiting, regurgitation, and hypersalivation. Severe esophagitis may progress to esophageal stricture [34,35]. In extreme cases, esophagitis may extend transmurally, resulting in fibrous adhesion between the esophagus and surrounding structures (such as the diaphragmatic hiatus), thereby reducing the elastic ability of the esophagus to stretch. This condition is termed "shortened esophagus syndrome" and carries a poor prognosis when addressed using normal surgical techniques [3,36].

Regurgitation

Abnormal and decreased esophageal motility may be primary or secondary to hiatal hernia and reflux esophagitis. Up to 60% of patients with hiatal hernias have signs of megaesophagus on plain or contrast radiographs [3,16,37].

Dysphagia in humans seems to result from obstruction to passage of a swallowed bolus by diaphragmatic impingement on the herniated stomach [38].

Dyspnea

Dyspnea may occur in animals with hiatal hernias as a result of an intrathoracic mass effect (gastric distention in Types 1 to 4 or herniated organs in Type 4 hernia, Fig. 27-2), failure of the thoracic bellows in animals with diaphragmatic dysfunction, or aspiration of gastric contents leading to bronchospasm or aspiration pneumonia.

Prognosis

Hiatal Hernia

Reflux esophagitis may be treated effectively with a variety of medical agents. However, surgery is indicated in animals with severe gastroesophageal reflux leading to chronic esophagitis, regurgitation, and airway disease. After surgical correction of hiatal hernia by use of an anatomic restoration technique, and with attention to exacerbating problems such as brachycephalic disease, uniformly good results may be expected.