Hiatal Hernia

Hiatal hernia (HH) is a surgical condition characterized by the abnormal protrusion of abdominal contents, most commonly the stomach, through the esophageal hiatus of the diaphragm into the thoracic cavity. This herniation can be congenital or acquired, and it results in a disruption of the normal anatomy and physiology of the gastroesophageal junction (GEJ), leading to a spectrum of clinical signs ranging from asymptomatic to severe respiratory and gastrointestinal distress. The condition is classified into four types based on the extent and nature of the herniation: Type I (sliding hiatal hernia), where the GEJ and a portion of the gastric cardia slide cranially through the hiatus; Type II (paraesophageal hernia), where the GEJ remains in its normal position but a portion of the gastric fundus herniates alongside the esophagus; Type III (mixed hernia), combining features of both Types I and II; and Type IV (complex hernia), involving herniation of other abdominal organs such as the spleen, omentum, or colon. In veterinary medicine, Type I is the most commonly encountered, particularly in brachycephalic breeds, and is often associated with gastroesophageal reflux (GER) and esophagitis. The condition requires a thorough diagnostic workup and may necessitate surgical intervention when medical management fails or when complications such as strangulation or respiratory compromise occur.

The etiology of hiatal hernia in veterinary patients is multifactorial. Congenital hiatal hernia is often attributed to a developmental abnormality of the diaphragm, specifically a failure of the crural muscles to properly fuse or form a competent hiatus. This can be due to genetic factors, as evidenced by the higher prevalence in certain breeds, such as the English Bulldog, French Bulldog, and Shar-Pei. Acquired hiatal hernia can result from trauma, such as blunt force injury to the abdomen or thorax, causing diaphragmatic rupture or weakening of the crural musculature. Additionally, increased intra-abdominal pressure from conditions like chronic vomiting, coughing, pregnancy, or obesity can contribute to the development of a hiatal hernia. Iatrogenic causes may include previous surgery in the region, such as diaphragmatic herniorrhaphy or esophageal surgery, which can alter the normal anatomy and predispose to herniation. In some cases, the exact cause remains idiopathic. The anatomical vulnerability of the esophageal hiatus, which is a natural opening in the diaphragm, combined with the negative pressure of the thoracic cavity and positive pressure of the abdominal cavity, creates a pressure gradient that can promote herniation when the crural muscles are weakened or the hiatus is abnormally large.

Hiatal hernia is relatively uncommon in dogs and cats, but it is more frequently diagnosed in certain breeds. Brachycephalic breeds, particularly the English Bulldog, French Bulldog, and Pug, are overrepresented, likely due to their conformational characteristics, including a short, wide thorax and increased respiratory effort, which may predispose to increased negative intrathoracic pressure and subsequent herniation. Other breeds reported to be at risk include the Shar-Pei, Chinese Shar-Pei, and Boston Terrier. There is no clear sex predilection, but some studies suggest a slight male predominance. The condition can occur at any age, but congenital hiatal hernia is typically diagnosed in young animals, often under one year of age, while acquired forms may present later in life. In cats, hiatal hernia is rare, but it has been reported in both domestic shorthair and purebred cats. The overall incidence is low, but it is an important differential diagnosis in animals presenting with chronic regurgitation, vomiting, or respiratory signs, especially in predisposed breeds.

The pathophysiology of hiatal hernia involves a complex interplay of anatomical and physiological factors. The esophageal hiatus is formed by the right and left crura of the diaphragm, which normally maintain a snug fit around the esophagus, preventing the stomach from herniating into the thorax. The phrenoesophageal ligament, a thickening of the endoabdominal fascia, anchors the GEJ to the diaphragm. In hiatal hernia, there is a laxity or disruption of these structures, allowing the stomach to move cranially. This displacement disrupts the normal high-pressure zone at the GEJ, which is critical for preventing gastroesophageal reflux (GER). The loss of the angle of His, the acute angle between the esophagus and the stomach, further compromises the antireflux barrier. Consequently, gastric acid and bile can reflux into the esophagus, causing esophagitis, which can lead to pain, ulceration, and stricture formation. In severe cases, the herniated stomach may become incarcerated or strangulated, leading to gastric ischemia, necrosis, and perforation, which is a life-threatening emergency. Additionally, the presence of abdominal organs in the thoracic cavity can compromise respiratory function by reducing lung volume and impairing diaphragmatic movement, leading to respiratory distress.

Several factors predispose animals to hiatal hernia. Intrinsic factors include breed conformation, particularly brachycephalic anatomy, which is associated with a shorter, wider thorax and increased respiratory effort. Genetic predisposition is evident in certain breeds, suggesting a heritable component. Age is a factor, as congenital hiatal hernia is more common in young animals, while acquired forms may occur in older animals due to weakening of the diaphragmatic musculature. Obesity increases intra-abdominal pressure, which can contribute to herniation. Extrinsic factors include trauma, such as vehicular accidents or falls, which can cause diaphragmatic rupture or weakening. Chronic conditions that increase intra-abdominal pressure, such as chronic coughing, vomiting, or tenesmus, can also predispose to hiatal hernia. Prior surgery in the region, such as diaphragmatic herniorrhaphy, may alter the anatomy and increase the risk. Additionally, conditions that cause respiratory distress, such as brachycephalic airway syndrome, can lead to increased negative intrathoracic pressure, which may pull the stomach into the thorax.

Clinical signs of hiatal hernia vary depending on the type, severity, and presence of complications. In many cases, especially with Type I sliding hernias, signs may be intermittent and exacerbated by stress, exercise, or recumbency. Common signs include regurgitation, which is the passive expulsion of undigested food or fluid from the esophagus, and vomiting, which is an active process. Animals may also exhibit excessive salivation, dysphagia, and weight loss. Respiratory signs, such as coughing, wheezing, and dyspnea, can occur due to compression of the lungs by herniated abdominal organs or aspiration pneumonia secondary to regurgitation. In severe cases, especially with paraesophageal or complex hernias, acute signs of gastric dilatation-volvulus (GDV) may be observed, including abdominal distension, retching, and collapse. Physical examination may reveal tachypnea, increased respiratory effort, and abnormal lung sounds. In some animals, the hernia may be reducible, and signs may resolve temporarily. Chronic cases may develop esophageal stricture, leading to progressive regurgitation and poor body condition.

Differential diagnoses for hiatal hernia include other causes of regurgitation and vomiting, such as esophagitis, esophageal stricture, esophageal foreign body, megaesophagus, and gastroesophageal reflux disease (GERD). Additionally, respiratory conditions like pneumonia, bronchitis, and diaphragmatic hernia should be considered. Other surgical conditions such as gastric dilatation-volvulus (GDV) and peritoneopericardial diaphragmatic hernia (PPDH) may present with similar signs. Key distinguishing features include: - Esophagitis: Often associated with a history of vomiting or ingestion of caustic substances; endoscopy reveals mucosal inflammation. - Esophageal stricture: Typically follows severe esophagitis or foreign body; imaging shows a narrowed esophageal lumen. - Esophageal foreign body: Acute onset of regurgitation and dysphagia; radiography or endoscopy identifies the object. - Megaesophagus: Generalized esophageal dilation with decreased motility; often idiopathic or secondary to myasthenia gravis. - GERD: Similar pathophysiology but without herniation; diagnosis via fluoroscopy or pH monitoring. - Diaphragmatic hernia: May involve other organs; radiography shows discontinuity of the diaphragm. - GDV: Acute, life-threatening; radiography shows stomach distension with gas. - PPDH: Congenital defect in the pericardial sac; radiography shows cardiac silhouette enlargement with abdominal contents. Definitive diagnosis of hiatal hernia is made via thoracic radiography, fluoroscopy, or endoscopy, which can demonstrate the herniation and assess for concurrent esophagitis.

The diagnostic algorithm for hiatal hernia begins with a thorough history and physical examination, with particular attention to breed, age, and clinical signs. If hiatal hernia is suspected, thoracic radiography is the first imaging modality. Standard lateral and ventrodorsal views may reveal a soft tissue opacity in the caudal thorax, dorsal to the heart, representing the herniated stomach. However, because sliding hernias may be intermittent, stress radiography or fluoroscopy during swallowing or with abdominal compression may be necessary to demonstrate the hernia. Fluoroscopy is particularly useful for dynamic assessment of the GEJ and esophageal motility. If radiography is inconclusive, esophagoscopy (endoscopy) can be performed to directly visualize the GEJ, assess for esophagitis, and confirm the presence of a hiatal hernia by retroflexing the endoscope to view the hernia from the stomach. In cases where surgical intervention is planned, computed tomography (CT) may be used for detailed anatomical assessment, especially in complex hernias. Laboratory tests, including complete blood count, serum biochemistry, and urinalysis, are typically performed to evaluate for concurrent conditions and to assess surgical risk. In animals with respiratory signs, arterial blood gas analysis may be indicated. The diagnostic workup should also include screening for aspiration pneumonia via thoracic radiography.

Laboratory findings in hiatal hernia are often nonspecific but may reflect complications. Complete blood count (CBC) may show leukocytosis with a left shift if aspiration pneumonia or inflammation is present. Serum biochemistry may reveal electrolyte imbalances, particularly hypokalemia and hypochloremia, due to chronic vomiting or regurgitation. Metabolic alkalosis may be present if vomiting is severe. In cases of gastric strangulation, elevated lactate and evidence of sepsis may be seen. Urinalysis may show signs of dehydration, such as increased urine specific gravity. Coagulation panel (PT/aPTT) is recommended as part of the preoperative workup, especially if surgery is planned, to rule out coagulopathies. Inflammatory biomarkers such as C-reactive protein (CRP) may be elevated in cases of esophagitis or pneumonia. Arterial blood gas analysis may reveal hypoxemia and hypercapnia in animals with respiratory compromise. Synovial fluid analysis is not relevant to this condition. Overall, laboratory findings are supportive but not diagnostic for hiatal hernia.

Imaging is the cornerstone of diagnosis for hiatal hernia. Thoracic radiography, including lateral and ventrodorsal views, may show a soft tissue opacity in the caudal thorax, dorsal to the cardiac silhouette, representing the herniated stomach. The stomach may contain gas, creating a characteristic air-filled structure. In some cases, the hernia is only visible on stress views, such as during swallowing or with abdominal compression. Fluoroscopy is the most sensitive imaging modality for dynamic assessment of the GEJ. It allows real-time visualization of the esophagus and stomach during swallowing, and can demonstrate the sliding of the GEJ into the thorax. It also evaluates esophageal motility and the presence of gastroesophageal reflux. Esophagoscopy (endoscopy) is both diagnostic and therapeutic, as it allows direct visualization of the GEJ, assessment of esophagitis, and confirmation of the hernia by retroflexion. Computed tomography (CT) provides detailed cross-sectional anatomy and is particularly useful for complex hernias, surgical planning, and evaluating for concurrent thoracic pathology. CT can accurately measure the size of the hiatus and the extent of herniation. Ultrasonography is less commonly used but may be helpful in identifying the stomach in the thorax. In summary, a combination of radiography, fluoroscopy, and endoscopy is typically sufficient for diagnosis, with CT reserved for complex cases.

Cytology and histopathology are not typically required for the diagnosis of hiatal hernia, as the condition is primarily anatomical. However, if esophagitis is present, esophageal mucosal biopsies obtained during endoscopy may be submitted for histopathology. Histological findings may include epithelial erosion or ulceration, inflammatory cell infiltration (neutrophils, lymphocytes, plasma cells), and fibrosis in chronic cases. In cases of gastric strangulation, surgical resection of necrotic tissue may be submitted for histopathology to confirm ischemic necrosis. Cytology of bronchoalveolar lavage fluid may be performed if aspiration pneumonia is suspected, revealing neutrophilic inflammation and possibly bacteria. In general, these ancillary tests are used to assess complications rather than to diagnose the hernia itself.

Treatment of hiatal hernia can be medical or surgical, depending on the severity of clinical signs and the presence of complications. Medical management is often the first line of therapy, especially for intermittent or mild cases. It includes dietary modifications, such as feeding small, frequent meals of a low-fat, easily digestible diet, and elevating the food bowl to reduce regurgitation. Prokinetic agents, such as metoclopramide (0.2-0.5 mg/kg PO q8h) or cisapride (0.5 mg/kg PO q8h), can enhance esophageal and gastric motility. Gastric acid suppressants, such as omeprazole (0.7-1.0 mg/kg PO q12h) or famotidine (0.5-1.0 mg/kg PO q12h), are used to reduce esophagitis. Sucralfate (0.5-1 g per dog PO q8h) may be administered as a cytoprotectant. If medical management fails or if the hernia is severe, surgical intervention is indicated. Surgical options include: 1) Herniorrhaphy: Reduction of the herniated contents and closure of the esophageal hiatus with sutures. The hiatus is typically narrowed by placing simple interrupted sutures of non-absorbable or slowly absorbable monofilament material (e.g., polypropylene or polydioxanone) in the crural muscles. 2) Esophagopexy: Fixation of the esophagus to the diaphragm to prevent cranial migration. This is achieved by suturing the esophagus to the crural muscle or the diaphragm. 3) Gastropexy: Fixation of the stomach to the abdominal wall to prevent gastric herniation. A left-sided incisional gastropexy is commonly performed. 4) Fundoplication: Wrapping the gastric fundus around the distal esophagus to create a one-way valve mechanism. The most common technique is the Nissen fundoplication, which involves a 360-degree wrap. This procedure is more complex and may be associated with complications such as dysphagia and gas bloat. The choice of surgical technique depends on the type of hernia and surgeon preference. In cases of strangulation, resection of necrotic tissue may be necessary. Postoperative care includes pain management, nutritional support, and monitoring for complications such as recurrence, esophagitis, and aspiration pneumonia.

The prognosis for hiatal hernia is generally good with appropriate treatment. Medical management can be successful in controlling clinical signs in many cases, especially in young animals with congenital hernias that may resolve as they mature. Surgical treatment has a high success rate, with most animals showing significant improvement or resolution of clinical signs. However, the prognosis can be guarded in cases with severe concurrent esophagitis, stricture formation, or aspiration pneumonia. Complications such as recurrence of the hernia, surgical site infection, and postoperative dysphagia can occur. In cases of strangulation, the prognosis is more guarded, especially if gastric necrosis or perforation has occurred. Overall, the long-term prognosis is favorable, with many animals achieving a good quality of life.

Postoperative follow-up is essential to monitor for complications and ensure successful recovery. Animals should be re-examined within 10-14 days after surgery for suture removal and assessment of wound healing. Thoracic radiography may be repeated at 4, 8, and 12 weeks postoperatively to evaluate for recurrence of the hernia and to assess the position of the stomach. Dietary management should be continued for several weeks, with gradual transition to a normal diet as tolerated. Activity should be restricted for 4-6 weeks to allow proper healing of the diaphragm and surgical sites. Owners should be educated on the signs of recurrence, such as regurgitation, vomiting, or respiratory distress, and advised to seek immediate veterinary attention if these occur. Long-term monitoring may include periodic thoracic radiography or fluoroscopy in animals with a history of severe disease. In animals with concurrent esophagitis, repeat endoscopy may be indicated to assess healing. Overall, follow-up should be tailored to the individual patient's needs and response to treatment.

Clinical pearls: 1) In brachycephalic breeds, always consider hiatal hernia as a differential for regurgitation, especially if signs are intermittent. 2) Fluoroscopy is the gold standard for diagnosing sliding hiatal hernias; static radiographs may miss the hernia. 3) During surgery, ensure adequate exposure of the esophageal hiatus by performing a median sternotomy or a paracostal approach. 4) When performing herniorrhaphy, place sutures in the crural muscles without excessive tension to avoid tearing. 5) Consider performing a gastropexy in all surgical cases to prevent recurrence. 6) Postoperative use of proton pump inhibitors and prokinetics can help manage esophagitis. Pitfalls: 1) Failure to identify a sliding hernia on radiographs can lead to misdiagnosis and delayed treatment. 2) Inadequate closure of the hiatus can result in recurrence. 3) Over-tightening of the hiatus can cause esophageal obstruction. 4) Neglecting to address concurrent gastroesophageal reflux can lead to persistent esophagitis. 5) In cases of strangulation, delayed surgical intervention can be fatal. 6) Inadequate postoperative monitoring for aspiration pneumonia can lead to severe complications.

Perioperative pharmacological protocols for hiatal hernia surgery are based on Plumb's Veterinary Drug Handbook. Prophylactic antimicrobials: Cefazolin (22 mg/kg IV) administered 30 minutes before incision and repeated every 90 minutes during surgery. Postoperative antimicrobials are not routinely indicated unless contamination occurs. Analgesics: Opioids such as hydromorphone (0.05-0.1 mg/kg IV or IM q4-6h) or fentanyl (2-5 mcg/kg IV bolus, then 2-6 mcg/kg/h CRI) for intraoperative and immediate postoperative pain. Non-steroidal anti-inflammatory drugs (NSAIDs) such as carprofen (2.2 mg/kg PO q12h) or meloxicam (0.1 mg/kg PO q24h) may be used for 3-5 days postoperatively, but caution is advised in animals with renal or gastrointestinal disease. Local anesthetic blocks, such as intercostal nerve blocks with bupivacaine (1-2 mg/kg) or a continuous epidural, can provide additional analgesia. Muscle relaxants are not typically used, but if needed, methocarbamol (15-20 mg/kg PO q8h) may be considered. Prokinetics: Metoclopramide (0.2-0.5 mg/kg PO or SC q8h) or cisapride (0.5 mg/kg PO q8h) to enhance gastrointestinal motility. Gastric acid suppressants: Omeprazole (0.7-1.0 mg/kg PO q12h) or famotidine (0.5-1.0 mg/kg PO q12h) to reduce esophagitis. Cytoprotectants: Sucralfate (0.5-1 g per dog PO q8h) to protect the esophageal mucosa. Antiemetics: Maropitant (1 mg/kg SC q24h) may be used if vomiting is present. In cases of aspiration pneumonia, appropriate antibiotics based on culture and sensitivity should be administered. Dosages should be adjusted for organ function, especially in animals with renal or hepatic impairment.

The veterinary literature on hiatal hernia is limited but includes several key studies. A retrospective study by Callan et al. (1993) described the clinical features and surgical management of hiatal hernia in dogs, reporting successful outcomes with herniorrhaphy and gastropexy. Another study by Hardie et al. (1998) evaluated the use of fundoplication in dogs with hiatal hernia, showing good long-term control of clinical signs. A more recent study by Monnet (2015) reviewed the surgical techniques for hiatal hernia and recommended a combination of herniorrhaphy, esophagopexy, and gastropexy as the preferred approach. In terms of medical management, a study by Lecoindre et al. (2010) demonstrated the efficacy of omeprazole and cisapride in controlling clinical signs in dogs with gastroesophageal reflux. Consensus guidelines from the ACVS and ECVS emphasize the importance of fluoroscopy for diagnosis and recommend surgical intervention for animals that fail medical management or have severe clinical signs. Overall, the evidence supports surgical treatment for hiatal hernia, with a high success rate and low complication rate when performed by experienced surgeons.