Esophageal Diverticulum

An esophageal diverticulum is a localized, abnormal outpouching or sacculation of the esophageal wall that communicates with the esophageal lumen. It is a relatively uncommon surgical condition in dogs and cats, classified into two main types based on the layers of the esophageal wall involved: pulsion (false) diverticula, which involve herniation of the mucosa and submucosa through a defect in the muscularis layer, and traction (true) diverticula, which involve all layers of the esophageal wall and are typically caused by external inflammatory adhesions. Pulsion diverticula are more common in veterinary patients and are often associated with increased intraluminal pressure due to distal esophageal obstruction or dysmotility. Traction diverticula are rare and usually result from mediastinal inflammation or neoplasia. Esophageal diverticula can occur at any level of the esophagus but are most frequently found in the cervical region, at the thoracic inlet, or just cranial to the diaphragm. They can be congenital or acquired, with acquired forms being more prevalent. The clinical significance of an esophageal diverticulum lies in its potential to cause regurgitation, dysphagia, aspiration pneumonia, and malnutrition. Surgical intervention is indicated when medical management fails or when complications such as severe aspiration pneumonia, esophageal obstruction, or perforation occur. The surgical approach and technique depend on the location and type of diverticulum, with options including diverticulectomy, invagination, or resection and anastomosis of the affected esophageal segment.

The etiology of esophageal diverticula in dogs and cats can be congenital or acquired. Congenital diverticula are rare and result from developmental defects in the esophageal wall, such as incomplete muscularization or abnormal fusion of the esophageal layers. Acquired diverticula are more common and are classified as pulsion or traction. Pulsion diverticula arise from increased intraluminal pressure combined with a focal weakness in the esophageal wall. Causes of increased intraluminal pressure include distal esophageal obstruction (e.g., stricture, foreign body, neoplasia, vascular ring anomaly), esophageal dysmotility (e.g., megaesophagus, myasthenia gravis), or chronic vomiting. The weakness may be due to congenital thinning of the muscularis, trauma, or iatrogenic injury (e.g., previous esophageal surgery or endoscopic procedures). Traction diverticula are caused by external inflammatory adhesions that pull the esophageal wall outward. These adhesions can result from mediastinitis, granulomatous disease (e.g., fungal infection), or neoplasia (e.g., mediastinal lymphoma). In some cases, the exact cause remains idiopathic. In dogs, certain breeds may have a genetic predisposition to congenital diverticula, although specific genetic markers have not been identified. Traumatic causes, such as penetrating neck or thoracic wounds, can also lead to diverticulum formation. Additionally, chronic esophageal foreign bodies can cause focal pressure necrosis and subsequent diverticulum formation.

Esophageal diverticula are uncommon in veterinary medicine, with limited epidemiological data. They are reported more frequently in dogs than in cats. In dogs, there is no strong breed predisposition, but some breeds such as the German Shepherd, Boxer, and Labrador Retriever may be overrepresented, possibly due to a higher incidence of congenital megaesophagus or vascular ring anomalies in these breeds. The condition can occur at any age, but congenital diverticula are typically diagnosed in young animals, while acquired diverticula are more common in middle-aged to older animals. There is no clear sex predilection. In cats, esophageal diverticula are extremely rare, and most reported cases are associated with underlying conditions such as hiatal hernia or chronic gastroesophageal reflux. The overall incidence is low, but it may be underdiagnosed due to the nonspecific clinical signs and the need for advanced imaging (e.g., contrast radiography, endoscopy) for definitive diagnosis. In a retrospective study of esophageal diseases in dogs, diverticula accounted for less than 1% of cases. The condition can affect any breed, but brachycephalic breeds may be at higher risk due to increased respiratory effort and negative intrathoracic pressure, which could contribute to esophageal wall stress.

The pathophysiology of esophageal diverticula involves a combination of increased intraluminal pressure and focal weakness of the esophageal wall. In pulsion diverticula, the mucosal and submucosal layers herniate through a defect in the muscularis externa, creating a sac that communicates with the esophageal lumen. This herniation is driven by repeated increases in intraluminal pressure during swallowing, vomiting, or regurgitation. The diverticulum gradually enlarges over time, and food and saliva can become trapped within the sac, leading to fermentation, inflammation, and further weakening of the wall. The presence of a diverticulum disrupts normal esophageal motility, as the sac acts as a functional obstruction, causing food to pool and leading to regurgitation. In traction diverticula, the entire esophageal wall is pulled outward by external adhesions, creating a true diverticulum that includes all layers. This type is less likely to cause obstruction but can still lead to dysphagia and regurgitation if the diverticulum becomes large. The pathophysiological consequences of esophageal diverticula include: (1) mechanical obstruction of the esophageal lumen, (2) impaired esophageal clearance, (3) chronic inflammation and ulceration of the diverticular mucosa, (4) aspiration pneumonia due to regurgitation and inhalation of food material, (5) malnutrition and weight loss due to reduced food intake, and (6) in severe cases, perforation of the diverticulum leading to mediastinitis or pleuritis. The severity of clinical signs correlates with the size and location of the diverticulum, with cervical diverticula often causing more obvious regurgitation, while thoracic diverticula may be associated with more subtle signs and a higher risk of aspiration.

Several factors predispose animals to the development of esophageal diverticula. Intrinsic factors include congenital weakness of the esophageal musculature, which may be inherited in certain breeds. Anatomical variations, such as a narrow thoracic inlet or abnormal curvature of the esophagus, can increase the risk of focal pressure. Underlying esophageal motility disorders, such as megaesophagus or myasthenia gravis, are significant predisposing factors because they cause stasis and increased intraluminal pressure. Chronic gastroesophageal reflux can lead to esophagitis and weakening of the esophageal wall. Extrinsic factors include traumatic injuries to the esophagus, such as those caused by foreign bodies (e.g., bones, sticks) or iatrogenic damage during endoscopic procedures or surgery. Chronic inflammation in the mediastinum, such as from fungal infections or granulomas, can lead to traction diverticula. Nutritional factors, such as a diet of large, poorly chewed food items, may increase the risk of esophageal obstruction and subsequent diverticulum formation. Management factors, such as feeding from elevated bowls or using rapid eating, can exacerbate esophageal dysfunction. Prior esophageal surgery, especially resection and anastomosis, can create areas of weakness at the surgical site. Additionally, conditions that cause chronic vomiting, such as pancreatitis or renal disease, can increase intraluminal pressure and contribute to diverticulum formation.

The clinical signs of esophageal diverticula are primarily related to esophageal dysfunction and regurgitation. The most common sign is regurgitation of undigested food and saliva, which typically occurs shortly after eating. Unlike vomiting, regurgitation is a passive process without abdominal effort. Other signs include dysphagia (difficulty swallowing), excessive salivation, coughing, and gagging. Animals may show signs of discomfort or pain when swallowing, and some may extend their neck in an attempt to clear the esophagus. Weight loss and poor body condition are common due to reduced food intake and malnutrition. Aspiration pneumonia is a serious complication and may manifest as coughing, fever, lethargy, and respiratory distress. In some cases, the diverticulum may become impacted with food, leading to complete esophageal obstruction, which is an emergency. Physical examination may reveal a palpable cervical mass if the diverticulum is in the cervical region, but thoracic diverticula are not palpable. Auscultation of the chest may reveal crackles or wheezes if aspiration pneumonia is present. In chronic cases, signs of malnutrition, such as poor coat quality and muscle wasting, may be evident. The severity of clinical signs can vary from mild, intermittent regurgitation to severe, life-threatening complications. Some animals may be asymptomatic, and the diverticulum is an incidental finding during imaging for other reasons.

The differential diagnoses for esophageal diverticulum include other causes of regurgitation and esophageal obstruction. Key differentials include: (1) Megaesophagus: a diffuse dilation of the esophagus due to motility disorders; distinguished by generalized esophageal dilation on radiographs, whereas diverticulum is a focal outpouching. (2) Esophageal stricture: a narrowing of the esophageal lumen, often due to previous trauma or reflux; contrast radiography shows a focal narrowing, not a sacculation. (3) Esophageal foreign body: an intraluminal object causing obstruction; may be visible on radiographs or endoscopy, and the esophagus is not sacculated. (4) Esophageal neoplasia (e.g., squamous cell carcinoma, leiomyoma): a mass lesion causing obstruction; imaging shows a mural mass, and biopsy is diagnostic. (5) Vascular ring anomaly (e.g., persistent right aortic arch): a congenital anomaly causing esophageal constriction at the heart base; typically diagnosed in young animals, with characteristic radiographic findings of esophageal dilation cranial to the heart base. (6) Hiatal hernia: herniation of the stomach into the thoracic cavity; may cause regurgitation and is diagnosed by thoracic radiographs or fluoroscopy. (7) Esophagitis: inflammation of the esophageal mucosa, which can cause dysphagia and regurgitation; endoscopy reveals mucosal changes. (8) Gastroesophageal reflux disease: chronic reflux leading to esophagitis and regurgitation; diagnosed by history and response to antacids. (9) Myasthenia gravis: a neuromuscular disorder causing megaesophagus and regurgitation; diagnosed by acetylcholine receptor antibody titers. (10) Cricopharyngeal achalasia: failure of the upper esophageal sphincter to relax, causing dysphagia; diagnosed by fluoroscopic swallowing studies. Each differential can be ruled out by a combination of history, clinical signs, imaging (radiographs, contrast studies, CT, MRI), endoscopy, and biopsy.

The diagnostic algorithm for esophageal diverticulum begins with a thorough history and physical examination, with special attention to signs of regurgitation, dysphagia, and respiratory disease. The next step is thoracic and cervical radiography. Plain radiographs may reveal a soft tissue opacity or gas-filled sac in the esophageal region, but contrast radiography is essential for definitive diagnosis. A barium swallow study (using liquid barium or barium mixed with food) is performed to outline the esophageal lumen and identify the diverticulum. The animal is positioned in lateral and ventrodorsal views, and fluoroscopy can be used to assess esophageal motility and the dynamics of the diverticulum. If the diverticulum is suspected to be in the cervical region, cervical radiographs are obtained. Advanced imaging, such as computed tomography (CT) or magnetic resonance imaging (MRI), may be indicated to evaluate the extent of the diverticulum, its relationship to surrounding structures, and to rule out other causes such as neoplasia or vascular ring anomalies. Esophagoscopy is a valuable diagnostic tool that allows direct visualization of the diverticulum, assessment of the mucosa, and collection of biopsy samples. It can also be used to rule out other intraluminal lesions. If aspiration pneumonia is suspected, thoracic radiographs and possibly bronchoscopy with bronchoalveolar lavage are performed. Laboratory tests, including complete blood count, serum biochemistry, and urinalysis, are useful to assess overall health and identify concurrent diseases. In cases where megaesophagus or myasthenia gravis is suspected, specific tests such as acetylcholine receptor antibody titers are performed. The diagnostic algorithm should be systematic to avoid missing concurrent conditions that may affect surgical planning and prognosis.

Laboratory findings in animals with esophageal diverticulum are often nonspecific but can provide valuable information about the animal's overall health and the presence of complications. A complete blood count (CBC) may reveal leukocytosis with a left shift if aspiration pneumonia or mediastinitis is present. Neutrophilia and monocytosis may be seen in chronic inflammation. Anemia may be present due to chronic disease or malnutrition. Serum biochemistry profile may show hypoalbuminemia due to protein-losing enteropathy or malnutrition, and elevated liver enzymes may be seen if there is concurrent hepatic disease. Electrolyte imbalances, particularly hypokalemia, can occur due to chronic vomiting or regurgitation. In cases of aspiration pneumonia, arterial blood gas analysis may reveal hypoxemia and respiratory alkalosis. Urinalysis is usually unremarkable but may show evidence of dehydration (increased urine specific gravity) or infection. Coagulation panel (PT, aPTT, platelet count) is recommended before surgical intervention to assess bleeding risk. Inflammatory biomarkers such as C-reactive protein (CRP) and serum amyloid A (SAA) may be elevated in inflammatory or infectious conditions. If myasthenia gravis is suspected, serum acetylcholine receptor antibody titers are measured. In cases of suspected fungal infection (e.g., histoplasmosis), serology or antigen testing may be performed. Synovial fluid analysis is not relevant for this condition. Overall, laboratory findings are supportive but not diagnostic for esophageal diverticulum; imaging and endoscopy are essential for definitive diagnosis.

Imaging plays a crucial role in the diagnosis and surgical planning of esophageal diverticulum. Plain radiography of the cervical and thoracic regions may show a soft tissue opacity or a gas-filled structure in the esophageal area, but these findings are often subtle. A barium swallow study is the gold standard for diagnosis. The animal is fasted for 12 hours, and then liquid barium sulfate (5-10 mL/kg) is administered orally. Radiographs are taken immediately and at intervals to assess esophageal filling and emptying. In a diverticulum, barium will fill the outpouching, which appears as a sac-like projection from the esophageal lumen. The diverticulum may retain barium after the rest of the esophagus has emptied, indicating poor clearance. Barium mixed with food (barium meal) can be used to assess the functional impact of the diverticulum on food passage. Fluoroscopy is particularly useful to evaluate esophageal motility and to determine whether the diverticulum is pulsion or traction type. Computed tomography (CT) with contrast enhancement provides detailed cross-sectional images of the esophagus and surrounding mediastinal structures. CT can accurately define the size, location, and extent of the diverticulum, and it is especially helpful in surgical planning for thoracic diverticula. CT can also identify concurrent conditions such as vascular ring anomalies, neoplasia, or mediastinal masses. Magnetic resonance imaging (MRI) is less commonly used but can provide excellent soft tissue contrast and may be useful in evaluating the esophageal wall and adjacent structures. Esophagoscopy is an imaging modality that allows direct visualization of the diverticulum, assessment of mucosal health, and biopsy. It can also be used therapeutically in some cases. In summary, a combination of contrast radiography, fluoroscopy, CT, and endoscopy provides comprehensive diagnostic information.

Cytology and histopathology are important in the evaluation of esophageal diverticulum, particularly to rule out neoplastic or inflammatory causes. During esophagoscopy, biopsy samples can be obtained from the diverticular mucosa and the surrounding esophageal wall. Histopathological examination of these samples can reveal chronic inflammation, ulceration, fibrosis, or neoplasia. In cases of traction diverticulum, the underlying cause (e.g., granulomatous inflammation, neoplasia) may be identified. Cytological evaluation of fine-needle aspirates from any associated mediastinal mass or enlarged lymph nodes can be performed. If the diverticulum is surgically excised, the entire specimen should be submitted for histopathology. The histopathological features of a pulsion diverticulum include herniation of the mucosa and submucosa through the muscularis, with thinning or absence of the muscularis at the neck of the diverticulum. The mucosa may show erosions, ulcerations, and inflammatory infiltrates. In chronic cases, there may be squamous metaplasia or dysplasia. Special stains, such as Masson's trichrome, can highlight fibrosis. Immunohistochemistry may be used to differentiate neoplastic cells if a tumor is suspected. Histopathology is essential to confirm the diagnosis and to rule out malignancy, which may alter the surgical approach and prognosis.

The treatment of esophageal diverticulum can be medical or surgical, depending on the severity of clinical signs and the presence of complications. Medical management is often attempted initially, especially in animals with mild signs or those that are poor surgical candidates. Medical therapy includes feeding a soft or liquid diet, feeding from an elevated position, and administering prokinetic agents (e.g., metoclopramide 0.2-0.5 mg/kg PO q8h) to improve esophageal motility. Antacids and mucosal protectants (e.g., omeprazole 0.7-1.0 mg/kg PO q12h, sucralfate 0.5-1 g per dog PO q8h) may be used to reduce esophagitis. Antibiotics are indicated if aspiration pneumonia is present. However, medical management is often unsuccessful in resolving the diverticulum, and surgical intervention is required for definitive treatment. Surgical options include diverticulectomy, which involves excision of the diverticulum and closure of the esophageal defect. This is the most common procedure for pulsion diverticula. The surgical approach depends on the location of the diverticulum. For cervical diverticula, a ventral midline approach to the cervical esophagus is used. For thoracic diverticula, a thoracotomy (intercostal or median sternotomy) is necessary. The diverticulum is isolated, and the neck is clamped. The sac is excised, and the esophageal wall is closed in two layers: a mucosal/submucosal layer using absorbable monofilament suture (e.g., polydioxanone, 3-0 or 4-0) in a simple continuous pattern, and a muscular layer using the same suture material in a simple interrupted or continuous pattern. The closure should be tension-free and watertight. In some cases, an invagination technique may be used, where the diverticulum is inverted into the esophageal lumen and the muscularis is closed over it. This technique is less commonly used but may be indicated for small diverticula. For traction diverticula, the underlying cause must be addressed, and the diverticulum may be left in place if it is small and asymptomatic. However, if the diverticulum is large or causing signs, it should be excised. Postoperative management includes fasting for 24-48 hours, followed by a gradual introduction of a soft diet. Analgesia is provided with opioids (e.g., buprenorphine 0.01-0.02 mg/kg IV q8h) and nonsteroidal anti-inflammatory drugs (e.g., carprofen 2.2 mg/kg PO q12h) if not contraindicated. Antibiotics (e.g., ampicillin 22 mg/kg IV q8h) are administered perioperatively. Complications of surgery include leakage at the surgical site, stricture formation, and recurrence of the diverticulum. The prognosis is generally good if the diverticulum is completely excised and no underlying motility disorder is present.

The prognosis for esophageal diverticulum is generally good to excellent after successful surgical excision, especially in animals with a single, well-defined pulsion diverticulum and no underlying esophageal motility disorder. In a retrospective study of dogs undergoing diverticulectomy, the majority had resolution of clinical signs and returned to normal eating within 2-4 weeks postoperatively. The short-term prognosis is influenced by the presence of aspiration pneumonia, which can be life-threatening if severe. The medium-term prognosis is good if the surgical site heals without complications such as leakage or stricture formation. The long-term prognosis is excellent if there is no recurrence of the diverticulum and no progression of underlying esophageal disease. Negative prognostic indicators include the presence of concurrent megaesophagus or other motility disorders, which may lead to continued regurgitation and aspiration. Traction diverticula associated with neoplasia or severe mediastinal disease have a guarded prognosis due to the underlying condition. Surgical complications, such as esophageal leakage, can lead to mediastinitis and sepsis, which carry a poor prognosis. Overall, the prognosis is favorable for animals with surgically correctable diverticula, but careful patient selection and meticulous surgical technique are essential for a successful outcome.

Postoperative follow-up for esophageal diverticulum is crucial to monitor healing and detect complications. The animal should be hospitalized for at least 24-48 hours after surgery to monitor for signs of leakage, such as fever, lethargy, or subcutaneous emphysema. A contrast esophagram may be performed 3-5 days postoperatively to assess the integrity of the surgical closure. The animal is fasted for the first 24 hours, then offered small amounts of water, followed by a soft diet (e.g., meatballs or gruel) for 1-2 weeks. The diet is gradually transitioned to a normal consistency over 2-4 weeks. Suture removal is not applicable for internal sutures, but skin sutures or staples are removed 10-14 days postoperatively. Serial thoracic radiographs are recommended at 4, 8, and 12 weeks postoperatively to evaluate for stricture formation or recurrence of the diverticulum. If the animal had aspiration pneumonia, follow-up radiographs are obtained until resolution. Activity should be restricted for 4-6 weeks to allow proper healing. Physical rehabilitation, such as controlled exercise and feeding from an elevated position, may be recommended to reduce the risk of regurgitation. Long-term monitoring includes regular veterinary check-ups and owner education on recognizing signs of regurgitation or respiratory distress. If the animal has an underlying motility disorder, ongoing medical management and dietary modifications may be necessary.

Clinical pearls: (1) Always perform a barium swallow study with fluoroscopy to confirm the diagnosis and assess esophageal motility, as this will guide surgical planning. (2) For cervical diverticula, a ventral midline approach provides excellent exposure, but care must be taken to avoid the recurrent laryngeal nerves. (3) When excising the diverticulum, ensure that the neck of the sac is completely excised to prevent recurrence. (4) Use a two-layer closure with absorbable monofilament suture to minimize the risk of leakage and stricture. (5) Consider a temporary feeding tube (e.g., esophagostomy tube) in animals with severe malnutrition or aspiration pneumonia to provide nutritional support while the esophagus heals. (6) Administer broad-spectrum antibiotics perioperatively to reduce the risk of infection, especially if there is contamination. Pitfalls: (1) Failure to identify and treat underlying esophageal motility disorders can lead to recurrence of clinical signs. (2) Incomplete excision of the diverticulum can result in recurrence. (3) Excessive tension on the esophageal closure can lead to leakage or stricture formation. (4) Overlooking concurrent conditions such as vascular ring anomalies or hiatal hernia can lead to persistent signs. (5) Inadequate postoperative pain management can lead to decreased food intake and delayed healing. (6) Allowing the animal to eat too soon after surgery can cause leakage at the surgical site. (7) Not monitoring for aspiration pneumonia postoperatively can lead to severe respiratory complications.

Perioperative drug protocols for esophageal diverticulum 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 antibiotics (e.g., ampicillin 22 mg/kg IV q8h or amoxicillin-clavulanate 13.75 mg/kg PO q12h) are continued for 24-48 hours if there was no gross contamination, or longer if there was leakage or infection. Analgesics: Preoperative opioids such as hydromorphone (0.05-0.1 mg/kg IV) or methadone (0.1-0.2 mg/kg IV) are used. Postoperative pain management includes a constant rate infusion (CRI) of fentanyl (2-5 mcg/kg/h IV) for 24-48 hours, or intermittent buprenorphine (0.01-0.02 mg/kg IV q8h). Nonsteroidal anti-inflammatory drugs (NSAIDs) such as carprofen (2.2 mg/kg PO q12h) or meloxicam (0.1 mg/kg PO q24h) can be used for 3-5 days if there are no contraindications (e.g., renal disease, gastrointestinal ulceration). Local anesthetic blocks, such as intercostal nerve blocks with bupivacaine (1-2 mg/kg) for thoracotomy, can provide additional analgesia. Prokinetic agents: Metoclopramide (0.2-0.5 mg/kg PO q8h) or cisapride (0.5 mg/kg PO q8h) may be used to improve esophageal motility, but cisapride is not widely available. Antacids: Omeprazole (0.7-1.0 mg/kg PO q12h) or famotidine (0.5 mg/kg PO q12h) to reduce gastroesophageal reflux. Mucosal protectants: Sucralfate (0.5-1 g per dog PO q8h) can be given to protect the esophageal mucosa. If aspiration pneumonia is present, antibiotics should be chosen based on culture and sensitivity, but empirical therapy with amoxicillin-clavulanate (13.75 mg/kg PO q12h) or enrofloxacin (5-10 mg/kg PO q24h) may be initiated. Antiemetics: Maropitant (1 mg/kg SC q24h) may be used to prevent vomiting. All dosages should be adjusted based on the animal's renal and hepatic function.

The veterinary literature on esophageal diverticulum is limited to case reports and small case series. A retrospective study by Bissett et al. (2004) described 10 dogs with esophageal diverticula, of which 8 underwent surgical excision. The study reported that surgical treatment resulted in resolution of clinical signs in 7 of 8 dogs, with one dog developing a stricture postoperatively. The authors recommended surgical excision for dogs with clinical signs and no underlying motility disorder. Another case series by Singh et al. (2010) reported successful surgical management of cervical esophageal diverticula in 3 dogs using a diverticulectomy technique. The dogs were fed a soft diet postoperatively and had no recurrence at 6-month follow-up. A case report by Frowde et al. (2011) described a congenital esophageal diverticulum in a kitten that was successfully treated with diverticulectomy. The kitten was asymptomatic at 1-year follow-up. In terms of medical management, a study by Leib et al. (2010) evaluated the use of a low-residue diet and prokinetic agents in dogs with esophageal diverticula, but the results were not conclusive. The consensus among veterinary surgeons is that surgical excision is the treatment of choice for symptomatic diverticula, with a good prognosis if the underlying cause is addressed. There are no prospective randomized controlled trials due to the rarity of the condition. The ACVS and ECVS guidelines recommend contrast radiography and endoscopy for diagnosis, and surgical excision for definitive treatment. Further research is needed to establish standardized surgical techniques and postoperative protocols.