Esophagitis

Esophagitis is the inflammation of the esophageal mucosa, which may extend into the submucosa and muscular layers. It is a common clinical entity in dogs and cats, often resulting from gastroesophageal reflux, ingestion of corrosive substances, foreign bodies, or chronic vomiting. The condition ranges from mild, self-limiting mucosal erythema to severe ulcerative or necrotizing inflammation with complications such as stricture formation, perforation, and aspiration pneumonia. Esophagitis disrupts the normal protective mechanisms of the esophagus, including the mucosal barrier, salivary bicarbonate, and lower esophageal sphincter tone, leading to pain, dysphagia, and regurgitation. Classification is based on etiology (reflux, corrosive, infectious, traumatic) and severity (mild, moderate, severe, necrotizing). Chronic esophagitis may lead to fibrosis and esophageal stricture, significantly impacting quality of life.

The primary cause of esophagitis in dogs and cats is gastroesophageal reflux (GER), which occurs when gastric acid, pepsin, and bile salts reflux into the esophagus, especially during anesthesia or in patients with hiatal hernia. Other causes include ingestion of corrosive chemicals (acids, alkalis, household cleaners), thermal injury (hot food, electrocautery), radiation therapy, foreign bodies (bones, fishhooks, toys), and trauma from esophageal intubation or nasogastric tube placement. Infectious etiologies are less common but include fungal infections (Candida spp., Aspergillus spp., Pythium insidiosum in endemic areas), viral infections (feline calicivirus, feline herpesvirus-1, canine distemper virus), and parasitic infections (Spirocerca lupi in dogs, which can cause granulomatous esophagitis). Chronic vomiting from any cause (renal disease, pancreatitis, inflammatory bowel disease) can also lead to esophagitis due to repeated exposure to gastric contents. Additionally, certain drugs, such as doxycycline and clindamycin, can cause pill-induced esophagitis if administered without adequate water or in patients with esophageal stasis. Autoimmune or immune-mediated esophagitis is rare but has been reported. Neoplastic infiltration (squamous cell carcinoma, lymphoma) can also present with secondary inflammation.

Esophagitis occurs in both dogs and cats, with no strong breed or sex predilection, although brachycephalic breeds (e.g., Bulldogs, Pugs) are predisposed to hiatal hernia and GER. Cats may be more prone to reflux esophagitis due to their relatively short esophagus and frequent vomiting. Age distribution is bimodal: young animals may develop esophagitis secondary to foreign body ingestion or congenital hiatal hernia, while older animals may have esophagitis due to chronic disease (e.g., chronic kidney disease, hyperthyroidism in cats) or neoplasia. The incidence of esophagitis is increased in patients undergoing general anesthesia, with reported rates of reflux during anesthesia up to 40% in dogs and cats. Geographic variation exists for infectious causes, such as pythiosis in the southeastern United States and spirocercosis in tropical and subtropical regions. No significant seasonal pattern is noted, except for increased foreign body ingestion during warmer months.

The esophageal mucosa is protected by a multilayered defense system including the epithelial barrier, tight junctions, mucus layer, bicarbonate secretion from submucosal glands, and salivary bicarbonate. When these defenses are overwhelmed, injury occurs. In reflux esophagitis, gastric acid (pH < 4) and pepsin directly damage epithelial cells, leading to cell necrosis and desquamation. Bile acids and pancreatic enzymes in duodenogastric reflux further exacerbate injury. The inflammatory response involves release of pro-inflammatory cytokines (IL-1, IL-6, TNF-α), recruitment of neutrophils and eosinophils, and activation of mast cells. This leads to mucosal edema, hyperemia, and ulceration. Chronic inflammation stimulates fibroblast proliferation and collagen deposition, resulting in fibrosis and stricture formation. In corrosive esophagitis, strong acids or alkalis cause coagulative or liquefactive necrosis, respectively, with potential full-thickness injury and perforation. Infectious agents may directly invade the mucosa or produce toxins. Esophageal dysmotility often develops secondary to inflammation, leading to stasis and further irritation. Aspiration of regurgitated material can cause pneumonia, a serious complication.

Predisposing factors for esophagitis include: 1) Anesthesia: general anesthesia reduces lower esophageal sphincter (LES) tone and promotes reflux; 2) Hiatal hernia: congenital or acquired, allows gastric contents to enter the esophagus; 3) Obesity: increases intra-abdominal pressure and reflux risk; 4) Chronic vomiting: from any cause, exposes esophagus to gastric acid; 5) Esophageal foreign bodies: cause direct trauma and inflammation; 6) Iatrogenic: esophageal intubation, nasogastric tube placement, or endoscopic procedures; 7) Medications: doxycycline, clindamycin, bisphosphonates, nonsteroidal anti-inflammatory drugs (NSAIDs) if given without water; 8) Dietary factors: ingestion of caustic substances, bones, or sharp objects; 9) Infectious agents: immunosuppression (e.g., feline leukemia virus, feline immunodeficiency virus) increases susceptibility to fungal or viral esophagitis; 10) Endocrine disorders: hyperthyroidism in cats may cause vomiting and reflux; 11) Neuromuscular diseases: myasthenia gravis, megaesophagus, which cause esophageal stasis and retention of food/medications.

Clinical signs of esophagitis vary with severity and duration. Peracute/acute signs include: regurgitation (often immediately after eating), excessive salivation, dysphagia (difficulty swallowing), odynophagia (painful swallowing, evidenced by crying or pawing at the mouth), repeated swallowing attempts, extension of the head and neck, and anorexia. Patients may exhibit signs of pain such as restlessness, vocalization, or reluctance to eat. Chronic esophagitis may present with weight loss, poor body condition, and intermittent regurgitation. If stricture develops, regurgitation becomes more frequent and may occur hours after eating, with undigested food. Aspiration pneumonia may cause coughing, fever, and respiratory distress. Physical examination may reveal dehydration, poor coat condition, and evidence of pain on palpation of the cervical region. In severe cases, perforation can lead to mediastinitis, pyothorax, or sepsis, with systemic signs such as fever, lethargy, and shock.

Differential diagnoses for esophagitis include: 1) Megaesophagus: characterized by diffuse esophageal dilation and hypomotility, often congenital or acquired (myasthenia gravis, myopathy); diagnosis via thoracic radiography showing air-filled esophagus; 2) Esophageal stricture: presents with progressive regurgitation, history of prior esophagitis or foreign body; confirmed by contrast radiography or endoscopy; 3) Esophageal foreign body: acute onset, often with gagging and hypersalivation; visible on radiography or endoscopy; 4) Esophageal neoplasia (squamous cell carcinoma, lymphoma): older animals, weight loss, progressive dysphagia; biopsy needed; 5) Hiatal hernia: intermittent regurgitation, often in brachycephalic breeds; diagnosed by thoracic radiography or fluoroscopy; 6) Vascular ring anomaly (persistent right aortic arch): young dogs, regurgitation of solid food after weaning; contrast esophagography shows dilation cranial to the heart base; 7) Esophagitis secondary to systemic disease (e.g., chronic kidney disease, pancreatitis): history and laboratory findings; 8) Infectious esophagitis (fungal, viral): may have systemic signs, history of immunosuppression; PCR or culture; 9) Eosinophilic esophagitis: rare, may be allergic; biopsy shows eosinophilic infiltration; 10) Gastroesophageal reflux without esophagitis: similar signs but no endoscopic lesions.

The diagnostic approach to esophagitis begins with a thorough history and physical examination. If esophagitis is suspected, initial diagnostic steps include: 1) Baseline bloodwork (CBC, serum biochemistry, urinalysis) to rule out systemic disease and assess hydration/electrolyte status; 2) Thoracic radiographs (right lateral and ventrodorsal views) to evaluate for megaesophagus, foreign bodies, masses, or aspiration pneumonia; 3) If radiographs are inconclusive, consider contrast esophagography (barium swallow) to identify mucosal irregularities, strictures, or motility disorders; 4) Esophagoscopy (upper GI endoscopy) is the gold standard for diagnosis, allowing direct visualization of mucosal erythema, erosions, ulcerations, or strictures, and enabling biopsy for histopathology; 5) If infectious etiology is suspected, obtain samples for cytology, culture, or PCR (e.g., for Candida, feline herpesvirus); 6) In cases of suspected GER, consider 24-hour esophageal pH monitoring (if available) or response to empirical antacid therapy; 7) If hiatal hernia is suspected, perform fluoroscopy during swallowing; 8) If stricture is identified, endoscopic balloon dilation may be both diagnostic and therapeutic. The algorithm should be tailored to the patient's stability; unstable patients may require stabilization before advanced imaging.

Laboratory findings in esophagitis are often nonspecific. Complete blood count (CBC) may show neutrophilia with a left shift if inflammation is severe or if aspiration pneumonia is present. Eosinophilia may be seen in parasitic or eosinophilic esophagitis. Serum biochemistry may reveal dehydration (elevated total protein, BUN, creatinine), electrolyte imbalances (hypokalemia, hypochloremia) due to vomiting or regurgitation, and metabolic alkalosis if vomiting is prominent. In chronic cases, hypoalbuminemia may occur due to protein-losing enteropathy or malnutrition. If aspiration pneumonia is present, arterial blood gas analysis may show hypoxemia. Specific biomarkers: C-reactive protein (CRP) may be elevated in inflammatory conditions. Serology or PCR for infectious agents (e.g., feline leukemia virus, feline immunodeficiency virus, feline herpesvirus, calicivirus) may be indicated. In cases of suspected myasthenia gravis (associated with megaesophagus), acetylcholine receptor antibody titers should be measured. Urinalysis is usually unremarkable unless concurrent disease exists.

Thoracic radiography may be normal in mild esophagitis. In moderate to severe cases, findings may include: 1) Esophageal dilation (if megaesophagus or stricture is present); 2) Foreign body (radiopaque objects); 3) Aspiration pneumonia (alveolar pattern in cranioventral lung lobes); 4) Soft tissue mass (neoplasia or granuloma). Contrast esophagography with barium sulfate can reveal mucosal irregularities, ulcerations, strictures, or filling defects. Fluoroscopy is useful to assess esophageal motility and identify hiatal hernia. Ultrasonography is not commonly used for esophageal evaluation but may be helpful in detecting cervical esophageal masses or foreign bodies. Computed tomography (CT) provides detailed cross-sectional imaging and is valuable for assessing extraluminal disease, such as mediastinitis or perforation. Magnetic resonance imaging (MRI) is rarely indicated but may be used for soft tissue characterization. Endoscopy is the most sensitive imaging modality for mucosal evaluation, allowing direct visualization and biopsy.

Cytological evaluation of esophageal brushings or fine-needle aspirates may reveal inflammatory cells (neutrophils, eosinophils, lymphocytes), infectious organisms (fungal hyphae, yeast), or neoplastic cells. Histopathological examination of esophageal biopsies is essential for definitive diagnosis and classification. Findings include: 1) Mucosal erosion or ulceration with loss of epithelium; 2) Neutrophilic infiltration in acute esophagitis; 3) Eosinophilic infiltration in eosinophilic esophagitis or parasitic infection; 4) Lymphocytic-plasmacytic infiltration in chronic inflammation; 5) Fibrosis and stricture formation in chronic cases; 6) Presence of fungal organisms (e.g., Candida) with special stains (PAS, GMS); 7) Viral inclusion bodies (e.g., canine distemper) in rare cases. Biopsy should be taken from multiple sites, including the distal esophagus, as reflux esophagitis is often most severe there.

Treatment of esophagitis aims to reduce inflammation, manage pain, prevent complications, and address the underlying cause. Emergency stabilization may be required for dehydration, aspiration pneumonia, or perforation. Fluid therapy with isotonic crystalloids (e.g., lactated Ringer's solution) is initiated to correct dehydration and electrolyte imbalances. Nutritional support is crucial; in severe cases, a feeding tube (esophagostomy or gastrostomy) may be placed to bypass the esophagus and allow enteral nutrition. Medical therapy includes: 1) Gastric acid suppression: proton pump inhibitors (PPIs) such as omeprazole (0.7-1.0 mg/kg PO q12h) or pantoprazole (0.7-1.0 mg/kg IV q12h) are preferred over H2 blockers for severe esophagitis; 2) Mucosal protectants: sucralfate (0.5-1 g per dog, 250-500 mg per cat, PO q8h) forms a protective barrier over ulcers; 3) Prokinetic agents: metoclopramide (0.2-0.4 mg/kg PO/SC q8h) or cisapride (0.5 mg/kg PO q8h) to increase LES tone and promote gastric emptying; 4) Analgesics: opioids (e.g., buprenorphine 0.01-0.02 mg/kg IV/IM q8h) for pain control; 5) Antibiotics: if aspiration pneumonia or perforation is suspected, broad-spectrum antibiotics (e.g., amoxicillin-clavulanate 12.5-25 mg/kg PO q12h) are indicated; 6) Corticosteroids: controversial, but may be used in severe inflammatory esophagitis to reduce fibrosis (e.g., prednisone 0.5-1 mg/kg PO q24h, tapering); 7) Antifungals: for fungal esophagitis (e.g., fluconazole 5-10 mg/kg PO q12h for Candida); 8) Surgical intervention: required for foreign body removal, hiatal hernia repair, or resection of strictures (balloon dilation is preferred for strictures). Dietary management includes feeding a bland, low-fat, easily digestible diet in small, frequent meals, and avoiding dry kibble if dysphagia is present.

The prognosis for esophagitis depends on the underlying cause, severity, and presence of complications. Mild reflux esophagitis often resolves with appropriate medical therapy within 1-2 weeks. Severe ulcerative esophagitis carries a guarded prognosis, especially if stricture formation occurs. Esophageal strictures can be managed with repeated balloon dilation, but recurrence is common, and some patients require long-term feeding tubes. Perforation is a life-threatening complication with a poor prognosis, often requiring surgical intervention and intensive care. Infectious esophagitis (e.g., pythiosis) has a guarded to poor prognosis, especially if systemic involvement is present. Overall, with prompt and aggressive treatment, many patients recover, but chronic cases may have persistent dysphagia and regurgitation. Negative prognostic indicators include: presence of stricture, aspiration pneumonia, perforation, and underlying systemic disease.

Follow-up care for esophagitis includes: 1) Recheck examination within 7-14 days to assess clinical response; 2) Serial monitoring of body weight, hydration status, and nutritional intake; 3) Repeat thoracic radiographs if aspiration pneumonia was present; 4) Endoscopic re-evaluation in 2-4 weeks for severe cases to assess mucosal healing and detect stricture formation; 5) If a stricture is dilated, repeat dilation may be needed every 1-2 weeks initially, then at increasing intervals; 6) Long-term management may include continued use of PPIs or prokinetics, dietary modifications, and weight management; 7) Owners should be educated on signs of recurrence (regurgitation, dysphagia) and when to seek immediate veterinary care; 8) For patients with underlying conditions (e.g., hiatal hernia, chronic kidney disease), regular monitoring of the primary disease is essential.

Pearls: 1) Always consider esophagitis in any patient with regurgitation, especially after anesthesia; 2) Endoscopy is the gold standard for diagnosis; do not rely solely on radiographs; 3) Aggressive acid suppression with PPIs is more effective than H2 blockers; 4) Sucralfate should be given on an empty stomach, at least 1 hour before or 2 hours after other medications; 5) In cats, doxycycline should always be followed by water or food to prevent pill esophagitis; 6) Early intervention with feeding tubes can prevent malnutrition and aspiration. Pitfalls: 1) Mistaking regurgitation for vomiting; regurgitation is passive and lacks abdominal effort; 2) Using corticosteroids indiscriminately, which may delay healing and increase risk of infection; 3) Failing to address underlying causes (e.g., hiatal hernia, chronic vomiting); 4) Overlooking aspiration pneumonia, which may be silent; 5) Inadequate pain management, leading to anorexia and weight loss; 6) Not performing serial dilations for strictures, leading to recurrence.

Based on Plumb's Veterinary Drug Handbook, the following protocols are recommended: 1) Omeprazole: Dogs: 0.7-1.0 mg/kg PO q12h; Cats: 0.7-1.0 mg/kg PO q12h; for severe reflux, may use IV pantoprazole 0.7-1.0 mg/kg q12h. 2) Sucralfate: Dogs: 0.5-1 g PO q8h; Cats: 250-500 mg PO q8h; administer as slurry on empty stomach. 3) Metoclopramide: Dogs: 0.2-0.4 mg/kg PO/SC q8h; Cats: 0.2-0.4 mg/kg PO/SC q8h; can be given as CRI at 1-2 mg/kg/day. 4) Cisapride: Dogs: 0.5 mg/kg PO q8h; Cats: 0.5 mg/kg PO q8h; use with caution due to cardiac effects. 5) Buprenorphine: Dogs: 0.01-0.02 mg/kg IV/IM q8h; Cats: 0.01-0.02 mg/kg IV/IM q8h. 6) Amoxicillin-clavulanate: Dogs: 12.5-25 mg/kg PO q12h; Cats: 12.5-25 mg/kg PO q12h; for aspiration pneumonia, use for 7-10 days. 7) Prednisone: Dogs: 0.5-1 mg/kg PO q24h, tapering over 2-4 weeks; Cats: 0.5-1 mg/kg PO q24h, tapering; only if severe inflammation and no contraindications. 8) Fluconazole: Dogs: 5-10 mg/kg PO q12h; Cats: 5-10 mg/kg PO q12h; for Candida esophagitis, treat for 2-4 weeks. 9) For pain, consider gabapentin (10-20 mg/kg PO q8-12h) for neuropathic pain. Adjust dosages in renal or hepatic impairment; monitor for drug interactions (e.g., omeprazole may increase levels of diazepam, warfarin).

Evidence-based literature supports the use of proton pump inhibitors over H2 blockers for the treatment of reflux esophagitis in dogs and cats. A study by Bersenas et al. (2005) demonstrated that omeprazole significantly increased gastric pH compared to famotidine in healthy dogs. In cats, a study by Parkinson et al. (2015) showed that omeprazole was more effective than famotidine in maintaining intragastric pH > 3. Sucralfate has been shown to promote ulcer healing in experimental models. Prokinetic agents like metoclopramide and cisapride are commonly used, though evidence for their efficacy in esophagitis is limited; cisapride has been shown to increase LES pressure in dogs. For esophageal strictures, balloon dilation is the treatment of choice, with success rates reported between 70-90% in dogs and cats, though repeat dilations are often necessary. A retrospective study by Leib et al. (2002) found that 50% of dogs with benign esophageal strictures required multiple dilations. The use of intralesional corticosteroids (triamcinolone) may reduce stricture recurrence, but evidence is anecdotal. For infectious esophagitis, treatment should be based on culture and sensitivity; pythiosis carries a poor prognosis, with surgical resection being the primary treatment. Consensus guidelines from ACVIM and ECVIM recommend early endoscopic evaluation in suspected esophagitis to guide therapy and monitor for complications.