Anesthesia and surgery in megaesophagus patients:
When a patient with megaesophagus requires anesthesia there are some precautions which are suggested to minimize reflux of stomach contents into the esophagus, therefore minimizing aspiration pneumonia. Pretreating one half hour before anesthesia induction with metoclopromide in those dogs who can tolerate it, will encourage the stomach to empty. Elevating the head end of the surgical table, or placing the patient on a slant, so that the head is above the rear end, minimizes reflux of stomach contents into the esophagus. Leaving the endotracheal tube in until the dog is very actively swallowing, to minimize aspiration, is important. Maintaining elevation of the front end of the pet, preferably in a vertical position (body perpendicular to the floor), while recovering from anesthesia allows any fluid that accumulates in the esophagus to “drain” into the stomach. Any fluid build-up in the esophagus can be easily refluxed and precipitate aspiration pneumonia in dogs with megaesophagus.

Some hospitals assign an assistant or technician to keep the pet elevated, others allow the owner to hold the pet as soon as it is extubated. Prevention of regurgitation, at all costs is paramount in these pets.

It may be a consideration to have the owner give liquid carafate for a few days after surgery, just in case of esophagitis secondary to unavoidable reflux.

Submitted by Dr. Kathy
November 29, 2007

Note from Dr. Kathy – thankfully, these complications occur very rarely, but, every veterinarian, technician and owner need to be aware that they can occur. We weigh the risks versus the benefits of the procedure.

Perioperative Gastrointestinal Complications:
by R M Bright

Every surgical or anesthetic experience has the potential for some form of gastrointestinal complication. The complication may or may not have some relationship with the primary disease of the patient. Gastroduodenal ulcers (GDU) & aspiration pneumonia are all complications that could be life threatening and therefore deserve our attention.

Benign gastroduodenal ulcers result when the aggressive effects of acid and pepsin overwhelm the protective factors related to mucosal resistance. Etiopathogenesis of ulcer disease focuses on 3 general areas: deficits in mucosal resistance to acid; hypersecretory acid state; defects in endocrine control mechanisms. All are known to predispose dogs to GDU. The recognition of GDU is likely increasing due to better means of diagnosis and the increased use of non-steroidal antinflammatory drugs ( NSAIDs). Ulcer perforation followed by septic peritonitis is the most common complications related to GDU.The frequent use of (NSAIDs) is a common and well-studied cause of GDU in the dog. Hepatopathy, uremia, compromised blood supply to the stomach (GDV, shock), spinal cord diseases, use of corticosteroids, hypoadrenocorticoidism, and increased duodenogastric reflux are all underlying factors related to GDU. A hypersecretory state related to a gastrinoma (Zollinger-Ellison syndrome) or mast cell tumor (hyperhistaminia) can also predispose the dog to GDU.

Clinical signs related to GDU include vomiting with or without blood, melena, inappetance, abdominal discomfort, and pale mucous membranes. Clinicopathologic data are not specific for GDU but may help identify an underlying cause. Hypoalbuminemia may be present and would be associated with blood loss,
hepatorenal disease or a malabsorption problem. A hypochromic microcytic anemia is seen in the vast majority of serious GDU cases and explains the pallor often seen with ulcer disease. Gastrin levels are elevated in the rare Zollinger-Ellison syndrome. This functional non-islet pancreatic tumor should be suspected in those dogs with confirmed GDU that do not respond to aggressive medical therapy.

Since clinical and laboratory evaluations are not specific for ulcer disease, additional diagnostic tests are necessary. Survey radiography is usually not helpful but the addition of a contrast agent (barium) may help outline an ulcer crater. It may assist in ruling out other diseases such as neoplasia, foreign bodies, etc. Endoscopy yields a more definitive diagnosis than does radiography. In addition, biopsies can be taken to rule out neoplastic disease.

Identifying potential predisposing causes of GDU aids therapeutic decisions. The goals of antiulcer therapy are to decrease secretion of stomach acid, maintain mucosal blood flow, stimulate normal secretion of bicarbonate and mucus and stimulate normal mucosal cell turnover and repair. Decreasing acid secretion is probably important in promoting ulcer healing. Other micro environmental factors that facilitate healing include healthy mucous cells, normal mucus, bicarbonate, and healthy capillaries.

Acid production is dramatically decreased when the histamine (H2) receptor on the parietal cell is blocked by an antagonist. H2 antagonists include cimetidine, ranitidine, and famotidine. All three are available in oral or injectable forms. The injectable form is indicated in those animals that are vomiting and hospitalized. The dose of ranitidine is 0.5 mg/kg IV or PO q 8-12 hours; for famotidine, the dose is 0.5 mg/kg q 12 hours, IV, SC or PO. The newer anti-ulcer agent, omeprazole, is a potent inhibitor of gastric acid secretion that works by interfering with the H+/K+ proton pump. The dose is 0.7 mg/kg once daily and inhibits acid secretion efficiently for 24 hours. I generally prefer to start with an H2 receptor antagonist and if after 48 hours there is no improvement in clinical signs, I will substitute omeprazole. Unfortunately, omeprazole is available only in the oral form.

Another form of therapy is aimed at cytoprotection. Sucralfate is a cytoprotective drug that exerts its effects locally by providing a gel-like barrier to the effects of acid and pepsin on the mucosa. In addition, it has the ability to decrease pepsin activity and adsorb bile acids. It also increases mucus bicarbonate secretion and blood flow to the mucosal cells. The effects are thought to be mediated by increasing the synthesis of the prostaglandin, PGE2.

NSAID-induced ulcers may benefit from the effects of misoprostol, a synthetic prostaglandin E analog. It has been shown to be effective against NSAID-induced injury in dogs, but does not protect against the effects of corticosteroid on the gastric mucosa at a dose of 4-6 ug/kg PO q8h (CR Rohrer et al, AJVR 60 1999, p.982). Prostaglandins have important regulatory functions for gastric flow, bicarbonate and mucus secretion, and epithelial cell hydrophobicity , all of which are necessary to maintain a healthy GI mucosa. The recommended dose is 2-5 ug/kg every 8-12 hours. Avoid its use in pregnant animals.

Aspiration pneumonia is one of the most feared complications that may accompany anesthesia and/or surgery. The awake dog is protected from aspiration by laryngeal closure, coughing, and breath holding. However, under the influence of drugs, these protective mechanisms are weak. Aspiration of esophageal or gastric contents can occur as a result of vomiting, an active process occurring in a light plane of anesthesia. Just prior to vomiting, swallowing or gagging movements may be noted.

There are a number of factors that increase the risk of regurgitation or vomiting. These include elevated intragastric pressure caused by insufficient duration of fasting; delayed gastric emptying associated with pregnancy and Caesarian section; recent injury; beta-adrenergic agents; narcotics; pain; anticholinergic agents. Increased intraabdominal can increase the risk of aspiration and can be associated with obesity, pregnancy, gastrointestinal distention, and a tight abdominal bandage. Other factors are related to esophageal retention of fluid associated with hiatal hernias, megaesophagus, or diaphragmatic hernias. Finally, other risk factors are associated with lower esophageal tone seen with the use of narcotics, beta-adrenergic drugs, anticholinergic agents, hiatal or traumatic diaphragmatic hernias, and certain tranquilizers.

Under anesthesia with the endotracheal tube in place, passive regurgitation results in the movement of gastric contents into the esophagus or pharynx. If  this is observed, steps can be taken to diminish the serious consequences related to aspiration. Raising the occiput and swabbing the oropharynx following gentle saline irrigation is recommended.

At the end of anesthesia, the endotracheal tube is removed with the cuff partially inflated. Silent regurgitation , because it goes unnoticed, can have more serious consequences.When regurgitation of material into the oropharynx occurs during induction or after the endotracheal tube has been removed, the occiput is again raised immediately, the pharynx is swabbed with a piece of cotton gauze, an endotracheal tube is placed again, and the pharynx irrigated gently with saline. If material is thought to be within the tracheobronchial tree, suction through the endotracheal tube should be done multiple times. Bronchial lavage is to be avoided! Surgery or the procedure that was to be done can be rescheduled at a later time allowing the patient to recover. The animal should be given aminophylline (15 mg/kg IV) to be given over 15 minutes; this is to be repeated as an oral form every 8-12 hours for a maximum of 48 hours. Oxygen is given as necessary. Intermittent positive pressure ventilation with the animal under anesthesia or awake via a tracheostomy may be done in cases that do not respond to supplemental oxygen. Empirical use of antibiotics is initiated. I prefer an injectable form of a first generation cephalosporin (cefazolin). Coupage (3X daily) and frequent walking should be encouraged. Humidification may help expectoration of the airways. Nebulization with saline or saline mixed with gentamicin may be indicated.

Although treatment has been outlined above, it is far better to identify those animals that may be at risk of aspiration BEFORE it occurs and attempt to protect them with the empirical and perioperative use of injectable metoclopramide (0.2-0.4 mg/kg subcutaneously) and an injectable antacid (famotidine, ranitidine). I like to use these drugs for an 18-24 hour period since the function of the glottis muscles can be impaired (EVEN after swallowing) for a prolonged period of time.

VCA-Veterinary Specialists of Northern Colorado
201 W. 67th Court
Loveland, Colorado
November 2004

All volatile anesthetics including Halothane, Isoflurane, Sevoflurane and depolarizing neuromuscular blocking agents (Succinylcholine)

Safe agents for induction and maintenance of anesthesia:
Benzodiazepines Phenothiazine
Barbiturates Etiomidate
Propofol Dissociative agents
Opioids Nitrous oxide
Local anesthetics Non-depolarizing neuromuscular blockers