Gastrointestinal Disease

Gastrointestinal Disease

Juliana Peboni Figueiredo

VCA West Coast Specialty and Emergency Animal Hospital, Fountain Valley, Orange County, CA, 92708, USA

Gastrointestinal (GI) Tract Function

The digestive system provides the body with a continual supply of water, electrolytes, and nutrients. To achieve these larger global functions, several physiological functions need to be occurring normally. Food must be appropriately taken, ingested, and moved through the gastrointestinal (GI) tract: the stomach must secrete digestive enzymes, and, at the same time, the homeostatic function of the stomach must be maintained. Nutrients, water, and electrolytes must be absorbed by the small intestines; circulation of the GI organs must be adequate to carry away the absorbed substances, and motility of the GI tract must be maintained [1].

Any alteration in function or structure in the segments of the GI tract can disturb these physiological processes, resulting in anorexia, dehydration, hypovolemia, acid–base and electrolyte disturbances, protein loss, abdominal pain, and patient emaciation. All these derangements can have significant implications in the anesthetic management of dogs and cats undergoing diagnostic procedures (e.g., endoscopy), feeding tube placement, or surgery.

Oropharyngeal Diseases

Anatomically, the oral cavity is generally composed of the lips, cheeks, hard and soft palates, lower and upper dental arcades and associated bones (i.e., incisive, maxillary, palatine, mandible), tongue, and oropharynx [2]. In dogs and cats, endotracheal (ET) intubation is commonly achieved orally, and injury or disease of the oral cavity can present unique challenges to accomplish this task, in addition to other complications during the perianesthetic period (Table 5.1). Oral cavity diseases in dogs and cats that require surgical intervention include congenital and traumatic abnormalities, infectious disorders, foreign bodies, neoplasia, and salivary gland and dental diseases.

Clinical Signs

Patients with oral disease may present with ptyalism, abnormal food prehension, dysphagia, inappetence, weight loss, and halitosis. Attempts to ingest food can cause trauma to the oropharyngeal mucosa, resulting in oral pain and bleeding [2, 3]. Patients with pharyngeal dysphagia may be more prone to regurgitation and aspiration, particularly in cases where a large space‐occupying mass is compressing cranial nerves IX and X. These nerves are responsible for a series of involuntary movements that transport food through the pharynx and cricopharyngeal sphincter into the esophagus and protect the airway during swallowing [4]. Patients with pharyngeal‐stage dysphagia have repeated unsuccessful attempts at swallowing and food may stay in the pharynx. Because the epiglottis relaxes at the termination of swallowing and leaves the airway unprotected, affected animals are at risk for aspiration pneumonia. Difficulty associated with eating and swallowing can lead to weight loss and poor body condition score, which can compromise redistribution of lipid‐soluble drugs such as propofol [2, 3, 5]. In addition, animals with large oropharyngeal neoplasia may be at risk of partial or complete airway obstruction, and anesthesia may have to be induced in an emergency in order to intubate the trachea and relieve the obstruction [3].

Table 5.1 Potential perianesthetic considerations in patients with oral cavity and oropharyngeal disorders undergoing anesthesia for surgical procedures.

Common oral surgical diseases Anesthetic considerations
Congenital Primary cleft palate Pediatric patient
Dysphagia—potential for preoperative aspiration pneumonia
Low body condition score (BCS)
Infectious Lingual abscesses Large ventral cervical swelling—potential for pain and airway obstruction
Trauma Lip avulsion, jaw fracture, tooth fracture Pain

Foreign body (tongue, palate, oropharynx) Difficult intubation (e.g., wood stick in oral cavity)
Surgical ventral midline approach of oropharynx—potential for laryngeal paralysis in recovery if laryngeal recurrent nerve is damaged

Chemical burns Careful handling of tongue with ET intubation
Neoplasia Oral melanomas, nontonsillar squamous cell carcinoma (SCC), fibrosarcoma, osteosarcoma, canine acanthomatous ameloblastoma (CAA) Potential for preoperative aspiration pneumonia when dysphagia is presenta
Difficult ET intubationa
Hemorrhage, painb
Postoperative aspiration of fluid and blood
Postoperative airway obstruction if gauze sponges are left in oropharynx

Tonsillar SCC Potential for preoperative aspiration pneumonia when dysphagia is presenta
Preoperative stridor, airway obstruction, dyspneaa
Difficult ET intubationa
Hemorrhage, pain, postoperative aspiration of fluid and bloodc
Postoperative airway obstruction if gauze sponges are left in oropharynx
Postoperative airway obstruction or dyspnea due to pharyngeal swelling secondary to tissue trauma
Sialocele Pharyngeal sialoceles Potential for preoperative aspiration pneumonia when dysphagia and regurgitation are presenta
Preoperative stridor, airway obstruction, dyspneaa
Difficult ET intubationa
Postoperative airway obstruction if gauze sponges are left in oropharynx
Feline orofacial pain syndrome (FOPS)
Neoplasia Oral SCC, mast cell tumor, fibrosarcoma, osteosarcoma, peripheral odontogenic fibroma (POF) Hemorrhage, paind
Postoperative aspiration of fluid and blood Postoperative airway obstruction if gauze sponges are left in oropharynx

a Large space‐occupying pharyngeal mass.

b In dogs, mandibulectomy or maxillectomy is recommended for the treatment of malignant oral neoplasms involving bones.

c Tonsillectomy.

d In cats, rostral mandibulectomy is recommended for the treatment of malignant oral neoplasms involving the rostral mandible.

Laboratory Data

Before anesthesia is performed, a thorough physical examination, complete blood count (CBC), serum biochemistry profile, and urinalysis should be performed. The prothrombin time, partial thromboplastin time, and buccal mucosal bleeding time tests should be considered when a coagulopathy is suspected, or a large, vascularized mass is to be resected. Blood typing should be performed before surgery in dogs and cats undergoing mandibulectomy or maxillectomy to ensure safety, in case blood product transfusion is necessary, and blood cross‐matching should always be performed in dogs and cats that have previously been transfused [3]. CBC and serum biochemical profile results can be nonspecific for these patients; however, low hematocrit values owing to continuous small bleeding from trauma of the oropharyngeal mucosa may be noted (Figure 5.1) [2, 3].

Anesthetic Management

Perianesthetic Considerations

Anemic patients with packed cell volume (PCV) lower than 20% should receive a packed red blood cell (pRBC) transfusion before surgery because the oxygen‐carrying capacity of blood and the oxygen delivery to tissues are significantly impaired below this point. pRBC transfusion must also occur in patients with severe anemia undergoing mandibulectomy and maxillectomy owing to the increased risk of hemorrhage during these procedures [2]. The inferior alveolar artery, a branch of the maxillary artery, runs through the horizontal ramus of the mandible and is almost always ligated and transected during mandibulectomy (Figure 5.1). Blood supply to the maxillary region is provided by two major arteries, the major palatine, and the infraorbital arteries, both branches from the maxillary artery. Depending on the location of the tumor, one or both arteries may be ligated before maxillectomy. Rostral maxillectomy can be accompanied by diffuse bleeding from the highly vascularized nasal turbinates [6]. In this regard, the placement of two intravenous (IV) catheters may be prudent, as this allows simultaneous administration of blood, fluids, and inotropic support, if necessary.

Photo depicts (a) Twelve-year-old male neutered Labrador Retriever presented for an actively hemorrhagic and necrotic rostral mandibular mass, previously diagnosed as osteosarcoma.

Figure 5.1 (a) Twelve‐year‐old male neutered Labrador Retriever presented for an actively hemorrhagic and necrotic rostral mandibular mass, previously diagnosed as osteosarcoma. On presentation, PCV was 30% and TP was 6.0 g dl−1. Surgery was scheduled on the following day. Preoperative PCV was 17% and TP 4.8 g dl−1. Patient received pRBCs prior and during surgery. (b) Rostral mandibulectomy. (c) Inferior alveolar artery ligation prior mandibular horizontal ramus resection.

Preoperative thoracic radiographs or computed tomography (CT) for the detection of pulmonary metastases is indicated for dogs and cats with oral neoplasia; the presence of visible pulmonary metastases may indicate an extremely poor prognosis and surgery may not be indicated [6]. Careful lung auscultation and thoracic radiographs are advised for evaluation of aspiration pneumonia in patients with clinical signs of dysphagia and diagnosed with large oropharyngeal masses or swelling [3].

Laryngeal visualization is often challenging in dogs and cats with large oral cavity masses (Figure 5.2) or masses located in the temporomandibular joint, which can complicate ET intubation and maintenance of a patent airway. General anesthesia without a secure airway may result in aspiration of gastric contents and blood, which can lead to pneumonia and small airway obstruction, respectively. In cases where ET intubation is expected to be difficult (i.e., patients with large pharyngeal masses, difficulty of opening the mouth, or for those already presenting dyspnea), preoxygenation with 100% oxygen via a tight‐fitting mask should be considered before anesthetic induction. In addition, diverse diameters of ET tubes, stylets, a laryngoscope with adequate lighting, and several laryngoscope blade sizes should be readily available. A flexible endoscope can also be valuable in visualizing the airway for ET intubation, if available. Alternatively, retrograde ET intubation can be performed in patients with restricted mouth opening. In this case, the anesthetist punctures the cricothyroid membrane with a needle or an IV catheter, a guide wire is inserted through the needle or catheter and advanced retrograde to the mouth opening. The guide wire is grasped with forceps once it is observed in the oral cavity and a cuffed ET tube is passed caudally over the wire into the larynx. The guide wire is removed, and the ET tube is advanced further caudally into the trachea [7]. Regardless of the selected ET intubation technique, a surgical tracheostomy pack should always be available, as tracheostomy may be necessary if several attempts at ET intubation fail.

Photo depicts (a) Oropharyngeal mass (black arrow) hindering laryngeal visualization. (b) Possible laryngeal visualization (white arrow) with the aid of a tie gauze around the muzzle to widely open the oral cavity and a long-blade laryngoscope. (c) Successful ET intubation.

Figure 5.2 (a) Oropharyngeal mass (black arrow) hindering laryngeal visualization. (b) Possible laryngeal visualization (white arrow) with the aid of a tie gauze around the muzzle to widely open the oral cavity and a long‐blade laryngoscope. (c) Successful ET intubation.

An orally placed ET tube can sometimes hinder oral cavity and oropharyngeal surgery. In these cases, the portion of the ET tube that remains in the oral cavity can be deviated through a pharyngotomy or tracheotomy incision (see Chapter 13; Figure 5.3). For all methods of intubation, it is important that the ET tube and its cuff are properly inflated and lubricated to prevent blood and fluid from entering the lower airways. Gauze sponges are frequently placed in the oropharynx around the ET tube to help absorb fluids. However, these gauze sponges must be removed before the end of anesthesia and removal of the ET tube to prevent airway obstruction [2, 3]. Tying umbilical tape around the gauze to stack them together in the oropharynx and leaving the other end of the umbilical tape long enough to exit the mouth is a common way to prevent leaving packing material in the pharynx (Figure 5.4) [3].

Photo depicts introduction of the proximal end of the ET tube through a pharyngotomy. After the ET tube is orally placed and connected to the breathing system, inhalational anesthesia is started. A pharyngotomy is performed, and the adaptor of the ET tube is removed.

Figure 5.3 Introduction of the proximal end of the ET tube through a pharyngotomy. After the ET tube is orally placed and connected to the breathing system, inhalational anesthesia is started. A pharyngotomy is performed, and the adaptor of the ET tube is removed. A hemostat is inserted through the skin at the entry site of the pharyngotomy. The proximal end of the ET tube (without the adaptor) is grasped with the hemostat and pulled through the pharyngotomy. The adaptor is reattached to the ET tube, and the latter is reattached to the breathing system. Inhalational anesthesia can be continued at this time.

Source: Photo courtesy of Dr. M. Martinez, Dr. V. Cairoli, and Dr. R. Bruhl Day.

Proper patient and anesthetic equipment positioning maximize the surgeon’s ability to visualize the surgical field. In some situations, the anesthetist and anesthetic equipment will be away from the patient head, which can make it difficult for the anesthetist to monitor the signs associated with anesthetic depth, and therefore changes associated with heart rate, arterial blood pressure, and respiratory rate and pattern should be used to help predict anesthetic depth.

A mouth gag is often needed to facilitate exposure of the oral cavity. However, in cats, spring‐loaded mouth gags have been associated with neurological deficits, including postoperative blindness. Blood flow to the feline brain is primarily supplied via the maxillary artery. The high and constant forces between the maxilla and the mandible applied by spring‐loaded mouth gags can compromise cerebral blood flow by stretching the maxillary artery. If a mouth gag is necessary, the use of a smaller and plastic mouth gag (e.g., a plastic needle cap or a 20 mm, cut 1 ml syringe barrel, depending on the size of the cat) between the upper and lower arcades is advised [8, 9]. Decreased duration of open‐mouth procedures should also be exercised during feline oral cavity surgery to minimize reduced maxillary artery blood flow.

Photo depicts laparotomy sponge used to pack oropharynx and prevent fluid from entering airway.

Figure 5.4 Laparotomy sponge used to pack oropharynx and prevent fluid from entering airway. The tie of the laparotomy sponge is left exiting the oral cavity to remind the anesthetist to remove it before anesthetic recovery.

Preanesthetic Medication

Sedative drug selection will depend on multiple factors, including patients’ signalment, temperament, physical status, and disease localization (Table 5.2). In patients with partial airway obstruction and those in whom preoxygenation is included before induction of anesthesia, sedative drugs that decrease anxiety may be desired.

The potential for severe pain exists in patients undergoing mandibulectomy and maxillectomy, as bone and nerves will be resected during these procedures. Therefore, these cases warrant a multimodal analgesic approach [10]. Full mu‐opioid agonist drugs should be included in the premedication with the goal of providing preemptive analgesia (Table 5.2).

Vomiting after premedication should be avoided in patients with an inability to open the oral cavity and with partial airway obstruction. Therefore, drugs such as alpha‐2‐adrenergic agonists [11] and full mu‐agonist opioids [12, 13] should be used with caution or via appropriate routes (e.g., IV versus IM). Meperidine and methadone are notable exceptions, as they are less likely to cause vomiting in small‐animal patients [14, 15]. The advantage of using full mu‐opioid agonists (i.e., intense analgesia) must be weighed against several factors, including options of opioids available, procedural pain level, and the risks associated with emesis. Therefore, in patients in whom vomiting is undesirable, but analgesia is required, methadone may be a better premedication drug to administer if the chosen route is IM [14].

Anesthetic Induction

In patients with airway obstruction or an inability to open the oral cavity, anesthetic induction should be rapidly achieved without excitement (Table 5.2). For this reason, IV anesthetic induction techniques with propofol (2.0–8.0 mg kg−1 IV), alfaxalone (0.5–4.0 mg kg−1 IV), or ketamine–diazepam or ketamine–midazolam (5.0 mg kg−1, 0.25 mg kg−1 IV) are overwhelmingly preferred to mask induction with inhalation anesthetics.

Anesthetic Maintenance

Anesthetic maintenance in patients undergoing oral cavity surgery should be achieved using inhalation anesthetics (e.g., isoflurane, sevoflurane, or desflurane) or injectable techniques (total or partial IV anesthesia; TIVA or PIVA). Intraoperative analgesia can be accomplished by combining nitrous oxide with the inhalation anesthetic or by using a multimodal approach. Local or regional blocks can be very effective for providing analgesia for mandibulectomy and maxillectomy. Depending on the resected area, regional blocks of the infraorbital, maxillary, mental, or mandibular nerves can be performed with the administration of 0.5–1.0 ml kg−1 of lidocaine, bupivacaine, or ropivacaine (Table 5.3) [16]. Ultrasound‐guided techniques can be used to allow local anesthetic visualization and distribution in the region of the maxillary nerve [17], and a nerve stimulator can aid in the localization of the proximal mandibular nerve [18]. Specific descriptions of these techniques can be found elsewhere [17, 18]. Intraoperatively, analgesia can also be achieved by a continuous rate infusion (CRI) of an opioid (e.g., fentanyl, morphine, hydromorphone, or methadone) or combined with multimodal CRIs such as IV lidocaine and/or ketamine (Table 5.2). This approach provides the additional benefit of reducing the amount of inhalation anesthetic required, which will improve hemodynamic stability for the patient and may also prevent central sensitization of pain [10, 19].

Table 5.2 Preanesthetic, induction, and adjunct agents used in the anesthetic management of patients with gastrointestinal diseases.

Dogs Cats
Dose (mg kg−1) and route LD (mg kg−1); CRI (mg kg−1 h−1) (IV route) Dose (mg kg−1) and route
 Acepromazine 0.02–0.05 IV, IM
0.05–0.1 IV, IM
Alpha‐2‐adrenergic agonists
  Dexmedetomidine 0.002–0.01 IV, IM
0.003–0.02 IV, IM
  Morphine 0.3–1.0 IM
0.1–0.3 IM
  Meperidine 1.0–5.0 IM
0.5–1.0 IM
  Methadone 0.1–1.0 IV, IM
0.1–0.3 IV, IM
  Hydromorphone 0.05–0.2 IV, IM
0.05–0.1 IV, IM
  Oxymorphone 0.05–0.2 IV, IM
0.05–0.1 IV, IM
  Buprenorphine 0.01–0.03 IV, IM
0.01–0.02 IV, IM
  Butorphanol 0.1–0.4 IV, IM
0.1–0.4 IV, IM
  Diazepam 0.2–0.4 IV
0.2–0.4 IV
  Midazolam 0.2–0.4 IV, IM
0.2–0.4 IV, IM
Propofol 2.0–8.0 IVa
2.0–8.0 IVa
 Alfaxalone 0.5–4.0 IVa
0.5–4.0 IVa
  Ketamine + diazepam OR midazolam K: 5.0 IV +
D/M: 0.25 IV

K: 5.0 IV +
D/M: 0.25 IV
Fentanyl + diazepam OR midazolam F: 0.005–0.01 IV +
D/M: 0.2–0.5 IV

Adjuncts and analgesics
CRI: 0.1–0.3
CRI: 0.01–0.05
CRI: 0.12–0.036
LD: 0.002–0.005
CRI: 0.002–0.04
LD: 0.002–0.005
CRI: 0.002–0.04
  Carprofen 2.0–4.0 SC
2.0–4.0 SCb
  Meloxicam 0.2 SC
0.1–0.2 SCb
  Robenacoxib 2.0 SC
2.0 SC
  Atracurium 0.1 IV
0.1 IV
  Vecuronium 0.1 IV
0.1 IV
Local anesthetics
LD: 1.0–2.0 IV
CRI: 3.0 IV
N‐methyl‐D‐aspartate receptor (NMDA) antagonist
LD: 0.5
CRI: 0.6 IV
Opioid antagonist or partial reversal
  Naloxone 0.001–0.002 IV
0.001–0.002 IV
  Butorphanol 0.1 IV
0.1 IV

LD: loading dose; CRI: continuous rate infusion; IV: intravenously; IM: intramuscularly; SC: subcutaneously.

a Administered to effect.

b Single dose in cats.

Table 5.3 Perineural anesthesia of the head according to the location of mandibulectomy and maxillectomy.

Surgery location Type of perineural block
Rostral hemimandibulectomy Ipsilateral mental nerve block
Rostral mandibulectomy Left and right mental nerve blocks
Central, caudal, or total hemimandibulectomy Ipsilateral mandibular nerve block
Rostral hemimaxillectomy Ipsilateral infraorbital nerve block
Rostral maxillectomy Left and right infraorbital nerve blocks
Central, caudal, or total hemimaxillectomy Ipsilateral maxillary nerve block

Although rarely reported in veterinary medicine, maxillofacial surgery can trigger the trigeminovagal reflex, which produces increases in vagal tone and bradycardia when a branch of the trigeminal nerve is stimulated [20, 21]. Therefore, anesthetic monitoring should include an electrocardiogram (ECG), a means to detect heart rate or pulse rate (e.g., Doppler oscillometry, pulse oximetry, esophageal stethoscope), and blood pressure measuring to accurately and rapidly diagnose severe hypotension that may be associated with bradycardia or asystole. Upon recognition of the trigeminovagal reflex, rapid communication between anesthetist and surgeon should occur in an attempt to discontinue the stimulation of the surgical region followed by IV treatment with anticholinergics (e.g., atropine or glycopyrrolate) or beta‐1‐adrenergic receptor agonists (e.g., dopamine, dobutamine) in case of a refractory response to anticholinergics (Table 5.4) [21].

Table 5.4 Fluids and therapeutic agents used to treat cardiovascular derangements during anesthesia in patients with gastrointestinal diseases.

Fluids and therapeutic agents Dose regimen
Maintenance fluid rate during anesthesia
Balanced crystalloid (e.g., LRS) 5–10 ml kg−1 h−1 IV
Fluids for hypovolemia
6% HES 20 ml kg−1 d−1 IVa
6% HES 1–2 ml kg−1 −1 IVa
6% HES bolus 3–5 ml kg−1 IVa
7% hypertonic saline 4–6 ml kg−1 IV
Isotonic crystalloid shock dose 60–90 ml kg−1 IV
Isotonic crystalloid bolus 10–20 ml kg−1
Treatment for intraoperative bradycardia
Glycopyrrolate 0.005–0.02 mg kg−1 IV
Atropine 0.02–0.04 mg kg−1 IV
Treatment for intraoperative hypotension
Dopamine 5–20 μg kg−1 min−1 IV
Dobutamine 1–10 μg kg−1 min−1 IV
Norepinephrine 0.01–2.0 mcg kg−1 min−1 IV
Phenylephrine 0.5–3.0 mcg kg−1 min−1 IV
Vasopressin 0.5–2.0 mU kg−1 min−1
Treatment for ventricular tachycardia
Lidocaine Bolus: 2–4 mg kg−1 IV
Infusion: 3.0–4.5 mg kg−1 h−1 IV
Procainamide Bolus: 2–8 mg kg−1 slow IV
Infusion: 1.5–2.4 mg kg−1 h−1

a Use is controversial; see text for details.

Intraoperatively, a balanced isotonic crystalloid solution (e.g., lactated Ringer’s solution [LRS]) should be administered IV at a rate of up to 5–10 ml kg h−1 (Table 5.4). The surgery magnitude and the likelihood of hemorrhage, due to the extensive vascular supply of the oral and nasal cavity, should be considered when selecting modalities of arterial blood pressure monitoring. Intra‐arterial catheter placement with invasive arterial blood pressure measurements is preferred when large, vascularized masses are excised. Hypertonic saline (7.0–7.5%), hydroxyethyl starches (HESs; 6% hetastarch 600/0.75 [Hespan®] or 6% tetrastarch 130/0.4 [VetStarch™]), a combination of 23.4% saline with HES, whole blood or pRBC, and fresh frozen plasma (FFP) should be available in the event of severe hemorrhage (Table 5.4) [2]. In situations of significant blood loss, an approach combining several types of fluids is desirable, since large volumes of crystalloids are required to replace intravascular volume. HES solutions are commonly used for the treatment of hemorrhagic shock in dogs and cats. In the recent years, controversies related to their use have been raised in both human and veterinary medicine, particularly in critically ill patients or patients with sepsis [2227]. Negative outcomes, such as acute kidney injury, need for renal replacement therapy, and mortality, have been associated with the administration of HES in critically ill human patients, but are likely related to HES solutions with higher concentrations, molecular weights (MWs), and molar substitutions (MSs), as well as administration of large cumulative doses over several days of hospitalization [28]. These conclusions have been extrapolated to veterinary medicine and prospective controlled studies are still lacking in critically ill dogs and cats. However, 6% tetrastarch (HES 130/0.4) in noncritically ill dogs and cats at recommended doses for intraoperative volume replacement (dogs: 5–20 ml kg−1, cats: 3–15 ml kg−1) has been shown to effectively expand plasma volume during anesthesia or in hemorrhagic shock states without evidence of acute kidney injury or long‐lasting effects on coagulation function [2935].

Anesthetic Recovery

On termination of inhalation anesthetics, gauze sponges should be removed from the caudal pharynx and the oral cavity [2]. Fluid evacuation with a suction tube before termination of anesthesia may also prevent fluid aspiration. Postoperative swelling of the oral mucous membranes may cause airway obstruction. This can be minimized by the administration of corticosteroids (e.g., dexamethasone 0.1–0.2 mg kg−1 IV).

Tracheal extubation should be delayed until a well‐developed swallowing reflex is present. When the patient is ready for extubation, the ET tube should be removed with the cuff at least partially inflated to help ensure that any blood clots and fluid left in the pharynx are expelled through the mouth rather than being aspirated or swallowed [36]. During recovery, these patients should be monitored for signs of airway obstruction or pain.

Analgesics such as opioids (e.g., fentanyl, hydromorphone, methadone) and nonsteroidal anti‐inflammatory drugs (NSAIDs) (e.g., carprofen [2.0–4.0 mg kg−1 in dogs; 2.0–4.0 mg kg−1 single dose in cats], meloxicam [0.2 mg kg−1 in dogs; 0.1–0.2 mg kg−1 single dose in cats], robenacoxib [2.0 mg kg−1 for up to 3 days in dogs and cats]) should be provided as needed. However, if corticosteroids have been previously administered to the patient, caution should be taken when deciding if NSAIDs are an appropriate analgesic to administer.

Esophageal Diseases

The esophagus carries food, water, and saliva from the pharynx to the stomach. Impairment of these functions can lead to gastroesophageal reflux (GER), esophagitis, regurgitation of the ingesta back to the oral cavity, and aspiration of this content, resulting in pneumonia [2].

Esophageal diseases in dogs and cats are related to obstructive, motility (e.g., megaesophagus), or inflammatory (e.g., esophagitis from chronic vomiting or GER) disorders [37]. In certain situations, these patients require anesthesia for feeding tube placement (e.g., percutaneous endoscopic gastrostomy [PEG] tube and gastrostomy tube), further diagnostics (e.g., esophagoscopy and biopsy), or treatment of the primary problem (e.g., esophagoscopy for foreign body removal, esophageal balloon dilation, and vascular ring anomaly correction).

Esophageal Anatomy

The esophagus connects the pharynx to the stomach and is responsible to transport ingesta and fluid. It is the only visceral organ that contains striated muscle. In the dog, the muscular layers of the esophagus are made entirely of striated muscle, whereas in the cat, only the proximal two‐ thirds contain striated muscle. The esophagus is divided into cervical and thoracic portions. The upper esophageal sphincter (composed of cricopharyngeus and thyropharyngeus muscles) is located at the proximal end of the esophagus. The lower esophageal sphincter (LES) is located at the distal end, at the gastroesophageal junction. In this area, dogs have a thick muscle layer created by a circular arrangement of striated muscle. Combined with the diaphragm crura and the angle at which the esophagus and stomach meet, a zone of higher intraluminal pressure at the gastroesophageal junction is created [3840].

Esophageal Obstruction

Esophageal obstruction usually occurs in dogs and cats because of foreign bodies, benign strictures, neoplasia, hiatal hernias, gastroesophageal intussusceptions, and vascular ring anomalies [2]. Depending on the degree of obstruction, food and secretions accumulate cranially to the obstruction leading to segmental distention of the esophagus, disruption of normal neuromuscular function, and decreased esophageal peristalsis [40].

Esophageal foreign bodies are relatively common in small‐animal patients. Foreign material usually lodges where the esophagus narrows. These locations include the thoracic inlet, the base of the heart, and the esophageal hiatus in the diaphragm. Dogs, particularly small breed and younger than 3 years old [41], are the most frequently diagnosed with esophageal foreign bodies. Esophageal injuries secondary to the foreign body can occur, and the extent of these injuries depends on the type of object, its size and shape, and the duration in contact with the mucosa [37]. Previous unsuccessful attempts at endoscopic foreign material removal can also lead to a significant increase in secondary esophageal injury. Esophageal perforation prior to or during foreign body removal can lead to significant morbidity and mortality due to pneumothorax, pleuritis, pyothorax, and respiratory distress [42].

Esophagitis is caused by esophageal mucosal inflammation and, in more severe cases, these lesions can extend into the submucosa and muscularis layers, leading to esophageal stricture formation. Causes associated with esophagitis include persistent vomiting, gastroesophageal emptying, hiatal hernia, ingestion of corrosive substances, thermal burns, and esophageal foreign bodies. However, esophagitis with resulting esophageal stricture related to GER during general anesthesia is the most common cause of benign esophageal stricture in dogs and cats (46–83%) [4347] and may occur when protective mechanisms are diminished (i.e., reduced LES pressure, absence of swallowing saliva, reduced esophagus clearance) by general anesthesia itself and anesthetic/analgesic drugs (Box 5.1). During anesthesia, the acidic gastric contents, particularly with pH ≤4.0, that contact the esophageal mucosa can severely damage the esophagus if they are not neutralized by saliva or removed by peristalsis within a few minutes. The most common signs of esophagitis/esophageal stricture include hypersalivation, dysphagia, esophageal pain, anorexia, weight loss, and regurgitation. These signs may take as little as a few days or up to 3 weeks after the general anesthetic event to present [44, 45, 47]. Despite the most common cause of esophageal stricture being associated with anesthesia, the overall incidence of esophageal stricture following anesthesia appears to be low (0.07–0.1%). However, when it occurs, the cost associated with diagnosis and treatment of this disorder is extremely large, with a subsequent high mortality rate (12–30%) [44, 45, 47]. These patients usually return for several subsequent anesthetic events in which esophageal bougienage or dilation with balloon catheters is performed to treat the strictures.

Brachycephalic dogs presented with signs of brachycephalic obstructive airway syndrome are known to have a higher incidence of gastroesophageal abnormalities due to the generation of high negative intrathoracic pressures during increased inspiratory effort [70]. Although they are at increased risk of GER, regurgitation, and vomiting preoperatively and postoperatively [70, 71], one study failed to show that they are at increased risk of GER and regurgitation during anesthesia [72]. However, this study was underpowered and brachycephalic dogs presented in respiratory distress were excluded from the data if they had received corticosteroids prior to anesthesia. Therefore, when anesthetizing brachycephalic breeds, the anesthetist should still closely monitor for intraoperative regurgitation and signs of esophagitis and aspiration pneumonia in the immediate postoperative period.


Megaesophagus may occur with esophageal motility disorders. The causes of esophageal hypomotility are extensive, varying from a primarily idiopathic origin in dogs (most common) or secondary to neuromuscular, muscular, infectious, or autoimmune disorders. Patients with megaesophagus may require anesthesia for esophagoscopy or other diagnostic tests and procedures for the suspected primary disease. These may include electromyography and nerve conduction velocity, muscle biopsy, cerebrospinal fluid collection, or thymoma removal [2, 37].

Clinical Signs

Clinical signs of esophageal diseases include abnormalities of prehension and swallowing, regurgitation, and ptyalism. Vomiting can occur if both the esophagus and stomach have significant disease such as with hiatal hernia, gastroesophageal intussusception, or GER [37]. It is important to differentiate regurgitation from vomiting because regurgitation is more likely to occur in patients with primary pharyngeal or esophageal disorders. In addition, the clinical consequences of vomiting and regurgitation may be different and, as such, can influence the clinician’s anesthetic plan. Regurgitation is a passive flow of food, water, or saliva from the esophagus to the oral cavity [73]. The primary complication of regurgitation is aspiration pneumonia. Alternatively, vomiting is a forceful expulsion of gastroduodenal contents mediated by the central nervous system. The presence of vomiting usually indicates the presence of GI or systemic disease [73, 74].

Chronic regurgitation can lead to anorexia, weight loss, stunted growth compared to littermates (e.g., vascular ring anomalies, congenital megaesophagus), depression, and emaciation [2]. Esophageal pain may be suspected when patients are observed having signs of neck stretching while swallowing and repeated swallowing [45, 47].

Respiratory distress, coughing, pulmonary crackles, and fever may suggest aspiration pneumonia secondary to regurgitation. In the case of foreign bodies, respiratory distress can also be associated with pneumothorax or compression of the upper airway by the foreign material. Therefore, it is recommended to closely examine thoracic radiographs, not only for the diagnosis of a foreign body but also to evaluate for signs of aspiration pneumonia, pleural effusion, pneumothorax, pneumomediastinum, or tracheal compression [40].

Patients with esophageal motility disorders (e.g., megaesophagus) can also present with generalized muscle weakness or atrophy, neurologic deficits, and/or oropharyngeal dysphagia when generalized myasthenia gravis is present [2, 37].

Laboratory Data

A minimum database of tests, including a CBC and serum biochemical profile, should be performed in patients with esophageal disease. PCV, total protein (TP), blood urea nitrogen (BUN), and creatinine may be elevated because of dehydration. A neutrophilia with left shift may be consistent with aspiration pneumonia. Metabolic acidosis with lactatemia can occur in dehydrated patients and metabolic alkalosis can be seen with gastroesophageal disorders (e.g., hiatal hernia) [37]. Patients with megaesophagus secondary to hypoadrenocorticism may have electrolyte disturbances such as hyperkalemia and hyponatremia [73, 75].

Anesthetic Management

Perianesthetic Considerations

The purpose of preoperative fasting is to withhold liquids and solids for a specified period before surgery to reduce gastric volume and acidity. These goals are particularly important for patients with gastroesophageal diseases that are prone to regurgitation. When considering preoperative fasting, one needs to balance the risk of dehydration, administration of preoperative oral medications, and hypoglycemia versus the risk of GER, regurgitation, esophageal injury, and aspiration pneumonia. Traditionally, in small‐animal medicine, preoperative fasting times have been 8–12 h for scheduled procedures with the rationale that the stomach would be empty prior to anesthetic induction, since complete gastric emptying in dogs and cats ranges from 7–15 h [76]. More recently, the American Society of Anesthesiologists (ASA) has modified their guidelines for preoperative fasting in healthy humans undergoing elective procedures; these guidelines may additionally need to be adjusted for people with coexisting diseases or conditions that can affect gastric emptying or fluid volume. With that in mind, the ASA Practice Guidelines for Preoperative Fasting recommend: (i) clear liquids may be ingested for up to 2 h before anesthetic procedures; (ii) a light meal may be ingested for up to 6 h before elective procedures; and (iii) fasting time of 8 h or more may be needed in cases of patient intake of fatty foods and/or meat. These conclusions were based on randomized clinical trials that showed no differences in findings regarding gastric volume and pH when people could have a light meal 4–6 h before a procedure compared to overnight fasting [77].

In veterinary medicine, the incidence of GER in healthy dogs after shorter fasting time has been reported (Box 5.1). When fed a light meal (one‐half of their daily ration in canned food) approximately 3 h before elective procedures, 3/60 dogs experienced GER during anesthesia compared to 12/60 dogs that were fed the same amount and type of food but 10 h prior to anesthetic induction [56]. These results were confirmed as dogs did not have significantly increased gastric volume when fed canned food at one‐half of their daily ration 3 h before anesthesia; in addition, the gastric acidity was reduced [54]. However, in a more recent report, dogs that were fed a light meal 3 h prior to anesthesia were associated with significantly greater odds of both GER and regurgitation compared to dogs fasted for 18 h [49]. The differences can be due to diet composition which may have different gastric emptying time or the preanesthetic administration of opioids (or other drugs) that could have also influenced gastric motor function and affected residual gastric volume content. While shorter preoperative fasting may be desirable in veterinary medicine and has been the new standard of practice in people, there have been no randomized controlled trials assessing the impact of preoperative fasting for dogs and cats with GI disorders, and veterinarians have followed recommendations based on small clinical studies and experience. Based on that, the American Animal Hospital Association (AAHA) has recommended shorter preoperative fasting times for water and food for healthy dogs and cats [78]. For patients with a history of, or at risk for, regurgitation, fasting times for food and water should be kept between 6 and 12 h. In addition, the clinician should consider feeding 10–25% of the normal amount of food in the form of a wet ration 4–6 h prior to induction. Regardless of fasting duration, the anesthetist should recognize that esophageal diseases can increase the likelihood of GER, regurgitation, and related morbidities, and that additional strategies may be appropriate, such as rapid induction and ET intubation, as well as readiness to suction the pharynx and airway. GI foreign bodies are considered medical emergencies, and fasting is usually not possible. If patients are not fasted, preoperative and intraoperative regurgitation may occur with potential of aspiration.

Preoperative fasting for young animals (i.e., 8–16 weeks of age) undergoing surgery, such as ligation and transection of the ligamentum arteriosum in puppies and kittens with persistent right aortic arch (Figure 5.5), should be kept to a minimum and limited to no greater than 4–6 h. In cases of malnourished animals, preoperative fasting should be decreased to 1–2 h [2, 39]. In these young animals, other anesthetic considerations regarding size and nourishment must also be considered. For example, blood glucose should be monitored during the procedure, maintenance fluids may have to be supplemented with dextrose, and hypothermia should be aggressively prevented [2, 42].

Photo depicts right lateral thoracic radiograph showing esophageal dilation cranial to the base of the heart (black arrow) secondary to a vascular ring anomaly.

Figure 5.5 Right lateral thoracic radiograph showing esophageal dilation cranial to the base of the heart (black arrow) secondary to a vascular ring anomaly (persistent right aortic arch in this case).

Source: Photo courtesy Dr. G. Sepulveda.

GER may still happen during anesthesia regardless the duration of food withholding. The incidence at which patients with esophageal diseases have GER during anesthesia is unknown, but one can assume that this occurs at higher rate than in patients without GI disease, especially in patients with clinical signs of esophagitis. In dogs and cats without history of esophageal or GI disorders, GER during anesthesia occurs frequently with an incidence rate varying from 12% to 67% [15, 48, 49, 5256, 5860, 66, 67, 69, 72, 7981]. However, clinically, GER is usually not diagnosed during anesthesia because it requires the use of an esophageal pH meter or a pH impedance catheter to be detected. Only a minority of patients that experience GER regurgitate (0–15%) during anesthesia [15, 48, 50, 53,5860, 66, 67, 69, 80, 81], making it an insensitive clinical sign for recognizing GER. For this reason, medications to prevent GER and reflux events, to increase the pH of gastric secretions, or to improve GI motility preoperatively have been advocated by some clinicians. It should be noted that the efficacy of these drugs, when administered preoperatively, in reducing the frequency of reflux events in healthy dogs and cats that experienced GER during anesthesia is equivocal. In part, the lack of drug efficacy in reducing reflux may be due to differences in methodology of measuring pH. In some cases, administration of these drugs preoperatively, particularly proton‐pump inhibitors (PPIs), may still be beneficial in reducing gastric acidity, helping to reduce esophageal mucosal and lung damage after aspiration if reflux or regurgitation does occur [2, 81, 82]. In humans, the ASA guideline for preoperative fasting and the use of pharmacologic agents found inconclusive evidence to routinely recommend administration of metoclopramide, histamine‐2 antagonists (H2As), PPIs, or antiemetics prior to anesthesia to reduce the incidence of GER, emesis, or pulmonary aspiration. As such, these drugs are only recommended in people at increased risk of aspiration pneumonia [77]. Similarly, the AAHA Anesthesia and Monitoring Guidelines for Dogs and Cats recommend antiemetic, antiacid, and promotility drugs prior to anesthesia for patients with history of, or at risk for, regurgitation [78]. Clinically, H2As and PPIs are commonly administered prior to anesthesia with the goal to decrease gastric acidity. Ranitidine (2 mg kg−1 IV) administered 6 h prior to anesthesia did not prevent or decrease the frequency of GER in dogs [83]. Although famotidine administered every 12 h is superior to famotidine every 24 h or ranitidine to decrease gastric acid secretion and increase gastric pH, H2As are overall less efficacious than PPIs in dogs and cats to treat gastroduodenal ulceration or reflux esophagitis [84]. In addition, H2A tachyphylaxis may occur within 3–13 days [85], which could give a false sense of security if patients with esophageal diseases receiving this therapeutic regimen for that period would reflux or regurgitate during anesthesia. Currently, there are no studies in dogs and cats that determine if the preanesthetic administration of H2As and, potentially, a short period of increasing esophageal pH present any benefit in the anesthetized patient [86]. Therefore, additional studies of H2As prior to anesthesia to reduce esophageal pH are warranted before they are routinely recommended. In clinically healthy dogs and cats, PPIs such as omeprazole and pantoprazole are the most effective in increasing gastric pH compared to H2As [86]. In addition, omeprazole administered orally to dogs as a single dose 4 h before anesthesia and to cats twice, 18–24 h and 4 h before anesthesia, decreased the incidence of GER with pH <4. However, reflux event frequency was not decreased in both dogs and cats that had GER [81, 82]. In addition, esomeprazole administration IV 12–18 h and 1.0–1.5 h before anesthetic induction in dogs undergoing orthopedic surgery significantly increased the gastric and esophageal pH. Like the studies with omeprazole, the preanesthetic administration of esomeprazole did not decrease reflux event frequency. By contrast, esomeprazole administration IV combined with cisapride, a prokinetic drug, before anesthesia significantly decreased GER events [87], likely due to increase in LES pressure [88]. Therapy with PPIs (omeprazole 0.5–1.0 mg kg−1 PO or pantoprazole 1.0 mg kg−1 IV) should be started at least 2 days before anesthesia in order to be most effective [82, 84]. Recently the American College of Veterinary Internal Medicine published a Consensus Statement on the administration of gastroprotectants to dogs and cats and has made several recommendations to the practice of acid suppressants for the management of GI diseases, including the prevention of reflux esophagitis. The consensus opinions on the use of acid suppressants for management and prevention of reflux esophagitis, which pertains to the scope of this chapter, including: (i) there is lack of benefit for administration of H2As on a once‐daily basis in dogs and cats to treat reflux esophagitis; (ii) monotherapy with an H2A given twice daily is inferior to PPIs given twice daily to dogs and cats; (iii) acid‐suppressing agents may be beneficial for prevention of esophagitis secondary to GER, particularly in animals when these are associated with an anesthetic procedure; and (iv) administration of PPIs does not decrease GER, but may prevent injury by increasing the pH of the refluxate [86].

Metoclopramide is a dopaminergic receptor antagonist with antiemetic properties. In addition, it is thought to increase the LES resting tone and promote gastroduodenal motility. However, metoclopramide at 0.5 mg kg−1 PO did not increase LES pressure measured by high‐resolution manometry in unpremedicated awake healthy Beagles [88]. Clinically, metoclopramide is recommended as a prokinetic in the treatment of esophagitis because esophageal inflammation may cause esophageal hypomotility. Also, it is routinely administered to patients who are at risk of GER and regurgitation during anesthesia; however, clinical studies are conflicting in this regard and there is no consensus if metoclopramide administration perioperatively decreases the risk of GER, esophagitis, and aspiration pneumonia. For example, high‐dosage IV administration (1.0 mg kg−1) followed by a high‐dosage CRI (1.0 mg kg−1 h−1) in healthy dogs undergoing orthopedic surgery decreased the risk of GER by 54% [79]. By contrast, the same high‐dosage CRI (1.0 mg kg−1 h−1) did not influence the incidence of GER in dogs undergoing ovariohysterectomy, which could have been a result of a small number of dogs experiencing GER in the studied groups [83]. Lower dosages similar to that required to attain an antiemetic and gastric prokinetic effect (0.4 mg kg−1 IV followed by a 0.3 mg kg−1 h−1 CRI) also did not decrease the incidence of GER compared to a negative control group [79]. Interestingly, preoperative metoclopramide at a lower dosage CRI (2.0 mg kg−1 d−1) combined with maropitant (1 mg kg−1 IV) did not decrease the incidence of postoperative clinical GER, defined in the study as passive gastric reflux observed in the oral cavity (i.e., regurgitation) combined with signs of nausea. The authors speculated that metoclopramide could also have increased gastro‐oral reflux due to anxiety from metoclopramide‐induced extrapyramidal effects [89]. When metoclopramide (0.5 mg kg−1) was administrated in combination with famotidine or omeprazole in brachycephalic dogs undergoing airway surgery, there was a lower incidence of postoperative regurgitation, and preoperative administration of these drugs is recommended for brachycephalic breeds. However, brachycephalic dogs with history of regurgitation are still more likely to regurgitate intraoperatively regardless of treatment with GI‐protectant drugs [71]. Therefore, it can be concluded that the risk of GER and regurgitation during anesthesia still exists when metoclopramide is administered regardless of the CRI dose in healthy patients, and observation of clinical signs for esophagitis is warranted postoperatively. Care must be taken when extrapolating these data from healthy patients to patients with esophageal disorders who already have a predisposition to GER and regurgitation (e.g., brachycephalic breeds), and, therefore, these patients, when receiving metoclopramide perioperatively, should be closely monitored for signs of regurgitation and aspiration pneumonia.

Maropitant (1.0 mg kg−1), an antiemetic drug that acts as a neurokinin‐1 receptor (NK1) antagonist, administered IV 45–60 min prior to anesthetic premedication with acepromazine and hydromorphone did not significantly decrease the incidence of GER in dogs undergoing elective surgical procedures when compared to dogs treated with saline [90]. Similarly, preoperative administration of maropitant (1.0 mg kg−1 IV) did not prevent postoperative GER/regurgitation in dogs [89]. Currently, there is not sufficient evidence that maropitant decreases the incidence of GER or regurgitation, and therefore maropitant should not be recommended with the intent to prevent anesthesia‐induced GER.

However, both metoclopramide (0.2 mg kg−1 IM) [91, 92] and maropitant (1.0 mg kg−1 SC or IV) [90, 91,9399] are effective antiemetics administered prior to opioids combined with dexmedetomidine or acepromazine in healthy dogs and cats. Their administration in dogs and cats with esophageal disease preoperatively may be desirable with the goal of preventing vomiting, thus decreasing further damage to the esophagus and the risk of aspiration pneumonia. Metoclopramide should be administered 30–45 min in dogs and maropitant 30–60 min in dogs and 20 h in cats before the administration of an opioid or an alpha‐2‐adrenergic agonist premedication to be most effective.

In cases where the patient is emaciated, anesthesia should be postponed until the animal has an improvement in body condition score. However, in certain situations, treatment for nutritional debilitation requires the placement of a gastrostomy or PEG tube, both of which require general anesthesia. In these situations, the anesthesia period should be kept as short as possible with perianesthetic considerations aimed at the individual patients’ physical status and comorbidities.

Since regurgitation is commonly associated with esophageal disease, thoracic radiographs should be taken preoperatively to evaluate for the presence of aspiration pneumonia. Patients with aspiration pneumonia should be treated aggressively before being anesthetized for esophagoscopy, surgery, or feeding tube placement. If anesthesia cannot be delayed until aspiration pneumonia resolves, preoxygenation with 100% oxygen before anesthetic induction is recommended [2]. In addition, the trachea should be immediately intubated after induction, and positive pressure ventilation should be instituted to maintain oxygen saturation above 90%.

Dogs presenting with esophageal diseases that appear to be dehydrated or hypovolemic based on physical examination, CBC, and serum biochemical variables should receive fluid resuscitation before anesthesia. Tachycardia, pale mucous membranes, prolonged capillary refill time, and cold extremities are signs of hypovolemic shock and should be treated with isotonic crystalloids (60–90 ml kg−1 in one‐quarter dose increments) and/or HES solutions (5–20 ml kg−1, when indicated) and reassessed before anesthetic induction (Table 5.4). It should be noted that cats in shock might present with bradycardia and hypothermia [100]. Treatment of acid–base and electrolyte disturbances should be initiated before anesthesia if possible (see the subsection titled “Laboratory Data ” under the section titled “Gastric and Small Intestinal Diseases ”).

In general, the anesthetic protocol is not aimed at avoiding drugs that decrease LES pressure because many of the drugs administered with the purpose of producing anesthesia or analgesia will interfere with protective mechanisms against GER (Box 5.1). Most drug selection is based on the physical status of the patient, mentation, pain level, and surgical procedure (Table 5.2). Whenever possible, drugs that produce emesis should be avoided to prevent further damage to esophagus and aspiration pneumonia.

Preanesthetic Medication

The GI effects of anticholinergic drugs have been well described. Atropine and glycopyrrolate decrease LES tone at doses commonly used for prevention or treatment of bradycardia [536163]. At high doses, they inhibit hydrogen‐ion secretion by gastric parietal cells, and at the standard recommended doses for preanesthetic medication, they have minimal effect on the pH of gastric secretions in dogs [101]. Therefore, the argument for including anticholinergic drugs in the preanesthetic medication is not justifiable due to their effect on the LES, likelihood of GER, and lack of effect to reduce gastric acidity at clinical doses.

The administration of drugs that may induce vomiting or GER (e.g., alpha‐2‐adrenergic agonists and full mu‐opioids) in the preanesthetic period of patients with an esophageal foreign body is questionable. Sharp foreign body objects may abrade or lacerate the esophageal mucosa, causing esophagitis. Sharp objects may also perforate the esophagus and, occasionally, the great vessels. If emesis is induced by preanesthetic drugs in these patients, further damage may occur [2, 102]. Acidic gastric‐fluid reflux can induce further damage to the esophagus. Even so, opioids are usually included in the preanesthetic medication of these patients to provide analgesia even if foreign body removal is performed with noninvasive techniques (e.g., esophagoscopy) wherein pain is less intense. However, opioids that do not cause vomiting such as butorphanol (0.1–0.4 mg kg−1), buprenorphine (0.01–0.03 mg kg−1), methadone (0.1–1.0 mg kg−1), and fentanyl (0.002–0.005 mg kg−1) have been recommended for this type of procedure [42]. The administration of morphine, hydromorphone, and oxymorphone has been shown to increase the risk of regurgitation, GER, or vomiting significantly [1315, 50, 60]. Therefore, methadone or fentanyl is preferred in the case of esophageal surgery where pain is more likely to be more intense. In addition, IV administration may result in less vomiting altogether, as drugs may bypass the chemoreceptor trigger zone (which induces vomiting) and act to suppress vomiting at the vomiting center [103]. Maropitant may be administered 30–60 min prior to opioid administration to prevent emesis [90, 91,9399].

Acepromazine (0.02–0.05 mg kg−1) can be administered to provide sedation in patients with esophageal foreign bodies that are hemodynamically stable. When administered before opioids, acepromazine decreases the incidence of vomiting [13], although it increases the chances of GER [53]. Diazepam or midazolam (0.2 mg kg−1) may be preferred in depressed and hypovolemic patients. Furthermore, diazepam has been associated with a significant reduction in GER episodes [53].

Intense sedation or muscle relaxation should be avoided in patients with megaesophagus. Muscle relaxation of the striated muscle layer of the esophagus can increase the likelihood of regurgitation before anesthetic induction. Intense sedation may impair the patients’ ability to protect their airway, increasing the chances of aspiration pneumonia. Acepromazine, alpha‐2‐adrenergic agonists, and benzodiazepines should be used with caution in these patients.

Anesthetic Induction

Dogs and cats with esophageal disease are at high risk of regurgitation and aspiration pneumonia. For this reason, it is advised to have a suctioning system set up during the induction period. Anesthetic induction should be rapid with immediate ET intubation. Therefore, mask induction with inhalation anesthetic should be avoided, and IV anesthetic techniques are preferred. Propofol (2.0–8.0 mg kg−1 IV) or alfaxalone (0.5–4.0 mg kg−1 IV) are rapid‐acting, and the airway can be immediately secured, particularly in patients with megaesophagus. Alternatively, other drugs with fast onset, such as ketamine–diazepam/midazolam, can be used in patients with esophageal disorders [42].

Endotracheal intubation should be performed with the patient in sternal recumbency with the head elevated. Application of pressure to the cricoid region has been documented in humans to reduce regurgitation [104]; however, this has not been advocated for dogs and cats. If regurgitation is observed during induction, the airway of the patient should be secured with a properly sized and lubricated cuffed ET tube and its cuff immediately inflated. Afterward, the patient’s head should be dropped below the thoracic inlet, and the airway and oropharynx should be suctioned. The ET tube should be connected to a breathing system and 100% oxygen supplemented. Oxygenation and ventilation with the aid of a pulse oximeter and capnograph should be monitored at this time. If the procedure can be delayed, it is advised to allow the patient to recover from anesthesia and be observed for signs of aspiration pneumonia.

Anesthetic Maintenance

Anesthetic maintenance in patients with esophageal obstruction or megaesophagus is achieved with inhalation anesthetics (e.g., isoflurane, sevoflurane, or desflurane) diluted in 100% oxygen. Nitrous oxide should be avoided in patients with esophageal obstruction, as it can accumulate in viscous organs and dilate the esophageal portion distal to the obstruction [2].

Owing to the striated muscle layer in the esophagus, especially in dogs, central muscle relaxant administration (e.g., diazepam and midazolam) or short‐acting neuromuscular blocking agents (e.g., atracurium 0.1–0.4 mg kg−1 IV) may be indicated for patients with esophageal foreign bodies. These drugs may help to relax the striated muscular layer of the esophagus, reduce esophageal tone, and facilitate endoscopic manipulations and foreign body removal [2, 42]. Positive pressure ventilation is required in patients that receive neuromuscular blocking agents, and, ideally, neuromuscular function should be monitored by accelerometry. Deep anesthetic planes required with inhalation anesthetics to achieve muscle relaxation are not recommended in patients who are hemodynamically unstable.

Intraoperatively, a balanced isotonic crystalloid solution (e.g., LRS) should be administered up to a rate of 5–10 ml kg−1 h−1. Supplemental fluid boluses of isotonic crystalloids may be indicated depending on the patient’s hydration and hemodynamic status. In most cases, blood pressure can be monitored noninvasively, and pulse oximetry and capnography can provide valuable information in the event of esophageal perforation or aspiration [42].

Most general anesthetics can increase the chances of GER or regurgitation because of their effects on the LES tone in dogs and cats [6569]. Although the incidence of regurgitation is low in healthy anesthetized patients [15, 48, 50, 53,5860, 66, 67, 69, 80, 81], it is more likely to occur in patients with esophageal disorders. Continuous monitoring for regurgitation during anesthetic maintenance, and immediate treatment if regurgitation occurs, can help prevent complications from occurring.

If regurgitation is observed during anesthesia, suctioning the refluxate from the oropharyngeal cavity and esophagus can minimize the chances of the patient aspirating and avoids damage to the esophageal mucosa, respectively. However, only suctioning of the refluxate from the esophagus has minimal impact in increasing the pH within the lumen of the esophagus. If regurgitation is observed, suctioning should be followed by esophageal lavage and sodium bicarbonate instillation [105]. Esophageal lavage with tap water can increase esophageal pH above 4.0, and infusion of a small volume of sodium bicarbonate can increase the pH above 6.0–7.0 for up to 3 h [105, 106]. However, esophageal lavage with tap water after esophageal suctioning may not be necessary if sodium bicarbonate is instilled, especially when all or most of the regurgitant volume is suctioned from the esophagus. Although esophageal lavage with tap water increases the esophageal pH, instillation of sodium bicarbonate after suctioning the esophagus readily buffers the pH of the esophageal lining, rendering any dilutional effect of the lavage inconsequential. The esophagus can be suctioned using a smooth tipped 8–12 Fr catheter. To ensure correct placement of the catheter and avoid suctioning from the stomach, the distance from the mandibular incisors to the 10th rib should be measured. Caution should be taken when inserting the catheter into the oropharynx to not enter the trachea. Therefore, it is critical that the airway is protected, and the ET tube cuff appropriately inflated. Esophageal suctioning should only be applied, as the catheter is withdrawn to avoid trauma to the esophagus. If the esophagus is lavaged with tap water, the lavage should be continued until clear fluid is retrieved. Sodium bicarbonate solution can be prepared using a 1:1 ratio of 8.4% sodium bicarbonate and water for injection; a volume of 0.6 ml kg−1 of this solution has been recommended for instillation into the esophagus [105, 106]. Pantoprazole (1.0 mg kg−1 IV) may be administered to dogs and cats following regurgitation.

If reflux aspiration is observed while the animal is anesthetized, the airway should be suctioned to remove irritants, and oxygen saturation and breathing patterns should be monitored. If oxygen saturation starts to drop, positive pressure ventilation should be instituted. Peak inspiratory pressure generated by a normal tidal volume (10–20 ml kg−1) should be observed. Generation of high peak inspiratory pressure (>20 cm H2O) with a normal tidal volume can indicate bronchospasm. Blood gas analysis can help assess the degree of oxygen exchange impairment.

Esophageal perforation with life‐threatening tension pneumothorax should be suspected with sudden changes in breathing patterns, subsequent drops in oxygen saturation, decreased breath sounds on thoracic auscultation, and increased resistance to manual ventilation [42]. If these occur, immediate thoracocentesis should be performed and positive pressure ventilation instituted. A decision of exploratory thoracotomy should then be made to remove the esophageal foreign body and repair the esophagus [2, 40]. In cases of thoracotomy for esophageal surgery, positive pressure ventilation must be continued, and appropriate pain management should be administered intraoperatively and postoperatively. Air and fluid must be evacuated via a thoracostomy tube or thoracocentesis after the procedure.

Anesthetic Recovery

Observing for regurgitation and airway protection during recovery is still crucial. Premature extubation can lead to aspiration if regurgitation occurs. Patients should be maintained in sternal recumbency, with the head elevated until the animal regains full consciousness and laryngeal reflexes. The ET tube cuff should be kept inflated (at least in part) during extubation to remove any fluid or content proximal to the ET tube cuff, which will minimize the chances of aspiration [36]. If the patient regurgitates on extubation, its head should be dropped below the thoracic inlet, and suctioning of the airway should be provided. Oxygenation with the aid of a pulse oximeter must be monitored during recovery from anesthesia.

Postoperative analgesia should be provided accordingly to the intensity of pain produced by the procedure and damage to the esophageal mucosa in the case of foreign bodies. NSAIDs have been identified as a factor associated with intraoperative regurgitation [50]; therefore, these drugs should be avoided in patients with esophageal disorders.

Gastric and Small Intestinal Disease

Gastric surgery is commonly performed to remove foreign bodies and to correct gastric dilatation–volvulus (GDV). Gastric foreign bodies usually cause vomiting and regurgitation because of mechanical irritation to the mucosa, outflow tract obstruction, or gastric distention. Vomiting often is intermittent, occurring when the object is forced into the pyloric antrum [2, 74].

Gastric ulceration, hemorrhage, and neoplasia are less common indications for surgery. However, patients with these disorders may require endoscopic diagnostic procedures or feeding tube placement. Gastric mucosal bleeding should be considered in patients with gastroduodenal ulceration or esophagitis due to chronic vomiting and, less often, due to malignancy [107].

Gastroscopy or gastrotomy is often indicated for the removal of large, sharp, or potentially toxic foreign bodies, whereas partial gastrectomy is performed for the removal of ulcers and neoplasms or necrosis from GDV. Pylorectomy with gastroduodenal anastomosis is indicated for the removal of the pylorus due to neoplasia, outflow tract obstruction caused by hypertrophic pyloric gastropathy, or gastric outflow tract ulceration [2, 74, 108].

Small intestinal surgery (enterotomy, intestinal resection, and anastomosis) is most often indicated for GI obstruction (i.e., foreign bodies). Foreign body material can result in partial or complete intestinal luminal obstruction, tissue necrosis, intestinal perforation, or a combination of these. With intraluminal GI obstructions, the intestine rostral to the lesion distends with gas and fluid. Fluid accumulation is caused both by fluid retention in the intestinal lumen and by fluid secretion by intestinal glands. During obstruction, secretion increases, and absorption diminishes; gas also accumulates. Eventually, fluid shifts not only into the lumen, but also from the serosa into the peritoneal cavity. Circulation in the mucosa and submucosa becomes impaired, and the mucosa becomes ischemic. Full thickness wall necrosis may occur at the obstruction site. Small intestinal stasis leads to luminal bacterial overgrowth. If the normal mucosal barrier is impaired by distention and ischemia, permeability may increase, with subsequent bacterial translocation, absorption of toxins into the systemic circulation or peritoneal cavity, or both [2].

Other indications for small intestine surgery include trauma (e.g., perforation, ischemia), malpositioning (e.g., volvulus, intussusception), neoplasia, and diagnostic procedures (e.g., full thickness biopsy). In addition, patients with suspected protein‐losing enteropathy require stomach and intestinal biopsies in order to confirm the diagnosis. These patients may undergo gastroduodenoscopy or exploratory laparotomy with gastrotomy and enterotomy [109].

Clinical Signs

Visual examination provides the following information about dogs and cats with GI disease: the animal’s mental state, temperament, nutritional state, and comfort. Most animals with gastric diseases have vomiting, regurgitation, anorexia, or depression, and, occasionally, abdominal pain and weight loss. Patients with primary small intestinal disorders usually present for signs of vomiting, diarrhea, anorexia, depression, and/or weight loss [2]. Fever and abdominal pain may result from severe GI disease such as complete GI obstruction or perforation [2, 74]. These patients usually become severely dehydrated due to fluid loss and a reduced fluid intake, resulting in acute volume depletion and signs of shock [2, 42, 73]. Abdominal distention may be evident if pyloric outflow obstruction or intestinal perforation is present.

Upper GI hemorrhage is an important cause of blood loss and anemia and is potentially life‐threatening in dogs [107]. Hematemesis or melena may indicate gastroduodenal ulceration or coagulopathy [2]. If blood loss exceeds 25% of total blood volume, these patients may experience hypotension and tachycardia and may be poor anesthetic candidates.

Coughing, dyspnea, and cyanosis can indicate that aspiration pneumonia has occurred in vomiting animals. However, aspiration pneumonia is a less common complication of vomiting than it is of regurgitation because reflex closure of the glottis occurs during emesis. Regurgitation may also occur because of esophagitis in animals that experience chronic vomiting [2, 73].

Laboratory Data

A full CBC, serum biochemistry profile, and venous blood gas (if possible) should be performed in any patient presenting with vomiting and/or diarrhea, as GI disease can lead to electrolyte and acid–base disturbances [42, 73, 109].

Laboratory parameters may be normal or may show only changes caused by dehydration (e.g., high PCV, TP, BUN, and creatinine), especially in animals with acute GI foreign bodies [2]. The metabolic consequences of vomiting due to foreign bodies are variable, but can be severe [74, 110]. The most common electrolyte and acid–base abnormalities, regardless of the site (stomach or small intestine) or type of foreign body, are hypochloremia, metabolic alkalosis, hypokalemia due to loss of acid‐rich gastric secretions, and hyponatremia. Paradoxical aciduria occurs in consequence of hypovolemia and hypokalemia [73, 74, 110]. This also suggests that foreign bodies distal to the duodenum can produce metabolic alkalosis by increased secretion of chloride and potassium into the intestinal lumen. This combined with vomiting of acid‐rich gastric secretions and volume contraction act to perpetuate any initial metabolic alkalosis [110]. However, metabolic acidosis might occur depending on the composition and volume of expelled GI contents and the degree of dehydration [73, 74]. In patients with more chronic vomiting, hyperlactatemia with subsequent metabolic acidosis may occur because of GI ischemia or systemic hypoperfusion [2, 73].

Hematocrit in patients with acute and severe gastric bleeding may be normal early during acute gastroduodenal hemorrhage due to insufficient time for plasma volume equilibration. Once plasma volume is equilibrated and fluid resuscitation is administered, anemia becomes more overt [74]. Acute upper GI bleeding is associated with a normocytic normochromic regenerative anemia, whereas chronic blood loss is characterized by iron deficiency and microcytic hypochromic anemia. In addition, a mild to moderate thrombocytosis may also be noted with chronic GI blood loss. With active bleeding, anemia is accompanied by hypoproteinemia [74]. BUN levels are typically increased in these cases because of the absorbed nitrogen load from the blood in the small intestine. A high BUN‐to‐creatinine ratio has been reported with upper GI hemorrhage [107].

Gastrointestinal loss accounts for approximately 40% of the normal daily turnover of plasma proteins, and, for this reason, protein‐losing enteropathy (e.g., inflammatory bowel disease) can lead to hypoproteinemia [111]. The mechanism of protein loss may be related to GI barrier inflammation or damage. Albumin is one of the proteins lost into the GI tract and, as it contributes significantly to oncotic pressure, intravascular fluid loss can occur second to hypoalbuminemia [73]. As albumin decreases (<1.5 g dl−1), effusions (e.g., pleural and peritoneal effusions) and edema can occur [111].

Anesthetic Management

Perianesthetic Considerations

The degree of dehydration should be evaluated based on physical examination and laboratory findings. Ideally, fluid deficit and electrolyte and acid–base abnormality correction should take place before anesthesia to improve the patient’s hemodynamic stability throughout the anesthetic procedure [42]. Isotonic (0.9%) saline is the fluid of choice for metabolic alkalosis. Since hypokalemia can lead to skeletal muscle weakness, decreased GI motility/ileus, and cardiac arrhythmias, it should be corrected with potassium chloride supplementation before anesthesia. When administered IV, potassium chloride generally should not be infused at rates >0.5 mEq kg−1 h−1 to avoid potential adverse cardiac effects [112]. Hypokalemia can also predispose the myocardium to the refractory effects of class I antiarrhythmic drugs such as lidocaine and procainamide. These drugs are commonly used during anesthesia in patients with diseases that can cause ventricular arrhythmias such as GDV. Hypokalemic patients in shock should be resuscitated with an isotonic crystalloid solution (e.g., 0.9% saline or LRS) before adding potassium chloride to the fluids. If a patient is severely hypokalemic (serum potassium <2 mEq), it is prudent to start potassium as a separate infusion and not with the resuscitation fluid bag to not exceed the recommended potassium infusion rate (0.5 mEq kg−1 h−1) [73]. Dehydration from vomiting in patients with metabolic acidosis should be corrected with a balanced isotonic crystalloid solution containing lactate or acetate as a buffer. The administration of sodium bicarbonate is necessary only in the treatment of patients with severe metabolic acidosis who have not responded to fluid therapy (pH <7.15) [113]. In these patients, bicarbonate deficit should be corrected with sodium bicarbonate according to the following equation:


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Oct 18, 2022 | Posted by in SUGERY, ORTHOPEDICS & ANESTHESIA | Comments Off on Gastrointestinal Disease

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