EMERGENCY SURGICAL PROCEDURES 0195--5616/00 $15.00 + .

00

GASTROINTESTINAL
EMERGENCIES
Lillian R. Aronson, VMD, Daniel J. Brockman, BVSc, CVR, CSAO,
and Dorothy Cimino Brown, DVM*

The animal that presents with a surgical gastrointestinal emergency typically

requires a rapid thorough physical examination with concurrent resuscitation.
As the diagnosis is being made, the animal must be made as stable as possible
before undergoing general anesthesia. During surgery, there must be a critical
evaluation of gastrointestinal viability and the use of precise technical skills to
achieve the best outcome. Adept postoperative management, including careful
monitoring and an index of suspicion for potential complications, is vital. 33

ESOPHAGUS
Esophageal Foreign Body

The normal esophagus has three distinct anatomic narrowings where in-
gested objects are likely to become lodged: the level of the cricopharyngeal
sphincter, the base of the heart, and the diaphragmatic hiatus. In addition,
foreign bodies tend to lodge at the thoracic inlet, where adjacent soft tissues
may impede esophageal dilation. 20, 33, 63 Many foreign bodies produce acute
clinical signs because of either complete obstruction or extreme partial obstruc-
tion. Ptyalism as a result of impaired swallowing of saliva, progressive dyspha-
gia, and persistent regurgitation of undigested food are the most common signs
of esophageal obstruction. 20' 33' 63 When foreign objects permit the movement of
liquid or semisolid food past them, producing only partial obstruction, it is
possible for these objects to be present for an extended period of time before
being diagnosed.
Radiopaque foreign bodies are visualized on plain radiographs. Nonradio-

*Authors are listed in alphabetical order.

From the Department of Clinical Studies, School of Veterinary Medicine, University of

Pennsylvania, Philadelphia, Pennsylvania

VETERINARY CLINICS OF NORTH AMERICA: SMALL ANIMAL PRACTICE

VOLUME30•NUMrnER3•MAY2~ 555
556 ARONSON et al

paque foreign bodies require a positive-contrast esophagram to be visualized.

Although barium may be used, if esophageal perforation is supected, an iodin-
ated contrast agent is indicated. Endoscopy is also a valuable tool for diagnosis
and, in many cases, treatment of the obstruction.
Esophageal foreign body obstruction is an emergency, and removal of the
foreign body should be immediate. The longer the duration of the obstruction,
the more chance there is of developing complications. Local changes occur in
the esophagus at the point(s) of contact with the foreign body, and mucosal
necrosis can occur. Necrosis may extend through the entire esophageal wall,
which can lead to perforation, mediastinitis, pleuritis, pyothorax, or esophageal
fistula. 21, 31, 32, 61, 79
Nonsurgical management of esophageal foreign bodies is generally the
treatment of choice. 20• 21 • 31- 33 Rigid proctoscopes or flexible fiber-optic endoscopes
and long blunt-ended forceps can be used to remove most foreign bodies.
Esophagoscopy is performed while the animal is under general anesthesia and
positioned in left lateral recumbency. Some instruments allow insufflation of air,
dilating the esophagus arolind the foreign body. Once the foreign body is
grasped, gentle twisting may help to disengage the foreign object and allow per
os removal. Some objects are too large and can be gently pushed into the
stomach. Once in the stomach, indigestible objects can be removed via gastrot-
omy. Bones generally do not need to be removed. After removal, the esophageal
wall is re-examined, and clean lacerations that do not extend to the full thickness
of the esophageal wall can be left to heal. Full-thickness tears or areas of necrosis
require surgical intervention.
Surgical removal of foreign bodies is necessary when endoscopic removal
fails or in cases with associated esophageal perforation. The cervical esophagus
is accessed via a ventral midline incision in the neck. For foreign bodies lodged
at or cranial to the heart base, a right third or fourth intercostal thoracotomy
provides the best exposure. For foreign objects lodged caudal to the heart base,
a left eighth intercostal thoracotomy is used. Foreign bodies in the distal esopha-
gus can often be retrieved by manipulation through a gastrotomy incision made
via laparotomy or a transdiaphragmatic approach through the eighth intercostal
space. For penetrating esophageal foreign bodies such as fishhooks and needles
that cannot safely be retrieved or pushed into the stomach, surgery can be used
to cut off the extraluminal portion of the object, and the remaining intraluminal
portion is recovered with an endoscope. 51 When an esophagotomy is necessary,
a longitudinal incision is made. The incision can be closed with a single layer of
interrupted, appositional, 3-0 or 4-0 monofilament sutures. 19• 33• 36 The combined
effects of absence of serosa and omentum, vulnerable intramural blood supply,
and motion at the incision site make the esophagus prone to wound healing
complications. 19• 21• 32
The major complication of esophageal surgery is cervical cellulitis or medi-
astinitis secondary to esophageal perforation. The diagnosis is confirmed via
repeated esophagoscopy or a contrast esophagram using a water-soluble iodin-
ated contrast agent. Establishing drainage, controlling infection, and repairing
the esophagus is the treatment for leakage of the cervical esophagus. Thoracic
esophageal perforation requires exploratory thoracotomy, removal of infected
debris, and repair of the damaged area. The chest cavity is thoroughly lavaged
and drained via chest tubes. After foreign body removal, animals are held off
food for 24 hours after uncomplicated endoscopic removal or for 48 to 72 hours
for cases requiring esophagotomy; a small amount of soft food or slurry can
then be fed. 32
The prognosis following uneventful endoscopic removal is generally good.
 GASTROINTESTINAL EMERGENCIES 557

During chronic partial obstruction, the esophagus proximal to the lesion may
dilate. A permanent megaesophagus of the affected region with poor esophageal
motility can remain even after the obstruction is relieved and may indicate a
more guarded prognosis. 87

STOMACH

Gastric Foreign Bodies

Many gastric foreign bodies are not true surgical emergencies. They cause
clinical signs if they lodge in the pylorus and trigger the vomiting reflex. Metallic
foreign bodies retained in the stomach may cause toxicosis associated with
aluminum or zinc absorption. 50• 81 This is particularly the case with pennies
minted after 1982. Sharp gastric foreign bodies should be removed as soon as
possible to prevent migration or perforation.
Radiopaque foreign bodies are visualized on plain radiographs. Nonradio-
paque foreign bodies require positive- or double-contrast studies to be visual-
ized. If gastric perforation is suspected, an iodinated contrast agent is indicated.
Many foreign bodies can be removed with a flexible endoscope. If endoscopic
removal of a foreign body is planned, it should be done as soon after diagnosis
as possible, before the object leaves the stomach and is no longer accessible.
Large or rough foreign bodies and those that are not successfully retrieved
via the endoscope can be removed via gastrotomy. The incision is made in a
relatively avascular area of the stomach, midway between and parallel to the
greater and lesser curvatures. The incision is made long enough to allow the
foreign body to pass without tearing. A two-layer technique, with the second
layer being an inverting pattern using a synthetic, monofilament, absorbable
suture material, can be used to close the incision. Small amounts of food can be
introduced 24 hours after surgery.
The prognosis following gastrotomy for the removal of foreign bodies is
good. It can be complicated by local or generalized peritonitis as the result of
spillage of gastric contents, but this is uncommon if moist laparotomy sponges
are used to wall off the stomach before the gastrotomy incision is made.

Gastric Bleeding

Occasionally, severe gastric ulceration and bleeding can become a surgical

emergency. If medical management, including volume replacement with fluid
therapy and whole-blood transfusion, H 2 receptor antagonists, proton pump
inhibition, and synthetic prostaglandins, is unsuccessful in stabilizing the animal,
surgical treatment is indicated, particularly when uncontrolled hemorrhage or
acute perforation occurs. 68• 71 • 80 Gastric ulceration and bleeding can be associated
with chronic renal and hepatic disease, gastric neoplasia, mast cell tumors,
gastrinomas, and corticosteroids. Cases of severe gastric hemorrhage occur most
frequently after the use of nonsteroidal anti-inflammatory drugs. 71 Characteristic
clinical signs are hematemesis and melena. If perforation occurs, collapse, ab-
dominal pain, and abdominal distention ensue. 55• 71 • 80
Several methods have been used to localize the site of bleeding. Endoscopy
can be useful in locating superficial erosions, but in cases of severe hemorrhage,
it may be difficult to visualize the lesion when the stomach is full of blood.
Positive- or double-contrast radiography may detect ulcer craters as outpouch-
558 ARONSON et a!

ings from the gastric lumen containing contrast material. 3 Despite these tech-
niques, or if the animal is deteriorating too rapidly to allow the performance of
these techniques, the diagnosis may not be confirmed until the time of surgery. 71
At surgery, the stomach is inspected from fundus to pylorus. Small ulcers
can be removed by elliptic incision and closed in two layers as described
previously. Multiple or large ulcers in the pyloric part of the stomach are
removed by gastrectomy and gastroduodenostomy (Billroth 1). 71 • 80 The prognosis
depends on the underlying cause for the bleeding. For neoplasia, chronic renal or
hepatic disease, or blood coagulation disorders, the prognosis is generally poor. 80

Gastroesophageal Intussusception

Intussusception is the invagination of one portion of the gastrointestinal

tract into the lumen of an adjoining segment. The stomach can invaginate into
the lumen of the esophagus and become trapped, resulting in acute respiratory
distress and rapid deterioration. Affected animals tend to be less than 1 year of
age, and German Shepherds are especially at risk. 42 Survey thoracic radiographs
reveal a soft tissue density within the thoracic esophagus adjacent to the dia-
phragm. A positive-contrast esophagram may help to delineate the apex of the
intussusceptum.
Emergency treatment is necessary to relieve the dyspnea and shock and to
prevent gastric necrosis secondary to strangulation. Fluid resuscitation is fol-
lowed immediately by exploratory laparotomy. The intussusception is reduced,
and if the stomach is still viable, a fundic gastropexy is performed to prevent
recurrence. The reported prognosis for this condition is grave. In one study, less
than 20% of affected dogs were diagnosed antemortem. 42

Gastric Dilatation with Gastric Volvulus

Gastric dilatation-volvulus syndrome comprises acute and chronic gastric

dilation, gastric dilatation with gastric volvulus (GDV), and chronic gastric volvu-
lus.72 GDV causes local and systemic pathophysiologic changes that are rapidly
fatal if left untreated. It is estimated that GDV affects approximately 60,000 dogs
in the United States every year; even with treatment, acute GDV has been
associated with reported mortality rates between 10% and 60%.5-7, 9• 24• 49• 52

Risk Factors
Over the years, many factors have been proposed as contributing to the
etiology of acute GDV Most research has focused on the influence of anatomy
and diet as well as on the possible influence of perturbations of gastric motility.
Such factors must individually or in combination result in failure of the normal
mechanisms of gastric decompression. The simultaneous failure of mechanisms
of eructation and pyloric outflow may result in an inappropriate accumulation
of gas, fluid, or both.
Anatomy and Breed. Because GDV is predominantly a disease of large- and
giant-breed dogs, it is reasonable to hypothesize that there are anatomic features
of large- and giant-breed dogs that may predispose them to GDV development.
Predisposed breeds demonstrated in various reports include Great Danes, Ger-
man Shepherds, Standard Poodles, Weimeraners, Saint Bernards, Gordon Setters,
Irish Setters, Borzois, and large mixed-breed dogs. 6• 23• 58• 65 Although large-breed
 GASTROINTESTINAL EMERGENCIES 559

dogs are most commonly affected, the syndrome has occasionally been docu-
mented in small breeds, with the Bassett Hound having the highest incidence in
dogs weighing less than 23 kg. Although rare, GDV has also been reported in
cats.74 In one epidemiologic study, increasing breed size, being purebred, and
increasing age were confirmed as significant risk factors in the development of
GDV. 23 In another study, purebred dogs were 4.4 times more likely to develop
GDV than mongrels. 9
A few authors have suggested that a relation exists between thoracoabdomi-
nal conformation and GDV. In a recent study evaluating Irish Setters, increased
thoracic depth-to-width ratios were associated with an increased risk of develop-
ment of GDV. It was suggested that selective breeding against deep-chested
conformation may decrease the prevalence of GDV. 65 As previously mentioned,
Bassett Hounds have the highest risk of GDV in breeds weighing less than 23
kg. They have also been shown to have the largest thoracic depth-to-width ratio
among the smaller breeds, suggesting that thoracic depth-to-width ratio may be
an important predictor of GDV risk. Others have suggested that thoracoabdomi-
nal dimensions could influence the relation between the stomach, esophagus,
gastroesophageal junction, and diaphragm. 72 The normal anatomic arrangement
of these organs is important in preventing gastroesophageal reflux. Any alter-
ation in this area may be a reason for failure of the gastroesophageal junction to
function normally, resulting in a dog's inability to eructate or vomit. 72 This could
also explain why animals may suffer from chronic gastric dilation after therapy
for acute GDV. The influence of the spleen on gastric position has also been
proposed; however, the fact that GDV can occur in splenectomized dogs suggests
that although it may contribute to the syndrome, it is not an essential factor. 14
In a recent report, dogs with GDV had significantly longer hepatogastric
ligaments than unaffected dogs. 27 It was suggested that the longer ligaments
may facilitate gastric rotation and predispose dogs to partial or complete GDV.
Unfortunately, no definitive conclusions could be drawn from this study, because
it is not known whether the ligaments were lengthened as a result of GDV or
whether the lengthened ligaments predisposed dogs to GDV.
Diet. The number of meals, type of diet, exercise after eating, overeating,
rapid ingestion of food, and consumption of large volumes of water have all
been implicated as playing a role in the development of GDV at some point.
More recently, the focus has been on the type of diet and feeding patterns of
domestication. The diet in domesticated dogs is lower in protein and roughage
and higher in carbohydrates78 than the diet of feral dogs. Additionally, domesti-
cated dogs are typically fed once or twice daily in comparison to feral dogs,
whose eating pattern is variable. Earlier studies suggested that dry dog foods,
particularly those containing soybean meal, may predispose dogs to GDV if fed
once a day. 77 In 1985, Burrows et aP1 evaluated dietary composition and its effect
on gastric emptying and motility in dogs. He concluded that dietary composition
did not affect motility and emptying and that these diets had been wrongly
implicated. In 1987, Van Kruiningen et aF8 evaluated the influence of diet and
feeding frequency on gastric function in normal dogs. Gastric motility was not
significantly different between dogs fed a commercial dry dog food or meat and
bone ration or between different feeding frequencies. The authors did comment
that once-daily feeding of a commercial dry dog food may cause a chronically
distended stomach that could predispose a dog to the development of GDV.
Gastric Motility. Gastric Myoelectric Activity. In human beings, gastric
dysrhythmias have been associated with nausea, vomiting, and bloating. 28• 73 In
the early 1980s, it was suggested that similar abnormalities may exist in the dog
and result in delayed gastric emptying with secondary GDV.U The role of
560 ARONSON et a!

myoelectric dysfunction in the pathogenesis of GDV is unclear. A study in

1992 evaluating gastric myoelectric activity after experimental GDV and tube
gastrostomy found that myoelectric activity was disrupted in normal dogs after
GDV with tube gastrostomy as well as after tube placement alone?0 It was
concluded from this study that GDV alone was not responsible for any signifi-
cant dysrhythmias. It seemed that myoelectric changes were induced by the
tube alone. A number of experiments have been performed to evaluate gastric
dysrhythmias in experimental and spontaneous GDV. Although dysrhythmias
were detected in both groups, it could not be determined if changes in myoelec-
tric activity were the cause or result of GDV. 10
Vomiting and Eructation. Abnormalities in the normal vomiting or eructa-
tion mechanism can also result in an abnormal accumulation of gas in the fasting
or postprandial stomach. It is not thought that a primary malfunction of the
gastroesophageal sphincter exists in these animals; however, alterations in ana-
tomic arrangement of the stomach, esophagus, and diaphragm in this area may
play a role in acute gastric dilatation.
Vagal innervation of the esophagus is essential for the normal vomiting
reflex. This has been shown in studies in which selective vagotomies have been
performed on the caudal canine esophagus, resulting in an inability to retract
the intra-abdominal segment into the thoracic cavity. 16 This finding could suggest
that failure of normal vomiting and eructation may be secondary to lack of
vagal innervation.
The role of gastrin has been evaluated for possible effects on both vomiting
and normal gastric emptying. Initially, it was suggested that dogs suffering from
GDV may have had a pre-existing high plasma gastrin concentration. 43 Gastrin,
a hormone secreted by the pyloric antrum, was proposed to play a role in the
development of GDV by increasing gastroesophageal sphincter pressure (GESP)
and by causing a delay in gastric emptying. An increase in GESP may prevent
vomiting during the development of GDV, and delayed gastric emptying may
result in gastric distention. In a later study by Hall et aF6 evaluating pre- and
postprandial GESP and plasma gastrin levels in normal dogs and dogs that were
treated for GDV, no significantly different values were detected between affected
and normal dogs.
Stress. Stress has been suggested by some authors to be a risk factor for the
development of GDV. Historical evaluation of some animals revealed a stressful
event preceding the onset of GDV. In other canine studies, stress was shown to
disrupt gastric motility and emptying. 25 The exact contribution of stress to the
development of GDV is unclear.
Pathoanatomy of Gastric Dilatation with Gastric Volvulus. If the dog is
positioned in dorsal recumbency and viewed caudocranially, the most common
rotation is clockwise. The pylorus and gastric antrum become displaced from
the right abdominal wall and move ventrally over the gastric fundus and body
to a position adjacent to the esophagus along the left abdominal wall (Fig. 1).
The maximum rotation in this direction is 270° to 360°. On the initial approach
into the abdomen, the ventral leaf of the omentum is seen covering the ventral
aspect of the displaced stomach (Fig. 2). Counterclockwise rotation is less com-
mon, with a maximum rotation of 90°. The pylorus and antrum move dorsally
along the right abdominal body wall, ending up adjacent to the esophagus.
Minimal ventral displacement of the gastric fundus and body occurs, and the
omentum is not visualized over the ventral aspect of the stomach.
The splenic position varies depending on the degree of gastric volvulus.
Occasionally, the spleen can undergo torsion around its vascular pedicle.
 GASTROINTESTINAL EMERGENCIES 561

Pyloric Fundus
Pyloric
antrum
antrum

Figure 1. Anatomic malpositioning of the stomach that occurs with gastric dilatation-
volvulus syndrome. The pylorus and gastric antrum become displaced from the right
abdominal wall and move ventrally over the gastric fundus and body to a position adjacent
to the esophagus along the left abdominal wall.

Figure 2. The ventral leaf of the omentum is seen covering the ventral aspect of the
displaced stomach.
562 ARONSON et al

Pathophysiology of Gastric Dilatation with Gastric Volvulus

Dogs that present with GDV are not only at risk for the development of
local complications involving the stomach and spleen but are at risk for the
development of systemic complications, which can be fatal if left untreated.
Cardiovascular Pathophysiology. As gastric dilatation progresses, the cau-
dal vena cava is occluded, reducing venous return to the heart. The portal
vein is also compressed, resulting in sequestration of blood in the splanchnic
parenchyma, which compounds poor venous return to the heart. Portal hyper-
tension can also cause movement of fluid into the gastrointestinal tract, resulting
in a reduction of circulating blood volume. 72 Compensation occurs with shunting
of blood through the intervertebral and azygous veins, but this collateral circula-
tion is not adequate to return blood flow to normal circulation, and the net
result is decreased cardiac output, arterial blood pressure, and coronary arterial
blood flow. 47• 72 Reduced coronary blood flow contributes to myocardial ischemia
and hypoxia with resultant cardiac dysrhythmias. 30• 34 With continued hypoten-
sion, systemic cellular hypoxia occurs with a shift to anaerobic metabolism.
Gastric and Splenic Pathophysiology. Gastric pathology ranges from mild
gastritis to necrosis and perforation. A number of factors contribute to gastric
mucosal and mural venous stasis in affected animals. An increase in gastric
intraluminal pressure may result in congestion because of interference with
normal venous drainage. 8• 48• 49• 85 The vascular stasis that occurs can then lead
to venous thrombosis. As gastric distention and malposition progress, portal
hypertension can occur, contributing to gastric congestion as well as causing a
decrease in gastric blood flow. The gastric mucosa receives 80% of the total
gastric blood flow. A decrease in mucosal blood flow in conjunction with gastric
acid production can result in gastric ulceration and necrosis. A decrease in
gastric circulation may also affect innervation to the stomach, occasionally re-
sulting in persistent gastric atony after recovery from gastric dilatation. 72 Avul-
sion of branches of the short gastric and right gastroepiploic vessels from the
gastric fundus results in hemoperitoneum and hypovolemia, which can exacer-
bate gastric ischemia. Splenic congestion can also occur secondary to portal
hypertension, and splenic torsion has been seen in some animals with GDV. In
experimental studies in which splenic arterial ligation was performed, a decrease
in coagulation factors VIII and IX was observed.75 This may be important in the
development of disseminated intravascular coagulation in some of these ani-
mals.
Respiratory Pathophysiology. Respiratory dysfunction occurs as a result of
decreased pulmonary compliance and restriction of diaphragmatic movement
secondary to gastric dilatation. Because the tidal volume is decreased, the respi-
ratory rate is increased so as to maintain minute volume. As dilatation worsens,
a normal minute volume cannot be maintained. As a result, blood oxygen
tension falls, exacerbating the already reduced oxygen delivery to tissue, and
tissue hypoxia occurs.
Pathophysiology of the Liver and Pancreas. With continued portal vein
occlusion and hypertension, there is a decrease in the ability of the reticuloendo-
thelial system to clear gram-negative endotoxins absorbed from the devitalized
gastric mucosa. This results in endotoxemia, which can further potentiate hypo-
tension, decreased cardiac output, and splanchnic sequestration. Mild to severe
elevations of serum alanine aminotransferase and alkaline phosphatase may be
detected. The pancreas is also quite sensitive to decreases in blood flow. Pancre-
atic ischemia can result in the release of proteolytic enzymes that can cleave off
biologically active peptides. One of these peptides is myocardial depressant
 GASTROINTESTINAL EMERGENCIES 563

factor, which has a direct cardiodepressant effect and causes vasoconstriction of

the splanchnic parenchyma and depression of the reticuloendothelial system. 40
Clinical Signs and Physical Examination Findings. Clinical signs are typi-
cally acute. Nonproductive retching, restlessness, depression, and hypersaliva-
tion are typically followed by progressive abdominal distention and tympany,
discomfort, and weakness. In animals with chronic GDV, a history of intermittent
vomiting, anorexia, and weight loss is more common. Clinical signs alone cannot
differentiate dilatation from dilatation and volvulus. In some giant-breed dogs,
the dilated stomach can remain within the rib cage, resulting in an inability on
the part of the clinician to observe the classic abdominal distention.
On initial physical examination, animals are often tachycardic with poor
peripheral pulses and a prolonged capillary refill time. Gastric distention may
also be evident along with tachypnea and dyspnea if gastric distention is re-
stricting diaphragmatic movement.

Initial Treatment and Stabilization

The initial goal in stabilizing these animals is treatment of hypovolemic
shock. On admission, two large-bore catheters (18-gauge) are placed in either
the cephalic or jugular vein. Placement of catheters in caudal veins may not be
sufficient because of decreased venous return to the heart secondary to the
dilated stomach compressing the vena cava. A blood sample is collected for
packed cell volume (PCV), total protein, acid-base analysis, and serum electro-
lytes. Blood is also collected for a complete blood cell count, chemistry profile,
and coagulation panel. An electrocardiogram (ECG) is placed to monitor for any
cardiac arrhythmias.
Isotonic fluids are started at a rate of 90 mL I kg I h. Animals are continuously
reassessed by monitoring parameters such as central venous pressure, arterial
blood pressure, PCV, total protein, heart rate, and capillary refill time, and
intravenous fluid rate and composition are adjusted accordingly. In some ani-
mals, hypertonic saline (7% sodium chloride in 6% dextran 70) at 5 mLikg
every 5 minutes may be more beneficial in combination with crystalloid adminis-
tration.66 Some animals also may benefit from blood product administration in
addition to standard fluid treatment.
The use of antibiotics in animals suffering from GDV is controversial.
Both aerobic and anaerobic bacteria can be absorbed in animals with gastric
compromise. Although not proven, antibiotics may be beneficial for prophylaxis
against gastrointestinal absorption of bacteria, abdominal contamination that
may occur during surgery, and treatment for endotoxic shock. Broad-spectrum
antibiotics are recommended.
Once hypovolemia is corrected, gastric decompression is performed either
by orogastric intubation or, if the veterinarian is unable to perform orogastric
intubation, by gastric trocarization. The tube length is measured from the exter-
nal nares to the last rib (Fig. 3). Oxymorphone (0.05-0.2 mglkg) intravenously
and diazepam (0.25-0.5 mglkg) intravenously can be used for sedation. A roll
of tape can be placed between the dog's teeth to aid in placement of the
orogastric tube. If resistance is met during placement, transabdominal gastro-
centesis using a large-bore needle at the site of gastric tympany may facilitate
intubation. The inability to pass a stomach tube is not diagnostic for volvulus.
It is also important to remember that the easy passage of the tube does not rule
out volvulus. In a few cases, adequate decompression cannot be performed until
surgical correction.
564 ARONSON et a!

Figure 3. Measurement of tube length from the external nares to the last rib.

Radiography
A radiograph of the animal positioned in right lateral recumbency is the
view of choice. 29 In a normal dog positioned in right lateral recumbency, fluid
collects in the most dependent portion of the stomach (pylorus), and gas fills
the fundus.4 6 In an animal with GDV, the pylorus is gas-filled and located
dorsally. A gas-filled fundus can also be detected along with a soft tissue
fold that seems to compartmentalize the gas-filled stomach (Fig. 4). 29 Other
radiographic observations include the location of the duodenum between the
liver and gastric fundus, splenic enlargement and malpositioning, and gas within
the gastric wall indicating gastric compromise; if rupture has occurred, free gas
may be seen in the abdominal cavity.

Anesthesia
Agents selected for anesthesia should have minimal effects on the cardiovas-
cular system. Drugs that are hypotensive, arrhythmogenic, or depress respiration
such as acepromazine and barbiturates should be avoided. Narcotics are appro-
priate for sedation and induction. Anesthesia can be maintained with isoflurane
in oxygen. Nitrous oxide should not be used until permanent gastric decompres-
sion is achieved. An arterial line is placed to facilitate intraoperative blood
pressure monitoring, and continuous ECG is performed because of the risk of
cardiac arrhythmias. Evaluation of PCV, total protein, electrolytes, and blood gas
analysis is done every hour during the procedure, and fluid and blood product
administration is adjusted accordingly.

Surgical Techniques
The goals of surgery are to correct gastric malposition, resect devitalized
tissue, and prevent recurrence of volvulus by performing a gastropexy. A cranial
 GASTROINTESTINAL EMERGENCIES 565

Figure 4. A lateral abdominal radiograph taken with the dog in right lateral recumbency. The
pylorus is gas-filled and located dorsally. A gas-filled fundus will also be seen caudoventrally.

ventral midline laparotomy is recommended. Any free peritoneal blood is evacu-

ated, and active sites of hemorrhage are ligated. Gastric decompression is
achieved by orogastric intubation or gastrocentesis to aid in the restoration of
normal gastric position. After decompression, downward displacement of the
fundus along with ventral retraction of the pylorus returns the stomach to its
normal position. The stomach and spleen are evaluated for viability. Infarction
and necrosis are most common along the greater curvature in the area of
attachment of the short gastric vessels39• 47 and occur in approximately 10% of
cases (Fig. 5). Determining the presence and extent of gastric necrosis can be
difficult. A pale greenish or grayish coloring to the serosal surface or areas that
remain black after repositioning of the stomach suggest ischemia that is likely
to proceed to necrosis. Palpation of gastric and splenic vessels a ls o may be
helpful in assessing viability. Because evaluation of tissue viability is often
subjective, the amount of gastric resection needed may be difficult to determine.
Partial gastrectomy can be performed using a suture technique or stapling
equipment. Before partial gastrectomy, the stomach is packed off from the
abdominal cavity with laparotomy sponges. For the suture technique, stay su-
tures are placed in healthy stomach to define the area of resection. The necrotic
stomach is excised u sing Metzenbaum scissors or a scalpel blade, and the
gastric wall is closed in two or three layers using absorbable suture material.
Alternatively, a GIA-50 or TA-90 surgical stapler can be used to perform the
partial gastric resection. The staple line is then oversewn using a continuous or
interrupted Cushing or Lembert inverting suture pattern. In cases of complete
gastric necrosis or necrosis of the cardia and abdominal esophagus, a poor
prognosis should be given to the owner.
Often, at the time of initial laparotomy, the spleen may look congested, and
566 ARONSON et al

Figure 5. Necrotic gastric wall is most common along the greater curvature.

its viability may be questioned. The stomach and spleen are repositioned, and
the splenic vasculature is evaluated before a decision is made to perform a
partial or complete splenectomy. Although initially congested, the spleen often
returns to its normal. size and color after repositioning. If torsion of the spleen
has occurred around its pedicle, a splenectomy should be performed before
reducing the twist to prevent the release of toxins into the systemic circulation.
To prevent recurrence, a gastropexy is performed. A gastropexy produces a
permanent adhesion between the stomach and the lateral body wall. Many
techniques have been described.22. 42• 62• 67• 82• 83 Two of the more common tech-
niques are an incisional gastropexy and a tube gastropexy.
To perform an incisional gastropexy, an incision is made in the serosal and
muscularis layers of the pyloric antral region of the stomach. An incision of
similar length is made into the peritoneum and internal fascia of the muscles of
the lateral abdominal wall. The edges of the gastric incision are sutured to the
abdominal incision using a simple continuous pattern (Fig. 6).
To perform a tube gastropexy, a large Foley catheter (24- or 26-gauge) or
Pezzar urologic catheter is placed through a stab incision in the ventrolateral
abdominal body wall approximately 2 em caudal to the last rib on the right side
and 2 em lateral to the ventral midline. A pursestring suture is placed in the
pyloric antrum using polypropylene, and a stab incision is made into the gastric
lumen. The catheter is placed into the gastric lumen, and the Foley catheter and
pursestring suture are tied (Fig. 7). Pexy sutures are placed to attach the pyloric
antrum to the body wall. Puncture of a Foley catheter balloon is carefully
avoided when placing the pexy sutures. Tube gastropexy allows for postopera-
tive decompression in animals that bloat following surgery and is a route for
feeding or administration of medication. Complications associated with this
technique include premature dislodgment of the tube, local and occasionally
generalized peritonitis, and cellulitis associated with leakage of gastric contents
around the gastropexy site.
 GASTROINTESTINAL EMERGENCIES 567

Figure 6. lncisional gastropexy. An incision is made in the serosal and muscularis layers
of the pyloric antral region of the stomach. An incision of similar length is made into the
peritoneum and internal fascia of the muscles of the lateral abdominal wall. The edges of
the gastric incision are sutured to the abdominal incision using a simple continuous pattern .

Figure 7. Tube gastropexy. A large Foley catheter or Pezzar urologic catheter is placed
through a stab incision in the ventrolateral abdominal body wall. A pursestring suture is
placed in the pyloric antrum and a stab incision is made in the center of the pursestring
suture into the gastric lumen. The catheter is placed into the gastric lumen and the
pursestring suture is tied. Although not shown, pexy sutures are placed to attach the pyloric
antrum to the body wall.
568 ARONSON et a!

Postoperative Management
Intravenous fluids are administered postoperatively until the animal is
eating and drinking. Immediately postoperatively, a balanced electrolyte solution
should be administered at a rate of 8 to 10 mL/kg/h. Fluid therapy should be
adjusted based on regular determinations of peripheral pulse quality, mucous
membrane color and refill time, hydration status, urinary output, PCV and total
protein. If indicated, a complete blood cell count and chemistry profile should
be performed. ECG monitoring should be performed for 48 to 72 hours postop-
eratively. Postoperative discomfort should be treated with the systemic admin-
istration of opioid analgesics such as morphine (0.5 mg/kg administered intra-
muscularly every 4-6 hours) or oxymorphone (0.05 mg/kg administered
intramusculary every 4-6 hours). If the animal is stable and not vomiting, water
can be offered 24 hours after surgery. If water is tolerated well, small amounts
of food can be offered 48 to 72 hours after surgery. Antibiotics may be indicated
postoperatively in animals that had abdominal contamination during surgery
secondary to gastric necrosis or in those animals in which endotoxic shock is
suspected.

Postoperative Complications
Cardiac Arrhythmias. Cardiac arrhythmias are a common complication and
occur 12 to 36 hours after the onset of GDV. 52 The arrhythmias are usually
ventricular in origin and have been reported to occur in 30% to 50% of animals
suffering from GDV. 64 Such arrhythmias include persistent or intermittent ven-
tricular tachycardia and multifocal premature ventricular conductions. 53 Al-
though less common, supraventricular arrhythmias such as atrial fibrillation and
atrial premature depolarization have been observed. 53' 54 Factors that may be
responsible include acid-base and electrolyte abnormalities (particularly hypoka-
lemia), myocardial ischemia, circulating cardiostimulatory substances such as
myocardial depressant factor, and an imbalance of autonomic function. 54, 6o Before
instituting antiarrhythmic therapy, all electrolyte and acid-base abnormalities
should be corrected. Treatment with antiarrhythmic drugs such as lidocaine
hydrochloride or procainamide is indicated if the arrhythmias are associated
with signs of reduced cardiac output or the R-on-T phenomenon and if acid-
base, electrolyte, and intravascular volume deficits have been restored. It is
administered initially as a bolus of 2 to 4 mg I kg and is continued as a constant-
rate infusion of 0.05 to 0.08 mg/kg/min. Signs of lidocaine toxicity include
vomiting, nausea, depression, and muscle tremors. If signs occur, either the
dosage of lidocaine should be lowered or a different antiarrhythmic instituted.
Reperfusion Injury. Standard treatment of animals suffering from GDV
involves aggressive fluid therapy and gastric decompression followed by surgi-
cal techniques to immobilize the stomach. The goal of this treatment is reversal
of hypovolemic shock by reperfusion of poorly perfused tissues. Unfortunately,
this can result in the production of highly reactive molecules derived from
oxygen reduction, including superoxide anions, hydroxyl radicals, and hydrogen
peroxide, which can cause significant cellular injury termed reperfusion injury. It
is possible that treatment directed toward preventing or controlling reperfusion
injury may improve survival rates in these animals. A few experimental studies
have evaluated the protective benefits of iron chelators (deferoxamine), xanthine
oxidase inhibitors (allopurinol), and free radical scavengers (dimethyl sulfoxide)
in animals with GDV. 2' 39 The results of one study suggested that deferoxamine
may have beneficial effects in reducing mortality by preventing or attenuating
 GASTROINTESTINAL EMERGENCIES 569

reperfusion injury. Although some of these drugs have shown beneficial effects
in the experimental situation, until prospective studies are performed on large
numbers of clinical cases, the information from these experimental studies
should be evaluated with caution.
Gastric Necrosis and Perforation. Gastric viability at the time of surgery is
subjective, and postoperative necrosis and perforation can occur postoperatively
in spite of careful assessment. 49 This complication should be suspected within
the first few days postoperatively in a dog with a deterioration of clinical
signs and abdominocentesis revealing a bacterial peritonitis. Treatment of these
animals involves exploratory laparotomy with resection of devitalized tissue
and repair of the gastric wall. In a recent study, the relations between plasma
lactate concentration and gastric necrosis and between plasma lactate concentra-
tion and outcome were evaluated. 15 It was found that the pretreatment plasma
lactate concentrations in dogs with gastric necrosis (6.6 mmol/L) were signifi-
cantly higher than those in dogs without gastric necrosis (3.3 mmol/L) and that
99% of the dogs in their retrospective study with plasma lactate less than 6
mmol/L survived compared with 58% of the dogs with concentrations greater
than 6 mmol/L. In animals suffering from GDV, gastric necrosis has been
associated with significantly higher mortality. 15
Hypotension. Hypotension in these animals has been associated with inade-
quate fluid therapy, anesthetic drugs, continued hemorrhage after surgery, gas-
trointestinal fluid loss, and poor cardiac function. Hemorrhage after surgery
may be the result of continued bleeding from the short gastric and gastroepiploic
vessels, disseminated intravascular coagulation, or. gastric mucosal ulceration.
Gastrointestinal fluid loss may be associated with hypoproteinemia. Treatment
should be based on the underlying cause of hypotension and often involves the
use of crystalloids, blood products, or synthetic colloids. In animals with primary
cardiac disease, appropriate drug therapy should be instituted, and fluid treat-
ment should be administered with caution.
Aspiration Pneumonia. Gastritis and esophagitis put these animals at risk
for the development of aspiration pneumonia during recovery. Aspiration pneu-
monia is suspected in any animal that is febrile, has an increased respiratory
effort, and has crackles or wheezes auscultated on thoracic auscultation. Thoracic
radiographs, arterial blood gas analysis, and a transtracheal wash are performed
to confirm the diagnosis, and a sample is collected for culture and sensitivity
testing. Treatment of these animals includes supportive fluid therapy, appro-
priate antibiotic treatment based on sensitivity test results, supplemental oxygen
and nebulization, and coupage.

SMALL INTESTINES

Foreign Body Obstruction

Small intestinal foreign bodies are a common condition requiring emergency

surgery. The clinical signs seen in animals with small intestinal obstructions vary
with the location, duration, and severity of the obstruction. Vomiting, anorexia,
depression, and abdominal tenderness are common. The vomiting may be pro-
fuse with complete proximal obstruction or more sporadic with distal or partial
obstruction.
Many foreign bodies can be detected on careful abdominal palpation. The
classic radiographic sign of mechanical obstruction is the presence of multiple
loops of gas-dilated small intestine of various diameters. Radiopaque foreign
570 ARONSON et a!

bodies are easily visualized on plain radiographs, although contrast radiography

is sometimes needed to provide confirmation of the diagnosis for radiolucent
foreign bodies. Most proximal small intestinal obstructions are evident within 6
hours after administration of barium suspension, but more distal obstructions
may require 24-hour study for effective diagnosis.
Surgery involves a thorough examination of the entire gastrointestinal tract.
In cases in which the bowel is healthy, the foreign body is removed through an
enterotomy incision made in the antimesenteric border of the bowel immediately
distal to the foreign body. This ensures that the suture line is placed in healthy
bowel. The enterotomy can be closed with single interrupted appositional su-
tures of 3-0 or 4-0 synthetic absorbable material. In cases where there has been
necrosis of the intestinal wall, the affected area of small intestine with normal
margins is resected, and an end-to-end anastomosis is performed. Omental
wrapping or serosal patching can be used to reinforce the area." The prognosis
following foreign body removal is generally good.

Linear Foreign Bodies

Linear foreign bodies (e.g., thread, nylon stocking, rope, string, carpet) are
a unique form of intestinal obstruction. The foreign body typically anchors itself
around the base of the tongue (Fig. 8) or at the pylorus. As peristaltic waves
attempt to move the foreign body along, the intestine progressively gathers itself
into accordion-like pleats (Fig. 9). The ensuing obstruction is typically incom-
plete, and vomiting tends not to be as severe or frequent as in the case of
complete obstruction. Although the foreign body itself is typically not palpable,
the irregularity of the small intestine caused by the pleating often is. Plain
radiographs often show pleating of the intestine with trapped intestinal gas
bubbles. If contrast is needed to confirm the diagnosis, along with the pleating
becoming more obvious, the foreign body may appear as a radiolucent object in
the barium-filled intestine. After the barium passes into the colon, the foreign
body may retain the barium, making it more apparent.

Figure 8. The linear foreign body typically anchors itself around the base of the tongue.
 GASTROINTESTINAL EMERGENCIES 571

Figure 9. The intestine often becomes plicated as peristaltic waves attempt to move the
foreign body along.

Conservative management for linear foreign bodies in cats has been re-
ported.• In these cases, the cats were stable and were treated soon after ingestion
of the foreign body (i.e., string). The string was freed from around the tongue,
and it passed through the gastrointestinal tract in 1 to 3 days. Although conser-
vative management was successful in these cases, delay in surgical removal may
result in serious morbidity and possibly mortality. As long as the ·foreign body
remains, peristaltic waves continue to attempt to move it along, eventually
causing the foreign body to saw through the mesenteric side of the intestine. If
the intestine is perforated, peritonitis and sepsis can develop.
At laparotomy, the plicated area of bowel is isolated from the peritoneal
cavity. An enterotomy incision is made midway along the site of the obstruction,
and the string is grasped. The anchor under the tongue or in the pylorus can
then be cut without losing control of the foreign body. The entire length of string
is removed, which may necessitate multiple enterotomies. The mesenteric areas
of the plica ted bowel can be perforated but do not leak until the tension on the
string is released and the plications relax. Large sections of the intestine may
have multiple mesenteric perforations, necessitating resection and anastomosis.
The prognosis after uncomplicated linear foreign body removal is generally
good, although it has been reported that the probability of morbidity and
mortality is higher in dogs than in catsY When localized peritonitis and fibrosis
of the mesenteric border occur, the intestine may not resume normal function
postoperatively. If the extent of intestine involved is so long that intestinal
resection would result in short bowel syndrome, the prognosis is more
guarded.ls, sa, 86

Intestinal Intussusception

Intussusception is the invagination of one portion of the gastrointestinal

tract into the lumen of an adjoining segment (Fig. 10). It occurs most commonly
572 ARONSON et a!

Figure 10. Intussusception in a dog.

in young animals. Although a cause is often not determined, many animals

have some degree of enteritis. Vomiting, depression, anorexia, and diarrhea are
common clinical signs.44• 45• 84
On abdominal palpation, a cylindric or "sausage-shaped" abdominal mass
is evident. Definitive radiographic diagnosis on plain films may be difficult. In
many cases, gas and fluid accumulate proximal to the intussusception and
produce the signs of small intestinal obstruction described previously. Contrast
studies can be used to differentiate an intussusception from other causes of
intestinal obstruction. Because most intussusceptions occur at the ileocecal junc-
tion, they are often better identified by barium enema than by upper gastrointes-
tinal studies. 45• 58 In recent years, ultrasonography has been used increasingly for
diagnosis. In most instances, the ultrasonographic appearance of an intussuscep-
tion is a series of concentric rings in a transverse image (Fig. 11) or parallel lines
in a longitudinal image that reflect the folded layers of the intestinal wall making
up the lesion. 37
At surgery, the entire gastrointestinal tract should be carefully examined,
because multiple intussusceptions can occur at the same time. Gentle traction
on the intussusceptum and pressure on the intussusceptions aid in reduction.
Resection and anastomosis are required in cases in which the lesion cannot be
reduced or if the involved bowel is necrotic. Many cases recur within a few
days postoperatively. By laying adjoining segments of intestine side by side in a
series of gentle loops, enteroplication can be performed at the time of surgery
to decrease the incidence of recurrence. The adjacent loops of intestine are
sutured to each other with absorbable or nonabsorbable sutures that penetrate
the submucosal layer and are placed midway between the mesenteric and
antimesenteric borders.57 The prognosis for uncomplicated reduction and enter-
oplication is good.

Mesenteric Volvulus

Mesenteric volvulus is a rare and usually fatal disease in the dog. It tends
to occur in young-adult, male, large-breed dogs, with German Shepherds and
 GASTROINTESTINAL EMERGENCIES 573

Figure 11. The ultrasonographic appearance of an intussusception is a series of concentric

rings in transverse image.

English Pointers possibly having a predisposition. The condition has been re-
ported in association with several other conditions, including recent gastrointes-
tinal surgery and exocrine pancreatic insufficiency.SQ. 69 The root of the mesentery
twists, completely occluding the mesenteric veins and partially to completely
occluding the mesenteric arteries. The intestinal mucosa is rapidly compromised
and undergoes ischemic necrosis, leading to gastrointestinal toxin release and
shock (Fig. 12).

Figure 12. Mesenteric volvulus in a dog. The root of the mesentery twists, completely
occluding the mesenteric veins and partially to completely occluding the mesenteric arteries.
The intestinal mucosa is rapidly compromised and undergoes ischemic necrosis.
574 ARONSON eta!

Clinical signs are peracute with rapidly progressive abdominal distention

and hematochezia. Vomiting may occur but is not present in all cases. Abdominal
radiographs show severely distended gas-filled loops of bowel and loss of
abdominal detail caused by peritoneal fluid. Treatment includes rapid fluid
resuscitation and immediate surgery to reduce the twisted mesenteric root.
Unless recognition and treatment of the condition are immediate, the prognosis
for recovery is grave.

LARGE INTESTINES

Cecal Inversion

Inversion of the cecum into the proximal colon can cause partial or complete
obstruction. If complete obstruction occurs, there is an acute onset of vomiting
and depression. On abdominal palpation, a firm painful mass is often obvious.
On plain radiographs, gas distention of the small bowel indicative of mechanical
obstruction can be seen. A definitive diagnosis can be made with an upper
gastrointestinal study or barium enema. The inverted cecum appears as a pleated
structure surrounded by contrast material within the first 4 to 6 em of the
barium-filled proximal colon. Treatment involves typhlectomy or resection of
the ileocolic junction. 1

Cecal-Colic Volvulus

Large intestinal volvulus is even more rare than small intestinal volvulus.
It has been reported in three Great Danes. 12• 35 The dogs presented with acute to
peracute vomiting, abdominal distention, and tenesmus. Abdominal radiographs
revealed severe fluid and gas distention of bowel segments. All dogs were
treated with fluid resuscitation and exploratory laparotomy. In all cases, the
distal ileum; cecum; and ascending, transverse, and proximal descending colon
were rotated 180° to 360° around the mesenteric root. In all cases, the bowel was
decompressed and replaced to its normal position, and in two of the three cases,
a colopexy was performed. Two of the three dogs recovered uneventfully, but
the third dog died 3 days postoperatively of cardiopulmonary arrest of unknown
cause. In this limited number of cases, it seems that large intestinal volvulus
has a better prognosis than small intestinal volvulus, which is the case in
human beings. 76

Rectal Prolapse

Rectal prolapse can occur secondary to parasitism and other conditions

causing tenesmus such as perineal hernia, prostatic disease, and colitis (Fig. 13).
In cats, rectal prolapse can also occur secondary to colonic or rectal lymphosar-
coma. It is important to differentiate simple rectal prolapse from small or large
intestinal intussusception with prolapse. With rectal prolapse, a blunt lubricated
probe does not pass into a "lumen," because the prolapsed tissue converges
with the mucocutaneous junction of the anus. In simple cases with viable rectum,
the prolapse is reduced digitally with the animal under general anesthesia. A
pursestring suture is placed, avoiding the anal sacs and ducts, and is tied loosely
to allow the passage of soft feces. An epidural anesthetic (2% lidocaine, 1 mL
 GASTROINTESTINAL EMERGENCIES 575

Figure 13. Rectal prolapse in a dog.

per 5 kg of weight) reduces immediate postoperative straining. In animals in

which manual reduction is difficult or has failed and in which the tissue is viable,
a colopexy is performed using a caudal midline approach to the abdomen. The
prolapse is reduced by gentle cranial traction on the colon, and the colon
is sutured to the transverse abdominus muscle to maintain reduction. Rectal
amputation is required in prolapse cases with necrotic rectal tissue. The animal
is placed on awell-padded rectal stand, with the area around the prolapse
clipped and prepared for aseptic surgery. Two stay sutures may be placed
through all layers of the prolapse: one dorsally and one ventrally, cranial to the
level of proposed resection. The dorsal half of the prolapsed rectum is incised
180° and the outer and inner layers of the prolapse are identified and anasto-
mosed with single interrupted 3-0 m onofilament absorbable sutures spaced 2 to
3 mm apart. The ventral half is then incised and sutured in a similar manner.
The anastomosis is carefully c hecked, the stay sutures are removed, and the
anastomosis is replaced in the pelvic canal.

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Veterinary Hospital
University of Pennsylvania
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