Oral Cavity and Gastro-intestinal Tract

1. Cleft Palate/ Oronasal Fistula

The palate (roof of the mouth) is a wall, partitioning the nasal and oral cavities. This
partition is made up of two parts: the hard palate and the soft palate. The hard palate forms the front
portion of this partition and is made up of two bony plates (one on each side) that are normally
fused together at their midline juncture. This fusion normally takes place during fetal development.
The soft palate forms the rear portion of the palate wall. Both palates are covered with a mucous
membrane.
The most common type of cleft palate results when the two bony palate plates fail to fuse.
The lack of bone fusion leaves a hole or slit in the roof of the mouth. The cleft (hole) drastically
impacts nursing; suction is affected, a portion of the food that the puppy is able to draw is passed
into the nasal cavity, the nasal cavity is highly prone to infection, and the puppy will literally wear
itself out trying to satisfy it's appetite. The cleft is present at birth and can usually be detected by
examining the roof of the mouth. Occasionally milk can be observed running from a puppy's nose
while it is nursing.
Types:
• Congenital
• Acquired
Congenital:
Congenital fistula results from fail in the fusion of palate roof. The closure of palate normally
occurs at 25th to 30th day of gestation. Any stressful including nutritional deficiency, intrauterine
trauma, hormonal imbalance, toxic including viral. Congenital is further classified as
• Primary fistula (lip, premaxilla, nostrils)
• Secondary fistula (Hard and soft palate)
Acquired:

Treatment:
Such individuals are normally culled or euthanized. Because they require excessive care feeding
with an orogastric tube or gastrotomy tube can be passed to give animal feed. Surgical repair of
acquired lesions, and closure of congenital defects is recommended. In all cases surgery should be
performed as soon as possible before secondary complications occur but surgical intervention is
not recommended in newborn pups because the tissue is friable, and suture tends to rip through
them. Surgical procedure is mostly followed when the animal is 8 to 12 weeks old because the
tissue is less friable and suture holds better. For fistula including soft palate and hard palate sliding
bipedicle flap (incision along the fistula edge and mucoperiosteal line is made a mucoperiosteum
flap on both side of the fistula then tissue is slided over the cleft to close the gap. Another method
that is practiced is overlapping flap technique ( flap from one side of fistula is made by incising
along the periosteal line and turning it over the cleft and suturing it along the other side of the cleft.
If both the hard palate and soft palate are involved the hard palate should be closed first, followed
by the soft palate. If necessary two separate procedures should be performed.
For small fistula direct opposition, buccal flap method, rotational flap method and cartilage implant
can be used.Severe defects may be very difficult or even impossible to repair and in severely
affected neonates euthanasia should be considered.
It is important to:
• Freshen the edges of all tissues being sutured together
• Avoid post-operative oral feeding/fluid
• Feed for 5-6 days using a nasogastric tube or (BETTER) a gastrostomy tube. The latter can
easily be positioned at the time of surgery.
Periodantal diseases:
Progressive, cyclic and inflammatory disease of supporting structure of teeth. Due to plaque
bactaria and host response to it. Gingivitis is most common response to plaque antigen. Leads to
dental disease and early tooth loss. Affects 87% dogs and 70 % cats over 3 years.
Periodantal tissue:
 Gingiva
 Cementum covers the root surface of dentin, periodontal ligament and gingiva anchors
fibers into cementum
 Alveolar bone roots are enclosed in alveolar process. Most thick bone and in dental
radiographs seen as lamina dura.
 Periodontal ligament ( tough collagen fibers) highly vascuarised contain nerves also.
 Mucogingival junction margin between the oral mucosa and attached gingiva
 Gingival sulcus invisible, space between oral tooth surface and internal epithelial
surface of free gingiva.
 Cemento-enamel junction line demarcates the shiny enamel of the crown and dull
cementum of the root.
Disease Process:
 Plaque formation
 Deepening of sulcus
 Proliferation of subgingival plaque
 Toxins lead to tissue damage
 Continued attachment loss
 Tooth loss

Stages of Periodantitis:
Stage 1: No Attachment loss:
Plaque and calculus deposit on the tooth. Marginal gingivitis. Gingivitis is because of plaque
deposition and lack of home care. Can be reversed by proper care or professional scaling and
polishing. No tooth loss but with no treatment it could progress to stage 2.

Stage 2: Early attachment loss: upto 25 %

Sulcus deepened by disease no periodontal tissue in the apical part of the tooth including
periodontal ligament, alveolar bone crest and cementum all exposed to bacteria. infection results
in recession of periodontal tissue.

Stage 3: Moderate attachment loss: 25-50 %

Moderate loss is represented by loss of 25 to 50 % of tooth attachment. It can be verified by
probing and Radiographs. Deepening of tooth pocket can be observed and measured by dental
probe gingival recession is very significant at this stage. Tooth attachment loss is also severe.

Stage 4: Severe Attachment loss:

Attachment loss is now more than 50 %. More likely there could be horizontal bone damage
(mandible). Localized lesions palatal aspect of maxillary canines may present infrabony pockets
with vertical bone loss. There could be pathological fracture in mandible or a fistula could form
due to maxillary pockets resorption known as periodontal fistula.
Predisposing Factors:
 Breed ( small and bracheocepalic breeds)
 Chewing behaviour abrasion and scrub, fences and odd objects, soft diet
 Developmetal defects retention of deciduous teeth.
 Disease any febrile disease lead to hypocalification during enamel development.
Treatment options
Non Surgical:
 Scaling
 Root planning
 Antibiotics
Surgical:
 Flap surgery or pocket reduction surgery
 Soft tissue graft
 Bone grafting
Dental Formula:
Canine:
 2 (I 3/3 C 1/1 P 3/3) = 28 for puppies,
 2 (I 3/3 C 1/1 P 4/4 M 2/3) = 42 for dogs,
Felines:
 2 (I 3/3 C 1/1 P 3/2) = 26 for kittens,
 2 (I 3/3 C 1/1 P 3/2 M 1/1) = 30 for cats
Signs: Generalized enlarged, swollen,
nonpainful salivary glands; retching,gulping,
Salivary glands. ptyalism Infarction Regional, firm swelling
of salivary glands, pyrexia, anorexia
1. Parotid
2. Mandibular Sialocele (mucocele):
3. Sublingual Sings: Regionally diffuse, nonpainful
4. Zygomatic flocculent swelling sublingually, rostro-
ventro cervically or submandibularly
Diseases:
Sialodenitis (necrosis) Sialolithiasis:
Signs: Enlarged, hard, painful glands; Signs: Painful, firm swelling of the salivary
retching, vomition, and/or regurgitation gland (usually parotid)
Neoplasia:
Sialodenosis: Signs: Usually nonpainful, firm enlargement
of a specific salivary gland

2. Salivary Mucocele
In a salivary mucocele (or sialocele), mucoid saliva accumulates in the subcutaneous tissue after
damage to the salivary duct or gland surrounded by granulation tissue.
This is the most common salivary gland disorder of dogs. While any of the salivary glands may be
affected, the sublingual and mandibular glands are involved most commonly. Usually the saliva
collects at the intermandibular or cranial cervical area (cervical mucocele). It may also collect in
the sublingual tissues on the floor of the mouth (ranula). A less common site is in the pharyngeal
wall.
The cause may be traumatic or inflammatory blockage or rupture of the duct of the sublingual,
mandibular, parotid, or zygomatic salivary gland. Usually, the cause is not determined, but a
developmental predisposition in dogs has been suggested. Mostly predisposed breeds to salivary
mucocele includes GSD, Dachshunds, and Australian silky terriers.

Signs depend on the site of saliva

accumulation. In the acute phase of saliva
accumulation, the inflammatory response
results in the area being swollen and painful.
Frequently, this stage is not seen by the owner,
and the first noticed sign may be a nonpainful,
slowly enlarging, fluctuant mass, frequently in
the cervical region. A ranula may not be seen
until it is traumatized and bleeds. A pharyngeal
mucocele may obstruct the airways and result
in moderate to severe respiratory distress.
A mucocele is detectable as a soft, fluctuant,
painless mass that must be differentiated from
abscesses, tumors, and other retention cysts of the neck. Pain or fever may be present if the
mucocele becomes infected. A salivary mucocele usually can be diagnosed by palpation and
aspiration of the characteristic golden or blood-tinged, stringy saliva. Usually, careful palpation
with the animal in dorsal recumbency can determine the affected side; if not, sialography may be
helpful.
Sialo graphs:
Normal survey radiographs can be used but rarely helpful other than sialoliths, foreign body or
neoplasia. Thoracic radio graphs in case metastization is suspected. Iodinated water soluble contrast
medium can be used for contrast radiography.

Surgery is recommended to remove the damaged salivary gland and duct, usually of the
mandibular-sublingual gland complex. Cervical mucoceles can be managed with periodic drainage
if surgery is not an option. Drainage, marsupialization, or gland removal has been recommended
for treatment of ranulas. Complete gland and duct removal is recommended for pharyngeal
mucoceles to avoid future life-threatening airway obstruction

3. Oral Neoplasia

Benign
Benign granulomas (peripheral odontogenic fibromas) are common and are usually the result of
periodontal disease or other irritation. Firm masses adjacent to tooth involve gingival tissue also.
These are responsive to local excision and removal of the originating cause. The formation of
hyperplastic gingiva is common among some breed lines. Pocket formation and periodontal disease
may be the result of this hyperplastic tissue. Epulides are characterized by the presence of tumor
arising from the periodontal ligament. The fibromatous epulis contains periodontal ligament stroma
as the primary cell type. These granulomas are responsive to excision. An ossifying epulis contains
large amounts of osteoid matrix. Animal will appear to you with facial deformation, dysphagia,
halitosis, excessive salivation, oral bleeding.

Malignant Neoplasms
The acanthomatous epulis is composed primarily of epithelial cells associated with the stroma.
Tendency of the acanthomatous epulis is to invade bone, which makes dental radiographic
evaluation mandatory for complete evaluation.

Malignant melanomas:
can form in many sites in the oral cavity (gingiva, buccal mucosa, hard and soft palate, and tongue)
and are locally invasive and highly metastatic to the lungs and regional lymph nodes as well as
bone. They may appear either darkly pigmented or nonpigmented. Rapidly growing, whie gray to
brown black vascular and firm. Regional involvment is in more than 80% of the cases. Clients may
complain about halitosis or oral bleeding. Loose teeth may result from bone involvement. Surgical
excision(mandibulectomy, tonsillectomy, or glossectomy), electrocautery, cryotherapy, radiation,
chemotherapy and immunotherapy have been used in treatment. Malignant melanomas carry a poor
prognosis, as reoccurrence is common.

Epulis alongside the premolar Resection of periosteal mucosa Removal of tooth along with curettage of

periodontal tissue.

Closure by opposition of periosteal mucosa

Squamous cell carcinoma:
These tumors occur on the gingiva, lip, tongue, or tonsil. The masses are red, friable, vascular, and
sometimes ulcerated. Most tumors in the rostral oropharynx are locally invasive, often invading .
A frequent site for fibrosarcoma is the maxillary gingiva or hard palate. They appear as a fleshy,
protruding, firm mass which may be friable. They may be ulcerated and infected. caudal
oropharynx tend to be more infiltrative and metastasize more rapidly. Canine gingival SCC tends
to be highly invasive and osteolytic but has a low rate of metastasis. Feline gingival SCC has a
poorer prognosis than canine SCC. Wide resection is recommended for gingival tumors. They are
radiosensitive, and combining radiotherapy with hyperthermia has been effective. Investigations
into the use of chemotherapy alone or as an adjunct to surgery continue. Generally, the farther away
from the tonsils or floor of the mouth, the better the prognosis.
Fibrosarcoma:
Fibrosarcomas are found primarily in dogs They most commonly occur on the maxillary gingiva
and hard palate and appear as pink-red, firm, smooth, multilobulated masses that often are attached
to underlying tissue. Local infiltration with bony involvement is common, but distant metastasis is
uncommon. Local recurrence is high with any treatment; wide surgical resection is recommended.
Most fibrosarcomas are poorly responsive to chemotherapy. Fibrosarcomas generally are
radioresistant, although the median tumor control time with radiation alone may be as long as 12
months. Aggressive postoperative radiation therapy has improved survival times, but cryotherapy
is believed to stimulate recurrence.

OESOPHAGUS
4. Megaesophagus
Megaesophagus is a condition in which the esophagus is enlarged or dilated. The results of this
condition are: regurgitation, loss of overall condition and frequently leads to aspiration pneumonia.
Megaesophagus interferes with effective peristalsis thereby preventing food from passing down
into the stomach. In practical fact, it is a really unpleasant condition for even the most tolerant of
pet owners to put up with. The dog `strenuous than getting off the couch. After having purchased
and lived with one dog with this condition, I wouldn't wish it on my worst enemy, let alone their
dog.
Megaesophagus can be congenital or acquired. Some of the causes of acquired megaesophagus are
: esophageal foreign bodies, esophageal tumors, strictures, neurological disorders, autoimmune
diseases and heavy metal poisoning. Treatment for acquired megaesophagus disorders are
dependent upon the causative factors.
In the case of congenital megaesophagus in puppies, the symptoms generally manifest shortly after
the puppies begin to eat solid foods. Affected pups will frequently begin to eat eagerly, then
suddenly back away from the food dish, regurgitate a small amount of food, which they will eat
again. By repeatedly eating the food, the meal is liquefied, thereby making it possible to be passed
into the stomach. Portions of the food can be aspirated into the lungs, making the puppy prone to
aspiration pneumonia.

Treatment for congenital megaesophagus in puppies is primarily directed toward maintaining and
improving the nutritional status of the pup. Food and water are usually given by raising the bowls
up off of the floor (raising the bowls helps facilitate swallowing). Many owners have reported that
feeding the pups a semi liquid or gruel mixture has shown good results. Other pups seem to respond
best to being fed solids. Treatment has to be based upon which method the individual pup will
respond to best. The first few weeks are the most critical. Pups that survive this critical time appear
to spontaneously improve. Any dog with congenital megaesophagus should be spay or neutered
regardless of how well it "outgrows" its conditions.

Oesophageal Diverticulum:
Esophageal diverticula are saclike dilatations that produce pouches in the wall of the oesophagus.
Pulsion diverticulum
herniation of the mucosa through the muscular layers of the esophagus. These diverticula are
produced by exaggerated intraluminal pressure in association with abnormal regional peristalsis
or when obstruction interferes with normal peristalsis. epiphrenic area but can form cranial to any
diseased esophageal segment. Formation of diverticula, including esophagitis, esophageal
stenosis, foreign bodies, vascular ring anomalies, neuromuscular dysfunction, and hiatal hernias.
Traction diverticula are distortions, angulations, or funnel-shaped bulges of the full-thickness
wall of the esophagus caused by adhesions resulting from an external lesion. occur after an
inflammatory process
involving the trachea, bronchi, lymph nodes, or other extraesophageal structures.

Oesophageal diverticulum types

Congenital (congenital weakness of the esophageal wall, abnormal separation of tracheal and
esophageal embryonic buds). Pulsation diverticulum wall comprises of esophageal epithelium and
connective tissue. Forms as a result of esophagitis, foreign body, vascular ring formation.

Acquired (Traction diverticulum) inflammation leads to the formation of fibrous tissue. As the
fibrous tissue matures it pulls down a part of esophagus and forms it into a pouch like structure.
The wall of traction diverticulum comprises of adventitia,, muscle, submucosa and mucosa.
Esophageal diverticulum either congenital or acquired are most commonly found in the cervical
part of eosphagus just cranial to thoracic inlet.
Diverticulum of smaller size can be asymptomatic but large and multiple lobulated are associated
with clinical signs i.e. mediastinitis formation of esophagotracheal bronchial fistula, fever,
respiratory distress, thoracic or abdominal pain. Physical examination could reveal only when
aspiration pneumonia has occurred.
Diagnostic imaging reveals an area food filled or air filled mass. An esophagogram shows a out
pouching or deviation of esophageal lumen that fills up with contrast medium.
Surgical intervention is prescribed in case of the detection of esophageal diverticulum in case of
adhesions to lungs a partial lobectomy can also be performed if separation of adhesions is not an
option. In case of no complication simply perform esophagotomy and remove the part that has
diverted then close the incision site by one or two layer oppositional pattern.
Oesophageal Foreign Bodies

Oesophageal foreign bodies mostly lodge • Fistulae

Proximal esophagus, thoracic inlet, base of • Esophageal diverticula
the heart, or the diaphragmatic hiatus. Perforation of the esophagus may lead to
mediastinitis, pyothorax, and pleuritis.
Clinical Signs: surgical approaches to the esophagus
• Difficulty in swallowing Ventral cervical or lateral thoracotomy or
• Excessive salivation paracostal approach
• Regurgitation
• Fever, malaise What methods have been described for
• Cervical swelling or drainage esophagotomy closure?
• Inappetence (cats) • Double-layer appositional
• Respiratory distress • Single-layer simple continuous
• Single-layer simple interrupted
Clinical sign could differ based on the
shape of foreign body. Gastrointestinal Foreign Body
1. Hollow bones may permit passage of Clinical signs:
fluids or semisolids. • Vomiting
2. Balls may completely obstruct the • Dehydration
esophageal lumen. • Anorexia
3. Hooks and needles cause perforation and • Depression
infection. • Fever
• Abdominal pain
Diagnosis
• Suspicion based on clinical signs and Characteristic radiographic findings in
history an animal with mechanical obstruction
• Survey or contrast radiography of the intestine.
(obstruction, air or dye leakage) • Multiple loops of gas-filled or fluid-filled,
• Endoscopy (direct visualization) dilated small intestine
Treatment • Radiopaque foreign material in the
Non Surgical approach: gastrointestinal tract
• Endoscopic retrieval • Delayed passage (or retention) of
• Balloon inflation to dislodge embedded gastrointestinal contrast material
objects ( catheter)
• Gentle aboral dislodgment into the
stomach Linear foreign:
String, fabric, thread, or other objects that
Indications for surgical removal of a become fixed proximally in the
foreign object: gastrointestinal tract, extend distally, and
• Embedded objects cause partial gastrointestinal obstruction.
• Suspected perforations greater than 3 mm
• Prolonged unsuccessful endoscopy Pathophysiology of a linear foreign body:
After the linear foreign body becomes fixed
Complications associated with foreign proximally, the intestine becomes plicated
body removal from the esophagus? on the string because of repeated peristaltic
• Esophagitis activity. The linear foreign body becomes
• Ischemic necrosis taut at the mesenteric border of the intestine
• Dehiscence of the suture line and eventually begins to cut into the
• Leakage mucosa. If the string is not removed or
• Stricture released, the foreign body eventually cuts
through the bowel. The end result is
localized or generalized peritonitis, with
extensive adhesions at the mesenteric
border.
Radiographic findings are characteristic
of linear foreign bodies:
• Plication of the intestine with sharp turns
and irregular gas bubbles
• Loss of serosal detail or free gas in the
abdominal cavity, which indicate bowel
perforation and peritonitis
• Failure to pass a foreign body per rectum in
36 hours
Surgical treatment for a gastric foreign
Gastrotomy:
The gastrotomy incision should be made in
an avascular region of the body of the
stomach and closed in one or two layers
using either an appositional or an inverting
pattern.

Linear foreign bodies typically lodge? Surgical treatments for an intestinal foreign
• Cats—around the base of the tongue body?
• Dogs—at the pylorus Enterotomy

Where do nonlinear gastric and intestinal Intestinal resection and anastomosis is

foreign bodies typically become lodged?
• Pylorus
• Transverse portion of the duodenum
• Ileocecocolic valve
Surgical approach:
• Complete gastrointestinal obstruction
• Increased vomiting or abdominal pain
• Fever, lethargy, or deterioration of patient
status
• Failure of a foreign body to move (based
on radiographs) for more than 8 hours
performed
• If the foreign body obstruction has caused
necrosis of the bowel
• If perforation and localized peritonitis are
present (i.e., linear foreign body)
• If the viability of the intestine is in
question
Rate o incidence of intestinal wound
dehiscence in dogs and cats?
7-26%.

Gastric Dilation Volvulus (GDV):

This is a life threatening condition involving severe gaseous distension of the stomach, with
varying degree of gastric displacement around the long axis of the body. It can lead to series of
pathological events, which if untreated results in the death of the patient.
The cause or causes of GDV are incompletely understood. Factors that have been implicated are
pica, overeating, eating dry dog food or spoiled food, bodily trauma, conditions causing abdominal
pressing, general anesthesia, spinal surgery, abdominal surgery, genetically altered
gastroesophageal angle in deep chested breeds, abnormal gastroesophageal sphincter and pyloric
stenosis.

Pathophysiology

Exact pathophysiologic events are unclear. During volvulus the pylorus migrates ventrally and
cranially. Stomach move in clock wise direction from 90 to 360 degrees around the distal or
abdominal oesophagus. The rotation leads to the displacement of pylorus to the left of midline,
leaving duodenum entrapped in between the distal esopagus and stomach.
 Pathophysiological changes occur as a result of distention of stomach and are related to
compression of the neighboring anatomical structures and to ischemia of the stomach itself.
Ischemia occurs when intralumenal gas pressure exceeds the systolic pressure of the blood in the
arteriols.
▪ The most immediate threat is shock due to several factors. Hypotension results from pressure
on caudal vena cava and the portal vein, causing arrest of the blood in the veins caudal to the
compression.
▪ Another contributing factor is endotoxic shock due to bacterial proliferation in the small bowel
and failure of the portal circulation to allow the detoxification of these endotoxins in the liver.
▪ Third factor is the release of the vasoective peptide called ‘Mycocardial depressant factor’
(MDF) from the ischemic pancreatic tissue, which is an arrhythmia inducing compound. The result
is decrease in the efficiency of myocardial contractions, resulting in the cardiogenic hypoperfusion.
▪ At a certain point the shock becomes irreversible to any form of treatment.

Clinical Pathology
▪ Hemoconcentration due to the sequestration of the blood flow in the gastrointestinal system.
▪ Changes in the electrolyte and blood pH are variable.
▪ Serum glutamic pyruvic transaminase (SGPT) can be elevated due to hepatic hypoxia and
necrosis.
▪ BUN and creatinine can be elevated greatly due to decreased renal perfusion.

Diagnosis
▪ Based on the physical examination, radiology and clinical pathology.
▪ Characteristically the patient will be presented to a veterinarian because it has an acute
abdominal distress, which is often accompanied by unproductive attempts to vomit. The anterior
abdomen is distended, and when percussion is performed, there is a characteristic ‘tympanic’ pong
sound. This indicates gastric dilatation but doesn’t confirm volvulus.
▪ Volvulus is diagnosed by taking the radiographs or visualizing the stomach while performing
the exploratory surgery.
▪ Shock is diagnosed on the basis of characteristic signs of shock e.g. mucous membranes etc.

Treatment

i. Conservative Treatment
▪ Evacuation of the gas from the stomach by passing of tube, gastrocentesis by 18 gauge or larger
needle, gestrotomy.
▪ Treatment of shock e.g. fluid therapy @90ml/kg/hr.
▪ Steroid therapy.
▪ Antibiotic therapy.
▪ If gastric decompression fails to correct cardiac arrhythmia administration of lidocaine
hydrochloride intravenously as a bolus of 4 mg/kg should be considered. An additional dose of 2
mg/kg can be given initial doses fails to correct the problem and maintenance dose of 25-50
mg/kg/min may be required.

ii. Surgical Treatment

▪ Temporary gastrotomy helps in the removal of gases from the stomach and allows the
examination of the gastric mucosa.
▪ The stomach should be examined for malpositioning. If it is in a state of volvulus, it should be
returned manually to its proper position. Once this has been accomplished it should be possible to
pass a large diameter stomach tube to evacuate it completely.
▪ The stomach should be examined carefully for the areas of ischemic necrosis. If there is any
doubt about a particular lesion it is better to resect it to normal.
▪ To prevent GDV recurrence, it is desirable to create an adhesion between the stomach and the
abdominal wall e.g. gastropexy. A suitable site for gastropexy is between the pyloric antrum and
the right flank region near the last rib.
▪ A very effective method of gastropexy is circumcostal gastropexy, a technique which utilizes a
muscular flap of the ventral pyloric antrum to anchor the stomach to the costochondral of one of
the last four ribs.

Management
Prevention is reasonable consideration in breeds or individual animals that may be predisposed to
GDV. Steps that can be taken are:
▪ Give multiple daily feedings.
▪ Feed natural rather than commercial diets.
▪ Prevent access to items not usually ingested such as garbage or spoiled food.
▪ Give surfactant with meals (e.g. simethicone).
▪ Limit postprandial activity.
▪ Perform prophylactic gastropexy.
Quick Reference to Gastric dilatation–
volvulus (GDV):
An acute, life-threatening, medical and
surgical emergency affecting primarily large
and giant breeds of dogs. The stomach of
affected dogs becomes distended with gas
and malpositioned, leading to shock and
rapid deterioration of the patient if not
properly treated.
Causes of GDV?
The exact cause of GDV is not known;
however, several risk factors have been
identified.
Specific risk factors associated with GDV
in dogs?
• Age—middle-aged and old dogs are at an
increased risk.
• Body weight—breeds with a higher
average adult body weight are at increased
risk of GDV. Obesity is not a risk factor.
• Body conformation—dogs with deep,
narrow thoracic conformation have an
increased risk of GDV.
Diet—dogs that eat few meals each day or
ingest meals rapidly have increased
susceptibility to GDV.
• Genetics—Purebred dogs have a higher
risk of GDV than mixed-breed dogs.
• History—dogs with a family history of
GDV have an increased risk of developing
the syndrome.
List the clinical signs:
• Restlessness and pain
• Increased respiratory rates
• Nervous pacing
• Abdominal distention (bloat)
• Repeated vomiting (often nonproductive)
• Hypersalivation (ptyalism)
What comes first, dilation or volvulus?
This is the proverbial chicken or the egg
question of the GDV syndrome.
Investigators believe that gastric dilation
precedes rotation of the stomach.
In which direction does the stomach
normally rotate during GDV?
Usually in a clockwise direction (to 270º) as
viewed ventrodorsally into the abdomen
(i.e., the position of the patient prepared for
a ventral midline laparotomy).
Pathophysiology:
a. Cardiovascular: ….
b. Respiratory: ….
c. Gastric: …
Diagnosed?
Signalment, clinical signs, and physical
examination.
Recommended radiographic view:
The right lateral recumbent view. Dogs with
gastric volvulus have a distinct
compartmentalization line between the
gasfilled fundus and pylorus (double bubble
or pillar sign).
Differential diagnoses:
• Mesenteric volvulus
• Splenic torsion
• Ascites
• Hemoabdomen
• Abdominal neoplasia
Case fatality rate of dogs with acute
GDV?
• 15-33%.
Emergency treatments:
• Aggressive shock treatment
• Gastric decompression with an orogastric
tube or via percutaneous trocarization
Goals of surgery:
• Gastric decompression and repositioning
• Assessment of abdominal organ viability
• Permanent gastropexy of the stomach to
the body wall
15. List methods for intraoperative gastric
decompression.
• Orogastric tube passed by an assistant and
guided through the gastroesophageal
junction by the surgeon.
• Trocarization with a large-bore needle (14-
18 gauge) attached to the surgical suction
hose.
• Temporary gastrostomy tube.
How to determine gastric and splenic
viability?
Evidence of gastric necrosis includes gastric
contents in the peritoneal cavity,
discoloration and thinning of the stomach
wall, and lack of active bleeding after gastric
incision.
Splenic necrosis, avulsion of splenic
mesenteric vessels, and thrombosis of the
splenic vessels are indications for
splenectomy. An engorged spleen may
return to normal size and color several
minutes after repositioning.
What techniques are commonly used for
permanent gastropexy?
• Tube gastropexy
• Circumcostal gastropexy
• Belt-loop gastropexy
• Incisional gastropexy
• Ventral midline gastropexy
• Laparoscopic gastropexy
Which gastropexy method creates the
strongest adhesion in experimental cases?
• Circumcostal gastropexy.
What factors are associated with an
increased risk of perioperative mortality:
• Poor physical condition on hospital
admission (i.e., depressed or comatose dogs)
• Gastric necrosis or gastric rupture
• Splenectomy or partial gastrectomy
• Preoperative cardiac dysrhythmias
• Disseminated intravascular coagulation
List the primary immediate postoperative
complications
• Shock
• Ventricular dysrhythmias
• Vomiting and gastritis
• Hypokalemia
• Hypoproteinemia
• Anemia
• Gastric atony
• Gastric necrosis
• Peritonitis
• Disseminated intravascular coagulation
• Death

Peptic Ulcers
These lesions in dogs and cats are often associated with some systemic disease. Gastric hyper
acidity is often associated with mastocytosis. The mast cells secrets high levels of histamine, which
enhances the increased production of acid by the oxyntic cells. The increased concentration of the
ulcer results in more pepsin being released from its precursor pepsinogen. This pepsin in high
concentrations is capable of attacking the mucosal barrier.
Anti inflammatory drugs such as salicylates and corticosteroids may damage the mucosa and allow
back diffusion of acid. Aspirin applied to gastric mucosa increases the flow of sodium into the
lumen and enhances the back-diffusion of H+. Cellular damage allows further back-diffusion of H+,
increased release of histamine, vasodilatation and subsequent bleeding. Corticosteroids are thought
to reduce the rate of renewal of gastric epithelial cells and thereby lowering the resistance of the
mucosal cells to acid pepsin digestion.
Direct trauma to the gastric mucosa from foreign bodies may cause ulceration. Ischemia due to
GDV may also contribute to this. In some reports, renal disease that cause an increase in circulating
gastrin levels (e.g., gastric ulcers of uremia) may also have a role in gastric ulcer formation. Gastric
neoplasms can also cause ulcers and some cases perforation.
Treatment
- Surgical treatment for an ulcer is indicated when severe hemorrhage, perforation, obstruction, or
a poor response to medical therapy occurs.
- Resection of the stomach wall containing the ulcer, partial gasterectomy used successfully in dogs.

Gastric Outlet Diseases

Gastric neoplasia and pyloric ulcer disease can cause gastric outlet obstruction. It can also be caused
by the foreign bodies, abscess. Although most foreign bodies results in emesis and a more acute
onset of signs, chronic signs are also seen in some cases. For most animals with foreign bodies,
surgical treatment is recommended and the prognosis is usually good
Pyloric Stenosis
Pyloric stenosis is considered to be most common cause of the gastric outlet obstruction disease.
This can be classified as congenital and acquired groups.

Congenital Pyloric Stenosis

This form mostly occurs in boxers and Boston terriers, with clinical signs being noted close to the
weaning, when solid food is introduced into the diet.
The obstruction is caused by a thickening of the pyloric musculature. Histologically hypertrophy
is seen along with some fibrosis of the muscle layers and degeneration of the myenteric plexus.
Acquired Pyloric Stenosis
Dogs of any age and breed my affected with this. This can be mechanical or functional. Functional
stenosis results from the diseases somewhere else in the body interfering with the stomach ability
to empty. Functional obstruction due to the iatrogenic cause can occur after surgical manipulation
anywhere in the cranial right quadrant of the abdominal cavity; it usually results from the
inflammation and pain. Sympathetic stimulation resulting from this pain can inhibit the contractility
of the stomach musculature. Delayed emptying over a prolonged period of time causes mils gastric
distention.

Treatment
▪ Resection of the affected mucosa and reapposing of healthy mucosa.
▪ Y-U pyloroplasty is indicated as a surgical treatment.
▪ After surgery animal is kept on the baby food for 48 hrs.

QUICK Reference Gastric outflow Obstruction

Common causes of gastric outflow

obstruction in dogs and cats.
• Foreign bodies
• Pyloric stenosis
• Chronic hypertrophic pyloric gastropathy
• Infiltrative fungal diseases
• Gastric neoplasia
• Pancreatic abscess or neoplasia
• Previous gastric surgery
2. What is pyloric stenosis?
A congenital lesion characterized by a
benign thickening of the circular smooth
muscle of the pylorus.
What is chronic hypertrophic pyloric
gastropathy?
An acquired, benign condition involving
hypertrophy (mucosal and/or muscular) of
the pylorus.
Typical signalment of a patient presenting
with chronic hypertrophic
pyloric gastropathy
Middle-aged to older, small-breed dogs
weighing less than 10 kg.
Gender predisposition in chronic
hypertrophic pyloric gastropathy
Male dogs are affected approximately twice
as often as female dogs.
Types of gastric neoplasia are seen in
dogs and cats:
• Gastric adenocarcinoma—the most
common type of gastric neoplasia in dogs.
• Leiomyomas and leiomyosarcomas—
smooth muscle tumors. Leiomyomas are the
most common benign gastric tumor in the
dog.
• Lymphoma—the most common type of
gastric neoplasia in the cat; also seen in
dogs.
Which portions of the stomach are
usually affected with gastric neoplasia?
• Adenocarcinomas—pyloric antral region
or along the lesser curvature
• Leiomyomas—the cardia
• Lymphoma—discrete masses of the gastric
wall or a diffusely infiltrative disease
What is a pyloroplasty?
One or more full-thickness incisions through
the pylorus with subsequent suturing of the
pyloric incisions together in a different
direction, widening the gastric outflow tract.
Pyloroplasty is indicated with mild pyloric
outflow obstruction, when full-thickness
excision of the gastric wall is not necessary
to relieve the obstruction.
Y-U pyloroplasty.
An advance flap pyloroplasty procedure in
which a full-thickness Y-shaped incision is
made over the duodenum, pylorus, and
pyloric antrum. The incision is then closed in
a U shape