Gastric Dilatation-Volvulus in Dogs
Acute gastric dilatation-volvulus (GDV) is a life-threatening
condition, with fatality rates ranging from 10% to 60%.1
The animals most commonly affected by GDV include older, large
or giant breed, deep-chested dogs, including Great Danes,
German Shepherds, Standard Poodles, and large mixed breed
dogs. Early diagnosis, medical stabilization, surgical intervention
and post-operative monitoring are important factors in reducing
the mortality rate.
Gastric dilatation-volvulus is the result of accumulation
of gas, fluid, or a combination of the two in the stomach.
Factors responsible for causing dilatation include aerophagia,
exercise after ingesting a meal, and overeating. The stomach
distends with gas or fluid, and rotation along the axis of
the esophagus and cardia follows. The rotation is generally
in the clockwise direction (when viewed in dorsal recumbency),
and can be up to a maximum
of 360°. A less common fate is a counter-clockwise rotation,
to a maximum of 90°. In addition to the accumulation of gas
and/or fluid, there is often an outflow obstruction due to
a mechanical or functional abnormality.2
The clinical signs associated with GDV are restlessness,
anxiousness, respiratory dysfunction, hypersalivation, retching,
abdominal distension and frequent attempts to vomit. The
animal may present weak, collapsed, or comatose, depending
on the degree of shock. Signs related to hypovolemic shock
are pale mucous membranes, prolonged capillary refill time,
rapid, weak, thready pulses, and tachypnea. Diagnosis of
GDV is based upon clinical signs, inability to pass a gastric
or nasogastric tube effectively, and consistent radiographic
findings.
The major life threatening abnormality associated with GDV
is shock. Shock is due to compression of the caudal vena
cava, from distension of the stomach, and the portal vein,
from distension and rotation of the stomach. As a result,
there is decreased tissue perfusion, which leads to hypoxia
and ischemia of tissues. Ischemia of cardiac muscles can
result in arrhythmias, and ischemia of abdominal organs can
lead to necrosis/death of affected organs/tissues.
The first priority for treatment of GDV is cardiovascular
stabilization. Dogs that have persistent circulatory collapse
are thought to be at greater risk of dying than those dogs
that are stabilized.1 Hosgood, et al, suggests
that intravenous therapy with 7% sodium chloride plus 6% dextran
initially, followed by 9% sodium chloride, is superior to
9% sodium chloride alone. Once the animal is stabilized the
stomach is decompressed using orogastricintubation or needle
gastrocentesis. Radiographs are taken prior to surgery to
determine if a volvulus is present. Broad spectrum antibiotics
are administered prophylactically. The use of corticosteroids
remains controversial, but have shown to be beneficial in
instances of septic or endotoxic shock.
The timing of surgery also remains controversial, as there
are advantages and disadvantages to early and late surgical
intervention. The surgical techniques used for repair of
GDV include tube gastrostomy, circumcostalgastropexy, belt-loop
gastropexy, and permanent incisionalgastropexy. Complications
associated with tube gastrostomy are peritonitis (due to premature
removal or loosening of the tube), cellulitis (due to gastric
content leakage), and alteration of gastric myoelectric activity.
There is some evidence suggesting gastropexy procedures lead
to chronic bloaters by altering gastric emptying.3
Perfusion of the tissues is maintained perioperatively and
post-operatively, using an intravenously administered, balanced
electrolyte solution. Perioperative and post-operative monitoring
of the patient for perfusion, as well as abdominal distension,
are important. The parameters used to assess tissue perfusion
include capillary refill time, blood pressure, peripheral
pulse pressures, arterial blood gas, urine output, PCV, and
total protein. Abdominal distension is monitored due to the
potential of re-bloating following surgery.
There are many complications that can occur postoperatively,
most of which are secondary to the initial problems associated
with GDV. Cardiac arrhythmias, usually of ventricular origin,
tend to occur in the first 12-36 hours following surgery.
A continuous ECG is recommended to monitor for arrhythmias,
and anti-arrhythmic drugs (lidocaine, procainamide) are used
when the arrhythmia is responsible for poor tissue perfusion.
Additional complications include disseminated intravascular
coagulation, sepsis caused by gastric leak or aspiration pneumonia,
protein loss, gastric ischemia and esophagitis.
Additional medical options available for the treatment of
GDV include: a lipid peroxidase inhibitor to prevent lipid
peroxidation secondary to reperfusion injury; cisapride, metoclopramide,
erythromycin, and ranitidine to facilitate gastric emptying;
and vasoactive intestinal peptide to facilitate eructation
and lower esophageal sphincter tone in animals which are chronic
bloaters. The effect of metoclopramide on gastric emptying
in dogs with GDV has been studied, and the results suggest
there is no improvement of gastric emptying.4
Left untreated, GDV can lead to multiple organ failure, circulatory
shock and death.4 Factors which contribute to a
higher mortality rate include gastric necrosis, gastric resection,
splenectomy and pre-operative cardiac arrhythmias.5
It is therefore important to be familiar with the clinical
signs of GDV in order to arrive at an early diagnosis, stabilize
the patient as soon as possible, surgically correct the volvulus,
and medically manage any additional complications.
-by Elizabeth Natz, Class of 1999
-Edited by Brad L. Njaa, DVM, MVSc
Post Publication Correction
The section discussing fluid therapy for gastric dilatation-volvulus in dogs should have read
intravenous therapy with 7% NaCl (5ml/kg) in 6% Dextran 70 (HS/D70) initially followed by 0.9% NaCl is superior to 0.9% NaCl alone. Resource is Section 7/Gastrointestinal Disorders, Chapter 4/Disease of the Stomach, pp. 675 of Saunders Manual of Small Animal Practice, edited by Stephen J. Birchard and Robert G. Sherding, W.B. Saunders Company, 1994. |