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Gastric dilation‐volvulus syndrome in dogs 1. Pathophysiology, diagnosis and

stabilisation

Article  in  In Practice · February 2009

DOI: 10.1136/inpract.31.2.66

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COM PA N I O N A N I M A L PR ACT I CE Giant-breed dogs are at
increased risk of gastric
dilation–volvulus

Gastric dilation–volvulus syndrome

in dogs 1. Pathophysiology, diagnosis
and stabilisation MICKEY TIVERS AND DAN BROCKMAN

GASTRIC dilation–volvulus syndrome (GDVs) comprises acute gastric dilation (GD), acute gastric
dilation–volvulus (GDV) and chronic gastric volvulus. This article, the first of two reviewing
the management of GDVs in dogs, discusses the pathogenesis, pathophysiology, diagnosis and
stabilisation of GDV. An article in the next issue will describe surgical and postoperative
management of the condition.

Mickey Tivers A CLINICAL CHALLENGE sion and tympany and can be in considerable pain. It is
graduated from
Bristol in 2002. He worth remembering that in very large dogs the stomach
is currently a staff Acute GDV is a rare condition affecting predominantly may be covered entirely by the ribs, potentially mask-
clinician in small
animal surgery at
large, deep-chested dog breeds. It is a potentially cata- ing abdominal distension. The degree of cardiovascu-
the Royal Veterinary strophic disease associated with rapid deterioration and lar compromise that an individual dog experiences will
College (RVC). He high mortality if it is not managed appropriately. Rapid be proportional to the duration and degree of gastric
holds the RCVS
certificate in small medical and surgical treatment together with intensive rotation and the pressure within the gastric lumen.
animal surgery. postoperative care are necessary to optimise the chance
of a successful outcome.
Despite extensive clinical research, the pathogenesis PATHOGENESIS AND RISK FACTORS
of GDV remains unclear. Hence, a variety of treatment
regimens have been recommended but several elements Although the underlying pathogenesis of GDV is poorly
remain controversial. Dogs suffering from GDV are fre- understood, a number of risk factors have been suggested
quently presented out of hours and represent not only a in the veterinary literature. These can be grouped as intrin-
genuine emergency but a difficult clinical challenge. If sic or extrinsic factors.
managed correctly, the condition can be associated with
Dan Brockman a good prognosis and affected animals can be extremely
graduated from rewarding to treat.
Liverpool in 1987. Key considerations
He is currently
professor of small
animal surgery at ■ Gas in the dilated stomach is due to aerophagia
the RVC. He holds HISTORY AND CLINICAL FEATURES rather than bacterial fermentation
RCVS certificates in
veterinary radiology
■ There is no evidence to suggest that torsion is
and in small animal
GDVs occurs most commonly in large or giant, deep- due to the influence of the spleen. GDV has been
orthopaedics. He is chested breeds, but has also been reported in small reported in splenectomised animals
a diplomate of the breeds of dog. The onset of clinical signs is usually acute
American College of ■ Pyloric surgery is not necessary to prevent GDV
Veterinary Surgeons and is often reported to follow a large meal and/or a recurrence
and the European period of exercise. Affected dogs typically demonstrate
College of Veterinary ■ The ability or inability to pass a stomach tube is
Surgeons. agitation, restlessness, lethargy, progressive abdomi- not helpful in distinguishing between GDV and GD
nal distension, unproductive vomiting or retching and, ■ Steroids are not indicated for the management
in extreme circumstances, collapse. Clinically affected of GDV
dogs present with signs of hypovolaemic shock, includ- ■ A gastropexy is essential in the management of
ing tachycardia, poor peripheral pulses, tachypnoea and dogs with GDV
pale mucous membranes. The degree of hypovolaemia ■ Presumed gastric necrosis must be treated with
In Practice (2009)
is variable and the associated clinical signs will thus partial gastric resection
31, 66-69 vary accordingly. Patients also exhibit abdominal disten-

66 In Practice ● FEBRUARY 20 0 9
Intrinsic risk factors HYPOTHESES FOR THE PATHOPHYSIOLOGY OF GASTRIC DILATION–VOLVULUS
Intrinsic risk factors include breed, body
size, thoracoabdominal dimensions, gastric 1 Normal stomach ➞ Gastric volvulus ➞ Sphincter dysfunction ➞ Gastric dilation/gastric dilation–volvulus

volume, gastric position, gastric ligament lax-

ity, control of eructation and pyloric canal 2 Normal stomach ➞ Sphincter dysfunction ➞ Gastric dilation ➞ Gastric volvulus/gastric dilation–volvulus

function.
Various factors have been described in
scientific reports as predisposing dogs to GDV. The reli- fundus more vulnerable to ischaemia. As tension in the
ability of this information, in terms of scientific rigor, is gastric wall increases and the perfusion pressure (sys-
variable and contradictory evidence is often presented. temic arterial pressure) falls, compression of intramural
Some factors do, however, seem to be repeatedly asso- blood vessels can occur. In addition, gastric and splenic
ciated with GDV. Great Danes, German shepherd dogs, displacement can cause mechanical obstruction of local
Irish setters and standard poodles have been consistently blood vessels (kinking) as well as obstruction by throm-
found to be over-represented in studies of dogs with GDV bus formation. Ischaemia-induced gastric necrosis is,
and are statistically known to be at increased risk. A sig- therefore, most frequently seen at the fundus but necrosis
nificant predisposition has been correlated with a high of the cardia can be seen, presumably as a result of long-
thoracic depth to width ratio. Increasing age, having a standing or extreme gastric rotation. Splenic displace-
first-degree relative with GDV, thin body condition and ment can, in turn, lead to venous congestion, thrombosis
a fearful or anxious temperament have also been shown and splenic artery avulsion. This can result in partial or
to be risk factors. complete splenic infarction or torsion.

Extrinsic risk factors Systemic effects

Extrinsic risk factors include diet, postprandial GD and
accumulation of gastric gas. The precise role of diet is
unclear although feeding a small number of large meals
and rapid speed of eating are likely to play a part in some
dogs.
It is clear that the development of GDV is influenced
by environmental, anatomical, physiological and patho-
logical risk factors, but their specific contributions are
likely to vary between individuals. Brockman and oth-
ers (2000) proposed a hypothesis for the pathogenesis of
GDV that relates all of these factors. In order for GDV to
occur there must be a failure of the gastro-oesophageal
and pyloric sphincter function, thus preventing normal
eructation and pyloric outflow. Thus, two scenarios can
occur, with dilation following volvulus or volvulus fol-
lowing dilation (see table, above right). This model can be
used to explain why some dogs experience dilation only,
whereby gas accumulates too quickly to permit rotation
of the stomach. It can also explain why some dogs have
chronic volvulus in which incomplete sphincter obstruc-
tion allows gas to escape and thus prevent dilation.
PATHOPHYSIOLOGY
Regardless of the underlying pathogenesis of GDV,
the end result is similar – a gas-distended and twisted
stomach. In most dogs with GDV, the stomach is rotated
between 180 and 360º in a clockwise direction. Although
there is significant overlap between the pathophysiologi-
cal events that result from GDV, it is helpful to divide
them into local and systemic effects.
Local effects
The local effects of GDV concern the stomach and
the spleen. GDV compromises the blood supply to
the gastric wall. Due to their close anatomical rela-
tionship and their attachment (via the gastrosplenic
ligament), displacement of the greater curvature of the
stomach results in displacement of the spleen and often
causes avulsion of the short gastric branches of the
splenic artery, which lie in the gastrosplenic ligaments
and supply the gastric fundus. Damage to these vessels
can result in significant haemorrhage and makes the
The main systemic effect is due to mechanical obstruction
of blood flow through the caudal vena cava and hepatic
portal vein. This leads to a rapid reduction in venous
return to the heart and a reduction in cardiac output result-
ing in hypotension. Compensatory tachycardia, prolonged
capillary refill time and elevated serum lactate levels are
all clinical evidence of these events. Compensatory tachy-
cardia preserves cardiac output initially, but increases
myocardial oxygen demand at a time when myocardial
oxygen delivery is falling because of reduced diastolic
arterial pressure. Poor tissue perfusion results in stasis of
blood within the abdominal organs associated with aci-
dosis, hyperlactataemia and the liberation of inflamma-
tory mediators and myocardial active substances such as
myocardial depressant factor and catecholamines. These
factors coupled with hypotension can lead to myocardial
ischaemia and cardiac arrhythmias. Evidence of myocyte
injury in the form of increased serum cardiac troponin
I and cardiac troponin T has been demonstrated in dogs
clinically affected by GDV. These arrhythmias can, in
turn, worsen cardiac performance.
Ischaemic reperfusion injury (IRI) is tissue dam-
age caused by reactive oxygen species that are released
by oxygen entering previously ischaemic tissue follow-
ing reperfusion. It has been suggested that IRI is partly
responsible for the morbidity and mortality associated
with GDV. IRI studies have
investigated treatment tar-
geting the tissue damage,
but have only demonstrated
an effect in experimental
models. Further research
may provide better under-
standing and treatment of
this aspect of the disease
in the future.
In addition, gastric per-
foration can occur second-
arily to necrosis, resulting
in septic peritonitis. Severe
Stomach of a dog with GDV during repositioning at
GDV can lead to systemic coeliotomy. Gastric dilation with volvulus causes local
inflammatory response damage to the gastric wall and the splenic vasculature
as well as systemic effects that are predominantly due
syndrome and disseminated to obstruction of blood flow through the caudal cava
intravascular coagulation. and portal vein

In Practice ● FEBRUARY 20 0 9 67
 DIAGNOSIS AND STABILISATION
Therapeutic goals
Treatment of GDVs aims to address a number of thera-
■ Restore and support circulation
peutic goals (see box on the right).
■ Decompress the stomach
■ Establish whether GDV or simple dilation
Emergency care
is present
Initial medical management should be aimed at address-
■ Rapidly correct the volvulus surgically
ing the dog’s hypovolaemic shock. Ideally, two large-
■ Provide prophylaxis
bore catheters (16 or 18 gauge) should be placed into
– Surgically
the cephalic veins to allow aggressive intravenous fluid
– Environmentally
therapy. Blood should be taken and a minimum database,
including packed cell volume (PCV), serum total solids
(TS), serum electrolytes and venous blood gas analysis,
carried out if available. Fluid therapy should be admin-
istered and the cardiovascular status reassessed regularly
(every 15 to 20 minutes). Initially, a balanced electro-
lyte solution such as Hartmann’s should be given. Based
on the dog’s clinical signs, a proportion of the ‘shock
dose’ (90 ml/kg) should be administered. For example,
in a dog showing moderate compromise, 20 to 25 ml/
kg should be administered over 15 minutes and the dog
reassessed after this time, following which further fluids
should be provided as necessary. This may be repeated
up to a total dose of 90 ml/kg. In very large dogs, rapid
fluid administration may be facilitated by using a pres-
sure bag. Synthetic colloids (pentastarch or hetastarch) or Oxygen therapy is helpful in stabilising dogs with GDV. This
dog is also being monitored for cardiac abnormalities
hypertonic saline may be indicated in particularly large
dogs or those that have not responded to an initial bolus
of a crystalloid. In addition, blood Gastric decompression
products (packed red blood cells or Gastric decompression should be performed following
whole blood) may be necessary to initial stabilisation of the dog. However, there is some
support a low PCV following the debate about the timing of this procedure. It has been
initial resuscitation. suggested that decompression should be delayed until
Dogs with GDV are often in adequate volume resuscitation has been performed but,
considerable discomfort. Analgesia in general, the authors favour early gastric decompres-
using a pure opioid should be sion following a period of aggressive fluid therapy. This
administered and will also provide usually results in an improvement in venous return and
some sedation for subsequent gas- also in the dog’s comfort level, and facilitates continued
tric decompression and radiogra- stabilisation and rapid surgical management.
phy. Morphine or methadone can be Decompression can be performed by passing an oro-
administered intramuscularly at a gastric tube. Many dogs will tolerate this although seda-
dose of 0·1 to 0·3 mg/kg once fluid tion may be necessary. Opioid analgesics may provide
therapy is underway. Alternatively, sufficient sedation or, alternatively, may be combined
fentanyl, given intravenously at a with diazepam intravenously at a dose of 0·25 mg/kg. A
dose of 2 to 4 μg/kg, can provide large-bore stomach tube, preferably with end and side
good short-term analgesia with holes, is premeasured and marked from the nostril to the
minimal detrimental effects on last rib. The dog’s mouth is closed around a bandage roll
the circulatory system, although it to facilitate passage of the tube. The tube is lubricated
may cause respiratory depression, and passed through the centre of the bandage and into the
bradycardia and apnoea. Oxygen oesophagus. The tube should not be advanced beyond the
supplementation may benefit these marked point. In some instances, it is not possible to pass
dogs if they will tolerate it. the tube through the caudal oesophageal sphincter.
If available, electrocardiogra-
phy should be performed in order
to assess the patient for cardiac
abnormalities. While arrhythmias
are often seen in dogs with GDV,
the authors do not recommend
antiarrhythmic therapy in the
absence of significant cardiovas-
cular compromise or underlying
heart disease. Correction of under-
lying hypoperfusion and electro-
lyte abnormalities may resolve
Intravenous fluids for resuscitation with a pressure
bag attached to facilitate fluid administration at
arrhythmias without the need for Stomach tubes should be premeasured before insertion
fast rates specific therapy. for gastric decompression

68 In Practice ● FEBRUARY 20 0 9
 If passage of the stomach tube is not possible, decom-
pression can be performed by percutaneous gastrocente-
sis. This involves placing a large-bore needle or catheter
(14 to 16 gauge) caudal to the ribs on the side with the
maximum distension and tympany. Needle gastrocentesis
may facilitate subsequent orogastric intubation.
Once decompression has been achieved, the dog
should be further stabilised as necessary before surgery,
which is mandatory in dogs with GDV. Gastric decom-
pression should be repeated, as appropriate, while prepa-
rations are made to perform surgery.

Radiography
Radiography is not generally necessary for the diagno-
sis of GDV, but can be useful to differentiate GD alone
from GDV. Radiography is commonly performed fol-
lowing fluid resuscitation and gastric decompression.
Some clinicians prefer to take radiographs while provid-
ing initial fluid resuscitation. A right lateral radiograph
of the cranial abdomen should be taken in order to diag-
nose volvulus, but further views may provide additional
information.
GD is obvious radiographically as a large gas-filled
gastric shadow occupying most of the cranial abdo-
Right lateral radiograph
men. Volvulus is characterised by division of the gas- of a dog with GDV. Note
tric shadow into two compartments. This characteristic the small gas-filled
appearance is due to air being trapped in the pylorus and compartment dorsally,
Gastric dilation only which represents air in
descending duodenum as a result of their abnormal posi- the pylorus
tion on the left side of the abdomen. This is not present A small number of dogs are presented with acute
on a left lateral view and reliance on this projection may GD without volvulus. In one study, approximately
lead to a misdiagnosis. Free peritoneal gas is indicative 22 per cent of dogs had GD alone (Brockman and
of gastric perforation. others 1995). GD can be distinguished from GDV
radiographically. The ability or inability to pass a
Anaesthesia stomach tube is not helpful in making this distinc-
Once stabilised, affected dogs should be anaesthetised. tion. Dogs with GD alone should respond well to
In dogs that are proving difficult to stabilise, rapid medical management and do not require emergen-
anaesthesia and surgical decompression of the stomach cy surgery, but an elective gastropexy would still be
are indicated following adequate fluid resuscitation. recommended as these animals would be at greatly
In most situations, the choice of anaesthetic protocols increased risk of subsequent GDV. However, surgery
is limited. Ideally, the protocol that has minimal delete- is indicated following appropriate stabilisation in
rious effects on cardiovascular and respiratory systems any dog with GD and in which it is not possible to Further reading
BROCKMAN, D. J. & HOLT, D. E.
should be used. The analgesic and sedative drugs outlined achieve adequate gastric decompression. Dogs with
(2000) Management protocol
above should provide adequate premedication. Induction recurrent GD often have underlying gastrointestinal for acute gastric dilatation–
of anaesthesia and endotracheal intubation may be disease and this should be investigated. volvulus syndrome in dogs.
Compendium on Continuing
achieved by a further bolus of the fentanyl and diazepam Education for the Practicing
combination described above. Propofol titrated to effect Veterinarian 22, 1025-1034
GOGGS, R., HUMM, K. &
may also assist in anaesthetic induction. It is important port adequate tissue perfusion and oxygen delivery by HUGHES, D. (2008) Fluid
to remember that, in most patients, a reduced volume of maintaining adequate mean arterial blood pressure therapy in small animals.
1. Principles and patient
induction agent is needed due to circulatory compromise. (above 65 mmHg). assessment. In Practice
Dogs should be maintained using isoflurane or sevoflu- Perioperative antibiotics are indicated in dogs with 30, 16-19
GOGGS, R., HUMM, K. &
rane in oxygen, but nitrous oxide should be avoided until GDV. Broad-spectrum antibiotics should be adminis- HUGHES, D. (2008) Fluid
permanent gastric decompression has been achieved. tered at induction and every two hours thereafter peri- therapy in small animals.
A urinary catheter and closed urine drainage sys- operatively. The authors commonly use cefuroxime 3. Colloid solutions.
In Practice 30, 136-142
tem should be inserted. This will allow both peri- and (Zinacef; GlaxoSmithKline) or amoxicillin/clavulanate HUMM, K., GOGGS, R. &
postoperative monitoring of urine production, which is (Augmentin; GlaxoSmithKline) both at a dose of 20 mg/ HUGHES, D. (2008) Fluid
therapy in small animals.
a good indicator of renal perfusion and acts as an indi- kg intravenously. Postoperative antibiotics are indicated 2. Crystalloid solutions.
rect marker of whole-body perfusion status. Ideally, in patients with contamination at the time of surgery (ie, In Practice 30, 85-91
RASMUSSEN, L. (2003)
direct or indirect arterial blood pressure and central in cases of gastric perforation). Stomach. In Textbook of
venous pressure should be monitored and continuous Small Animal Surgery,
electrocardiography carried out during general anaes- References 3rd edn. Ed D. Slatter.
BROCKMAN, D. J., HOLT, D. E. & WASHABAU, R. J. (2000) Philadelphia, W. B. Saunders.
thesia. Evaluation of PCV, TS, serum electrolytes and Pathogenesis of acute canine gastric dilatation–volvulus pp 592-643
blood gases should be performed at regular intervals syndrome: is there a unifying hypothesis? Compendium WILLIAMS, J. M. (2005) Gastric
on Continuing Education for the Practicing Veterinarian dilatation and volvulus. In
(every 30 to 60 minutes). Intraoperative intravenous flu- 22, 1108-1113 BSAVA Manual of Canine and
ids should be maintained at a high rate (10 to 20 ml/kg/ BROCKMAN, D. J., WASHABAU, R. J. & DROBATZ, K. J. (1995) Feline Abdominal Surgery.
Canine gastric dilatation–volvulus syndrome in a veterinary Eds J. M. Williams and J. D.
hour) and supplemented with synthetic colloids or blood critical care unit: 295 cases (1986-1992). Journal of the American Niles. Quedgeley, BSAVA
products, as necessary. Fluid therapy should aim to sup- Veterinary Medical Association 207, 460-464 Publishing. pp 80-95

In Practice ● FEBRUARY 20 0 9 69

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