Gastric Dilatation-Volvulus Syndrome in Dogs

Introduction

Gastric dilatation-volvulus (GDV) syndrome is an acute, life-threatening condition requiring immediate emergency surgical intervention.

Intervention includes stabilization, decompression, derotation, and gastropexy. Every second counts!

It is most commonly seen in large to giant breed dogs, particularly in deep-chested dogs, although any breed may be at risk.

It can occur when the stomach fills with gas, food, and/or fluid, resulting in gastric dilatation, or otherwise known as “bloat”. Gastric dilatation can then progress further into a volvulus. Volvulus is when the stomach “flips” or twists upon itself (i.e. gastric rotation). Once a volvulus has occurred, the stomach continues to fill with gas, and thereby continuing to dilate/distend.

Note that the pathophysiology involves two theories: gastric rotation followed by gastric dilatation versus gastric dilatation followed by gastric rotation.

A GDV not only obstructs the stomach’s inflow and outflow, but additionally, the enlarged gas-filled stomach presses dorsally against the caudal vena cava, resulting in cutting off blood circulation throughout the entire body, known as obstructive shock. This obstructive shock leads to decreased cardiac output, reduced blood flow, hypovolemia, and hypotension. Blood flow is further reduced by fluid entrapment within the stomach and third space shifting, leading to hypovolemic shock. Reduced blood flow and oxygen delivery results in compromise to vital tissues and organs. The increased pressure within the stomach can additionally cause stomach wall destruction, tissue necrosis, stomach perforation, and peritonitis. Tissue necrosis and toxin buildup can lead to distributive shock. Immediate emergency surgical intervention is required to help prevent and/or treat life-threatening sequelae such as shock, cardiac arrhythmias, ventilation/perfusion mismatch, organ damage, electrolyte disturbances, acid-base derangements, tissue necrosis, sepsis, and/or disseminated intravascular coagulation. Sequelae are described in more detail below in the “Pathophysiology” section.

Incidence

The incidence of GDV is 2.4 to 7.6 for every 1,000 dogs admitted to a hospital, and it is the second leading cause of canine death with 15% dying due to the condition within their lifetime.

Large to giant breed dogs have a 3.9% to 36.7% lifetime risk.

Risk Factors

Some factors that can increase GDV risk include:

• Ingesting a large amount of food or food particles less than 30 mm in size
• Eating only one meal a day
• Running/exercise after eating a large meal or drinking a large volume of water
• Anxiety or having a nervous temperament (suspected due to increasing the amount of swallowed air)
• Advanced age: risk by a factor of one
• Giant breed status: in urban residences, 22% of cases
• Large breed status: in rural residences, 24% of cases, a risk factor of one
• Having a history of GDV in a first degree relative
• Having a history of a splenic torsion/splenectomy: 3% to 8% incidence
• Presence of a gastric foreign body: by a factor of five, a 98% increase
• Splenectomy: intact male in 25% of cases
  • Higher body weights or older age are more likely to have a history of a splenectomy
  • GDV without a history of splenectomy: 1% to 6% of cases
  • GDV with a history of splenectomy: 3% to 6% of cases, risk factor of 5.3 (GDV develops 350 days post-operatively (PO)) with GDV by 1yr, 3yrs, & 6yrs PO having a 65%, 20%, & 15% incidence respectively, versus no GDV by 1yr, 3yrs, & 6yrs PO having a 50%, 30%, & 20% incidence respectively

Predisposition

Single-nucleotide polymorphism array genotyping found the most significant signal in Collies, German Shorthaired Pointers, and Great Danes. Genes for gastric tone and motility were involved (VHL, NALCN, and PRKCZ).

Higher-risk breeds include (but not limited to):

• Airedale terrier
• Akita
• Basset Hound
• Borzoi
• Bull Mastiff
• Chow Chow
• Collie
• Doberman Pinscher (4% incidence)
• German Shepherd (12% to 25.8% incidence)
• Gordon Setter
• Great Dane (11% incidence, 42% life-time risk)
• Irish Setter
• Irish Wolfhound
• Rottweiler (4% life-time risk)
• Saint Bernard
• Standard Poodle (5% incidence)
• Weimaraner

Males (overall 59.25%, intact 53.1%), older dogs (5 to 10 years of age make up 55% of dogs, dogs 6 to 7 years of age are 2x as likely to be affected compared to those 3 to 4 years of age), and dogs with higher body weights are over-represented.

Pathophysiology

The pathophysiology involves two theories: gastric rotation followed by gastric dilatation versus gastric dilatation followed by gastric rotation.

With either, the stomach rotates about its long axis in a clockwise direction, with the pylorus and proximal duodenum displacing ventral and cranial, from right to left, and finally positioning dorsal to the esophagus.

The gastroesophageal sphincter is obstructed and pyloric dysfunction is evident.

Eructation, vomiting, and pyloric outflow is inhibited, resulting in aerophagia, bacterial fermentation, and rapid gas buildup, and progressive gastric dilatation.

GDV physiologic changes include the following in sequential but also overlapping phases:

• Increased intra-abdominal pressure, decreased venous blood flow, caudal vena cava compression, and obstructive shock
• Poor splanchnic circulation causing small intestinal compromise, increased endotoxin absorption, villi injury, and jejunal mucosal changes
• Decreased pancreatic perfusion, gastric/splenic displacement, and decreased portal venous return; causes pancreatitis and portal hypertension causing decreased hepatic reticuloendothelial function, poor bacterial/endotoxin hepatic clearance, and hepatic ischemia
• Increased gastric volume/abdominal pressure decreases total thoracic volume, increases diaphragmatic pressure and decreased excursions, decreased inspiratory effort, partial lung collapse, ventilation/perfusion mismatch, hypovolemia, decreased pulmonary blood flow, and poor oxygen delivery
• Cardiac dysfunction from poor coronary flow (decreased by 50%), myocardial depressant factor, cardiac arrhythmias (40 to 70% incidence overall, incidence of ventricular arrhythmia 13% to 100%), decreased cardiac output, and increased cardiac oxygen extraction by 30%
• Shock results in poor tissue perfusion and hypoxemia, promotion of anaerobic metabolism with tissue acidosis (hyperlactatemia)
• Full thickness gastric wall necrosis (10% to 37% incidence) from avulsion of the splenic artery and short gastric arteries along the greater curvature (causing a hemoperitoneum), collapsed capillaries (from increased intragastric pressure), and decreased systemic blood pressure (hypotension), causing ischemia, hyperlactatemia, submucosal/mucosal gastric edema, and gastric necrosis
• Other factors include the degree of gastric rotation, duration of GDV, intragastric pressure, gastric wall tension, and systemic arterial pressure
• Splenomegaly from venous congestion/vessel occlusion, intravascular thrombosis, splenic infarction, and splenic necrosis

Ischemic reperfusion injury, sepsis (2.4% incidence), systemic inflammatory response syndrome, and acute respiratory distress syndrome due to reactive oxygen species, directly by lipid peroxidation, and indirectly by neutrophil activation. Poor cardiovascular stability, hypotension, multiple organ failure, and finally death results.

Degree Rotation

Clinical presentations include acute gastric dilation, or gastric dilatation with gastric volvulus.

The former is defined as a 90° counterclockwise gastric rotation around the gastroesophageal junction.

The latter is defined as simultaneous dilation and clockwise 180° to 360° rotation at the gastroesophageal junction. Average rotation reported is between 180° and 270°.

Abdominal Radiography

Findings with the patient in right lateral recumbency include pyloric air entrapment and pyloric
malpositioning that is described as a “double bubble” sign, “reverse C” sign, “boxing glove” sign, “Popeye’s arm” sign, or “Smurf’s hat” sign.

Pneumoperitoneum indicates gastric perforation or gastric trocarization.

Gastric Decompression

Decompression may be via orogastric tube, percutaneous over-the-needle catheter, or trocar.

Delayed Surgery

There is no survival difference for dogs whom received gastric decompression and placement of an indwelling nasogastric tube for 90 minutes prior to surgery versus those with surgery after 5 to 13.7 hours of stabilization.

Of dogs that had surgery in the same anesthetic session as for decompression/stabilization, 33% had gastric necrosis.

Of dogs with surgery at a second anesthetic episode at a mean of 22.3 hours after presentation, 5.7% had gastric necrosis.

Surgical Management

Surgical intervention creates a permanent adhesion between the gastric pyloric antral wall and the right abdominal body wall.

The stomach is retracted to the right abdominal wall and the body of the stomach is pushed dorsally for evaluation of the gastroesophageal junction.

Gastric viability is determined via color, thickness, integrity, and near-infrared fluorescence.

The ideal gastropexy would restore normal anatomic positioning, maintain normal gastric function, is permanent, predictable, simple with minimal complications, and requiring minimal post-operative management.

Surgical Approaches

Surgical approches include:

• Total laparotomy: strength 24.04 N to 106.5 N
• Mini-laparotomy
• Grid approach
• Total laparoscopic: intracorpeally stapled or sutured gastropexy
• Laparoscopic-assisted: Hasson or Veress needle techniques. Strength 45 to 100 N at 30 to 50 days, 51.1 N at 10 weeks.
• Modified laparoscopic-assisted: Strength 35.86 N
• Endoscopic-assisted

Gastropexy Types

Gastropexy types (with associated strengths to the abdominal wall) include:

• Belt loop: seromuscular flap created along the greater curvature of the stomach (gastroepiploic artery), extending to the antrum. A tunnel is created in the abdominal wall, parallel to the gastric incision. Strength 109 N at 50 days
• Modified belt loop
• Circumcostal: single- or double-hinged seromuscular flap is created over the lesser curvature of the stomach or the antrum, by undermining below the muscularis layer. Strength 109 N at 21 days.
• Gastrocolopexy: attaches the greater curvature of the stomach to the transverse colon
• Incisional: most common. Strength 35 to 38 N.
  • 59 to 60 N at 3 weeks
  • 62 to 106 N at 4 weeks
  • 60 to 85 N at 21 to 58 days
  • 53 N at 8 weeks
• Modified incisional
• Incorporating: incorporates the line alba laparotomy closure with the gastropexy. Strength 60 to 110 N.
• Muscular flap
• Tube

Splenectomy (15% to 20% need it) and/or gastric resection/invagination (up to 20% need it) may be considered on a case by case basis.

Board Certified Surgeon vs General Practitioner

Deciding to opt for a board certified surgeon versus general practitioner (GP) can be challenging.

The survival rates of patients operated on by GP versus specialists were 81.7% and 88.7%, respectively.

Intraoperative mortality rates for GP versus specialists were 7.0% and 2.9%, respectively. The odds of mortality in dogs operated on by GP were approximately 2x those operated by specialists.

Post-Operative Recovery and Possible Complications

As with other surgical procedures, GDV procedures come with possible complications, including:

• Cardiac arrhythmias: 30% to 50% incidence
• Hemostatic derangements: 20%
• Recurrence of disease: 4% to 10.6%
  • Gastrocolopexy: 15%
  • Circumcostal: 0% to 7%
  • Incorporating: 6.5%
  • Incisional: 5%
  • Belt loop: 0%
• Coagulopathy: 8%
• Acute renal injury: 3% to 8%
• Peritonitis: 5% (gastric necrosis)
• Splenic thrombosis: 3%
• Pancreatitis: 1.5%

Mortality and Prognostic Factors

Some mortality and prognostic factors include:

• Overall mortality: 10% to 68% (50% due to gastric necrosis)
• Overall survival: 75% to 97%
• No treatment/medical therapy alone: 81% die within one year
• Recurrence rate without gastropexy: 56% within 3 months, 80% long-term
• Splenectomy mortality: 32%
• Partial gastrectomy and splenectomy mortality: 55%

Some high mortality factors include:

• Clinical signs duration > 5 hours: 46% mortality rate
• Depressed/coma at admission: 3x to 36x risk of death
• Coagulopathy: associated with gastric necrosis
• Pre-operative cardiomegaly: survival decreases by 10x
• Survival without gastric resection: 100%, mortality without gastric necrosis: 2% to 14%
  • Gastric necrosis: 11x increased mortality
  • Gastric necrosis/partial gastrectomy mortality: 31% to 98%, 6x increase in mortality

Prevention

The GDV risk with at-risk patients decreases from 4% to 54.5% to 0.3% to 8% with prophylactic gastropexy.

Mortality decreases by 2x (Rottweilers) to 29.6x (Great Danes) with prophylactic gastropexy.

Gastric motility does not change after prophylactic laparoscopic gastropexy.

Preoperative euthanasia (non-survival without intent to treat) is the majority of GDV mortality. Disease prevention will improve disease mortality greater than improving treatment.

The majority of non-insured dogs (37% to 63%) are euthanized pre-operatively (5 to 7.4x risk), while 0 to 10% of insured dogs are euthanized pre-operatively.

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