Acute gastric dilatation volvulus is a life-threatening emergency characterised by a distended stomach and rotation on its mesenteric axis (Monnet, 2003). The cause is unknown, but it is vital to promptly recognise the condition and initiate effective stabilisation (Monnet, 2003).
Another presentation is a chronic or partial gastric volvulus (Radlinsky and Fossum, 2013). This affects dogs in a more subtle way and prolonged clinical signs can be recognised (Paris et al, 2011; Radlinsky and Fossum, 2013).
This article provides theoretical and practical advice about acute gastric dilatation volvulus syndrome. It gives information about triage and recognition of the symptoms, diagnosis and haemodynamic stability before surgical intervention. Surgical considerations and postoperative care are also described, along with client education and communication about this syndrome.
Pathophysiology
Gastric dilatation volvulus is characterised by gastric distension and pyloric rotation, most commonly clockwise, between 90 and 360°. Often the spleen is displaced concomitantly to the right ventral side of the abdomen (Radlinsky and Fossum, 2013). Gastric rotation will lead to the inability to eructate (belch). Additionally, gas accumulation could come from aerophagia, bacterial fermentation of carbohydrates, diffusion from bloodstream or metabolic reactions. Meanwhile, fluid accumulates in the lumen from normal gastric secretions and from transudation secondary to venous congestion (Radlinsky and Fossum, 2013).
Haemodynamic effects
Decrease venous return will cause hypoperfusion of venous abdominal flow. Consequently, a decrease in mean arterial pressure and in cardiac output is detected. This will affect the haemodynamics of multiple systems, such as cardiovascular, respiratory, gastrointestinal and renal systems. It will also lead to coagulation dysfunction, and acid–base and electrolyte abnormalities (Sharp and Rozanski, 2014).
Cardiovascular system
Hypoperfusion of the myocardium leads to ischaemia. This will damage the tissue and can cause arrhythmias, in approximately 40% of dogs with gastric dilatation volvulus (Brockman et al, 1995; Bebchuk et al, 2000). Ventricular arrhythmia, specifically ventricular premature complexes, are most commonly seen (Figure 1) (MacPhail et al, 2006).
Respiratory system
Respiratory compromise may occur as a result of gastric dilation and increased intra-abdominal pressure. These will cause decreased total thoracic volume and abnormal excursion of the diaphragm, inhibiting initiation of inspiration. Hypoventilation and reduced pulmonary perfusion are seen. A compensatory increased respiratory rate is noticed at this point. When compensatory mechanisms become inadequate, hypercapnia and hypoxaemia can occur. An increased risk of aspiration pneumonia (Bruchim and Kelmer, 2014) and development of respiratory distress syndrome have also been reported (Santoro Beer et al, 2013).
Gastrointestinal system
The distended stomach compresses the caudal vena cava and the portal vein, which causes hypoperfusion of the gastric wall. This will be more severe with increasing degrees of rotation, resulting in stasis and possible thrombosis. Consequently, necrosis and gastric perforation can occur. The short gastric arteries can be stretched and subsequently avulsed causing intra-abdominal haemorrhage. As the rotation occurs, the omentum and spleen can also be rotated and become compromised (Brockman et al, 1995).
Renal system
Renal dysfunction is a significant risk, with potential mechanisms including hypoperfusion, inflammatory injury and renal microthrombosis (Bruchim and Kelmer, 2014; Sharp and Rozanski, 2014).
Coagulation dysregulation
Dysfunction of the coagulation system can occur and may affect primary haemostasis, secondary haemostasis and/or fibrinolysis. Dogs presenting with gastric dilatation volvulus have an hypocoagulable state, which can result in consumption of platelets and clotting factors in disseminated intravascular coagulation. The presence of three or more coagulation parameters is consistent with disseminated intravascular coagulation (thrombocytopenia, prolonged prothrombin/activated partial thromboplastin time, hypofibrinogenaemia, elevated levels of fibrin degradation products and depletion of antithrombin). Apart from the hypocoagulable state, studies have also reported macrothromboses in dogs with gastric dilatation volvulus (Sharp and Rozanski, 2014).
Acid–base and electrolyte abnormalities
Mixed acid–base status is commonly seen in dogs with gastric dilatation volvulus. A high anion gap can be explained by the higher level of lactate (caused by hypoxia and hypoperfusion). Metabolic acidosis is usually a result of low global oxygen delivery. Hypochloraemic metabolic alkalosis is a consequence of gastric hydrochloric acid. Hypoventilation and hypercapnia can lead to respiratory acidosis. As there can be concurrent and opposing primary disorders, the pH can be normal (Hornbuckle et al, 2008).
Electrolyte abnormalities are variable. The most common alteration is hypokalaemia (Radlinsky and Fossum, 2013) caused by sequestration of potassium in the stomach, loss of potassium through vomiting or stomach lavage, hyperchloraemic metabolic alkalosis, activation of the renin–angiotensin–aldosterone system and catecholamine-induced intracellular shifting of potassium. Hypokalaemia is further compounded by the administration of large volumes of low potassium fluids (Sharp et al, 2014).
In a final phase, shock can be identified (Cornell, 2018). Different types of shock can occur (and usually more than one is associated with gastric dilatation volvulus): obstructive, distributive, hypovolaemic and/or cardiogenic shock, as demonstrated in Figure 2 (Sharp and Rozanski, 2014).
The cause of gastric dilatation volvulus is not well understood. The literature suggests risk factors include large and pure breed (German Shepherd dogs, Great Danes, standard poodles, and Irish setters are overrepresented), male dogs, and those with deep-chested conformation, a history of gastric dilatation volvulus in first-degree relatives, increased length of the hepatogastric ligament or nervous temperament. Other proposed risk factors are a low number of meals per day, eating too quickly or from elevated bowls, decreased food particle size or exercising after meals. In older dogs, being underweight and exposed to stressful events were also related to development of gastric dilatation volvulus (Radlinsky and Fossum, 2013; Sharp, 2015; Cornell, 2018).
Clinical presentation
Signalment and history
Common clinical signs include progressive abdominal distention and tympanic abdomen, unproductive vomiting or retching, restlessness, discomfort and hypersalivation. In more severe cases collapse can be seen (Sharp, 2015; Cornell, 2018).
Complete history taking can be challenging because of the acute nature of the condition.
Physical examination
Abdominal palpation can reveal different degrees of tympany and distention. This can be obscured by an obese, heavily muscled or deep-chested conformation (Radlinsky and Fossum, 2013). As the disease progresses, signs of compensatory shock and decompensatory shock are seen, as described in Table 1 (Cornell, 2018).
Table 1. Signalments of compensatory and decompensatory shock in a patient
| Compensatory shock | Injected mucous membranes |
| Tachycardia | |
| Weak pulses | |
| Decompensatory shock | Pale mucous membranes |
| Bradycardia | |
| Cold extremities | |
| Depressed mentation | |
| Hypothermia |
Diagnosis and laboratory findings
Gastric dilatation volvulus is diagnosed by taking a single right lateral abdominal X-ray. This view allows differentiation between gastric dilatation volvulus and a simple gastric dilation. In gastric dilatation volvulus, the pylorus will be malpositioned. Air in the pylorus is seen separated from the air in the stomach by soft tissue density which cause the appearance of a sign which is known as the ‘double bubble’, ‘reverse C’ or ‘Popeye sign’ (Figure 3). If pneumoperitoneum is noticed, it likely indicates gastric perforation (Cornell, 2018).
There are some laboratory abnormalities that are expected with gastric dilatation volvulus. An emergency minimum dataset should include packed cell volume, total protein (both may be elevated as a result of haemoconcentration), glucose, urea and lactate measurement. If possible, blood should also be collected for a complete blood count, biochemistry profile and coagulation panel (Tivers and Adamantos, 2016).
Hyperlactataemia is related to the prediction of non-survival in dogs, to gastric perfusion (and therefore necrosis) and to the success of resuscitation efforts (Santoro Beer at al, 2013). Increased levels of hepatic enzymes and azotaemia can be seen, and electrolyte abnormalities can vary (Cornell, 2018).
Some clinicians also opt to perform preoperative thoracic X-rays, to screen for neoplasia, aspiration pneumonia, hypovolaemia, oesophageal abnormalities or cardiac disease. The cardiovascular status of the animal needs to be taken into account when considering additional diagnostic tests (Green et al, 2012).
Treatment
Stabilisation
Large-bore catheters should be placed at least in two veins, either cephalic or jugular. Initial fluid therapy is crucial as hypotension is expected. Shock doses of isotonic crystalloid solutions (up to 90 ml/kg boluses), or a combination of isotonic crystalloids at a lower dose (20–40 ml/kg) along with 7% hypertonic saline (2–4 ml/kg), can be considered (Tivers and Adamantos, 2016). Other resuscitation protocols are described in Table 2.
Table 2. Type of fluid for resuscitation and related dose
| Type of fluid | Dose |
|---|---|
| Sodium chloride | 45–90 ml/kg/h |
| Lactated Ringer's solution | 45–90 ml/kg/h |
| Hypertonic saline 7% | 4–5 ml/kg over 5–15 minutes |
| Hydroxyethyl starch | 10–20 ml/kg |
| Isotonic crystalloids and hydroxyethyl starch | 10–40 ml/kg + 10–20 ml/kg |
| 7% hypertonic saline in 6% dextran-70 | 5 ml/kg over 5–15 minutes |
An electrocardiogram is an easy and non-invasive diagnostic test that is recommended as soon as possible since arrhythmias can be seen preoperatively (Figure 1) (Beck et al, 2006; Mackenzie et al, 2010). Treatment for ventricular arrhythmias is advised when there are arrhythmias with cardiovascular compromise (hypotension, pulse deficits, poor pulse quality), sustained tachycardia (heart rate above 150 bpm) or multiform ventricular premature contractions. The described dose is a slow bolus of 1–2 mg/kg and then to continue a constant rate infusion of 50–70 µg/kg/min over the first 24 hours of presentation.
If any side effects of lidocaine are noticed, such as nausea or seizures, the drug must be stopped and the side effects treated appropriately (Tivers and Adamantos, 2016).
Gastric decompression is attempted after beginning cardiovascular resuscitation. Figure 4 shows the steps for gastric decompression by orogastric tube placement or percutaneous trocar insertion. Box 1 gives some tips to try if this procedure is not effective.
Box 1.Tricks and tips for gastric decompression
- When the orogastric tube is passed during surgery, the endotracheal cuff should be well inflated and the oesophagus should be suctioned after the procedure to minimise the risk of aspiration pneumonia (Cornell, 2018).
- When trocarisation is performed, the most tympanic site, identified by palpation or auscultation, should be tapped. If the clinician is inexperienced, ultrasound can be used to aid trocarisation (Goodrich et al, 2013).
- During trocarisation, gentle inward pressure can be applied to the trocar (catheter) to aid air evacuation from the stomach (Goodrich et al, 2013).
If the orogastric tube is successfully passed (Figures 5 and 6), a delay in corrective surgery is possible in selected cases. Close monitoring, fluid therapy and repeated gastric decompression will be required to avoid cardiovascular compromise. If percutaneous decompression (trocarisation) is performed (Figure 7), surgery should not be delayed (White et al, 2021).
Surgery
Surgical goals are gastric decompression, inspection of viability of the stomach and the other organs involved, and minimising recurrence by performing a gastropexy (Radlinsky and Fossum, 2013).
To prepare the dog for surgery, the abdomen needs to be clipped and aseptically prepared for a full ventral midline celiotomy. When in the abdominal cavity, further gastric decompression can be achieved by passing an orogastric tube (nurse or anaesthetist, aided by the surgeon) after de-rotation of the stomach (Box 1). The stomach and spleen are then investigated to assess the viability of these organs. Subjective parameters are often used for this.
Some of the parameters are discolouration (green, purple, black), the existence of seromuscular tearing and thinning on palpation; these indicate that ischaemia and necrosis is likely. Gastric vessels can be palpated and the tissue examined for active bleeding to investigate perfusion (if there is no active bleeding, resection will be necessary). Objective assessment of gastric viability using fluorescein dye, scintigraphy or laser Doppler flowmetry (Tivers and Adamantos, 2016) are possible but may be impractical or not available.
Non-viable or possibly non-viable areas of the stomach can be resected by performing a partial gastrectomy or through invagination. To help manipulation, stay sutures 2-0 or 3-0 polypropylene are placed in healthy stomach wall. For partial gastrectomy, the portion affected is resected until the cut edges are actively bleeding. The stomach is closed in two layers using absorbable suture material. When doing an invagination, the affected portion is folded inward and healthy tissue is sutured in two layers of a simple continuous or inverting suture pattern using absorbable suture material. The affected tissue will become necrotic and be digested in the gastric lumen (Tivers and Adamantos, 2016).
Gastropexy is performed between the pyloric antrum and the right abdominal wall to minimise recurrence. Different gastropexy techniques have been described, most relying on adherence of the muscular layers between the stomach and the abdominal wall (Cornell, 2018). The choice of technique depends on each surgeon, but the most commonly used is the incisional gastropexy. This is performed by creating a 4–5 cm seromuscular incision in the gastric antrum and another one through the peritoneum and transversus abdominis muscle on the lateral or ventrolateral right abdominal wall (caudal to the last rib). Starting in the craniodorsal edges of the incision, both incisions are placed, using a 2-0 monofilament absorbable suture, in a simple continuous suture pattern incision (Cornell, 2018).
The remainder of the abdominal contents should be inspected and the abdominal cavity lavaged with warm sterile saline followed by routine closure (Radlinsky and Fossum, 2013).
Postoperative management
The first 48–72 hours are important for close monitoring. Fluid therapy and frequent assessment of mucous membrane colour, capillary refill time, packed cell volume, total protein, urine output, electrocardiogram, blood pressure and acid–base balance are advisable (Sharp, 2015).
Patients should be monitored with an electrocardiogram as arrhythmias are more common post-surgery (12–24 hours after intervention), with an incidence of 50–77% (Beck et al, 2006; Mackenzie et al, 2010). If present, arrhythmias should be treated as described for stabilisation.
Feeding can start 12–24 hours after surgery (Cornell, 2018).
Complications reported include arrhythmias, gastric necrosis or dehiscence, acute kidney injury, peritonitis, sepsis, disseminated intravascular coagulation, ileus and vomiting. It is also reported that dogs that undergo partial gastrectomy have an increased risk of developing peritonitis, disseminated intravascular coagulation, sepsis and arrhythmias. However, it has not been proven that those dogs are at increased risk of death (Beck et al, 2006).
Prognosis and recurrence
Mortality rate has improved down to 10%, likely as a result of better understanding of the disease and quicker diagnosis. Poor prognostic indicators include duration of clinical signs (more than 6 hours before examination), hypotension, lactate concentration, peritonitis, and development of disseminated intravascular coagulation or sepsis (Cornell, 2018). Preoperative measurement of lactate levels is a good predictor of prognosis and gastric necrosis, with a cut-off of 7.4 mmol/litre (Santoro Beer at al, 2013). Also, an absolute change in lactate concentration lower than 42.5% and a final lactate concentration higher than 6.4 mmol/litre were associated with lower survival rates in dogs with gastric dilatation volvulus (Zacher et al, 2010).
Dogs who respond to decompression and are treated with medical stabilisation alone have a reported recurrence rate of 80%. For this reason, all patients with gastric dilation and/or partial rotation (less than 180°) should have gastropexy performed (Radlinsky and Fossum, 2013).
Client education (prophylaxis)
Owners of large or giant breed dogs should be educated regarding gastric dilatation volvulus. Some management strategies have been reported and are included in Table 3 (Sharp, 2015).
Table 3. Strategies to reduce the likelihood of developing gastric dilatation volvulus for owners of dogs predisposed to this condition
| Not feeding from raised food bowls |
| Ensure that they eat slowly |
| More than one meal during the day |
| Avoid extreme exercise after meals |
| Avoid giving food that has larger particles |
| Avoid stressful events |
| Prophylactic gastropexy |
Mortality from gastric dilatation volvulus can be decreased to 0.3% with prophylactic gastropexy (Ward et al, 2003). However, cost, lifetime probability of morbidity and risk of death from gastric dilatation volvulus are factors that influence breeders and owners' decision to have prophylactic surgery (Ward et al, 2003). Laparoscopy gastropexy can be an alternative to open abdominal prophylactic gastropexy. This technique is considered quicker and easier to perform for one experienced surgeon and less stressful for the dog (Rawlings, 2002). There is no difference in tensile load to failure after 30 days compared with the conventional technique. Laparoscopic-assisted gastropexy is another technique that requires less specialised equipment and can be performed in a significantly shorter time (Mayhew and Brown, 2009).
Conclusions
Gastric dilatation volvulus syndrome leads to rapid development of systemic haemodynamic abnormalities in dogs. Urgent treatment is essential to maximise therapeutic success. This includes prompt recognition and stabilisation through fluid resuscitation and gastric decompression. Close monitoring postoperatively is crucial as complications can arise. It is important to educate clients to recognise the condition and minimise possible risk factors.
KEY POINTS
- Gastric dilatation volvulus is a life-threatening emergency that must be promptly recognised in order to have a better outcome.
- The pathophysiology of this syndrome causes systemic haemodynamic abnormalities.
- Cardiovascular resuscitation and decompression of the stomach are important stabilisation steps before surgery.
- Surgery is done with the aim of decompression, inspection of organs' viability and minimising recurrence by gastropexy.
- Owners of large to giant breed dogs should be educated, with some management strategies and/or prophylactic gastropexy advised.