Aloha! You're speaking to Dr. Michael Salkin
I'm sorry that your question wasn't answered in a timely manner. I'm necessarily constrained to tell you why Rascal is bloating. It can be a precursor to GDV, however - particularly in the German shepherd - and so I'm going to post a thorough synopsis of bloat/GDV for you taken from Clinical Veterinary Advisor, 3rd Ed., Cote', 2015. Not all of what you read will pertain to Rascal presently but you're likely to receive guidance on how you might proceed with him...
Rotation of the stomach on its mesenteric axis associated with gastric distention; well-recognized in large- and giant-breed dogs
Bloat, gastric torsion, gdv
Species, Age, Sex
Risk of gdv increases with age; rarely reported in small dogs and cats
Genetics and Breed Predisposition
Large- and giant-breed dogs
Purebred dogs at greater risk than mixed breeds
Great Dane, German shepherd, Weimaraner, Saint Bernard, Gordon setter, Irish setter, Doberman pinscher, Old English sheepdog, and standard poodle are overrepresented.
Having a first-degree relative with gdv confers an increased risk.
Increased risk may be associated with:
Narrow and deep thoracic cavity
Long hepatogastric ligament
Nutritional risk factors include once-daily feeding, feeding dry dog food, rapid ingestion of food, consumption of large volumes of food, and eating from a raised feeding bowl.
Geography and Seasonality
Possible increased incidence in the months of November, December, and January (United States)
Inflammatory bowel disease
Gastric foreign body
Reports regarding previous splenectomy are conflicting as to risk
History, Chief Complaint
Retching or vomiting (may be nonproductive)
Physical Exam Findings
Abdominal distention and tympany:
Simultaneous auscultation and percussion of the abdomen may reveal a tympanic sound, indicating the presence of a taut, gas-filled stomach.
Clinical signs of hypovolemic shock: weak pulses, tachycardia, pale mucous membranes, prolonged capillary refill time, dyspnea
Etiology and Pathophysiology
In most cases, the pylorus moves ventrally and from right to left; the rotation may be 90°-360°.
Gastric dilation occurs secondary to failure of eructation and pyloric outflow obstruction. Dilation can occur before or after gastric rotation.
The distended stomach results in caudal vena cava and portal vein compression, causing decreased venous return to the heart.
Decreased venous return results in decreased cardiac output, decreased arterial blood pressure, and myocardial ischemia.
Myocardial ischemia causes cardiac arrhythmias.
In the case of volvulus, increased intraluminal gastric pressure, portal hypertension, and avulsion of the short gastric vessels compromise blood flow to the gastric wall. Gastric necrosis and perforation can result. Breakdown of gastrointestinal mucosa allows bacterial translocation.
Portal vein compression/hypertension causes sequestration of splanchnic blood and decreased ability to clear Gram-negative endotoxins.
Endotoxemia further potentiates hypotension and decreased cardiac output.
Pressure on the diaphragm, decreased lung perfusion, and decreased lung compliance cause respiratory dysfunction and exacerbate tissue hypoxia.
gdv should be suspected in large- or giant-breed dogs presenting with an acute history of a distended or painful abdomen, often with preceding or concurrent attempts at vomiting. Physical examination usually reveals a tympanic abdomen and often signs of shock. Treatment for shock is initiated; then diagnosis is confirmed with radiography.
Gastric bloat associated with overeating
Diaphragmatic hernia with stomach herniation
Right lateral view is preferred.
Shows gas-filled pylorus cranial and dorsal to the fundus (“Popeye sign,” “C sign,” or “double bubble”)
Free abdominal air suggests gastric perforation.
Quick assessment tests:
Packed cell volume/total solids (PCV/TS): often increased due to hypovolemia
Serum electrolyte and glucose concentrations: hypokalemia and hypoglycemia may be seen.
Acid-base analysis: metabolic acidosis due to lactic acidosis is frequently present.
Coagulation panel and platelet count: thrombocytopenia, increased prothrombin time/activated partial thromboplastin time/fibrinogen concentration and/or fibrin degradation product concentration associated with disseminated intravascular coagulation
Electrocardiogram (ECG; see p. 1147): ventricular arrhythmias are common.
Advanced or Confirmatory Testing
Diagnosis confirmed at surgery
Plasma lactate concentration: may assist in determining prognosis. In dogs, a cutoff of 7.4 mmol/L at admission correctly predicts presence or absence of gastric necrosis with 82% accuracy, and survival versus euthanasia/death with 88% accuracy.
GASTRIC DILATION/VOLVULUS: Lateral abdominal radiograph of a dog with gastric dilation/volvulus. Characteristic septation (arrows) of the gastric shadow is seen; a displaced, gas-filled antrum is cranial to the arrows (to the left on this image), whereas a gas-filled fundus is caudal (arrows are within it). A gas-filled esophagus and evidence of ileus in the form of distended, gas-filled small intestine are also present.
The initial therapeutic goal is to manage hypovolemia with intravenous (IV) fluids and to decompress the stomach to re-establish systemic and gastric perfusion. Definitive treatment involves surgery to correct the position of the stomach, remove devitalized tissue, and perform a gastropexy to prevent recurrence.
Acute General Treatment
Place large-bore IV catheters in both cephalic veins or cephalic and jugular veins and infuse isotonic crystalloids at an initial rate of 90 mL/kg/h. Colloids can be administered in combination with crystalloids at 5-20 mL/kg over 15-30 minutes. For severe shock, hypertonic saline can be administered at 4 mL/kg over 5 minutes followed by crystalloids.
Administer parenteral prophylactic antibiotics.
Decompress the stomach by orogastric intubation (see p. 1174).
If orogastric intubation is not possible and patient has visible abdominal distention with a radiographically confirmed gdv, perform percutaneous trocarization of the stomach:
Aseptically clip and prepare an area on the dorsolateral abdomen, just caudal to the last rib and ventral to the hypaxial muscles over the region of most obvious distention.
Using a large-bore needle or needle-styleted catheter (e.g., 16- or 14-gauge) directed ventrally and slightly cranially, penetrate all layers of the body wall and stomach. When successful, the procedure should produce a hissing sound associated with a release of fetid-smelling gas through the needle.
Immediate surgery to derotate the stomach and return it to a normal position:
Placing traction on the pylorus and elevating it while putting downward (dorsal) pressure on the fundus will aid derotation in a counterclockwise direction (most but not all cases will have rotated clockwise).
Evaluate stomach and spleen for irreversible vascular compromise and necrosis.
Perform partial or complete splenectomy if splenic necrosis, infarction, or torsion. Perform resection or invagination of necrotic areas of stomach.
Perform gastropexy of pyloric antrum to the right body wall.
Medical treatment alone (repeated intubation, trocarization) has been uniformly ineffective and is not recommended.
Postoperative potassium supplementation if hypokalemic (do not exceed 0.5 mEq/kg/h IV; see p. 528).
If ventricular arrhythmias are noted on the ECG (see p. 1065):
Is hypokalemia present? If so, institute potassium replacement immediately. Ventricular arrhythmias are caused by hypokalemia, and ventricular arrhythmias are refractory to treatment with lidocaine, procainamide, and other antiarrhythmics when hypokalemia is present.
Hypomagnesemia may also predispose patient to ventricular arrhythmias.
Is anemia, hypoxemia, or acidosis present? Many ventricular arrhythmias will resolve spontaneously if systemic abnormalities are corrected.
Is the rate rapid (>160 bpm) or is the pulse weak, despite addressing the systemic abnormalities? If so, consider treatment with lidocaine (see p. 1505).
Treat peritonitis (see p. 798) if gastric perforation has occurred (fluids, antibiotics, abdominal lavage ± drainage).
Treat gastric ulceration: H2 receptor antagonists (famotidine 0.5-1 mg/kg IV, IM, SQ, or PO q 12-24h; or ranitidine 0.5-2 mg/kg IV, IM, SQ, or PO q 8-12h) and/or proton pump inhibitors (omeprazole 0.7 mg/kg PO q 24h or pantoprazole 0.7 mg/kg IV q 24h) and/or sucralfate slurry (0.5-1 gram/dose PO q 6-8h)
Use drugs that increase gastric motility (i.e., metoclopramide 0.2-0.4 mg/kg PO, SQ, or IM q 6h, or 1-2 mg/kg/d IV as a continuous infusion; or cisapride 0.1-0.5 mg/kg PO q 8h) if recurrent bloating occurs after gastropexy, without evidence of gastric outflow obstruction.
Enteral/oral feeding can begin the day after surgery if the patient is not vomiting.
Several recommendations are made to prevent gastric bloat after discharge or to prevent gdv in dogs that have not had a gastropexy:
Divide feedings into several small meals a day.
Do not feed dry kibble.
Avoid stress during feeding.
Do not elevate feeding bowl during eating.
Regular moderate activity outside may decrease risk.
Gastric necrosis, perforation, and peritonitis can occur if devitalized gastric tissue is not excised.
Esophagitis and regurgitation
Gastroparesis and ileus
Disseminated intravascular coagulation
Recurrence of dilation
Recurrence of volvulus if gastropexy is not performed properly
ECG: ventricular arrhythmias common within 36 hours of surgery
Electrolyte concentrations: hypokalemia
Blood glucose concentration: hypoglycemia
PCV/TS: hemoconcentration indicates need for increased fluid therapy. Anemia can occur from bleeding of torn short gastric vessels.
Physical parameters: mucous membrane color, capillary refill, pulse quality, temperature, respiratory effort, lung auscultation, abdominal distention, bruising
Prognosis & Outcome
gdv patients treated surgically have ≤ 15% mortality rate.
Gastric necrosis and need for gastric resection or splenectomy with or without partial gastrectomy are associated with increased mortality.
Increased risk of death if
Clinical signs are present for > 6 hours before examination
Hypothermia is present
Hypotension is present
Peritonitis is present
DIC is present
Preoperative arrhythmias are present
Serum lactate level in dogs with gdv (see above):
99% survival if 6.4 mmol/L, absolute change < 4 mmol/L, or a percentage change < 42.5% of the original value; or < 50% decrease in lactate within 12 hours of presentation.
Pearls & Considerations
Begin fluid resuscitation before abdominal radiography.
Do not assume the stomach is not rotated just because a stomach tube can be passed.
Assess suspect areas of stomach for viability 10-15 minutes after derotation by palpation, evaluating blood flow and stomach wall color. If stomach wall is green or gray or the wall is thin on palpation, this area will need to be resected.
The presence of ventricular arrhythmias indicates the need to evaluate for hypokalemia, anemia, hypoxemia, pain, or acidosis that must be corrected for the arrhythmia to resolve.
See Nutrition/Diet, above.
Do not breed dogs with history of gdv.
Prophylactic gastropexy is recommended in breeds at high risk for gdv.
Performed during ovariohysterectomy, during splenectomy, or as an elective procedure
Commonly performed via laparoscopy
Place large-bore catheters in cephalic or jugular veins immediately for fluid therapy.
Monitor for pulse deficits and rapid heart rate with weak pulses.
Beck JJ, et al: Risk factors associated with short-term outcome and development of perioperative complications in dogs undergoing surgery because of gastric dilatation-volvulus: 166 cases (1992-2003). J Am Vet Med Assoc(###) ###-####1939, 2006.
Additional Suggested Readings
Beer KA, et al: Evaluation of plasma lactate concentration and base excess at the time of hospital admission as predictors of gastric necrosis and outcome and correlation between those variables in dogs with gastric dilatation-volvulus: 78 cases (2004-2009). J Am Vet Med Assoc 242(1):54–58, 2013.
Buber T, et al: Evaluation of lidocaine treatment and risk factors for death associated with gastric dilation and volvulus in dogs: 112 cases (1997-2005). J Am Vet Med Assoc(###) ###-####1339, 2007.
De Papp E, et al: Plasma lactate concentration as a predictor of gastric necrosis and survival among dogs with gastric dilatation-volvulus: 102 cases (1995-1998). J Am Vet Med Assoc 21549–52, 1999.
Green TI, et al: Evaluation of initial plasma lactate values as a predictor of gastric necrosis and initial and subsequent plasma lactate values as a predictor of survival in dogs with gastric dilatation-volvulus: 84 dogs (2003-2007). J Vet Emerg Crit Care 2136–44, 2011.
Mackenzie GB, et al: A retrospective study of factors influencing survival following surgery for gastric dilatation-volvulus syndrome in 306 dogs. J Am Anim Hosp Assoc 4697–102, 2010.
Pipan M, et al: An internet-based survey of risk factors for surgical gastric dilatation-volvulus in dogs. J Am Vet Med Assoc(###) ###-####1462, 2012.
Raghavan M, et al: Diet-related risk factors for gastric dilatation-volvulus in dogs of high-risk breeds. J Am Anim Hosp Assoc 40192–201, 2004.
Raghavan M, et al: The effect of ingredients in dry dog foods on the risk of gastric dilatation-volvulus in dogs. J Am Anim Hosp Assoc 4228–36, 2006.
Santoro KA, et al: Evaluation of plasma lactate concentration and base excess at the time of hospital admission as predictors of gastric necrosis and outcome and correlation between those variables in dogs with gastric dilatation-volvulus: 78 cases (2004-2009). J Am Vet Med Assoc 24254–58, 2013.
Zacher LA, et al: Association between outcome and changes in plasma lactate concentration during presurgical treatment in dogs with gastric dilatation-volvulus: 64 cases (2002-2008). J Am Vet Med Assoc 235892–897, 2010.
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