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GASTRIC DILATION AND VOLVULUS

Introduction
  • Gastric Dilatation-Volvulus (GDV) is a rapidly progressive life-threatening condition of dogs that requires immediate medical attention.

  • The condition is multifactorial but is commonly associated with rapid ingestion of large meals. The presence of food and gas causes the stomach to significantly dilate and expand (dilation), which may have several severe consequences, including:

    • obstruction of venous return to the heart from the abdomen

    • pooling of blood inside the stomach

    • rupture of the stomach wall

    • dyspnea due to increased pressure on diaphragm

  • Additionally, the stomach can become dilated enough to rotate on itself (volvulus). The rotation can lead to blockage in the blood supply to the spleen and the stomach.

  • Diminished respiration and cardiac output throughout the course of the disease leads to poor oxygen delivery to many tissues (hypoxia). This leads to cell death in the liver, kidneys, and other vital organs.

  • Cardiac arrhythmias (abnormal heart beats) are commonly seen because of the hypoxia.

  • The lining of the entire gastrointestinal tract is at risk of cell death and sloughing.

  • Devitalization of the gastrointestinal tract can allow bacteria to access to the bloodstream and lead to bacteremia (bacteria in the blood) and sepsis.

  • Several studies have been published that have evaluated risk factors and causes for gastric dilatation and volvulus in dogs. This syndrome is not completely understood; however, it is known that there is an association in dogs that:

    • have a deep chest (increased thoracic height to width ratio)

    • are fed a single large meal once daily

    • are older

    • are related to other dogs that have had the condition

  • Nearly all breeds of dogs have been reported to have had gastric dilatation with or without volvulus, but many of the commonly seen breeds are Great Danes, Weimaraners, St. Bernards, Irish setters, and Gordon setters.

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Clinical Signs​
  • The onset of clinical signs is typically peracute or acute.

  • Initial clinical signs include

    • restlessness,

    • hypersalivation and

    • non-productive retching

    • followed by gradual abdominal distension

    • Eventually, pain along with weakness and abdominal tympany.

  • Physical examination findings reflect

    • gastric dilation,

    • circulatory shock, and

    • dyspnea.

  • Therefore, a distended abdomen,

    • tachycardia,

    • poor peripheral pulse quality,

    • a prolonged capillary refill time,

    • pale and dry mucus membranes,

    • tachypnea, and

    • dyspnea are expected.

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Diagnosis ​
  • Suspicion of gastric dilation and volvulus is usually high after considering the history, signalment, and clinical signs.

  • Radiographs help distinguish simple gastric dilation from GDV.

  • The preferred radiographic views for identification of GDV are right lateral and dorsoventral recumbency.

  • Ventrodorsal positioning must be avoided because of the potential for aspiration of gastric contents.

  • The right lateral radiograph usually reveals a large, distended, gas-filled gastric shadow with the pylorus located dorsal and slightly cranial to the fundus. The gastric shadow is frequently compartmentalized or divided by a soft-tissue “shelf” between the pylorus and fundus. This shelf, or reverse "C” or double bubble sign, is created by the folding of the pyloric antral wall onto the fundic wall. Splenic enlargement or malposition may be noted on radiographs. Gas within the gastric wall is suggestive of tissue compromise, whereas free gas within the abdomen indicates gastric rupture.

  • PCV, total solids, electrolytes, blood glucose, and serum lactate levels should be evaluated, and blood drawn for a CBC, serum biochemical profile, and coagulation assays. Continuous ECG and blood pressure monitoring are recommended.

  • Prerenal azotemia is a common finding in animals with GDV and is secondary to systemic hypotension. Increased CK levels may be present due to striated muscle damage, and serum potassium levels may increase subsequent to cell membrane damage.

  • Serum ALT and AST levels may increase secondary to hypoxic damage. Increased lactate is a common finding and is secondary to systemic hypotension and inflammation.

  • Hyperlactatemia (>6 mmol/L) is associated with an increased likelihood of gastric necrosis and the need for partial gastric resection.

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Management of Suspected Acute GDV
  • Therapeutic goals:

    • Restore and support the circulation

    • Decompress the stomach

    • Establish whether GDV or simple dilation is present

    • Rapid surgical correction if volvulus has occurred

    • Prophylaxis:

      • a.  Surgical

      • b.  Environmental

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Emergency Care
  • Management of hypovolemia

    • ​ to prevent or treat shock, is the primary goal of emergency treatment.

    • Two large bore catheters (ideally 16g or 18g) should be placed in cranial veins (cephalic or jugular).

    • If the facility for rapid results is available, a blood sample should be taken for packed cell volume (PCV), serum total protein estimation (TP), serum electrolyte levels and evaluation of coagulation parameters.

    • Fluid therapy should be started at a rate of 90 ml/kg/hr using a balanced electrolyte solution.

    • In giant breeds, an hypertonic saline-dextran (HSD) combination (7% NaCl in 6% dextran 70), administered at 5ml/kg over a five minute period, may provide more rapid initial circulatory resuscitation.

    • Both the high volume crystalloid and low volume HSD fluid resuscitation protocols should be followed by high volume crystalloid administration (20 ml/kg/hr) for maintenance of resuscitation.

    • The decision to introduce blood products or a synthetic colloid to provide further circulatory support and improve oxygen delivery to tissues should be influenced by subsequent PCV, TP and circulatory stability estimations.

    • If available, continuous ECG should be started or a baseline recording made.

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  • Gastric decompression

    • Should only be attempted once correction of the intravascular volume deficit is well underway.

    • Delaying decompression beyond this time could have an important influence on gastric wall integrity and the ultimate systemic levels of inflammatory mediators released from the splanchnic circulation.

    • In most instances, gastric decompression can be achieved by orogastric intubation of the conscious or sedated animal. For sedation, a combination of fentanyl (2-4 micrograms/kg) or oxymorphone (0.1 mg/kg IV) followed by diazepam (0.25-0.5 mg/kg IV) can be used.

    • The tube selected should be measured from the external nares to the caudal edge of the last rib and marked. If tube passage is not possible, it may help to place the dog in a sitting position and gently rotate the tube in a counterclockwise direction.

    • If orogastric intubation is still impossible, gastrocentesis using a large bore needle in the right or left paracostal space at the site of greatest tympany will usually facilitate orogastric intubation and avoid inadvertent splenic damage.

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Surgical Therapy
  • The immediate aim of surgery is to return the stomach to its normal position and evaluate it and the spleen for signs of irreversible vascular compromise. If present, necrotic portions of stomach and spleen should be removed. The stomach should be emptied completely. Finally, a gastropexy should be performed in an attempt to prevent recurrence of the volvulus.​

  • Following routine aseptic preparation, a cranial ventral midline laparotomy is performed.

  • In cases of a clockwise volvulus of 180°–270°, the stomach is typically immediately visible and covered by the greater omentum. Gastric decompression at this stage will facilitate the subsequent manipulation and relocation of the stomach.

  • If the stomach is still tightly distended, decompression can be achieved intraoperatively via needle gastrocentesis. For a less distended stomach, a non-sterile assistant can gently place an orogastric tube under the surgeon's guidance.

  • After decompression, the pylorus should be identified and gently grasped. If the stomach is twisted clockwise, downward pressure on the right side of the visible portion of the stomach, along with gentle traction on the pylorus, will help facilitate counterclockwise rotation.

  • The spleen should follow passively during this process. A thorough evaluation of the abdomen should then be conducted.

  • Hemoperitoneum is common, often resulting from the avulsion of the short gastric branches of the splenic arteries. Active sites of hemorrhage should be identified and ligated.

  • The stomach and spleen should be carefully inspected for any signs of damage. If the organs appear grossly normal, an assistant should lavage the stomach using clean, warm water via the orogastric tube.

  • The most common sites of gastric necrosis following GDV are the junction between the fundus and body, and the greater curvature.

  • Evaluating tissue blood flow remains somewhat subjective; however, gentle palpation of the gastric and splenic vessels for pulsation can be helpful.

  • If the serosal surface appears torn, grey, green, or black ten minutes after anatomical reduction of the stomach, ischemia is suspected, and tissue necrosis is likely. In these cases, resection of the affected portion of the stomach should be performed.

  • Determining how much of the stomach to remove can be challenging. A full-thickness gastric wall resection should be carried out until the cut edges are actively bleeding to ensure proper healing and prevent further necrosis.

  • Stomach closure following partial resection should be done in two or three layers. A simple continuous suture pattern in the submucosa is followed by a simple interrupted pattern in the muscularis and serosa. To reinforce the closure, the suture line can be oversewn with a continuous or interrupted inverting pattern, such as a Cushing or Lembert.

  • Occasionally, the cardia or the abdominal esophagus will become necrotic due to prolonged or severe twisting. This area should be carefully examined. Resection of the abdominal esophagus and gastric cardia is technically demanding, and the prognosis following such a resection, even in healthy animals, is uncertain. Since necrosis at this site is typically observed in already severely compromised animals, the prognosis for recovery is poor.

  • The spleen may sustain vascular damage or occlusion following GDV. Therefore, the spleen and associated vasculature should be carefully examined for thrombi and signs of irreversible vascular compromise. Any necrotic portions of the spleen should be resected. If the spleen has undergone torsion around its pedicle, splenectomy should be performed before reducing the twist to minimize the risk of releasing toxins, myocardial active substances, and thromboemboli into the systemic circulation.

  • A gastropexy should be performed to prevent recurrence. Many techniques are available, but tube gastropexy is commonly used as it is simple to perform, creates strong adhesions, and offers the additional benefit of providing enteral access.

  • Closure of the abdominal incision is routine.

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Postoperative Care
  • Fluid therapy should be maintained at a rate of 8–10 ml/kg/hr using a balanced electrolyte solution during the first 24 hours.

  • Systemic opioid analgesics should be administered to reduce postoperative discomfort and support recovery.

  • Throughout this period, it’s important to monitor the patient’s packed cell volume (PCV), total protein (TP), peripheral pulse quality, mucous membrane color, and urine output. If available, continuous ECG monitoring should be utilized, or intermittent ECG recordings should be made.

  • If a stomach tube is present, it should be vented as needed. No food or water should be given by mouth during this initial period.

  • If no complications arise, water can be offered starting on the second day after surgery, and the intravenous fluid rate should be reduced to 4 ml/kg/hr.

  • The patient’s comfort level should be regularly reassessed, and additional analgesia provided as needed.

  • Small amounts of food can be introduced by the end of the second day. Dogs that have undergone partial gastrectomy may take longer to resume normal gastric motility.

  • In such cases, medications like metoclopramide or low-dose erythromycin may help stimulate gastric motility.

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Postoperative Complications

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  • Recurrent GDV
    The stomach may twist again after surgery if a gastropexy wasn’t performed or fails. This is a serious risk requiring immediate intervention.

  • Shock and Hypovolemic Shock
    GDV causes significant blood loss and low blood pressure, and the shock may persist postoperatively, requiring fluids and monitoring.

  • Gastric Necrosis and Perforation
    Prolonged twisting can lead to tissue death in the stomach. This can cause infection (peritonitis) if the stomach wall is perforated.

  • Splenic Injury
    The spleen may become damaged during GDV, potentially requiring removal (splenectomy) if it’s necrotic or twisted.

  • Cardiac Arrhythmias
    GDV and surgery can lead to abnormal heart rhythms due to electrolyte imbalances, which require monitoring and treatment.

  • Infection (Peritonitis, Wound Infection)
    Bacterial infections can develop in the abdomen or surgical wound, necessitating antibiotics and possibly further surgery.

  • Respiratory Complications
    GDV and anesthesia can cause breathing issues like fluid accumulation or restricted lung function, requiring oxygen therapy.

  • Electrolyte Imbalances and Metabolic Derangements
    GDV disrupts electrolytes and metabolism, leading to issues like weakness or muscle tremors, often needing IV fluid therapy.

  • Delayed Gastric Emptying or Ileus
    The stomach or intestines may not function properly after surgery, causing bloating or vomiting until normal motility returns.

  • Pain and Discomfort
    Post-surgery pain is common, and pain management is crucial for comfort and healing.

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