gastric Dilatation­volvulus syndrome

bassets, bulldogs, miniature poodles, dachshunds, and Pekingese are affected. GDV is rare in cats. GDV occurs in animals ranging in age from 2 months to 15 years, with a mean of about 6 years.

No single cause of GDV has been identified; however, several risk factors are thought to be of importance for the development of this condition. Deep-chested breeds of dogs appear to have an increased potential for rotational instability of the stomach, in part because of laxity of hepatoduode­nal and hepatogastric ligaments. Large-volume intake of food and water causes chronic gastric distention that can potentially impair gastric emp­tying. Exercise with a distended stomach, particu­larly in deep-chested dogs, might subsequently cause the stomach to become displaced and result in volvulus. Dietary composition, particularly feeding dry-food diets, has also been suggested as a contributing factor to GDV; however, a direct relationship has not been established. The inci­dence of GDV was reported to decline when dry food was dampened before feeding, presumably preventing swelling of dry food with water in the stomach. Aerophagia from rapid eating, hyperven­tilation, and esophageal motility abnormalities have also been associated with recurrent GDV. Impaired eructation may result from an anatomi­cally or functionally abnormal gastroesophageal junction (GEJ) in deep-chested dogs. The oblique angle of the GEJ may become exaggerated, espe­cially if the stomach is distended following a large meal, preventing normal eructation.

Pathophysiology of Gastric Dilatation-Volvulus

GDV traps ingesta, fluid, and gas in the stomach, which rapidly causes extreme increase of intragas- tric pressure. A cascade of life-threatening effects develops that, if not corrected rapidly and aggres­sively, will cause death. The most immediate effect is impedance of gastric blood flow by increased intragastric pressure, gastric wall edema, vasocon­striction, and thrombosis.

Vascular collapse, disseminated intravascular coagu­lation (DIC), and sepsis occur. Treatment by gas­tric deflation and derotation and by the rapid administration of fluids, although very necessary, can have further detrimental effects on the patient. Reperfusion injury and release of endo­toxins and cardiodepressant factors, hemodilu­tion, and metabolic acidosis further contribute to metabolic dysfunction and cardiovascular com­promise.

The metabolic consequences of GDV are vari­able but can be severe, depending on the duration of the problem. Acid-base and electrolyte imbal­ances may initially be absent but usually develop during treatment. Frequent monitoring of these parameters is necessary until the patient is stabi­lized. Metabolic acidosis occurs commonly in the GDV patient from decreased circulating blood vol­ume, arterial hypoxemia, and lactic acidosis. Metabolic alkalosis, caused by fluid sequestration in the stomach and by loss of gastric H⁺, Cl^-, and K⁺, occurs less frequently. Hyperventilation can cause respiratory alkalosis, whereas hypoventilation from gastric distention can interfere with diaphragmatic function and cause respiratory acidosis. Electrolyte abnormalities occur less frequently than acid-base imbalances, with hypokalemia being the most common.

Presumptive diagnosis of GDV is made on the basis of clinical findings and is confirmed by radio­graphic findings and gastric decompression. Clinical features of GDV are listed in Table 5-9. The most characteristic clinical signs are an acute onset of retching, but without vomiting, rapidly developing abdominal distention and tympany, and depression.

Radiographs taken following initiation of fluid therapy and decompression are necessary to deter­mine if volvulus is present. Radiographic determi­nation of the location of the pylorus is the key feature to differentiate gastric dilation from gastric volvulus. This is best accomplished by comparing left and right lateral recumbent views (see Figure 5-2). Gastric volvulus usually results in displace­ment of the pylorus dorsally and to the left, creat­ing a shelflike partition of soft tissue that appears to compartmentalize the stomach. With the pylorus shifted to the left and the patient in left lateral recumbency, the pylorus fills with fluid and gas fills the rest of the stomach. However, when the patient

is in right recumbency, gas fills the pyloric portion and fluid shifts to the fundus or body of the stom­ach. The finding that the pylorus fills with fluid when in the left lateral recumbent position and fills with gas when in the right lateral recumbent position indicates that the pylorus has rotated to the left. The presence of abdominal fluid is suggestive of peritonitis or hemorrhage, and air in the abdominal space indicates that perforation has occurred. Megaesophagus is a common finding.

Treatment

Successful treatment begins with rapid fluid ther­apy and gastric decompression, followed by surgi­cal repositioning of the stomach and gastropexy. Concurrent therapy for electrolyte imbalances, arrhythmias, and DIC are necessary.

Initial Stabilization

Fluid therapy should be started immediately. A balanced crystalloid such as lactated Ringer's solution should be given intravenously (25 ml/lb) within the first 15 minutes to reestablish cardiac output; an additional 25 ml/lb is then given over the next 30 to 45 minutes. After this initial bolus, a colloid such as hetastarch should be given at a dose of 5 ml/lb as a slow intravenous bolus over

CBC, Complete blood count; PCV, packed cell volume; TP_r total plasma protein; CVP_r central venous pressure; BP_r blood pressure; IV, intravenously; prn, as needed; GDV, gastric dilatation-volvulus.

10 to 15 minutes. Depending on patient response, crystalloid fluid should be resumed at a rate of 10 to 20 ml/lb/hr for the next 2 hours and then decreased to 5 to 10 ml/lb/hr. Pulse quality, capil­lary refill, central venous pressure, and urinary out­put should be used as a guide for continued fluid needs. The packed cell volume and plasma total protein concentration should be monitored hourly to avoid hemodilution (total plasma protein con­centration should not decrease to less than

3.5 g/dl). Following gastric decompression, the fluid rate can usually be decreased to 5 ml/lb/hr, depending on patient stability. Hetastarch can be repeated within 6 to 12 hours if needed to main­tain perfusion. If the plasma protein concentration decreases to less than 3.5 g/dl, a plasma transfusion (10 ml/lb) should be given.

Gastric decompression must be accomplished immediately, occurring as soon as intravenous fluid therapy has begun. Decompression is achieved either by passage of a stomach tube or by gastric trocarization. Trocarization is easier and better tolerated by the patient than gastric intubation; rarely does it cause peritonitis. A 16-gauge 2-inch needle or 14- to 16-gauge over-the-needle catheter is used to trocarize the stomach on the left side at the site of maximal distention.

Surgical Correction

As soon as the clinical condition has been stabi­lized, surgery should be done to reposition and stabilize the stomach (Box 5-10). The optimal time for surgery to occur is variable, depending on patient condition and response to initial therapy. In general, surgery should not be delayed beyond the initial period of time required for stabilization. If gastric contents are noted to contain digested blood suggestive of gastric ulceration and/or necrosis, if there is radiographic evidence of perfo­ration or peritonitis, if decompression cannot be achieved, or if decompression is difficult to main­tain, surgery should not be delayed for more than 1 or 2 hours.

A gastropexy should be done to prevent recur­rence of volvulus. A recent study determined that 55% of dogs that did not have gastropexy following surgery had a recurrence, compared with 4% recur­rence for dogs that did have gastropexy. Median survival time was 188 days for dogs not having gas- tropexy, compared with 547 days for dogs that did have a gastropexy. Several types of gastropexy done through laparotomy have been described and include incisional gastropexy, circumcostal gas- tropexy, belt-loop gastropexy, and tube gastropexy. The benefit of doing a prophylactic gastropexy to prevent GDV in a dog that is conformationally or genetically predisposed has not been scientifically proven. It is logical, however, that gastropexy would be of benefit to prevent a first episode of GDV in such patients, as well as for patients in which an episode of GDV was managed medically. A rapid laparoscopic gastropexy technique that provides a strong fibrous adhesion between the stomach and abdominal wall has recently been described that could be used for this purpose, thereby eliminating the need for laparotomy.

BOX 5-10

Surgical Correction of Volvulus

1. Anesthetic induction: Repeat intravenous oxymorphone-diazepam combination used for sedation (see Box 5-9).

Lidocaine (1 mg/lb IV) to facilitate intuba­tion and decrease cardiac arrhythmia.

2. Anesthetic maintenance: Halothane, isoflurane, or sevoflurane and oxygen; nitrous oxide should not be used until permanent gastric decompression is achieved.

3. Monitor continuous ECG, BP, and urine output. Maintain mean arterial BP greater than 65 mm Hg and a urine output greater than 1 ml/lb/hr.

4. Reposition stomach, and evaluate stomach and spleen for vascular compromise; remove necrotic portions. A gastropexy should then be performed to prevent recurrence of the volvu­lus. Basic details are given below; refer to sur­gical text for description of surgical procedure.

Ventral midline laparotomy incision; an omentum-covered stomach is usually the first structure visible when a clock­wise volvulus has occurred.

Decompress stomach by gastrocentesis or by orogastric intubation.

Retract pylorus in the counterclockwise direction; downward pressure on the right side of the visible portion of stomach will facilitate repositioning of the stomach and spleen.

Examine stomach and spleen for signs of irreversible vascular compromise. Pal­pate gastric and splenic vessels for pulse.

If organs look grossly normal, lavage stomach with warm water via orogas- tric tube.

Ligate sites of active hemorrhage; hemo­peritoneum usually occurs from avul­sion of short gastric branches of splenic arteries.

If gastric serosal surface is dark purple to green-black after 10 minutes of normal gastric position, irreversible ischemic damage has likely occurred and resec­tion of that portion of stomach should be performed.

5. Gastropexy should then be performed to prevent recurrence of the volvulus. Refer to surgical texts for detailed description of vari­ous procedures.

IV, Intravenously; ECG, electrocardiogram; BP_r blood pressure.

Medical Management (Box 5-11)

Antibiotics should be given to dogs with GDV because shock, mucosal damage, and portal hyper­tension predispose to sepsis. Antibiotics should be effective against gram-positive, gram-negative, and anaerobic organisms. A combination of ampi­cillin (10 mg/lb intravenously) and enrofloxacin (2.5 mg/lb intramuscularly) is a good choice. Second-generation cephalosporins (e.g., cefox­itin 10 mg/lb every 8 hours intravenously) or trimethroprim-sulfa antibiotics are reasonable alter­natives. Corticosteroids may be beneficial for the initial management of shock to improve capillary blood flow, to decrease capillary permeability, to reduce intestinal absorption of endotoxin, and to inhibit tissue-damaging phospholipases. Short­term, high-dose therapy is recommended; pred­nisolone sodium succinate (20 mg/lb intravenously, given every 1 to 3 hours as needed) or dexametha­sone sodium phosphate (5 mg/lb intravenously, given every 3 to 6 hours as needed) is recom­mended to treat shock. H₂-receptor antagonists can be given to help diminish gastric ulceration. This therapy can be started during initial therapy and continued for 7 to 10 days. If gastric mucosal dam­age has been severe, omeprazole should be used as soon as oral medication can be tolerated because it is a more potent gastric antisecretory drug.

Management of Complications

Cardiac arrhythmias, DIC, and GI motility disor­ders are common complications occurring during the acute and convalescent phases of disease. Cardiac arrhythmias can occur at the time of pres­entation but may not develop until as long as 72 hours after onset of GDV. Continuous electro­cardiographic (ECG) monitoring is required from presentation until the dog is discharged from the hospital. Ventricular premature contractions (VPCs), paroxysmal ventricular contractions, and ventricular tachycardia are common. Correction of acid-base, electrolyte (especially potassium), and fluid balance is the first step in control of arrhyth­mias. Antiarrhythmic therapy is indicated if ven­tricular tachycardia with a heart rate of 150 beats

BOX 5-11

Postoperative Treatment of the GDV Patient

1. Monitoring

CBC, serum electrolyte levels, acid-base and coagulation tests every 12 to 24 hours until stable.

Pulse, respiration, and temperature, blood pressure, urine production, and contin­uous ECG monitoring are necessary to detect hypoperfusion, electrolyte and acid-base imbalances, infection, DIC, and aspiration pneumonia.

2. Maintain Perfusion

Fluid therapy with a balanced electrolyte solution at a rate of 3 to 5 ml/lb/hr for 24 hours.

If PCV and TP are low and the patient is hypotensive, blood products or colloids should be given to correct the deficits.

If perfusion is good and the patient is stable 24 hours postoperatively, IV flu­ids can be decreased to 2 ml/lb/hr for the next 24 hours.

If the patient is stable, small amounts of water and food can be offered 48 to 72 hours postoperatively.

3. Analgesia

Systemic opioids such as morphine at 0.2 mg/lb IM given every 4 to 6 hours for 12 to 24 hours postoperatively will relieve pain and improve recovery.

Butorphanol tartrate at 0.1 mg/lb IV or 0.2 mg/lb IM every 4 to 6 hours can be used as an alternative for mild pain and for longer-term analgesia.

NSAIDs should be avoided because of potential to cause GI ulceration.

4. Treat Cardiac Arrhythmias

Correct acid-base and electrolyte imbal­ances and fluid deficits.

If cardiac function is poor (hypotension, sustained ventricular tachycardia), attempt should be made to abolish the arrhythmia with lidocaine infusion at a rate of 10 to 20 μg∕lb∕min.

5. Postoperative Complications

Esophagitis, gastric hypomotility, aspiration pneumonia. Metoclopramide is effec­tive in restoring gastric motility, dimin­ishing gastroesophageal reflux, and controlling vomiting.

Ranitidine or omeprazole help reduce gastritis and enhance gastric mucosal healing.

Aspiration pneumonia is treated with broad-spectrum antibiotics and pul­monary therapy with nebulization, coupage, and supplemental oxygen.

DIC is treated with fresh frozen plasma (10 ml/lb) and heparin (100 units/lb every 8 hours) until platelet count and coagulation times begin to normalize.

Local cellulitis and peritonitis around the tube gastropexy site occur from leakage of gastric contents.

If this occurs within 2 to 3 days post- operatively, replace the tube under anesthesia.

If this occurs 5 to 7 days postopera- tively, the tube can usually be left in place.

Thrombosis or avulsion of splenic vessels, or splenic infarction is indication for partial or complete splenectomy. If splenic torsion has occurred, splenec­tomy should be done before reducing the twist to lessen the release of throm- boemboli and toxins to the circulation.

A three-layer closure of the stomach using polypropylene suture or surgical sta­pling should be done following partial gastric resection.

CBC, Complete blood count; ECG, electrocardiogram; DIC, disseminated intravascular coagulation; PCV, packed cell volume; TP_r total plasma protein; IV, intravenous; IM, intramuscularly; NSAID, nonsteroidal antiinflammatory drug; GI, gastrointestinal.

per minute or greater is present or if multifocal VPCs are occurring. Ventricular arrhythmias are initially managed using lidocaine (1 to 2 mg/lb as a slow intravenous bolus followed by infusion of 25 to 40 μg∕lb∕min). Lidocaine infusion can also be used as an excellent adjunct to other analgesics for the control of postoperative pain. Procainamide is used as a supplement to lidocaine if the arrhythmia is refractory to lidocaine, or as longer-term mainte­nance therapy (5 to 10 mg/lb intramuscularly or orally every 6 hours). DIC is a frequent complica­tion of GDV and is detected initially by presence of progressively worsening thrombocytopenia and prolonged coagulation times. If DIC is sus­pected, treatment with plasma (10 ml/lb) in com­bination with heparin (45 units/lb every 8 hours subcutaneously) should be initiated. Heparin is continued until platelets begin to increase and other coagulation parameters stabilize; plasma transfusions should be repeated if the platelet count continues to decline or if coagulation times become more prolonged. When platelet counts and coagulation times normalize, heparin should be decreased gradually by giving doses every 12 hours for 24 hours and then every 24 hours for the next day to avoid rebound hypercoagulation.

Gastric atony, delayed gastric emptying, and ileus frequently occur following GDV; in most instances these are transient. If intermittent vomiting persists, therapy with promotility drugs (metoclopramide or erythromycin) is helpful to reestablish gastric emp­tying. Treatment with antisecretory drugs and sucralfate may also be beneficial.

The prognosis for GDV is guarded, especially if gastric damage is severe and requires gastrectomy. Mortality is reported to be from 23% to 60%. Poor prognostic signs at presentation include a pulse rate greater than 180 beats per minute, arrhythmia, cyanotic mucous membranes, prolonged capillary refill time, and severe coagulopathy.