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Vol. 22, No. 11 November 2000 CE Refereed Peer Review FOCAL POINT ★Improved knowledge about
Vol. 22, No. 11 November 2000
Refereed Peer Review
★Improved knowledge about
the pathophysiology of acute
gastric dilatation–volvulus (GDV)
and recent advances in critical
care services have led to more
successful treatment of this
condition in dogs.
Management Protocol
for Acute Gastric
Syndrome in Dogs
University of Pennsylvania
Daniel J. Brockman, BVSc
David E. Holt, BVSc
■ Restoration of intravascular
volume deficits, gastric
decompression, and confirmation
of the diagnosis are the goals of
initial emergency GDV therapy.
■ Because a dilated stomach can
remain within the rib cage in
giant-breed dogs, abdominal
distention may not be seen.
■ Sedative and anesthetic protocols
that have minimal deleterious
effects on cardiovascular and
respiratory system functions
should be used in patients with
ABSTRACT: Canine acute gastric dilatation–volvulus (GDV) is a potentially catastrophic condi-
tion in which emergency medical and surgical therapy and intensive postoperative care are
needed to optimize the chance of a successful outcome. The events that precede an episode of
GDV vary. Clinical features of the disease include restlessness; retching; and abdominal dis-
tention, discomfort, and tympany. Initial patient evaluation and treatment should be aimed at
determining the degree of cardiovascular compromise and restoration of intravascular deficits
by intravenous fluid administration. Dogs with GDV should receive prompt surgical attention
to permit gastric decompression, removal of any devitalized tissue (e.g., stomach, spleen),
and gastropexy. Intensive postoperative care is essential for dogs recovering from surgery for
GDV. The majority of animals will recover without complications. Some animals, however, will
develop potentially life-threatening complications. Although GDV is a challenge to treat, a good
survival rate can be achieved.
G astric dilation and gastric volvulus can occur independently, 1,2 but to-
gether they represent a potentially catastrophic disease that is referred to
as the gastric dilatation–volvulus syndrome (GDV). GDV is most likely
a polygenic disease with strong phenotypic and environmental influences. 3,4
■ Persistent hypotension,
hypovolemia, and hypoxia
secondary to the systemic
inflammatory response
syndrome are the most severe
complications of GDV and often
result in death.
Most episodes of GDV result from a single overwhelming factor or several com-
bined risk factors. 5 Simultaneous gastric dilation and volvulus result in patho-
physiologic changes that create a medical and surgical emergency. 6,7 Dogs with
GDV develop local and systemic consequences that result in hypovolemia, plac-
ing them at risk for gastric and splenic vascular compromise, focal and general-
ized bacterial infections, initiation and propagation of local and systemic inflam-
mation, disseminated intravascular coagulation, shock, and death. 6–9
The overall incidence of GDV in dogs is low. 5,8 This condition remains an im-
portant syndrome, however, because successful management requires intensive
emergency, surgical, and postoperative care. Despite what some consider optimal
medical management, the mortality rate for this syndrome can be as high as

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Compendium November 2000

15% to 20%. 8,9 Consequently, many treatment regi- mens have been recommended and management of GDV remains controversial. This article discusses a practical and clinically proven protocol 8 for the man- agement of this condition. A companion article will ex- plore the pathogenesis of GDV, including an examina- tion of recent scientific and clinical literature.

tial circulatory resuscitation. 11 Both the high-volume crystalloid and low-volume hypertonic saline–dextran fluid resuscitation protocols should be followed by high-volume crystalloid administration (20 ml/kg/ hour) for maintenance of resuscitation. The decision to introduce blood products or a synthetic colloid to pro- vide further circulatory support and help improve oxy- gen delivery to the tissue should be influenced by sub- sequent PCV, TP, and circulatory stability estimations. If available, a continuous electrocardiogram (ECG) should be started or a baseline recording made. Gastric decompression should only be attempted af- ter correction of the intravascular volume deficit is well under way. Close patient monitoring is essential. Fur- ther delay of decompression could influence gastric wall integrity and the amount of inflammatory media- tors that are released from the splanchnic circulation. Gastric decompression can usually be achieved by orogastric intubation of the conscious or sedated ani- mal. For sedation, a combination of fentanyl (2 to 4 µg/kg intravenously [IV]) or oxymorphone (0.1 mg/kg IV) followed by diazepam (0.25 to 0.5 mg/kg IV) can be used. A selection of smooth-surfaced equine naso- gastric tubes with large end and side holes can be used. The tube selected should be measured from the exter- nal nares to the caudal edge of the last rib and marked. The tube should not be inserted beyond this mark. A bandage roll placed between the dog’s teeth can aid pas- sage of the lubricated tube. If tube passage is not possi- ble, the dog should be placed in a sitting position and the tube gently rotated in a counterclockwise direction. If orogastric intubation is still impossible, gastrocente- sis—using a large-bore needle in the right or left para- costal space at the site of greatest tympany—will usual- ly facilitate orogastric intubation and avoid inadvertent splenic damage. Routine aseptic technique should be used. The patient should be assessed frequently by collec- tion and analysis of subjective and objective clinical data (i.e., peripheral pulse pressure and quality, heart rate, mucous membrane color, CRT, PCV and TP concen- tration, degree of abdominal distention, ECG). To opti- mize tissue perfusion and oxygen delivery, IV fluid type and composition should be tailored to the patient’s needs.


Gastric dilatation–volvulus syndrome occurs most commonly in large or giant, deep-chested breeds 3,4 of dogs but has also been reported in small breeds. 10 The onset of clinical signs is typically peracute or acute. Ini- tial signs include restlessness, hypersalivation, and retching. These signs are usually followed by further discomfort and gradual abdominal distention. Eventu- ally, pain becomes evident, along with weakness and abdominal tympany. Physical examination findings reflect gastric dilation and circulatory and respiratory compromise. Therefore,


distended abdomen, tachycardia, poor peripheral

pulse quality, prolonged capillary refill time (CRT), pale and dry mucous membranes, tachypnea, and dys- pnea may occur depending on the duration and severi- ty of the episode. Because a dilated stomach can remain within the rib cage in giant-breed dogs, classical ab- dominal distention may not be seen in these breeds.



The therapeutic goals in cases of suspected acute

GDV are to restore and support the circulation, de- compress the stomach, establish whether GDV or sim- ple dilation is present, perform rapid surgical correction


volvulus has occurred, and determine environmental

influences that may have triggered the condition.

Emergency Care

Management of hypovolemia—to prevent or treat shock—is the primary goal of emergency treatment of GDV. Two large-bore catheters (ideally 16 or 18 gauge) should be placed in the cephalic or jugular veins. If a facility for rapid results is available, a blood sample should be taken for packed cell volume (PCV), serum total protein (TP) estimation, and serum electrolyte

levels. Sufficient blood should also be drawn for subse- quent performance of full serum chemistry, hematolog-



evaluation, and evaluation of coagulation parameters. Fluid therapy should be started at a rate of 90 ml/kg/

Radiography is not necessary to diagnose gastric dila- tion but is an invaluable aid in diagnosing volvulus. 12,13 When considering the need for radiography, it is impor- tant to remember that the easy passage of an orogastric tube does not rule out volvulus. A lateral view of the cra- nial abdomen taken with the animal in right lateral re-

hour using a balanced electrolyte solution. In giant- breed dogs, a hypertonic saline–dextran combination (7% sodium chloride in 6% dextran-70) administered at 5 ml/kg over 5 minutes may provide more rapid ini-





Compendium November 2000

Small Animal/Exotics

cumbency is the initial exami- nation of choice. 12,13 If the diagnosis remains uncertain, additional radiographs (e.g., ventrodorsal, left lateral) should be obtained. The radiographic features of GDV include a large, dilated, gas-filled gastric shadow, which may be divided into two compartments by the soft tissue of the lesser curva- ture and the proximal duode- num, which courses caudally from the abnormally posi- tioned pylorus in the cran- iodorsal quadrant of the ab- domen (Figure 1). If stomach rotation is not severe, the ab- normal position of the pylorus (dorsal and to the left of the fundus) is diagnostically help- ful, although the pylorus may not be visible on left lateral ra-

although the pylorus may not be visible on left lateral ra- monitoring should be done during

monitoring should be done during anesthesia. Intraopera- tive fluids should remain at a high rate (10 to 20 ml/kg/hour) to offset further deterioration in hemodynamics during surgery. A catheter should be placed in the urinary bladder and connected to a closed urine collection system. PCV and TP should be evaluated intraoperatively at 30- to 60- minute intervals. Again, IV fluid type and composition should be tailored to the pa- tient’s needs in an attempt to ensure adequate tissue perfu- sion and oxygen delivery by maintaining a mean arterial blood pressure above 65 mm Hg and a hematocrit at or above 25% to 30%.

Figure 1—Right lateral radiograph of a dog with gastric dil- atation–volvulus. The gastric shadow is dilated with gas and divided into dorsal (malpositioned pylorus) and ven- tral (fundus and corpus) compartments by soft tissue of the folded lesser curvature of the stomach wall. There is generalized intestinal dilation, suggesting ileus. The metal- dense objects seen on this radiograph are the surgical sta- ples that remain in the peritoneal cavity following splenec- tomy, performed 6 months before this episode.

diographs. Splenic enlarge- ment and malposition may be evident. Gas within the gastric wall may indicate gastric wall compromise; if gastric rupture has occurred, free gas will be present in the abdominal cavity.



Surgical Therapy

The immediate aim of sur- gery is to return the stomach to its normal position and evaluate it and the spleen for signs of irreversible vascu- lar compromise. Any necrotic portions of stomach and spleen should be removed and the stomach emptied com- pletely. Finally, a gastropexy should be performed in an attempt to prevent recurrence of the volvulus. Following routine aseptic preparation, a cranioventral midline laparotomy should be performed. The stomach is usually immediately visible and covered by greater omentum when a clockwise volvulus of 180˚ to 270˚ has occurred. At this stage, gastric decompression will help subsequent manipulation and relocation of the stomach. This can be achieved intraoperatively by nee- dle gastrocentesis if the stomach is still tightly distend- ed. Alternatively, for a less distended stomach, an assis- tant (with the intraoperative guidance of the surgeon) can gently place an orogastric tube. After decompres- sion, the pylorus should be identified and grasped gen- tly with the hand. If the gastric rotation is in a clock- wise direction, downward pressure on the right side of the visible portion of the stomach along with gentle traction on the pylorus will aid counterclockwise rota- tion. The spleen should follow passively. Systematic evaluation of the abdomen should then be performed. Hemoperitoneum often results from avulsion of the short gastric branches of the splenic arteries. Active sites of hemorrhage should be identified and ligated. Careful inspection of the stomach and spleen should be per-

In practice situations, the choice of anesthetic agents may be limited. If the previously mentioned sedative combination has been used preoperatively, endotracheal intubation may be achieved after another IV infusion of the same cocktail. The inclusion of IV lidocaine (2 mg/kg) into the induction protocol will help desensitize the larynx and facilitate endotracheal intubation as well as enhance the overall state of anesthesia. In addition, if a different induction agent is to be used, the quantity required will be reduced because of residual effects of the sedative. Circulatory compromise will influence the speed and efficiency of drug distribution. Because IV access should already be established, small amounts of induction agent should be given to effect. Maintenance should be with halothane or isoflurane and oxygen. Ni- trous oxide should not be introduced until permanent gastric decompression is achieved. The placement of additional IV and intraarterial catheters in the pelvic limbs following the induction of anesthesia will facilitate intraoperative blood pressure monitoring and the addition of blood products (e.g., to the intraoperative fluid therapy regimen). Continuous ECG and continuous or intermittent blood pressure





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Compendium November 2000

formed. If all organs look grossly normal, an assistant should lavage the stomach us- ing clean, warm water via the orogastric tube. The junction between the fundus and body along the greater curvature of the stom- ach is the most common site of gastric necrosis following GDV. 14 Evaluation of tissue blood flow remains subjec- tive; however, gentle palpa- tion for pulsation in the gas- tric and splenic vessels can be helpful. If the serosal surface is either torn, gray–green, or black 10 minutes after ana- tomic reduction of the stom- ach, ischemia should be sus- pected and subsequent tissue necrosis anticipated (Figure 2). In these situations, resec- tion of the affected portion of the stomach should be per- formed. It may be difficult to determine how much of the stomach to remove. A full- thickness gastric wall resec- tion is carried out until the cut edges are actively bleeding to ensure healing without fur- ther necrosis. Closure of the stomach fol- lowing partial resection should be in two or three layers. A simple continuous suture pat- tern in the submucosa should

A simple continuous suture pat- tern in the submucosa should The cardia or the abdominal esophagus

The cardia or the abdominal esophagus will occasionally become necrotic secondary to longstanding or severe twist- ing; therefore, this area should be examined carefully. Resec- tion of the abdominal esopha- gus and gastric cardia can be technically demanding, and the outcome following such a resection, even in healthy ani- mals, is unknown. Because necrosis at this site is usually seen in animals that are already severely compromised, the prognosis for recovery is poor. The spleen can sustain vas- cular damage or occlusion following GDV. The spleen and associated vasculature should, therefore, be carefully evaluated for the presence of thrombi and irreversible vas- cular compromise. Any devi- talized portion of splenic tis- sue should be resected either by hand or using a surgical stapling device (Figure 3). If the spleen has undergone tor- sion around its pedicle, sple- nectomy should be performed before reducing the twist to lessen the risk of releasing tox- ins, myocardial active sub- stances, and thromboemboli into the systemic circulation. A gastropexy should be per- formed. 1620 Tube gastropexy is

Figure 2—Partial gastric resection using stapling equip- ment. The stomach has undergone spontaneous perfor- ation. The demarcation between viable and nonviable tissue (blackened area being removed) is clear. Despite successful partial gastric resection, this patient subse- quently died of systemic inflammatory disease.

subse- quently died of systemic inflammatory disease. Figure 3— Partial splenic infarction in a patient with

Figure 3—Partial splenic infarction in a patient with gastric dilatation–volvulus. The demarcation between viable and nonviable splenic tissue is indicated by a color change. The vascular pedicle at the ventral extremity of the spleen is torn and partially avulsed from the hilus. Partial splenecto- my was performed, and the dog recovered.

be followed by a simple inter- rupted pattern in the muscularis and serosa. Oversewing the suture line with a continuous or interrupted invert- ing pattern (e.g., Cushing, Lembert) can reinforce this closure. Polydioxanone, polyglactin 910, polyglycolic acid and polyglyconate are all suitable suture materials. Alternatively, surgical stapling devices can be used to per- form partial gastric resection. The use of a GI anastomo- sis instrument (GIA-50, US Surgical, Norwalk, CT) has been described for this purpose 15 ; however, we prefer to use a thoracoabdominal stapler (TA-90, US Surgical) with a 4.8-mm (green) staple cartridge. Again, this clo- sure should be reinforced using a continuous or inter- rupted Cushing or Lembert inverting pattern to oversew the staple line.

easy to perform, creates strong adhesions, and has the additional advantage of provid- ing enteral access. 20 A large (24 or 26 gauge) Foley or Pezzer’s urologic catheter is placed through a stab inci- sion in the body wall approximately 2 cm lateral to the ventral midline and 2 cm caudal to the last rib on the right side. The catheter is then passed through a loop of omentum and into the stomach via a purse-string suture through a small incision in the pyloric antrum. The bal- loon on the Foley catheter is then inflated but kept away from the stomach wall to avoid inadvertent puncture while pexy sutures of polypropylene are preplaced around the abdominal and gastric wall incisions in an overlapping mattress pattern. The sutures are then tied and the balloon or mushroom tip drawn up to the




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Compendium November 2000

  be kept clean and protected by a bandage. After removal of the tube, the gastrostomy

be kept clean and protected by a bandage. After removal of the tube, the gastrostomy is left to heal by second intention. Clients should be in- formed of the signs of recurrence and encour- aged to seek veterinary attention as soon as pos- sible if these signs occur.

Figure 4—Electrocardiogram (top) and direct arterial pressure trace (bottom) from a 5-year-old spayed Great Dane recovering from gastric dilatation– volvulus, 1 day after surgery. During the early (rapid) phase of this multi- form ventricular tachycardia, there is disparity between the ventricular de- polarization and ejection rates. The pulses formed, however, are strong and adequate. This arrhythmia does not require treatment if all other aspects of patient care are appropriately managed.


Persistent hypotension may be suspected if peripheral pulse quality is poor, tachycardia and poor CRT are evident, and urine output is low. This hypotension is usually caused by hypo- volemia secondary to inadequate fluid therapy

stomach wall and the tube is secured with either a Chi- nese finger trap suture or tape tabs sutured to the skin. Alternatively, an incisional gastropexy is simple and effective. 21 With this technique, a 5-cm seromuscular incision is made in the pyloric antrum, and a matching incision is made in the parietal peritoneum and trans- verse abdominal muscle, just caudal to the 13th rib on the right body wall. The edges of the gastric wall inci- sion are sutured to the edges of the body wall incision using either polydioxanone or polypropylene. Care must be taken not to penetrate the gastric lumen. Closure of the abdominal incision is routine. A ban- dage is placed around the abdomen to protect a gas- tropexy tube.

Postoperative Care

Fluid therapy should be maintained at a rate of 8 to 10 ml/kg/hour using a balanced electrolyte solution for the first 24 hours. Systemic administration of opioid analgesics (e.g., intramuscular morphine at 0.5 mg/kg every 4 to 6 hours) will reduce postoperative discom- fort and facilitate recovery. During this period, it is use- ful to monitor PCV and TP intermittently; peripheral pulse quality, mucous membrane color, and urine out- put should also be monitored. Again, continuous ECG should be used if available or intermittent records made. The stomach tube, if present, should be vented as needed. Nothing should be given by mouth. If complications do not occur, water can be offered the second day after surgery and the IV fluid rate re- duced to 4 ml/kg/hour. Patient comfort level should be assessed and additional analgesia provided as needed. Small amounts of food can be offered by the end of the second postoperative day. Animals that have undergone partial gastrectomy may take longer to regain normal gastric motility. IV metoclopramide (1 to 2 mg/kg/day) or low-dose oral erythromycin (0.5 to 1.0 mg/kg every 8 hours oral) might be beneficial. 22,23 The gastropexy tube should remain in place for 7 to 10 days. It should

following surgery. Hypotension may also devel- op if the IV crystalloid fluid therapy is failing because of inadequate primary surgical hemostasis, subsequent whole blood deficits, reduced colloid osmotic pressure, or abnormal body fluid distribution. Occasionally, hy- potension in post-GDV surgery patients is caused by poor cardiac function. If PCV and TP levels reveal hemoconcentration, a return to high-volume, rapid crystalloid infusion may be necessary for a short time (i.e., 1 hour at 90 ml/kg) followed by a return to 10 to 15 ml/kg/hour. If PCV or TP is low, blood products or synthetic colloid should be administered to correct the deficit(s). The patient should be reevaluated frequently following any change in fluid therapy. Cardiac arrhythmias are common following an acute episode of GDV. 8,9,24 They are usually ventricular in ori- gin and range from intermittent ventricular premature conductions to sustained ventricular tachycardia. Supra- ventricular abnormalities (e.g., atrial fibrillation) are oc- casionally seen. 9,25 Cardiac arrhythmias may need to be treated if they are associated with primary heart disease (e.g., dilated cardiomyopathy) or if there is evidence of poor cardiac performance. If continuous ECG and si- multaneous blood pressure monitoring are available, a decision about cardiac function with regard to arrhyth- mia is relatively easy (Figure 4). An attempt to abolish a cardiac arrhythmia that is associated with hypotension using antiarrhythmic drugs is considered only if acid– base and electrolyte imbalances have been corrected and intravascular volume replenishment is adequate. The most common complications of tube gastropexy are local cellulitis caused by leakage of gastric contents around the tube or premature tube dislodgment. 18 Occa- sionally, the balloon of a Foley catheter can be eroded by the acidic gastric fluid, causing early loosening of the tube. Usually this occurs after 5 to 7 days, as the animal becomes more active, and will spontaneously resolve. If it occurs in the first 48 hours, the risk of peritonitis sec- ondary to leakage of gastric contents mandates tube re- placement with the patient under general anesthesia.




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Preoperative retching and vomiting, and postopera- tive esophagitis and regurgitation put these animals at risk for aspiration pneumonia. 8 Alterations in breathing rate and pattern coupled with crackles and wheezes on thoracic auscultation are suggestive of pneumonia. Thoracic radiography, arterial blood gas evaluation, and tracheal/bronchoalveolar wash fluid cytology and cul- ture will help confirm this diagnosis. Treatment with the appropriate antibiotic(s), local fluid therapy (nebu- lization), thoracic coupage, supplemental oxygen, and frequent short periods of exercise should aid recovery. Gastric necrosis and perforation can occur up to 5 days after surgery, especially if resection was performed and despite careful intraoperative assessment of gastric wall viability. 14,15 Although this complication may be difficult to confirm without surgical exploration of the abdomen, it may be suspected on the basis of clinical progression of disease, radiographic and ultrasono- graphic findings, and cytologic evaluation of peritoneal fluid. Treatment is by debridement and repair of the gastric wall defect followed by continued intensive sup- portive care. If gastric necrosis and perforation occur, the prognosis is grave. Persistent ongoing hypotension, despite appropriate fluid therapy, is a serious concern. Serum electrolyte concentrations (i.e., sodium, potassium, chloride, mag- nesium, calcium) should be measured, coagulation pa- rameters assessed, acid–base status evaluated, and blood gas levels determined before further altering therapy. Electrolyte abnormalities should be corrected. An ab- normal hemostatic profile or a clinical bleeding tenden- cy should be interpreted as evidence of disseminated in- travascular coagulation. Replacement of consumed coagulation factors using fresh-frozen plasma should be considered in addition to continued therapy for the un- derlying cause of shock. Hypoxemia may occur secondary to pneumonia or pulmonary edema. Pulmonary edema may develop sec- ondary to overzealous IV fluid administration, primary cardiac dysfunction, or reduced colloid osmotic pres- sure or following acute lung injury as a component of the systemic inflammatory response syndrome. In turn, the systemic inflammatory response syndrome can be triggered by several factors, including endotoxemia, organ reperfusion injury, and local inflammatory con- ditions (e.g., peritonitis, pneumonia, pancreatitis). Thoracic and abdominal radiography, cardiac and ab- dominal ultrasonography, abdominocentesis, tracheal/ bronchoalveolar wash sample cytology and culture, and further hematologic and serum chemistry evaluation should be considered to assist future therapeutic deci- sion making. Persistent hypovolemia despite aggressive fluid therapy and the development of pulmonary com-



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plications in which systemic inflammation is suspected are poor prognostic signs. Therapy for such patients may include oxygen supplementation and ventilator-as- sisted breathing as well as continued intensive circula- tory support. The prognosis for animals with these complications is poor.



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About the Authors

When this article was submitted for publication, Drs. Brockman and Holt were affiliated with the Department of Clinical Sciences and the Center for Veterinary Critical Care, School of Veterinary Medicine, University of Penn- sylvania, Philadelphia. Dr. Brockman is now affiliated with the Department of Small Animal Medicine and Surgery, The Royal Veterinary College, University of London. Both are Diplomates of the American College of Veterinary Surgeons. Dr. Brockman is also a Diplomate of the Euro- pean College of Veterinary Surgeons.



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