For dogs suspected to have GDV (gastric dilation – volvulus syndrome), circulatory support is paramount.
For dogs suspected to have GDV, circulatory support is paramount. This is commonly initiated before attempts at gastric decompression. Crystalloid fluid therapy (90ml/kg) is instituted with baseline parameters checked after every quarter-dose. These parameters include heart rate, pulse quality, capillary refill time, packed cell volume, and total protein.
Gastric decompression can be achieved through orogastric intubation or gastric trocharization. For orogastric intubation, a large bore gastric tube is selected and a length is measured from the dog's nose to the last rib. A roll of 2" tape is placed in the dog's mouth and the tube is gently passed through the tape roll and into the dog's esophagus. Passage can be facilitated by using a small amount of lubricant on the end of the tube. Changing the position of the dog (from sternal to sitting to standing to standing with feet elevated) can often help get the tube through the cardia into the stomach. Once in the stomach, the other end of the tube should be submerged in a bucket of water to roughly estimate successful gas decompression. The stomach is then lavaged with warm water until the fluid returns back clear. Retrieval of large amounts of blood or necrotic tissue may suggest gastric necrosis.
If an orogastric tube is unable to be passed, gastric trocharization may be performed. This should be performed with extreme care to avoid inadvertent laceration of the spleen. Trocharization is classically performed with a 14- or 16-gauge needle on the right side, but in the individual patient, it should be performed at the point of greatest tympany.
Dogs identified to have GDV require immediate surgical interventions. Preoperative diagnostics may include minimum database, clotting profile, serum lactate, electrocardiogram, and abdominal radiographs. Once in surgery, an exploratory should be performed first as a general assessment of the abdomen and to make sure other possible problems are not missed. This is often not possible in dogs with GDV as the stomach bloated and malpositioned. An exploratory is performed following derotation as this gives the stomach and spleen some time before assessing tissue viability. Subjective parameters are most reliable in assessing organ viability. These include color, thickness, peristalsis, arterial pulses, and capillary (or cut surface) bleeding. Large splenic vessels can be palpated for the presence of a pulse or thrombosis. A necrotic stomach will rapidly lose the characteristic mucosal slip. If indicated a splenectomy or partial gastrectomy should be performed. The decision to perform either of these procedures should not be taken lightly, as both have been showed to be associated with increased mortality.
Gastropexy is performed before closure to prevent recurrence. Recurrence rates following gastropexy range from 5 to 10% compared to an 80% recurrence rate without a gastropexy. Belt-loop, incisional, or circumcostal gastropexy should be performed and the choice is often based on surgeon preference. The author prefers to use an incisional or belt-loop gastropexy. An incisional gastropexy should not be confused with a midline, incorporating gastropexy, which the author does not recommend. For an incisional gastropexy, a 3 cm longitudinal incision is made through the seromuscular layer of the pyloric antrum. A matching incision is made in the transversus abdominus muscle on the right side of the abdomen caudal to the last rib. These incisions are then sutured together using 2-0 monofilament absorbable or nonabsorbable suture.
There are multiple causes of death for dogs with gastric dilatation-volvulus syndrome (GDV) including shock, disseminated intravascular coagulation, sepsis, and cardiac dysfunction. Overall mortality for dogs with GDV is approximately 12 to 18%. The animal's state at presentation has also been shown to be a highly predictive risk factor with dogs that present comatose 35 times more likely to die than dogs that walk in. The mortality rate in one study (Brourman et al, 1996) also increased with the presence of preoperative arrhythmias, the presence of gastric necrosis, or the need to perform a partial gastrectomy or splenectomy. However, a more recent study (Beck et al, 2006) showed no increase in mortality when partial gastrectomy was performed.
Beck JJ, Staatz AJ, Pelsue DH, et al. Risk factors associated with short-term outcome and development of perioperative complications in dogs undergoing surgery because of gastric dilatation-volvulus syndrome: 166 cases (1992-2003). J Am Vet Med Assoc 2006; 229:1934-1939.
Brourman JD, Schertel ER, Allen DA, et al. Factors associated with perioperative mortality in dogs with surgically managed gastric dilatation-volvulus: 137 cases. J Am Vet Med Assoc 1996;208:1855-1858
Glickman LT, Lantz GC, Schellenberg BD, et al. A prospective study of survival and recurrence following the acute gastric-dilatation volvulus syndrome in 136 dogs. J Am Vet Med Assoc 1998;34:253-259
Removal of the spleen is most often performed due to splenic masses, however torsion, infarction, thrombosis, and necrosis are also indications for splenectomy. Splenic tumors occur far more frequently in the dogs than in the cat. Hemangiosarcoma, hemangioma, and hematoma are the most common lesions requiring splenectomy. Other less common splenic tumors include fibrosarcoma, leiomyosarcoma, mast cell tumor, and lymphoma. Dogs with large splenic tumors or with splenic torsion may present with vague clinical signs (anorexia, lethargy, intermittent vomiting) associated with discomfort from the mass effect in the abdomen. However, dogs may present in an emergency state with hemoabdomen if the spleen ruptures.
Splenectomy requires a generous ventral midline abdominal incision. The spleen can be removed with traditional methods using suture to ligate small bundles of the splenic vessels. The main splenic artery and vein should be ligated separately and often a circumferential and transfixing sutures are used to ligate the artery.
As an alternative, a ligating-dividing stapler (LDS®) or vessel-sealing system (Ligasure®) can be used to expedite spleen removal, but the large vessels should still be ligated individually. The LDS simultaneously places two U-shaped vascular clips across a small vascular pedicle and transects in-between the two clips. The main disadvantage of the LDS is that it is more expensive to use than suture ligation. However, this may be offset by the reduction in surgical and anesthetic time. The Ligasure uses an optimized combination of pressure and energy to permanently fuse vessels up to 7mm in diameter with minimal injury to surrounding tissues.
Diaphragmatic hernias can be congenital or traumatic in origin, and acute or chronic in duration. Dogs and cats with acute traumatic diaphragmatic hernias have typically sustained significant blunt vehicular trauma. The degree of respiratory compromise depends on the amount of abdominal viscera displacement and the presence and severity of other thoracic injuries.
Thoracic injury in a dogs and cats is a common cause of death following trauma. Of cats involved in motor vehicle accidents in the United States, 39% sustain thoracic injuries. Of animals with radiographic evidence of thoracic trauma, 43 to 62% have more than one type of thoracic injury. A large percentage of injured animals do not outwardly demonstrate the clinical signs connected with thoracic injury. A potentially devastating mistake is to presume there is no thoracic injury following trauma based on the lack of clinical signs and presence of injury only in caudal half of the body. The thoracic wall is an inherently resistant structure and it is often spared from significant injury even if there are significant injuries to the internal thoracic structures. Also, there is no correlation between the pattern of appendicular injury and the existence of thoracic trauma. Common thoracic injuries include pleural space lesions (pneumothorax, hemothorax), chest wall injuries (rib fractures, flail chest), mediastinal injuries, cardiac injury, pulmonary injury, and diaphragmatic herniation. Respiratory compromise may result from direct pulmonary injury, pulmonary compression, loss of intrathoracic negative pressure, and pain. Early recognition of thoracic trauma through clinical signs, radiography, and blood gas analysis will help these animals receive appropriate therapy.
Thoracic radiography may demonstrate obvious organ herniation in the thoracic cavity. Radiographic signs include loss of diaphragmatic outline and cardiac silhouette, displacement of lung fields, presence of gas filled viscera, and pleural effusion. Effusion is usually associated with liver entrapment and venous occlusion. Abdominal radiographs may demonstrate cranial displacement of abdominal organs. Identification of stomach or intestines within the thoracic cavity makes the diagnosis of diaphragmatic hernia uncomplicated. However, if there is a large amount of pleural fluid or if the soft-tissue parenchymal organs are herniated the diagnosis of diaphragmatic hernia may be less obvious. Repeating radiographs following thoracocentesis may identify an underlying cause that was not apparent before. Performing all radiographic views (right lateral, left lateral, ventrodorsal, and dorsoventral) may shift herniated viscera and allow better visualization.
Mortality associated with diaphragmatic hernia is reportedly higher when surgery is performed less than 24 hours or more than 1 year after injury. This theory has been challenged in more recent literature. Anesthesia and surgery should be delayed until the animal can be adequately stabilized. Stabilization includes shock therapy, oxygen supplementation, and antibiotic administration. However, emergency surgery is indicated is there is gastric herniation or if the animal respiratory status deteriorates. Gastric herniation is a surgical emergency because these animals are at risk for acute gastric distension, severe respiratory compromise, and death.
The goals of surgery are to reduce the herniated organs back into the abdominal cavity, examine the organs for any vascular compromise or perforation, and repair the diaphragmatic defect. Occasionally the diaphragmatic tear needs to be enlarged or the incision extended cranially through the sternum to allow reduction of abdominal contents and improve visualization. Tears are sutured from dorsal to ventral using an absorbable or nonabsorbable monofilament suture in a simple continuous pattern. Use care when suturing near the caval, esophageal, or aortic foramina. If the diaphragm has been avulsed from its thoracic wall insertions, incorporate the ribs into the closure. Defects too large to close are rarely encountered; however, if faced with this situation autogenous flaps or synthetic implants may be used. Autogenous flaps include a sliding transverse abdominus muscle flap or an omental pedicle flap. Examples of synthetic materials include polypropylene mesh and silastic sheeting. Following repair of the diaphragm, air is removed from the thoracic cavity by needle thoracocentesis or placement of a thoracostomy tube.
The most serious complication associated with surgical repair of diaphragmatic hernias is re-expansion pulmonary edema, which follows rapid reinflation of atelectatic lungs. Pulmonary edema occurs as capillary integrity has been altered due to an anoxic environment in the atelectatic lung. Reperfusion of damaged vessels directs fluid in to the interstitium. Although this is an uncommon complication, it most often occurs in cats with chronic herniation. Ways to prevent this complication is to avoid aggressive positive pressure lung expansion during anesthesia once the hernia has been reduced and to avoid aggressive removal of air through the thoracostomy tube in the postoperative period. The animal should be allowed to gradually reinflate their lungs on their own. Other less common complications include pneumothorax, hemothorax, liver lobe necrosis, gastrointestinal vascular compromise, and reherniation.
If the animal survives for the first 12 to 24 hours after surgery, the prognosis is very good. Reported survival rates range from 80 to 90% following surgical correction. Deaths are usually due to concurrent injury or pulmonary edema.
Boudrieau RJ, Muir WM. Pathophysiology of Traumatic Diaphragmatic hernia in dogs. Compend Contin Educ Pract Vet 1987;9:379-386
Gibson TWG, Brisson BA, Sears W. Perioperative survival rates after surgery for diaphragmatic hernia in dogs and cats: 92 cases (1990-2002). J Am Vet Med Assoc 2005;227:105-109
Schmiedt CW, Tobias KM, McCrackin Stevenson MA. Traumatic diaphragmatic hernia in cats: 34 cases (1991-2001). J Am Vet Med Assoc 2003;222:1237-1240
Septic peritonitis is a life-threatening condition in dogs and cats that causes serious metabolic alterations and organ dysfunction. Bacterial contamination of the peritoneal cavity results from a primary disease process or from a traumatic insult to the abdomen. The source of infection is most commonly perforation or rupture of the gastrointestinal tract secondary to ulceration, gastric dilatation-volvulus (GDV), erosive neoplasia, mechanical obstruction, or dehiscence of a previous intestinal surgical site. Other causes of contamination include rupture of infected hepatic, pancreatic, prostatic, or uterine tissues. Animals with chemical peritonitis caused by urine, bile, or pancreatic enzyme leakage may develop septic peritonitis from the combination of the marked inflammatory reaction, inhibition of peritoneal clearing mechanisms and defense systems, and bacterial translocation from an inflamed and static gastrointestinal tract. Surgery is always indicated in the management of septic peritonitis and any delay in providing appropriate treatment will dramatically increase the morbidity and mortality associated with this condition.
Aside from standard laboratory evaluation, including complete blood count, biochemical profile, electrolyte panel, and urinalysis, an abdominocentesis should also be performed. Collected fluid should be examined cytologically. Protein quantitation, hematocrit and total nucleated cell counts should also be performed. Other biochemical analyses that may be indicated include BUN, creatinine, cholesterol, triglycerides, lipase, and total bilirubin. A sample of the abdominal fluid is saved for aerobic and anaerobic cultures. Abdominal radiographs may be of value, even in patients where there is a large amount of abdominal fluid. Although the ground-glass appearance of abdominal fluid will obscure serosal detail, the presence of free gas or intestinal ileus may be demonstrated. Abdominal ultrasound may be helpful in finding pockets of localized peritonitis associated with the prostate, pancreas, liver, or retroperitoneal space, as well as locating intra-abdominal masses. Contrast studies, such as cystourethrogram, excretory urogram, or upper gastrointestinal barium series, are ideal and may confirm your diagnosis, but more often are unnecessary and may delay much needed therapy. Thoracic radiographs should be performed prior to surgery if the animal is showing signs of respiratory distress. Conditions that may affect treatment options and prognosis include pleural effusion, pulmonary edema, aspiration pneumonia, and metastatic neoplasia.
Treatment: Aggressive intravenous fluid administration should be initiated as soon as possible. Up to 90ml/kg/hr in dogs and 60 ml/kg/hr in cats of crystalloid fluids may be administered to animals in hypovolemic shock. Administration of synthetic colloids (dextrans, Hetastarch) or hypertonic saline may also be considered for a more sustained effect on intravascular volume.
Initial empirical administration of antibiotics should be begun as soon as a sample of abdominal fluid is obtained for culture and sensitivity. Escherichia coli and anaerobes are the most common organisms associated with septic peritonitis since the gastrointestinal system is the most common source of contamination. Therefore, antibiotics must be chosen that have a good gram-negative and anaerobic spectrum.
Every patient with septic peritonitis should be surgically explored to locate and correct the underlying cause and source of contamination. Other therapeutic goals may also be accomplished at surgery including removal of foreign material, debridement, copious lavage of the peritoneal cavity, peritoneal drain placement and feeding tube placement. Abdominal lavage aids in diluting the bacterial population, facilitates the removal of blood and necrotic debris, and potentially reduces adhesion formation. Surgical procedures performed depend on the cause of peritonitis and viability of tissues. Abdominal structures should be evaluated for blood supply based on color, thickness, temperature, and perfusion (arterial pulse; bleeding of incised surface). Peristalsis is also a good indicator of viability of the stomach and intestines. Techniques utilized to reinforce enterotomy or anastomosis sites include serosal patching and mobilization of the omentum. The omentum can also be used to strengthen urogenital repairs or handled as a "physiologic drain" for intraperitoneal abscesses; it has a large absorptive capability due to its excellent vascular and lymphatic supply.
Peritoneal drainage allows for further removal of fluid, bacteria and cellular debris. Closed peritoneal drains are particularly useful for management of intra-abdominal abscesses or other pockets of localized peritonitis. For generalized conditions, abdominal drainage is beneficial in allowing for continuous effusion of fluid, bacteria, and cellular debris; unfortunately most closed systems are sealed over by omentum and fibrin within 6 hours. Open abdominal drainage provides a more rapid and effective means of draining the peritoneal cavity, however the patient requires a tremendous amount of post-operative intensive care. An additional surgical procedure is also required to complete abdominal closure, yet this provides an opportunity for additional abdominal lavage and a "second look". The animal needs to be anesthetized on a daily basis to reexplore the abdomen, reassess organ viability and surgical repairs, sample the abdominal fluid for cytology and culture, copiously lavage, and to replace sterile bandages. The most common complications include infection and massive fluid loss resulting in hypovolemia, anemia, and hypoproteinemia.
Lanz OI, Ellison GW, Bellah JR, et al. Surgical treatment of septic peritonitis without abdominal drainage. in 28 dogs. J Am Anim Hosp Assoc 2001;37:87-92
MacPhail CM: Peritonitis. In WE Wingfield (ed): Veterinary emergency medicine secrets. Philadelphia, Hanley & Belfus, 1997, pp. 267-272.
Mueller MG, Ludwig LL, Barton LJ. Use of closed suction drains to treat generalized peritonitis in dogs and cats: 40 cases (1997-1999). J Am Vet Med Assoc 2001;219:789-794
Staatz AJ, Monnet E, Seim HB, et al. Open peritoneal drainage versus primary closure for the treatment of septic peritonitis in dogs and cats. Vet Surg 2002;31:174-180