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Liver, Biliary System, Pancreas
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Robert Martin and Mike King
The liver is the largest glandular organ in the body, consisting of between 3% and 5% of bodyweight in dogs and cats. Blood draining from the gastrointestinal tract passes through hepatic cells prior to returning to the general circulation of the body.
Positioned in the cranial abdomen, the canine liver is bound by the diaphragm cranially, and the stomach, intestines and spleen caudally, and lies transversely within the abdomen, with a slight majority of its mass located on the right of midline. The organ is divided into 6 lobes: left lateral, left medial, quadrate, caudate, right medial and right lateral (Figure 21-1A). The caudate lobe is further divided into caudate and papillary processes and is positioned transversely across the abdomen. The papillary process extends to the left where it lies in the lesser curvature of the stomach and the caudate process to the right where it contacts the cranial aspect of the right kidney. The portal vein lies ventrally and the vena cava dorsally to the caudate lobe. The quadrate lobe is situated between the right medial and left medial lobes, with the gallbladder located in a fossa formed between the quadrate and right medial lobes.1,2
The cranial surface of the liver follows the curve of the diaphragm, and the right and left coronary ligaments attach it to the diaphragm caudolateral to the vena cava. The right and left triangular ligaments extend from their respective crus of the diaphragm, attaching to the adjacent lateral lobes. The visceral surface consists of several visceral impressions; the most prominent is to the left of midline, formed by the stomach. The dorsal border extends more caudally than the ventral border, with the cranial pole of the right kidney located within a renal impression formed on the caudate process of the caudate lobe. The normal liver does not usually extend caudal to the costal arch.1,2
Bile is secreted by the hepatocytes into canaliculi within hepatic lobules. Canaliculi drain into interlobular ducts which unite to form lobar ducts that exit from each liver lobe as extrahepatic bile passages termed hepatic ducts. Hepatic ducts may vary in number and terminate in the bile duct (Figure 21-1B).
In addition to the production of bile the liver has other functions, including metabolism of protein, fat, carbohydrates, as well as many drugs. Patients with liver disease may suffer from hypoproteinemia, hypoglycemia, and decreased levels of clotting factors. Patients with liver disease to be treated surgically are less than ideal anesthetic candidates, as hypotension, increased risk of hemorrhage, and more profound reaction to many anesthetic agents may be seen. Preoperative hemogram, serum chemistries, strict attention to intravenous fluid support (often with colloids to maintain osmotic pressure in a hypoalbuminemic patient) and careful attention to hemostasis are essential as is formulation of an appropriate anesthetic protocol.
Cytological evaluation of samples obtained by fine needle aspiration can be useful in diagnosis of some diffuse diseases. Care should be taken in the interpretation of such samples because the accuracy of liver cytology is markedly less than that of histopathological evaluation, especially in inflammatory hepatic disease.3-5
Ultrasound-guided needle biopsy is a commonly used technique for percutaneous liver biopsy (Tru-cut biopsy instrument).6,7 This allows the clinician to obtain multiple samples for histopathological assessment with low risk of complications such as excessive hemorrhage.8 Needle biopsy samples are not as accurate in yielding a diagnosis as larger wedge biopsies and laparoscopic liver biopsy is currently the best percutaneous technique.9 Laparoscopic biopsy allows direct visualization of the liver, especially when the disease is not generalized, and provides for a larger sized tissue sample.7 General anesthesia, specific equipment and expertise is required for the procedure.
A variety of techniques have been described for obtaining a liver biopsy during celiotomy. In cases of generalized disease or where a lesion exists at the apex of a lobe, the guillotine method is useful.6,7 A single loop of absorbable suture material is placed around the tip of a lobe and tightened (Figure 21-2A and B). The suture cuts through the parenchyma and tightens around the resulting pedicle of tissue which contains any vessels large enough to require ligation. A scalpel or dissecting scissors are used to transect the liver tissue distal to the ligature, producing the biopsy sample. A 2 to 3 mm tag of tissue should remain distal to the suture to avoid it loosening and becoming dislodged when the biopsy sample is excised. The edge of the lobe at the transection site should be examined for excessive hemorrhage. Hemorrhage can be controlled with direct electrocoagulation or placement of additional ligatures. For a larger biopsy sample along a lobe margin, a series of multiple interlocking sutures or a mattress suture pattern can be used. These can provide greater hemostasis than a single encircling ligature.6 The sutures should be pre-placed across the lobe or around the lesion and tightened before removing the biopsy sample.
In cases where a biopsy of a specific region or lesion is required, or when the disease process is not located at the margin of a lobe, a punch biopsy may be useful.6,7 Once the region of interest has been identified on the convex (ventral) surface, a 6 mm cutaneous biopsy punch is directed into the lesion, taking care to not penetrate more than 50% of the thickness of the lobe. This avoids larger hepatic veins situated near the concave surface of the lobe. To complete the biopsy the punch is positioned at a slight oblique angle to the direction it was first inserted and then driven a short distance further. The resulting defect in the liver defect can be filled with absorbable gelatin foam (Gelfoam, VetSpong) or omentum to contain hemorrhage. Placement of a mattress suture around the defect can also provide hemostasis, if necessary.
Regardless of technique employed, care is taken to avoid crushing the sample with tissue forceps or other instruments since this can cause histological alterations, possibly affecting the diagnosis.
Complete or partial liver lobectomy is indicated in a variety of clinical situations such as hepatic abscess, neoplasia, lobe torsion, and vascular alterations.6,7,10,11
For partial lobectomy the liver capsule is sharply incised along the planned point of resection. The parenchyma is bluntly dissected using a Bard scalpel handle, Doyen clamp, or digital pressure, leaving isolated vascular structures intact.6,7 Small structures can then be occluded by electrocoagulation while larger vessels (> 2 mm in diameter) should be ligated with suture or vascular occluding staples before transection.7 Surgical suction is useful in maintaining a hemorrhage-free field during dissection, allowing better visualization of vessels that require ligation. More pronounced hemorrhage can be controlled by temporary vascular inflow occlusion using the Pringle maneuver.12 A finger is passed around the free edge of the lesser omentum into the epiploic foramen where the hepatic artery, portal vein, and bile duct can be compressed between the thumb and forefinger. Occlusion of the hepatic artery and portal vein can be maintained safely in this manner for up to 15 minutes while the hemorrhage is controlled.12 A bulldog vascular clamp can be used to occlude these vessels, providing less interference to surgical exposure of the liver. Upon completion of a partial lobectomy the exposed parenchyma should be free of hemorrhage. Omentum can be sutured over the raw hepatic surface, though this is not necessary as omental adhesions will form spontaneously.7
Partial liver lobectomy can also be performed with specialized surgical stapling equipment, though this is dependent on lobe thickness and width.7,13,14 The Thoracoabdominal (TATM) series of stapling instruments were designed for use in pulmonary and gastrointestinal surgery and are also effective for hepatic surgery.7,13 Stapling devices are faster, provide more complete hemostasis, and are thought to cause less tissue inflammation than dissection and ligation techniques.13 The TA stapling instruments use preloaded disposable cartridges that produce a staggered double row of staples 30, 55, or 90 mm in length.14 The appropriate size instrument is selected based on lobe width at the desired point of transection. The liver capsule is incised, and the stapler is used to crush the parenchyma, compressing vessels and bile ducts between the jaws of the instrument. The staples are discharged and the parenchyma excised distal to the staple line.7,14 Application of the TA stapler can be simplified by crushing the liver parenchyma digitally or with a crushing instrument (Carmalt or Doyen intestinal forceps), leaving the vascular pedicle intact for stapling.
Complete liver lobectomy can be a challenging procedure. For complete lobectomy of the left liver lobes, the triangular ligament is transected, allowing surgical access to the hilus. In small dogs and cats the tissue around the hilum can be crushed using digital pressure, and a single encircling ligature placed, prior to transection of the lobe distal to the suture.6,7 Mass ligatures are not recommended for use in central or right division lobectomy or in larger dogs for left liver lobectomy as severe hemorrhage can occur should the ligature become dislodged.6,7 Complete lobectomy of central or right division lobes requires dissection of hepatic parenchyma from the caudal vena cava. Care must be taken to not damage this structure. The lobe must be freed from attachments to surrounding tissues or organs, and any parenchyma remaining at the hilus is crushed. If the right medial and/ or quadrate lobes are to be removed, the gallbladder has to be preserved.7,14 Once the vascular supply and biliary duct(s) of the lobe to be removed have been identified, they should be isolated and individually ligated. The lobe is then transected distal to these ligatures and removed. The hilus is examined for any signs of persistent hemorrhage and additional ligatures placed, if necessary.
Use of surgical stapling devices can avoid the need for individual dissection and ligation of hilar vessels. Once the lobe has been freed from its attachments the instrument can be applied at the hilus and the staples deployed. After the lobe has been excised and the stapler removed, the hilus should be assessed for any persistent hemorrhage which may require additional attention with suture or large vascular clips.7,13,14
Extrahepatic Biliary Tract Surgery
Anatomy of the Extrahepatic Biliary System
The gallbladder, a pear-shaped structure located between the quadrate and right medial liver lobes, varies in size depending on the size of the dog. Cats have a relatively consistent gallbladder size but are more prone to anatomic variations. In a beagle-sized dog, the gallbladder measures 5 cm long and 1.5 cm wide at its widest area with an approximate 15 ml volume storage capacity of bile.15 Anatomic regions of the gall bladder include a fundus, body, and a neck that continues as a cystic duct, the first structure of the biliary duct system (Figure 21-3).15 The bile duct is the main excretory channel to the duodenum that begins where the cystic duct joins with the first biliary tributary (hepatic duct) from the liver.15 Four hepatic ducts drain functional divisions of the liver and empty into the bile duct along its free portion (5 or more cm) as it courses to the duodenum through the hepatoduodenal ligament and lesser omentum (Figure 21-4).7,15 The central liver division (right medial and quadrate lobes) usually contribute 2 hepatic ducts that empty into the origin of the bile duct along with the cystic duct. The left division (left lateral and medial lobes, papillary process of the caudate lobe) usually gives rise to a single hepatic duct that enters midway along the free portion of the bile duct. The right division (right lateral and caudate lobes) usually gives rise to a single duct that is the last hepatic duct to enter the bile duct before it enters the duodenal wall where it courses for about 2 cm through the duodenal wall as the intramural portion of the bile duct. The intramural bile duct is surrounded by a double layer of smooth muscle as it passes terminally into the major duodenal papilla through a smooth muscle funnel. Bile is discharged into the duodenal lumen primarily as a result of duodenal motility with digestion but also by a coordinated active gallbladder contractile process.7,15 Variations in hepatic duct number (usually 3 to 5), liver division drainage, and hepatic duct entry into the bile duct can occur.
The frequent use of abdominal ultrasound (U/S) examination in dogs and cats has led to identification of asymptomatic biliary conditions such as gallbladder sludge (up to 50%), choleliths (about 5%), mucocoele (1 to 2%), and gallbladder wall thickening (1 to 2%) as incidental findings in dogs that do not have clinical signs of biliary tract disease.a Abnormal ultrasound findings can be significant if accompanying clinical signs and laboratory abnormalities (hemogram, serum chemistries) support a diagnosis of biliary tract obstruction. Only when ultrasonographic evidence of biliary obstruction (dilatation of the extrahepatic biliary system) is seen in a clinically ill patient does the role of infection become a likely contributor to biliary tract disease.
Surgical manipulation of the extrahepatic biliary tract is only part of the overall management of patients with clinical evidence of an extrahepatic biliary tract disease. The decision for surgical exploration should be made cautiously in clinically ill patients where morbidity has been induced by a biliary obstructive process (cholecystitis, inspissated bile, cholelithiasis, mucocoele, neoplasia, fibrosing pancreatitis, other).7,16 The selection of a surgical procedure and timing of intervention become critical factors that often affect patient survival. Stress of disease, anesthesia and prolonged surgery in these patients frequently results in death. Cholecystocentesis with U/S guidance is a minimally invasive procedure that can provide temporary biliary decompression for management of biliary obstructive disease in a sick patient.17 If patient stabilization can be achieved by fluid and electrolyte replacement, appropriate antibiotic administration, and nutritional support, then definitive surgical management can be undertaken with a better prognosis. In diseases such as cholecystitis with gallbladder necrosis and septic peritonitis, the surgeon may have little choice but to operate on an unstable patient. Even these patients could possibly be better managed by ingress/egress abdominal infusion of warm balanced electrolyte fluids after placement of a multifenestrated catheter for fluid retrieval. These patients have a guarded prognosis with immediate surgical intervention whereas stabilization over a period of hours or days prior to surgery might improve survival. In stable patients that show only mild to moderate clinical signs of biliary tract disease, surgery can be performed before the patient status deteriorates.
Surgical diseases of the extrahepatic biliary system can be divided into traumatic or obstructive processes. While sharp or missile-penetrating trauma can lacerate the biliary system, blunt force trauma (automobile, kick) is the most frequent cause of traumatic disruption. A delay of days to weeks between blunt trauma and recognition of bile peritonitis is a common occurrence.7 Animals are either presented in a stable state with abdominal effusion (chemical peritonitis only) or with varying degrees of illness and abdominal effusion (mixed chemical/bacterial peritonitis likely). Abdominocentesis is most often diagnostic when bilious fluid (green-tinged) is aspirated. The Ictotest® (Bayer HealthCare, Elkhart, IN) reagent tablets for detection of bilirubin in urine can be used to confirm the presence of bile in an abdominal fluid aspirate as can the less sensitive Multistix® 9 and Bili-Labstix® reagent strips (Bayer HealthCare, Elkhart, IN) used for standard urinalysis screening of bilirubin. Direct measurement of the bilirubin level may also be performed; if the bilirubin concentration of the effusion is at least twice that of peripheral blood, a diagnosis of biliary disruption is confirmed.7 Surgical exploration is indicated either immediately in a stable patient or should be delayed (hours) while steps are taken to improve the unstable patient’s surgical status. Most frequently, omentum will have formed adhesions in the vicinity of the biliary rupture that must be broken down to identify the site of rupture to determine what appropriate surgical steps should be taken.16
Bile peritonitis can also occur following gallbladder rupture from obstruction or infarction.7,18 These patients are often very ill and have a high mortality rate as a result. Surgical timing should coincide with an initial delay while attempts are made to improve patient stability over a period of hours, not days. A delay in owner recognition and subsequent presentation of a pet becoming ill from a biliary obstruction with bile peritonitis usually exists and time becomes a critical factor for patient survival in making the diagnosis and electing surgical intervention.18
Extrahepatic biliary obstruction occurs when disease processes interfere with the normal flow of bile from the liver and gallbladder into the duodenum. Biliary obstruction without rupture can occur from benign or neoplastic causes (benign – pancreatitis with periductal fibrosis7,8 edema, and/or abscess obstructing the bile duct, sludge, mucocoele, choleliths/choledocholiths, cysts, parasitic [flukes in cats in tropical zones], congenital cysts or atresia, and granulomas; inspissated bile, suppurative cholangitis; neoplastic–gastric, pancreatic, duodenal, biliary, and hepatic).7,16 Obstruction may be partial or complete, and intermittent or continuous. Consequences of extrahepatic biliary tract obstruction include impaired function of the reticuloendothelial system, increased absorption of endotoxins into the portal and peripheral circulations, depletion of coagulation factors, acquired platelet dysfunction, and an increased incidence of postoperative renal failure.17 Bile salts enhance absorption of the fat-soluable vitamins (A, D, E, and K) and chronic biliary obstruction can result in prolongation of coagulation related to vitamin K-dependent coagulation factor deficiencies (Factors II, VII, IX, and X).7,17 However, obstruction-related coagulopathy is unlikely in most cases of biliary obstruction in dogs and cats.7 Parenteral vitamin K administration should be considered for 8 to 12 hours prior to surgery when PT and PTT are prolonged.7,17,19 If coagulation is abnormal at the time of surgery, fresh whole blood (cross-matched) or fresh frozen plasma should be administered.7 Clinical signs include icterus, abdominal pain, vomiting, anorexia, depression, fever, dehydration, acholic feces, and weight loss.17 Most patients are debilitated on presentation from a chronic obstructive process.7,16,17 In general, diseases involving the gallbladder should be treated with cholecystectomy rather than cholecystotomy with content evacuation unless the gallbladder wall is healthy and it is required for construction of a bile flow diversion procedure.
Primary obstructive diseases of the bile duct can be treated primarily (choledochotomy or cholecystotomy for stone removal, with anthelmintics for flukes in cats, using stents for temporary obstructions and primary repair) or by bile flow diversion (neoplasia, traumatic avulsion, fibrosing pancreatitis and granulomas). Either stents or bile flow diversion procedures can be used for both palliative and curative intent. A bile sample is always taken for routine culture and antibiotic sensitivity testing and a liver biopsy is standard for biliary tract surgery. Moist laparotomy sponges are routinely used to pack around the surgical site to contain bile spillage. Gauze sponges with a radiopaque marker (Vistec X-ray Detectable Sponges, Tyco Healthcare/Kendall, Mansfield, MA) are counted immediately prior to a celiotomy and immediately prior to closure to prevent leaving a sponge in the abdomen. Abdominal lavage with warm physiologic fluid is a standard part of surgical management of extrahepatic biliary tract disease prior to celiotomy closure. The surgeon should consider use of supplemental feeding techniques postoperatively (esophageal feeding tube, gastrostomy tube, jejunostomy tube; jugular catheter for total parenteral nutrition) to promote nutritional health. Laparoscopic equipment, if available, can be used efficiently to visualize the extrahepatic biliary system and assist in performing temporary decompression procedures, liver biopsy, or cholecystectomy.
a Personal Communication, Dr. Martha M. Larson and Dr. Colin C. Carrig
Ultrasound-guided Percutaneous Cholecystocentesis
Goals of percutaneous cholecystocentesis are to provide rapid preoperative relief of jaundice, to allow control of biliary sepsis, and to allow time to improve the nutritional status of the patient before definitive surgery, especially in severely ill patients.17 Evidence of a ruptured gallbladder is a contraindication for percutaneous cholecystocentesis. Recent reports of percutaneous cholecystocentesis have demonstrated the value of temporary decompression in patients until stabilized by fluid, electrolyte, antimicrobial, and nutritional management, resulting in a more favorable risk/benefit ratio for a successful surgical outcome.19 Repeated cystocentesis can eliminate the need for definitive surgery in acute, temporary obstructions (e.g. acute pancreatitis) that resolve after intermittent biliary decompression.17,19 An 18- or 20-gauge, 3.5 inch spinal needle (Becton Dickinson, Franklin Lakes, NJ), is easily inserted into a dilated gallbladder under U/S guidance and usually has a large enough internal diameter to allow aspiration of tenacious bile without leaving a large hole that results in excessive bile leakage once the biliary tract is decompressed and the needle is removed. Leakage always occurs to some degree and resulting morbidity is partially dependent upon patient status, amount of bile leakage, and bile sepsis. Daily or even twice daily cholecystocentesis should be employed over 3 or more days in sick patients with biochemical and ultrasonographic evidence of obstructive biliary tract disease until patient stability can be achieved to improve the prognosis for surgical intervention.
A CookTM spiral catheter is attractive as a temporary percutaneous implantable catheter for use over several days in selected patients to minimize the necessity of multiple sedations and percutaneous needle placements but its use for percutaneous cholecystocentesis has not been reported. Accordion-type catheters have been described for use as an indwelling catheter after percutaneous placement.17 An esophageal feeding tube should also be considered for nutritional support in the initial preoperative management of these patients.
Hepatic Duct Ligation
Avulsion of a single hepatic duct can occur following blunt abdominal trauma. Bile peritonitis results and a significant delay (10 to 20 days) between the time of trauma and onset of clinical signs is common.7,16 Surgical management usually involves ligation of the avulsed duct.7 Marked elevation in serum alkaline phosphatase will result (usually present with bile peritonitis), peaking at 10 to 14 days, and declining subsequently.20 In some cases, an auxiliary retroportal network of bile ducts will develop to drain bile from the affected liver lobe (s) whereas, in other cases, diffuse microscopic biliary cirrhosis results.7,16,20 If the avulsion is directly off the bile duct (often), either the bile duct tear is oversewn with 6/0 monofilament suture with or without a stent or the bile duct is ligated and a bile flow diversion procedure is performed.7,16
In situations where the clinician does not have the capability of providing frequent cholecystocentesis, tube cholecystostomy can be employed as a percutaneous placement or by relatively quick surgical intervention to achieve biliary decompression without performing a prolonged definitive corrective procedure (Figure 21-5).16,17,20 Because surgical time can be a critical factor in a patient’s survival, tube cholecystostomy should be selected only as a temporary procedure for rapid surgical biliary decompression until patient stabilization permits a definitive correction of extrahepatic biliary tract obstruction. The Hawkins needle-guide system (22-ga cannulated needle with stylet and guidewire; Cook, Inc., Bloomington, IN) and a 6.5-Fr polytetrafluoroethylene self-retaining accordion catheter with side holes has been described for percutaneous placement through the right abdominal wall caudal to the costal arch.17 The catheter is secured to a Tuohy-Borst fitting and functions as a self-retaining catheter.17
A right paracostal celiotomy provides direct access to the gallbladder but ventral midline celiotomy is the more common approach for biliary surgery. Following creation of a cranial midline celiotomy, the falciform ligament is separated but not removed to minimize surgical time and blood loss. A self-retaining retractor (Gelpi for small dogs and cats; Balfour [pediatric and standard]) is used most efficiently to maintain body wall retraction for access to the gallbladder. A cutaneous incision is made ventral to the tip of the 13th rib on the right lateral body wall and a hemostatic forceps (Crile, Kelly, mosquito) is pushed with its tip from intraabdominal toward the skin incision. A Bard scalpel blade is used to sharply incise over only the tip of the forceps until its jaws pass completely through the body wall at that site. The tip of a 7- to 14-Fr balloon catheter (Foley catheter, Tyco Healthcare/Kendall, Mansfield, MA) or mushroom-tipped catheter (Bard Urological Catheter, CR Bard, Inc, Covington, GA; excise the tip of the mushroom catheter to improve bile drainage) is grasped with the forceps and pulled through the body wall and into the abdomen. The catheter is then passed through a layer of omentum.7,16,17 Avoid bunching omentum such that it impairs surgical manipulation of the gallbladder. Using 3/0 monofilament absorbable suture material, a pursestring suture is placed in the fundus of the gallbladder. The gallbladder is not dissected from its hepatic fossa7,16 nor is it necessary to pexy the gallbladder fundus to the body wall at the site of tube entry into the abdomen.7 Once the pursestring suture is placed, a stab incision (caution to avoid cutting the pursestring suture) is made with an 11 Bard blade into the center of the pursestring suture and bile is aspirated using suction. Alternatively, a large bore needle (14 gauge or teat cannula) connected to a 35 ml syringe can be introduced into the gallbladder from inside the pursestring suture to aspirate bile sufficiently to avoid leakage when the cholecystotomy is made for catheter tip introduction. Insert the catheter tip, inflate the balloon with sterile saline if a Foley® catheter is used, and tie the pursestring suture securely. Using a 4mm skin biopsy punch, take a liver biopsy from the ventral surface of a liver lobe, place a gelatin foam hemostatic sponge (Gelfoam®, Upjohn Company, Kalamazoo, MI; VETSPON®, Ferrosan A/S, Soeborg, Denmark) plug in the biopsy site to control hemorrhage, and close the celiotomy wound with an appropriate size absorbable monofilament suture material in a simple continuous pattern. The tube is secured to the skin at the exit site using 2/0 nylon in a finger- trap suture pattern. Avoid placing excessive external tension on the tube. The tube is occluded (use a 3 ml syringe placed into the tube end) and bandaged to the dorsal aspect of the patient for easy access for intermittent drainage multiple times daily. Gravity flow into a sterile collection system can also be used. The wound at the tube exit site is cleaned daily. The procedure should be accomplished in about 15 minutes in an attempt to minimize patient morbidity.
If the bile is not septic and the patient is eating or being fed through a tube (esophagostomy, gastrostomy), collected bile can be returned to the patient in gelatin capsules or directly into the tube to support digestion of dietary fats if prolonged drainage is anticipated.7,16,20 In cases of temporary bile duct obstruction, biliary tract patency can be determined with cholangiography by injecting radiographic contrast media (Conray® 400) through the tube and into the gallbladder, taking a radiograph immediately after injection. If biliary patency is confirmed, the patient is sedated and the tube removed by firm traction five or more days postoperative without concern for bile leakage into the abdomen.7,16 If at the time of tube placement the surgeon anticipates tube removal without further definitive biliary tract surgery, a balloon-tipped catheter (Foley catheter, Tyco Healthcare/ Kendall, Mansfield, MA) is preferred since it can be deflated and more easily removed by traction than a mushroom-tipped catheter. The omentum forms a fibrous tract around the tube that collapses and seals off the gallbladder stoma after the tube is extracted. The cutaneous stoma is cleaned daily and allowed to heal by second intention.
After stabilization of a patient requiring definitive biliary surgery, the tube is removed under direct visualization following a second celiotomy. Tube cholecystostomy does not hinder subsequent cholecystectomy or biliary diversion using the gallbladder for a cholecystoenterostomy. In either procedure the tube should be cut several cm distal to the pursestring suture site to extract it externally from the body wall. The tube stump can be used to apply traction while the surgeon dissects the gallbladder from its hepatic fossa.
Choledochal Tube Stenting
Use of a choledochal tube stent has been previously described in individual case reports in the veterinary literature and in experimental studies however only recently has its use in a series of dogs with clinical biliary tract obstruction been reported,including long-term outcome.7,21 Indications include short-term stenting for reversible disease processes (acute pancreatitis with temporary obstruction), internal support after primary repair of bile duct trauma, palliation of bile duct obstructing malignancy, and drainage of an obstructed bile duct prior to definitive surgical management in the severely compromised patient.21 We prefer tube cholecystostomy over choledochal tube stenting for temporary decompression of biliary obstruction in the severely compromised patient because tube cholecystostomy is a more rapid surgical technique that does not require an enterotomy. Advantages of choledochal tube stenting include decompression for temporary obstructive diseases (pancreatic inflammation, edema, or abscesses) without altering the normal anatomic features of the biliary tract, support for primary repair of a bile duct tear, and possibly preventing stricture during the early phases of healing (controversial).7,21
An antimesenteric duodenotomy is made 3 to 6 cm distal (aborad) to the pylorus over the major duodenal papilla. A red rubber catheter (Feeding tube, Tyco Healthcare/Kendall, Mansfield, MA) is used because of its availability in a variety of sizes to accommodate variable diameters of a bile duct opening.21 An appropriate diameter catheter is selected and passed retrograde from the bile duct opening at the major duodenal papilla. The biliary tract is flushed with a balanced electrolyte solution or sterile saline (0.9% NaCl) solution. If patency can be established, either by flushing through the stent only or by concurrent removal of choledocholiths/ cholecystoliths through a choledochotomy, cholecystotomy or cholecystectomy, the stent is left with its tip midway in the free portion of the bile duct. The remaining tube is cut to leave 3 to 5 cm of stent extending through the major duodenal papilla and into the duodenal lumen. The stent is secured in place by passing a monofilament absorbable suture through the stent wall and through the submucosa of the duodenal wall just distal (aborad) to the major duodenal papilla and tying the suture routinely.21 A monofilament nonabsorbable suture material should be used when a stent is placed for palliation of malignancy. Because of likelihood for stent occlusion to occur postoperatively, removal of the tip of the red rubber catheter while preserving the side openings should be considered even though bile can be expected to flow freely around the stent and into the duodenum.21 The duodenotomy is closed routinely. The stent can be expected to pass through the feces months later or it can be electively removed by endoscopic retrieval 3 to 6 months later after clinical and biochemical evidence of biliary tract obstruction has resolved.
An alternate placement of a red rubber catheter stent is by direct introduction through the body wall and duodenum and through the major duodenal papilla into the bile duct. A large bore needle is passed from within the abdominal cavity through the right body wall at a point equidistant between the tip of the last rib and ventral midline. The tip of an appropriate size red rubber catheter is passed from outside into the needle lumen and into the abdomen. The needle is removed from the body wall and catheter and it is next passed from the lumen of the duodenum 5 to 10 centimeters distal (aborad) to the major duodenal papilla (at a point in the descending duodenum that can be easily approximated to the right body wall) through the bowel wall on the antimesenteric surface of the duodenum. The tip of the red rubber catheter is again passed through the needle lumen and into the duodenal lumen. The needle is withdrawn and the catheter is passed into the bile duct through the major duodenal papilla to the midpoint in the free portion of the bile duct proximal to the level of obstruction or tear. The duodenotomy is closed routinely. The descending duodenum is sutured to the right body wall to fix the points of tube entry and prevent potential leakage. The red rubber feeding tube (Tyco Healthcare/Kendall, Mansfield, MA) is fixed to the skin by a finger-trap suture pattern with 3/0 nylon suture material. Bile can be drained passively from the tube externally or aspirated intermittently and returned to the animal through feeding as described above, if appropriate. Once serum bilirubin concentrations return to a normal level, a cholangiogram is performed by injecting contrast material (Conray 400®) through the stent and into the biliary system. If contrast can be seen flowing around the stent and into the duodenum, then the tube can be removed by cutting the fingertrap suture and placing gentle traction on the catheter.
Choledochal stenting may provide a less invasive and less time-consuming option for palliation of malignancies, compared with rerouting procedures.21 Duodenobiliary reflux with subsequent cholangiohepatitis does not seem to be a consequence of stenting.21
Cholecystotomy has limited indications in biliary surgery (removal of inspissated bile or biliary sludge, gelatinous bile, cholecystoliths/choledocholiths, and possibly to cannulate the bile duct to confirm its patency).7,16 A bile sample for culture analysis can be obtained as an attempt is made to aspirate bile (20 to 35 ml syringe, 14- or 16-ga needle) before cholecystotomy is performed.7 The bile duct is difficult to catheterize through a cholecystotomy because of the acute angle formed by the cystic duct as it joins the bile duct. An angiographic flexible-tipped guidewire is usually necessary to first pass around the sharp angle, followed by catheter passage over the guidewire to explore and flush the bile duct and its branches from this approach.16 Diseases of the gallbladder are usually best managed by cholecystectomy and not just evacuation of gallbladder contents (stones, mucocoele, and sludge) although stones can be successfully removed via cholecystotomy.7 It is imperative to insure that the bile duct is patent and a biopsy of the gallbladder wall is taken before a cholecystotomy is closed.7 Closure is best achieved by using small-gauge monofilament absorbable sutures in a simple interrupted or continuous, inverting suture pattern (Lembert or Cushing). A two-layer closure is not necessary or recommended.7 The primary indication for a controlled surgical opening of the gallbladder is in preparation for tube cholecystostomy or cholecystoenterostomy.
Gallbladder removal is the treatment of choice for diseases of the gallbladder.7 Secondary changes of inflammation, fibrosis or necrosis of the gallbladder wall are common. Removing the gallbladder eliminates a potential source of disease and a reservoir for subsequent stone formation.7 An intact distended gallbladder is more easily dissected from its hepatic fossa than a flaccid one and stay sutures or tissue clamp become useful in manipulating the structure (Figure 21-6).16 With gallbladder necrosis and/or rupture, cholecystectomy becomes more difficult to perform because stay sutures are no longer useful.
Omental, liver lobe, and diaphragmatic adhesions often require dissection to expose the gallbladder.7 Traumatic rupture of the gallbladder is uncommon, and by the time of diagnosis, omental adhesions have usually formed so that primary closure is a less likely consideration, necessitating cholecystectomy.7
The gallbladder is covered by a layer of visceral peritoneum over its free (abdominal) surface that is confluent with the liver surface (tunica serosa or Glisson’s capsule). This layer requires sharp dissection along the complete margin of the gallbladder and hepatic fossa. Some surgeons inject fluid beneath this layer to make it more distinct and to improve ease of dissection (Figure 21-7).7,16 Once this layer of peritoneal reflection is partially disrupted, the gallbladder can be sequentially removed from its intimate attachment with hepatic parenchyma in the hepatic fossa, either by precise blunt scissor dissection or by more crude but rapid finger dissection. As this separation progresses, the peritoneal reflection can be continued sharply until the gallbladder is completely freed from its hepatic fossa, down to the junction of the cystic duct and the bile duct. With precise dissection, the hepatic fossa is minimally disturbed so that hemorrhage from a raw liver surface is minimal. With finger dissection, increased hepatic hemorrhage can be expected.7 Because hemorrhage is not usually a major concern, blunt finger dissection of the gallbladder from the liver after peritoneal incision is a rapid method of mobilizing the gallbladder.7 Any hepatic hemorrhage is controlled with pressure by packing with a moist laparotomy sponge.7 In the normal dog, the cystic artery can be identified and ligated or coagulated directly. In clinical obstructive disease this structure can be ligated or coagulated when it is encountered. After gallbladder dissection is complete, the cystic duct can be cross-clamped and severed between the clamps (Figure 21-8). Our preference is to place a single clamp midway on the cystic duct to prevent spillage of gallbladder contents while leaving a sufficient stump (5 to 10 mm) attached to the bile duct to manipulate with Debakey tissue forceps for cannulation with an appropriate size catheter (5- to 8-Fr red rubber feeding tube, Tyco Healthcare/Kendall, Mansfield, MA). Once patency of the bile duct is confirmed by flushing and passing a catheter through the bile duct, a circumferential ligature is placed on the stump with 3/0 monofilament absorbable suture material or a hemoclip is applied. Double ligation or transfixation is not necessary when an adequate cystic duct stump is preserved although either can be employed, based on a surgeons’ discretion. With a very short stump or with friable tissue, transfixation becomes more important to avoid suture slippage or tissue tearing and subsequent bile leakage. Because bile is soluble in saline or balanced electrolyte solutions, any spillage not contained by laparotomy sponges during the cholecystectomy can be removed during abdominal lavage. Sponges are removed from the hepatic fossa at completion of the procedure. Omentum can be placed in contact with the raw liver surface if leakage is a concern.
Drainage of the area is unnecessary. The bile duct will dilate 2 to 3 times its normal diameter and remain dilated after cholecystectomy.7 Cholecystectomy performed by beginning the dissection at the cystic duct has been described.16
The normal bile duct in dogs and cats is usually too small (2.5 mm in diameter15) to consider an elective choledochotomy because of risk of either stricture and/or leakage after closure. However, in cases of bile duct obstruction in the distal free portion or in the intramural portion, dilation can result in a duct of sufficient size to make choledochotomy practical if needed to remove an intraluminal obstruction such as a choledocholith.7 Biliary flushing and tube exploration in both directions is achieved through the choledochotomy.
Solitary choledocholiths located in the free portion of the bile duct can occasionally be removed via a linear choledochotomy directly over the stone. Bile duct patency is confirmed using a catheter inserted through the choledochotomy site with flushing of the bile duct in both directions. Primary closure with small-gauge (5/0 or 6/0) monofilament absorbable suture in a simple interrupted or continuous pattern is used to close the incision. A continuous cruciate pattern is leak proof when the bile duct is of sufficient diameter and thickness to employ the suture pattern.
Traumatic tears of the bile duct may be amenable to primary repair followed by placement of a stent tube21 or a cholecystoenterostomy can be performed after ligation of the bile duct proximal to the tear. Primary closure of a choledochotomy or laceration by application of collagen biomaterial (fibrin-glued, sutured collagen patch) has been described; fibrin sealant alone was not reported to be effective.7
The bile duct is used in humans to bypass distal benign obstructions, usually stones, by creating a choledochoenterostomy (duodenal or jejunal). The procedure is described as a viable option in dogs and cats (Figure 21-9) when the duct is of sufficient size and the obstruction is distal.16 There is little indication for this procedure electively in dogs and cats. Choledochoduodenostomy is not recommended unless the gallbladder must be removed, the bile duct is dilated to at least 1 cm in diameter, and a stoma of at least 2.5 cm can be created.7
When the intramural portion of the bile duct contains an intraluminal obstruction (choledocholith), antimesenteric duodenotomy is used to access the major duodenal papilla where a blade of a blunt-tipped iris scissors or 60° Potts scissors can be introduced across the sphincter of Oddi to incise the intramural bile duct and duodenal mucosa sufficiently to remove the obstruction.7 Because of its small size, creation of a sphincteroplasty (suturing bile duct mucosa to duodenal mucosa; (Figure 21-10) to permanently enlarge the opening of the intramural bile duct is not usually practical in the dog or cat. Following a sphincterotomy, the biliary system is catheterized and flushed but no further manipulation of the intramural bile duct is required. The duodenotomy is closed routinely with 3/0 monofilament absorbable suture in a simple continuous pattern that captures the submucosal layer of the bowel wall. The major pancreatic duct empties into the duodenal hillock with the bile duct in approximately 50% of dogs and in nearly all cats yet iatrogenic pancreatic insufficiency has not been reported.16
Rarely, a pancreatic abscess22 or carcinoma of the intramural bile duct or major duodenal papilla can cause biliary obstruction. Drainage and stent management of a pancreatic abscess has been described in a dog.21 Duodenal resection and anastomosis with biliary diversion using a cholecystoenterostomy is required for definitive treatment of a neoplasm in this location. The first author (RAM) has seen one case of obstruction caused by a solitary tumor of the major duodenal papilla. A stent could be considered for palliative management of neoplastic obstruction of the intramural portion of the bile duct if it can be introduced into the bile duct successfully.21
Biliary-enteric Anastomosis for Bile Flow Diversion
Rerouting the flow of bile is necessary when its normal course is disrupted, either by traumatic rupture or benign or malignant obstruction. Obstruction of the distal part of the free portion of the bile duct that cannot be relieved by other means becomes the most common reason to reroute bile through an anastomosis surgically created between the gallbladder and duodenum or jejunum. Occasionally, traumatic rupture of the bile duct by avulsion of its free portion from its intramural junction or a tear in its free portion occurs and is managed by bile flow diversion. Normally, the anatomic arrangement of smooth muscle layers around the intramural portion of the bile duct and around its terminal opening at the major duodenal papilla prevents reflux of duodenal contents into the biliary system.15 However, reflux of intestinal contents (chyme and bacteria) into the biliary system occurs when the gallbladder is anastomosed to the small bowel. While long-term hepatic enzyme values (SAP, SGPT) and histological changes reflect subclinical reflux cholangitis, clinical signs of cholecystitis/cholangiohepatitis (fever, vomiting, anorexia, depression, abdominal pain and icterus) do not occur as long as the anastomosis remains sufficiently patent for ingress of contents to egress with the flow of bile.
Cholecystoduodenostomy is the most common bile flow diversion procedure used in veterinary medicine.7,16 Cholecystojejunostomy has been reported in dogs and cats as a viable technique for bile flow diversion but postoperative complications are more common. Increased alkaline phosphatase and alanine aminotransferase hepatic enzymes and subclinical periportal inflammation and fibrosis result following biliary enteric anastomosis in normal and clinical dogs but these changes may already exist with bile duct obstruction in most clinical patients. Serum hepatic enzyme levels remain elevated for at least 6 months after cholecystoduodenostomy but may return to normal within 1 to 2 years.7
The gallbladder is dissected from its hepatic fossa down to the junction of the cystic duct and the bile duct, as for cholecystectomy. Partial dissection of the gallbladder from the hepatic fossa has been described to minimize trauma to the cystic artery nourishing the gallbladder and to prevent cystic duct torsion.7,16 Decreased tension on the anastomosis is achieved by complete dissection of the gallbladder from the hepatic fossa without loss of its viability. Use of two full-thickness stay sutures, one in the fundus and the other in the neck on the free surface, prevent iatrogenic gallbladder torsion. These retraction sutures are then used to stabilize the gallbladder for anastomosis to the antimesenteric border of the duodenum at its most tension-free location, typically 3 to 6 cm distal to the pylorus, depending on patient size (Figure 21-11). Similarly, two full-thickness stay sutures are placed in antimesenteric surfaces of the duodenum to stabilize this portion of small intestine. Doyen intestinal forceps can be used across the gastric antrum and distal to the right limb of the pancreas after the descending duodenum has been manually “milked” to empty lumen contents in an aborad direction to prevent leakage of fluid into the abdomen following duodenotomy. This step is usually not necessary. Packing clean, moist laparotomy pads dorsal to the gallbladder and duodenum also helps contain any bile or gastrointestinal fluid spillage in the region of the anastomosis.
The gallbladder is opened sharply from its fundus toward its neck for 4 cm or to the level of the neck in smaller gall bladders in order to create a stoma that will remain patent after it contracts up to 50% as it heals.7 An incision of this length permits the maximum stoma size in small patients and an adequate stoma size in all patients. Using 3/0 monofilament absorbable suture on a tapered needle, a U-suture is placed between the proximal (orad) apex of the duodenotomy and the opposing apex at the neck of the cholecystotomy. A second U-suture is placed at the distal (aborad) apices of each structure. A single square knot is used to secure each U-suture to avoid a “daisy chain” effect created by multiple knots that potentially could leave enough space to allow for anastomosis leakage. The needle and suture of the proximally placed U-suture are brought back through the gallbladder wall and into its lumen immediately adjacent to the U-suture knot. A continuous suture pattern is employed to appose the dorsal (deep) margins of the stoma in a distal direction toward the second U-suture. When the suture line reaches the distal apices and U-suture, the needle and suture are brought through the gallbladder wall adjacent to that U-suture knot and the suture is tied securely to the free tag of that U-suture. At this point, the deep margin of the stoma is complete as a single-layer, simple continuous suture anastomosis that should be leak-proof if suture bites are placed appropriately (2 to 3 mm apart). The needle limb of the distal U-suture is now used to place a full-thickness simple continuous suture line through the ventral (superficial) margins of the gallbladder and duodenum, ending this suture pattern by tying to the free limb of the first U-suture on the external surface of the completed anastomosis. The deep stoma margin is inverted since it was created by suturing from within the lumen of the stoma whereas the superficial margin with be everted since it was created by suturing from the external surface of the stoma. The surgeon can digitally palpate the stoma through the walls of the gallbladder and duodenum to assess the opening created. The anastomosis is lavaged locally, followed by complete abdominal lavage prior to body wall closure.
This technique is employed when a surgeon either elects to perform the procedure or circumstances (gastric, duodenal, pancreatic, or biliary masses) require its performance. When bile is diverted from the proximal duodenum, normal physiology of gastric acid production and fat digestion is altered. Bile is required in the proximal duodenum to activate duodenal mechanisms responsible for inhibition of gastric acid secretion. Excessive gastric acid production can lead to peptic ulceration of the pyloric antrum and/or, more commonly, the proximal duodenum.7 Fat digestion is also disrupted since bile salts enhance both the hydrolysis and absorption of fats. Weight loss can result. No long-term reports exist on outcomes of cholecystojejunostomy in a series of dogs or cats to recommend the procedure.
Two techniques can be employed. A loop cholecystojejunostomy between the gallbladder and proximal jejunum is the simpler technique to perform. Noncrushing intestinal forceps (pediatric Doyen) should be applied proximal and distal to the selected jejunotomy site to minimize intestinal fluid spillage. Without dissecting the gallbladder from its hepatic fossa, a cholecystotomy is created in the free portion of the gallbladder from its fundus toward the neck and a loop of proximal jejunum is brought into proximity. An antimesenteric jejunotomy of equal length to the cholecystotomy is created and the two structures are anastomosed in a side-to-side fashion, using a continuous suture pattern with U-sutures as described for cholecystoduodenostomy. Stoma size should be either 4 cm in length or as long as the cholecystotomy will accommodate in patients too small to achieve this length. Reflux of jejunal contents will occur.
An alternate technique requires construction of an isoperistaltic antireflux limb of jejunum 40 to 50 cm long, according to the Roux-en-Y principle. The proximal jejunum is divided transversely, and the distal (aborad) segment is advanced to the gallbladder and anastomosed end to end with the gallbladder fundus. The proximal (orad) jejunal segment is anastomosed in an end-to-side manner 40 to 50 cm distal (aborad) in the distal (aborad) jejunal segment. This distance, considered necessary to prevent reflux of chyme into the gallbladder, is greater than half the length of the jejunoileum in all cats and most small dogs. A short bowel syndrome (maldigestion due to lack of small intestinal mucosal surface area) or stagnant bowel syndrome (overgrowth of bacteria in refluxed intestinal contents that stagnate in the limb) could result. This technique has only been reported in dogs experimentally where reflux occurred in all dogs having only a 15 cm Roux-en-Y jejunal limb.7
- Dyce KM, Sack WO, Wensing CJG: In Dyce KM, ed.: Textbook of Veterinary Anatomy. 2nd ed. Philadelphia: WB Saunders, 1996, p
- Evans HE, deLahunta A: Millers’ Guide to the Dissection of the Dog. 4th ed. Philadelphia: WB Saunders, 1996.
- Weiss DJ, Blauvelt M, Aird B: Cytologic evaluation of inflammation in canine liver aspirates. Vet Clin Pathol 30:193, 2001.
- Roth L: Comparison of liver cytology and biopsy diagnoses in dogs and cats: 56 cases. Vet Clin Pathol 30:35, 2001.
- Wang KY, et al: Accuracy of ultrasound-guided fine-needle aspiration of the liver and cytologic findings in dogs and cats: 97 cases (1990-2000). J Am Vet Med Assoc 224:75, 2004.
- Bjorling DE: Partial hepatectomy and hepatic biopsy. In Bojrab MJ, ed.: Current Techniques in Small Animal Surgery. Philadelphia: Williams & Wilkins, 1998, p 287
- Martin RA, Lanz OI, Tobias KM: Liver and biliary system. In Slatter D, ed.: Textbook of Small Animal Surgery. Philadelphia: WB Saunders, 2003, p 708.
- Bigge LA, Brown DJ, Penninck DG: Correlation between coagulation profile findings and bleeding complications after ultrasound-guided biopsies: 434 cases (1993-1996). J Am Anim Hosp Assoc 37:228, 2001.
- Cole TL, et al: Diagnostic comparison of needle and wedge biopsy specimens of the liver in dogs and cats. J Am Vet Med Assoc 220:1483, 2002.
- Farrar ET, Washabau RJ, Saunders HM: Hepatic abscesses in dogs: 14 cases (1982-1994). J Am Vet Med Assoc 208:243, 1996.
- Schwartz SG, et al: Liver lobe torsion in dogs: 13 cases (1995-2004). J Am Vet Med Assoc 229:242, 2006.
- Bjorling DE, Prasse KW, Holmes RA: Partial hepatectomy in dogs. Compend Contin Educ Pract Vet 7:257, 1985.
- Lewis DD, et al: Hepatic lobectomy in the dog. A comparison of stapling and ligation techniques. Vet Surg 19:221, 1990.
- Lewis DD, Ellison GW, Bellah JR: Partial hepatectomy using stapling instruments. J Am Anim Hosp Assoc 23:597, 1987.
- Evans HE, Christensen GC: Miller’s Anatomy of the Dog. 2nd ed. Philadelphia: WB Saunders, 1979, 499.
- Breznock EM: Surgical procedures of the hepatobiliary system. In Bojrab MJ, Ellison GW, Slocum B, eds.: Current Techniques in Small Animal Surgery, 4th ed. Williams & Wilkins, Baltimore, 1997, p 298
- Lawrence D: Percutaneous biliary drainage (cholecystostomy). In Bojrab MJ, Ellison GW, Slocum B (eds): Current Techniques in Small Animal Surgery, 4th ed. Baltimore: Williams & Wilkins, 1997, p 398
- Church EM, Matthiesen DT: Surgical treatment of 23 dogs with necrotizing cholecystitis. J Am Anim Hosp Assoc 24:305, 1988.
- Martin RA: Biliary obstruction/stones. In Bojrab MJ, ed.: Disease Mechanisms in Small Animal Surgery. Philadelphia: Lea & Febiger, 1992, p 306
- Martin RA, MacCoy DM, Harvey HJ: Surgical management of extrahepatic biliary tract disease: A report of eleven cases. J Am Anim Hosp Assoc 22:301, 1986.
- Mayhew PD, Richardson RW, Mehler SJ, et al: Choledochal tube stenting for decompression of the extrahepatic portion of the biliary tract in dogs. J Am Vet Med Assoc 228:1209, 2006.
- Matthiesen DT, Rosin E: Common bile duct obstruction secondary to chronic fibrosing pancreatitis: Treatment by use of cholecystoduodenostomy in the dog. J Am Vet Med Assoc 189:1443, 1986.
- Herman BA, Brawer RS, Murtaugh RJ, et al: Therapeutic percutaneous ultrasound-guided cholecystocentesis in three dogs with extrahepatic biliary obstruction and pancreatitis. J Am Vet Med Assoc 227: 1782, 2005.
Congenital Portosystemic Shunts in Dogs and Cats
Karen M. Tobias
Portosystemic shunts (PSS) are abnormal vessels that divert blood from the abdominal viscera to the heart, bypassing the hepatic sinusoids and carrying intestinal absorption products directly to the systemic circulation.1 Portosystemic shunts can occur as congenital anomalies, or may develop secondary to liver disease and portal hypertension. Congenital PSS usually occur as single large vessels, while acquired shunts are numerous and often small in size. Common types of single congenital portovascular anomalies include intrahepatic portocaval shunts, such as patent ductus venosus, and extrahepatic portocaval or portal-azygos shunts. Shunts may connect the portal vein with the caudal vena cava directly, or may originate from a portal tributary, such as the left gastric vein, and terminate on a caval tributary, such as a phrenic or hepatic vein. In a small percentage of dogs, the prehepatic portal vein is also congenitally absent.1,2
Signalment, History, and Clinical Signs
Congenital intrahepatic and extrahepatic PSS are usually diagnosed in immature animals. No sex predilection is evident. Intrahepatic PSS are found primarily in large breed dogs such as Irish Wolfhounds, Bernese Mountain dogs, Old English sheepdogs, Golden and Labrador Retrievers, and Samoyeds, and in medium-sized breeds such as Australian shepherds and Australian Cattle dogs.1,3 Extrahepatic PSS occur primarily in small breed dogs such as Yorkshire terrier, Maltese, pug, Schnauzer, Cairn terrier, Shih Tzu, and dachshund.3 In cats, PSS are most often extrahepatic. Congenital shunts are hereditary in Irish Wolfhounds, Yorkshire Terriers, Cairn Terriers, and several other breeds.3-6
Clinical signs associated with portosystemic shunts commonly involve the nervous system, gastrointestinal tract, and urinary tract.1 General clinical signs include poor growth rate, weight loss, fever, and anesthetic or tranquilizer intolerance. Neurologic dysfunction is seen in most animals with PSS and includes lethargy and depression, ataxia, behavioral changes, and blindness (especially cats).1,7,8 Animals with severe hepatic encephalopathy may develop head pressing, circling, dementia, stupor, muscle tremors, motor abnormalities, focal and generalized seizures, or coma. Hepatic encephalopathy may be precipitated by drugs (i.e.diuretics or sedatives), protein overload, hypokalemia, alkalosis, transfusion of stored red cells, hypoxia, hypovolemia, gastrointestinal hemorrhage, infection, and constipation.1,9,10 Gastrointestinal clinical abnormalities in animals with PSS include anorexia, vomiting, and diarrhea. Some dogs have no apparent clinical signs or are presented only with signs of cystitis or urinary tract obstruction. Seizures and hypersalivation are the most common clinical sign in cats, and some have unusual copper colored irises.7,8
The most common abnormality found on hemograms of animals with PSS is microcytosis.1,11 Up to half of dogs with congenital PSS have prolonged PTTs;12 however, this does not usually result in clinically significant hemorrhage. Biochemical abnormalities in dogs with PSS include decreases in blood urea nitrogen, protein, albumin, glucose, and cholesterol; and increases in serum alanine aminotransferase and alkaline phosphatase.1 An increase in alkaline phosphatase is most likely from bone growth, since cholestasis is not usually a problem in animals with PSS. Cats with PSS often have increased liver enzymes but may have normal albumin and cholesterol concentrations.7,8 Urine abnormalities may include low urine specific gravity and ammonium biurate crystalluria, and inflammatory urine sediment in animals with cystitis or urolithiasis.
Animals with portosystemic shunting will have decreased protein C activity and increases in fasting and 2-hour postprandial bile acids and in ammonia after an ammonia challenge (ammonia tolerance test). These tests are not specific for shunting, since they can occur with many liver diseases.
Hepatic histologic changes in animals with PSS include generalized congestion of central veins and sinusoids, lobular collapse, bile duct proliferation, hypoplasia of intrahepatic portal tributaries, proliferation of small vessels and lymphatics, diffuse fatty infiltration, hepatocellular atrophy, and cytoplasmic vacuolization.1,11,13 These pathologic changes are often termed “hepatic microvascular dysplasia” and can also be seen in dogs with congenital portal vein hypoplasia (without macroscopic shunting) or noncirrhotic portal hypertension. Pathologic changes may be present in the central nervous system, especially in encephalopathic animals with shunts.
On plain radiographs, microhepatica and renomegaly may be present. Urate calculi normally are radiolucent but occasionally will be seen in the renal pelvis, ureter, or bladder on survey films when combined with struvite or other radioopaque material. Portosystemic shunts may be definitive diagnosed with angiography, ultrasonography, scintigraphy, computed tomography, or magnetic resonance angiography.1 Mesenteric portography provides excellent visualization of the portal system but usually requires an abdominal incision. Water-soluble,sterile, iodinated contrast medium is injected into a catheterized jejunal or splenic vein (Figure 21-12), and one or more radiographs are taken during completion of the injection. Sensitivity of the test is greatest when performed with the animal in left lateral recumbancy.14
Single congenital portosystemic shunts must be differentiated from multiple acquired shunts secondary to portal hypertension, and from congenital portal vein hypoplasia (PVH); previously known as hepatic microvascular dysplasia or MVD). Congenital portal hypoplasia signifies a disorganization of the liver’s microscopic architecture that is similar to that of dogs with single congenital shunts.11,13 Congenital portal hypoplasia has been reported primarily in small breed dogs such as the Yorkshire terrier, Cairn terrier, Maltese, Cocker spaniel, and papillon. Dogs with PVH display biochemical, hematologic, and clinical changes consistent with portosystemic shunting but lack a macroscopic portosystemic shunt. Therefore, in dogs with PVH, portograms and scintigrams are normal. Signs of PVH are managed with a protein restricted diet. Lactulose is added if clinical signs are not controlled with diet alone. Some clinicians may administer nutriceuticals (milk thistle, denosyl) to improve hepatic function.
Medical Management of PSS
Medical management of animals with PSS includes correction of fluid, electrolyte, and glucose imbalances and prevention of hepatic encephalopathy by controlling precipitating factors.1 Dietary protein is restricted (protein content 18-22% in dogs; 30-35% in cats) to reduce substrates for ammonia formation by colonic bacteria, and any sources of gastrointestinal bleeding must be treated. Antibiotics that are effective against urease producing bacteria, such as neomycin or metronidazole, can be administered to decrease intestinal bacterial populations. Enemas and cathartics may be used to reduce colonic bacteria and substrates and are especially important in animals with hepatic encephalopathy. Lactulose is administered to reduce ammonia absorption and production. Cystitis is treated with an appropriate antibiotic based on urine culture and sensitivity; response may be poor if uroliths are present. Urate uroliths may respond to low protein diets; renal calculi have reportedly dissolved after shunt ligation.
With proper medical management, weight and quality of life stabilize or improve with treatment in most animals. In one study,15 one third of dogs did well with medical management as the sole method of treatment, with many living to 7 years of age or older. Duration of survival with medical management alone was correlated to age at initial onset of clinical signs and with BUN concentration: dogs with extrahepatic PSS that were older at presentation or had a higher BUN lived longer. Over half of dogs treated with medical management alone were euthanized, usually within 10 months of diagnosis, because of uncontrollable neurologic signs and, in some cases, progressive hepatic fibrosis and subsequent portal hypertension.15 In another study16 long term survival rate was 88% for dogs that underwent surgical treatment and 51% for dogs that were managed medically. In that study, age was not correlated with length of survival.16 To the author’s knowledge, no studies have evaluated survival of cats treated with only medical management. Of 4 cats managed medically by the author, 3 died or were euthanized less than 3 years after diagnosis because of neurologic disease or recurrent urinary tract obstruction. For animals with congenital PSS, particularly those that are symptomatic, surgery is considered the treatment of choice; however, surgery should be delayed until the animals are clinically stable.
Most patients are premedicated with an opioid and a sedative. Low dose acepromazine (0.1 to 0.25 mg total dose) can be used for sedation before or after surgery since it does not increase the risk of seizures in these patients.1 Animals can be induced with intravenous propofol or by mask induction with isoflurane or sevoflurane in oxygen.
Definitive diagnosis of extrahepatic PSS can usually be made during exploratory laparotomy if the veterinarian is thoroughly familiar with the vascular anatomy of the abdomen.17,18 In a normal dog, there are no large vessels entering the caudal vena cava between the renal and hepatic veins. Many extrahepatic PSS terminate on the caudal vena cava cranial to the renal veins at the level of the epiploic foramen. The caudal vena cava will appear dilated and contain turbulent flow at the level of the shunt terminus. Portocaval shunts entering near the epiploic foramen may be difficult to see if the terminus of the PSS is obscured by an overlying artery, liver lobe, or the pancreas. Occasionally, portocaval shunts will traverse along the lesser curvature of the stomach and the ventral surface of the distal esophagus before joining the left phrenic vein. Portoazygos shunts traverse the diaphragm at the level of the crura or aortic hiatus and are obscured by overlying viscera.17 To improve detection of and access to these shunts, it may be necessary to open the omental bursa (Figure 21-13) by tearing a hole in the superficial, ventral leaf of the greater omentum and retracting the stomach cranially and intestines caudally. Any vein of significant size that visibly penetrates the diaphragm at its lumbar attachments is likely to be a portoazygos shunt. Shunts that traverse the diaphragm through the esophageal hiatus may be easier to approach outside of the omental bursa by retracting the liver and stomach to the dog’s right so that the cardia and esophagus are visible. Thorough exploration is warranted in all dogs with single congenital PSS because of the possibility, though rare, of a second shunt.
Intrahepatic PSS are more difficult to detect and treat. Experienced surgeons will note enlargement of the portal vein branch to, or hepatic vein draining, the lobe containing the shunt.18 The liver lobe containing the intrahepatic shunt may have a visible, aneurysmal dilation of the shunt near the diaphragmatic surface of the parenchyma or may be palpably softer than the other lobes. When the shunt is a patent ductus venosus, it can occasionally be seen as it traverses between the left lateral and medial lobes. Because intrahepatic shunts are difficult to find and treat, preoperative dual phase contrast computed tomography is recommended in all large breed dogs and any other dog in which an intrahepatic shunt is suspected. Intrahepatic shunts can be occluded with interventional techniques (placement of a caval stent, followed by coils within the shunt); facilities that perform this procedure will utilize fluoroscopic and computed tomographic imaging as part of their diagnostic and therapeutic planning.
When a shunt is not found, the surgeon should obtain a liver biopsy to rule out other hepatic diseases such as PVH and perform intraoperative mesenteric or splenic portography to definitively rule out a PSS.
Porsostystemic Shunt Occlusion
Once the PSS is identified and presence of a prehepatic portal vein is verified, shunt occlusion can be attempted. It is critical to attenuate the shunt as close to its insertion site as possible so that all tributaries of the shunt are upstream from the occlusion. Portocaval shunts should be occluded at their terminus on the caudal vena cava. Portoazygos shunts can be occluded on the abdominal side of the diaphragm. Thorough examination is warranted before ligature placement as portoazygos and portophrenic shunts frequently have small branches from gastric veins that enter the PSS just before it traverses the diaphragm. The diaphragm may be opened if more exposure is needed.
Shunts can be occluded with suture or constricting devices. Most surgeons prefer to use devices that result in gradual occlusion of the shunt (e.g. ameroid constrictors or cellophane bands) or that are less invasive than open abdominal surgery (e.g., coiling of intrahepatic shunts). Suture attenuation is occasionally necessary when occlusive devices are not available. It is critical for veterinarians undertaking shunt ligation to understand that over half of animals with congenital shunts will die if the shunt is acutely ligated; therefore, partial ligation is necessary in most animals that undergo suture attenuation. If suture is to be used to ligate the shunt, then a small opening is made through the fascia around the shunt by dissecting adjacent to the PSS at its terminus. Silk suture (2-0) is frequently used in dogs because of ease of handling and knot security; however, a nonabsorbable monofilament suture is recommended in cats. The shunt should be temporarily occluded for 5 to 10 minutes while the surgeon evaluates the viscera for evidence of portal hypertension, including pallor or cyanosis of the intestines, increased intestinal peristalsis, cyanosis or edema of the pancreas, and increased mesenteric vascular pulsations.19 Additionally, the surgeon can measure portal and central venous pressures.18,20 To measure portal pressure, a catheter is placed directly into a jejunal vein or through the splenic parenchyma and into a splenic vein (See Figure 21-13).21 The catheter is secured in place with gut suture and is attached to an extension set, 3-way stopcock, and syringe. A water manometer is attached to the 3-way stopcock, which is rested on the inguinal region of the patient to provide consistent readings during portal pressure measurements.
Recommendations for postligation pressures are to limit the maximum portal pressure to 17 to 24 cm H2O, maximal change in portal pressure to 9 to 10 cm H2O, and maximal decrease in central venous pressure to 1 cm H2O.1,17,18,20 Partial ligation should be performed if evidence of portal hypertension is noticed during surgery. Objective pressure measurements should not be used as the sole criteria for degree of shunt attenuation, since blood pressures can vary with depth of anesthesia, hydration status, phase of respiration, degree of splanchnic compliance, and other systemic factors. To perform partial ligation, choose a cylinder (a piece of tubing, steel pin, or rod) that is the approximate diameter that you wish to achieve during shunt occlusion.22 Place the cylinder next to the shunt and wrap the ligature around the shunt and the cylinder. Tie the ligature and remove the cylinder, then recheck portal pressures and evaluate the color of the viscera.
Abrupt occlusion and partial ligation of PSS have been associated with serious postoperative complications, including perioperative death in 14 to 22%, seizures in 7.5 to 11%, recurrence of clinical signs in 40 to 41%, and development of multiple PSS in 7%.1,17,22,23 Therefore, many surgeons prefer gradual, complete shunt ligation with devices such as ameroid constrictors, cellophane bands, or hydraulic occluders.1,24-27 An ameroid constrictor (Research Instruments N.W., INC, Lebanon Oregon, 97355; researchinstrumentsnw.com) is an inner ring of casein that is surrounded by a stainless steel sheath. Casein is a hygroscopic substance that swells as it slowly absorbs body fluid; the stainless steel sheath forces the casein to swell inwardly, partially compressing the shunt. Ameroid constrictors cause shunt occlusion over 2-3 weeks by direct pressure and by stimulation of a fibrous tissue reaction. Ameroid constrictors are gas sterilized and therefore should not be used until 12 to 24 hours after sterilization to allow residual ethylene oxide to be released from the casein.
Ameroid constrictors with a 5 mm internal diameter are most frequently used for extrahepatic PSS ligation. The choice of ameroid constrictor size for PSS occlusion is based on shunt diameter; therefore, the surgeon should have a selection of sizes available at each surgery. To avoid postoperative portal hypertension, choose a constrictor that does not compress the shunt vessel during initial placement.1,17 In case where larger constrictors are not available, portal pressures can be measured during partial shunt occlusion and viscera can be evaluated subjectively for signs of portal hypertension to determine whether a smaller constrictor could be used.
Before constrictor placement, the “key”, a small column of stainless steel that completes the constrictor ring, is removed from the ameroid constrictor and set aside. The ameroid constrictor is held securely by a pair of Allis tissue forceps, which prevent rotation of the casein inside of the stainless steel ring. Dissection of the supporting fascia around the PSS should be kept to a minimum when placing an ameroid constrictor to prevent postoperative movement of the ring and acute obstruction of the shunt (Figure 21-14). Once an opening has been made through the fascia around the PSS, the shunt is flattened by elevating it with open right angle forceps or two silk sutures. The constrictor ring is slipped over the shunt and, with a hemostat, the key is replaced within the constrictor to complete the circle (Figure 21-15). Anti-inflammatory doses of steroids should not be administered for 1 month after ameroid constrictor placement since they reduce the amount of tissue reaction and may prevent shunt closure. Complication and mortality rates after ameroid constrictor occlusion of extrahepatic PSS were 10% and 7%, respectively, in one study.25 Excellent outcomes were seen in 80% to 85% of patients, although persistent shunting on scintigraphy was seen on recheck scintigraphy in 17 to 21% of animals in earlier studies.1,17,24,25 Causes of persistent shunting include development of multiple acquired shunts, presence of a second shunt, inadequate fibrosis of the original shunt, or inappropriate location of the constrictor. Multiple acquired shunts are less common when shunt diameter is smaller than the constrictor ring internal diameter at the time of surgical placement.
Gas sterilized strips of cellophane have been used to provide partial occlusion of shunts in dogs.26 Because the strips are flexible, they are easier to place around intrahepatic shunts than ameroid constrictors. The strips are wrapped once around the shunt and an adjacent stainless steel pin, and the ends of the band are held together with 4 alternating 11.5 mm surgical clips. Portal pressures are measured for several minutes after banding, and the viscera are evaluated for subjective signs of portal hypertension. Originally, animals required placement of bands with a final internal diameter of < 3 mm in diameter in animals to induce complete shunt closure.26 In more recent studies, however, PSS closure occurred after bands were placed without intraoperative shunt attenuation.27 Inflammation caused by the cellophane results in complete occlusion of most shunts in dogs in less than 4 to 6 weeks.24,26 Mortality rates are 6% to 9% after cellophane banding, and persistent hepatic dysfunction was evident on bloodwork in 16% of animals.26,27
Hydraulic occluders have been used for gradual extravascular occlusion of intrahepatic portosystemic shunts.24,28 The silicone and polyester cuff of the occluder is placed around the shunt, and the attached access port is inserted under the skin. The cuff is gradually inflated postoperatively by intermittent injections of a solution into the subcutaneous port until the shunt is closed.
Blood flow through intrahepatic PSS may be reduced by occluding the portal vein branches leading to, or hepatic veins draining, the shunt using the above described extravascular techniques.1,18 Alternatively, the shunt can be approached intravascularly during inflow occlusion. Most surgeons prefer minimally invasive extravascular techniques when possible to reduce the risk of complications.
Minimally invasive techniques for shunt occlusion are showing great promise for treatment of intrahepatic PSS. Thrombogenic coils have been placed via catheter access into the shunt to gradually obstruct PSS.24,29,30 Coil migration is prevented by placement of a caval wall stent.24 Under fluoroscopic guidance, a catheter is inserted through the mesh wall of the stent and into the shunt, and coils are placed via the catheter until portal pressure increases. Initially, complication rates were high with this technique; however, complication rates have been reduced to < 5% since initiating lifelong antacid therapy in dogs undergoing this procedure.29
After surgery, animals are monitored closely for seizures, hypothermia, hypoglycemia, and signs of portal hypertension, including shock, pain, and abdominal distension.1,9 Most animals will need analgesics; opioids are used most frequently. Carprofen and meloxicam have been used safely in dogs with extrahepatic shunts but, in rare instances, may precipitate gastrointestinal ulcerations. Antacid therapy is recommended in all dogs with intrahepatic shunts. Sedation with a low dose (0.1 to 0.25 mg total dose) of acepromazine or dexmedetomidine 1-3 mcg/kg IV may be necessary if dogs are vocalizing or abdominal pressing, since these activities will increase portal pressure. Dogs with ameroid constrictor occlusion usually experience minimal discomfort.
A protein restricted diet and lactulose are continued after surgery until liver function improves. Frequently the animals can be gradually weaned off of the lactulose 4 to 6 weeks after the surgery. Bile acids and albumin are evaluated 3, 6, and 12 months after the surgery or until liver function is improved. Protein in the diet can be gradually increased once bile acids are improved. In dogs with mildly elevated bile acids and normal albumin, it may be necessary to monitor clinical response to diet change to determine whether dietary protein content can be gradually increased, since many dogs with PSS also have PVH and, therefore, will always have mildly increased bile acids.
Treatment of postoperative portal hypertension includes intravenous fluid administration for hypovolemic shock, systemic antibiotics, and immediate surgery to remove the constrictor or ligature.1,9 Factors that may increase portal pressure postoperatively include excessive intraoperative fluid administration, increased systemic blood pressure from anesthetic recovery, and increased intra-abdominal pressure from bandages, pain, or vocalization.
Between 0 and 18% of small breed dogs develop seizures after shunt ligation.1,25,26,30,31,32 The etiology is unknown, and affected animals usually do not respond to fluids, dextrose, or enemas. Seizures are treated with an IV bolus of diazepam to effect or propofol to induce anesthesia and blood glucose is measured and corrected if low. The patient is started on intravenous levetiracetam and switched to an oral form once the animal is able to swallow. If the animal continues to seizure, the animal is placed on a continuous intravenous infusion of propofol to maintain light anesthesia and treated with IV mannitol and phenobarbital. Levetiracetam is continued, and intensive nursing care is provided. Propofol is discontinued after 12 hours; sedation with dexmedetomidine or acepromazine may be required during propofol recovery. If seizures occur after anesthetic recovery, the CRI is reinstated for another 12 hours. Prognosis is poor for animals with postoperative seizures, and those that survive usually continue to have neurologic problems.
Animals with persistently elevated bile acids should be re-evaluated by ultrasound, scintigraphy, or portography. Persistent shunting is usually from development of multiple acquired shunts but can occur with lack of closure of the shunt within the constricting device, or because of presence of a second shunt. If no shunting is detected, a liver biopsy is performed to determine the underlying pathology.
The prognosis for successful surgical treatment is best for dogs with extrahepatic shunts, for animals that undergo complete suture ligation or gradual occlusion with ameroid constrictors or cellophane bands, and for those animals that are presented with urinary tract signs and no hepatic encephalopathy.1,25,33-35 Mortality rates after surgery are higher in animals with low albumin, high white blood cell counts, seizures, or intrahepatic shunts and in those that undergo acute partial shunt ligation.1,25,26
Half of dogs that undergo partial shunt ligation with suture develop clinical signs of portosystemic shunting within 2 years after ligation.34 Some of these animals will respond to further ligation, while others have developed multiple acquired shunts or cannot tolerate further PSS occlusion. Clinical signs in these patients are controlled with lactulose and a protein restricted diet.
Cats commonly develop neurologic signs after surgery and may require continued treatment with phenobarbital. The prognosis is variable depending on the severity of preoperative clinical signs. After ameroid constrictor placement, acute complications occur in 25% to 75% of cats and excellent long term outcome is seen in 33% to 77%.7,8 The mortality rate was 20% and recurrence of hepatic encephalopathy was noted in 30% to 40% of cats after acute suture ligation.22
- Berent A, Tobias KM: Hepatic Vascular Anomalies. In Tobias KM, Johnston S: Veterinary Surgery: Small Animal. St. Louis IL, Elsevier, 2011, pp1624-1658.
- Hunt GB, Bellenger CR, Borg R, et al. Congenital interruption of the portal vein and caudal vena cava in dogs: six case reports and a review of the literature. Vet Surg 1998;3:203-215.
- Tobias KM, Rohrbach BW. Proportional Diagnosis of Congenital Portosystemic Shunts in Dogs Accessed by Veterinary Teaching Hospitals: 1980-2002. J Am Vet Med Assoc 2003;223:1636-1639.
- Tobias KM. Determination of heredity of single congenital portosystemic shunts in Yorkshire terriers. J Am Anim Hosp Assoc 2003;39:385- 389.
- van Straten G, Leegwater PAJ, de Vries M, et al. Inherited congenital extrahepatic portosystemic shunts in Cairn terriers. J Vet Intern Med 2005;19:321-324.
- Ubbink GJ, van de Broek J, Meyer HP, et al. Prediction of inherited portosystemic shunts in Irish Wolfhounds on the basis of pedigree analysis. Am J Vet Res 1998;59:1553-1556.
- Lipscomb VJ, Jones HJ, Brockman DJ: Complications and long-term outcomes of the ligation of congenital portosystemic shunts in 49 cats. Vet Rec 2007;160:465-470.
- Kyles AE, Hardie EM, Mehl M, et al. Evaluation of ameroid ring constrictors for the management of single extrahepatic portosystemic shunts in cats: 23 cases (1996-2001). J Am Vet Med Assoc 2002;220:1341-1347.
- Holt D. Critical care management of the portosystemic shunt patient. Compend Contin Educ Pract Vet 1994;16:879...892.
- Maddison JE. Hepatic encephalopathy. Current concepts of the pathogenesis. J Vet Int Med 1992 ;6:341-353.
- Allen L, Stobie D, Mauldlin, et al. Clinicopathologic features of dogs with hepatic microvascular dysplasia with and without portosystemic shunts; 42 cases (1991-1996). J Am Vet Med Assoc 1999;214:218-220.
- Niles JD, Williams JM, Cripps PJ. Hemostatic profiles in 39 dogs with congenital portosystemic shunts. 2001;30:97-104.
- Phillips L, Tappe J, Lyman R, et al. Hepatic microvascular dysplasia in dogs. Progr Vet Neurol 1996;3:88-96.
- Scrivani PV, Yeager AE, Dykes NL, et al. Influence of patient positioning on sensitivity of mesenteric portography for detecting an anomalous portosystemic blood vessel in dogs: 34 cases (1997-2000). J Am Vet Med Assoc 2001;219:1251-1253.
- Watson PJ, ME Herrtage. Medical management of congenital portosystemic shunts in 27 dogs–a retrospective study. J Small Anim Pract 1998;39:62-68.
- Greenhalgh SN, Dunning MD, McKinley TJ, et al: Comparison of survival after surgical or medical treatment in dogs with a congenital portosystemic shunt. J Am Vet Med Assoc 236:1215, 2010.
- Tobias KMS, Seguin B, Johnston G. Surgical approaches to single extrahepatic portosystemic shunts. Compend Contin Educ Pract Vet 1998;20:593-601.
- Tobias KMS, Rawlings CA. Surgical techniques for extravascular occlusion of intrahepatic shunts. Compend Contin Educ Pract Vet 1996;18:745-755.
- Mathew K, Grofton N. Congenital extrahepatic portosystemic shunt occlusion in the dog: gross observation during surgical correction. J Am Anim Hosp Assoc 1988;24:387-394.
- Swalec KM, Smeak DD. Partial versus complete attenuation of single portosystemic shunts. Vet Surg 1990;19:406-411.
- Schulz KS, Martin RA, Henderson RA. Transplenic portal catheterization. Surgical technique and use in two dogs with portosystemic shunts. Vet Surg 1993;22:363-369.
- Wolscrijn CF, Mahapokai W, Rothuizen J, et al. Gauged attenuation of congenital portosystemic shunts: Results in 160 dogs and 15 cats. Vet Quart 2000;22:94-98.
- Kummeling A, van Sluijs FJ, Rothuizen J. Prognostic implications of the degree of shunt narrowing and of the portal vein diameter in dogs with congenital portosystemic shunts. Vet Surg 2004;33:17-24.
- Sereda CW, Adin CA. Methods of gradual vascular occlusion and their applications in treatment of congenital portosystemic shunts in dogs: a review. Vet Surg 2005;34:83-91.
- Mehl ML, Kyles AE, Hardie EM, et al. Evaluation of ameroid ring constrictors for treatment for single extrahepatic portosystemic shunts in dogs: 168 cases (1995-2001).
- Hunt GB, Kummeling A, Tisdall PLC, et al. Outcomes of cellophane banding for congenital portosystemic shunts in 106 dogs and 5 cats. Vet Surg 2004;33:25-31.
- Frankel D, Seim H, MacPhail C, et al. Evaluation of cellophane banding with and without intraoperative attenuation for treatment of congenital extraheptaic portosystemic shunts in dogs. J Am Vet med Assoc 2006;228:1355-1360.
- Adin CA, Sereda CW, Thompson MS, et al. Outcome associated with use of a percutaneously controlled hydraulic occluder for treatment of dogs with intrahepatic portosystemic shunts. J Am Vet Med Assoc 2006;229:1749-1755.
- Weisse C, Berent AC, Todd K, et al. Endovascular evaluation and treatment of intrahepatic portosystemic shunts in dogs: 100 cases (2001-2011). J Am Vet Med Assoc 2014;244:78-94.
- Fryer KJ, Levine JM, Peycke LE, et al: Incidence of postoperative seizures with and without levetiracetam pretreatment in dogs undergoing portosystemic shutn attenuation. J Vet Intern Med.
- Tisdall PLC, Hunt GB, Youmans KR, et al. Neurological dysfunction in dogs following attenuation of congenital extrahepatic portosystemic shunts. J Small Anim Pract 2000;41:539-546.
- Heldmann E, Holt DE, Brockman DJ, et al. Use of propofol to manage seizure activity after surgical treatment of portosystemic shunts. J Small Anim Pract 1999;40:590-594.
- Harvey J, Erb HN. Complete ligation of extrahepatic congenital portosystemic shunts in nonencephalopathic dogs. Vet Surg 1998;27:413-416.
- Hottinger HA, Walshaw R. Long-term results of complete and partial ligation of congenital portosystemic shunts in dogs. Vet Surg 1995;24:331-336.
- Murphy ST, Ellison GW, Long M, et al. A comparison of the ameroid constrictor versus ligation in the surgical management of single extra-hepatic portosystemic shunts. J Am Anim Hosp Assoc 2001;37:390-396.
Cellophane Banding of Portosystemic Shunts
Geraldine B. Hunt
Most congenital portosystemic shunts cannot be completely ligated at the time of surgery because of the risk of inducing life-threatening portal hypertension. Placement of devices to produce gradual progressive occlusion is now considered by most surgeons to be the treatment of choice. A variety of methods of gradual occlusion have been evaluated clinically and experimentally, including cellophane bands,1-3 ameroid constrictors,4-9 thrombogenic coils2,10 and hydraulic occluders.11
Cellophane is a transparent flexible cellulose sheeting widely used in the packaging industry. It creates a foreign body reaction when implanted into the body of dogs. When placed around a blood vessel, cellophane promotes gradual progressive occlusion of the vessel by direct pressure of the developing fibrous tissue. Cellophane has been used for vessel occlusion in experimental animals for many years12 and had a role in human surgery at one stage, as a means of supporting vascular aneurysms and as a non-permeable barrier to discourage adhesions around joints.13 Cellophane was first reported for attenuation of a congenital portosystemic shunt in a dog in 199014 and its use has been reported subsequently in larger case series.1,3 Studies by Youmans and Hunt showed progressive reduction in diameter of the femoral vein from 5 mm to 2 mm in dogs after application of cellophane bands.2 For this reason, cellophane band diameters of no more than 3 mm are usually applied to the target vessel. However, a previous report,15 anecdotal observations and the author’s own experiences indicate that larger bands are capable of promoting complete vessel occlusion in some animals.
Cellophane is acquired in sheet form from a stationer or paper company. It should be strong enough to withstand handling, but not sufficiently thick to cause kinking of the fragile shunt vessel. Recent work has shown that the clear films reported for portosystemic shunt attenuation are not always cellophane.18 Nevertheless, polypropylene and polyethylene have yielded similar results, possibly due to the irritant effect of chemicals used during processing. Prior to implantation, the surgeon should check which particular clear film they are using. Cellophane strips should be cut parallel to the fiber orientation to preserve its breaking strength. Cellophane should be sterilized by autoclave, as this best preserves its strength once the band becomes wet with saline or body fluids. The best method of sterilization for synthetic polymers has yet to be determined. Gauging devices of various diameters are fashioned from surgical pins or connecting bars, bent at right angles and with their ends filed to a blunt tip if necessary. In most cases, a range between 2 mm and 1 cm is satisfactory. Medium-sized titanium surgical ligating clips are used to secure the cellophane band around the shunt. A water manometer is used to monitor changes in portal pressure during cellophane application in dogs weighing more than 10 kg. Right angled dissecting forceps (Debakey bile duct forceps) and Adson tissue foceps assist mobilization of the shunt and passage of materials around it.
Surgery is performed through a ventral midline celiotomy incision. The incision extends ventral to the xiphoid process of the sternum and the linea alba is divided to expose the xiphoid at the level of its cranial connection to the pectoral muscles. Care is taken when dividing the falciform ligament as shunts have occasionally been encountered in this location.
Initially, the abdominal viscera is retracted to the right using the mesocolon and the paravertebral gutter and left kidney are examined to rule out the presence of multiple acquired shunts that result from portal hypertension. The crura of the diaphragm is examined to determine whether a portoazygous shunt is present.
The abdominal viscera is then retracted to the left using the mesoduodenum and the caudal vena cava examined for the presence of abnormal veins emptying into it. The cava should be visualized from its origin at the confluence of the common iliac veins to the area cranially where it deviates to pass dorsad to the liver. The right and left renal veins, gonadal veins and phrenicoabdominal veins should be the only vessels entering the caudal vena cava within the cranial abdominal cavity. Any vessel terminating in the vena cava cranial to the phrenicoabdominal veins is abnormal. Dilation and obvious turbulence visualized through the thin wall of the cava may be indicative of an abnormal vessel. However, turbulence can occur as a normal finding at the point of entry of the renal veins in some animals. The caudal vena cava should be inspected as it crosses the liver to ensure that it does not continue forward as the azygous vein.
Particular attention is directed to the area of the epiploic foramen. The epiploic foramen is dorsal to the duodenum and is created by the fold of tissue containing the hepatic artery and portal vein ventrally and bounded by the vena cava dorsally. A small, flat-bladed retractor is placed dorsal to the hepatic artery into the foramen and elevated to visualize the left side of the vena cava. Extrahepatic portosystemic shunts are commonly detected entering the vena cava in this location.
The hepatic portal vein should be examined as it courses adjacent and ventral to the hepatic artery to arborize at the porta hepatis of the liver. Portal vein branches can be identified that supply the right lateral, right medial and left liver lobes. Dilation of one of these branches may indicate the presence of an intrahepatic shunt. Dilatation of all portal vessels simultaneously may signify portal hypertension, rather than increased portal flow.
If a shunt has not been identified within the epiploic foramen, the abdominal viscera are returned to their normal position and an opening created in the ventral leaf of the omentum to visualize the omental bursa. The stomach is retracted cranially to inspect the left gastric, splenic and pancreaticoduodenal veins. Dilation of one of these vessels usually indicates the presence of an extrahepatic shunt. Identify the portal branch giving rise to the dilated vessel and follow it to its point of entry into the systemic circulation.
If it is not possible to confidently identify an extrahepatic shunt, consider the likelihood of an intrahepatic shunt, or microvascular dysplasia. If a portoazygous shunt is suspected, the crura of the diaphragm may be divided to allow visualization of the caudal mediastinum.
Once the shunt has been identified, the viscera should be retracted so as to provide maximum access for dissection and attenuation of the vessel. Exposure of the shunt varies according to specific shunt anatomy but in most cases, portocaval shunt
dissection is easiest when performed through the epiploic foramen. For portoazygous shunts, dissection is usually easiest from a left approach with the viscera retracted to the right. Attenuation of any shunt should take place as close as possible to the systemic vascular system so as to ensure that small portal branches do not enter distal to the attenuation point.
Determining Cellophane Band Diameter
The shunt vessel should be dissected free from surrounding fat and connective tissue. A suture of 2-0 or 0 polypropylene is passed around the vessel to facilitate further attenuation at a later date should the cellophane band not promote complete shunt occlusion. Baseline physiologic parameters are measured including heart rate, direct or indirect systolic arterial pressure and central venous pressure. The color of the pancreas and intestines, and intestinal motility are assessed prior to placement of the cellophane band. In dogs heavier than 10 kg, and those with intrahepatic shunts, a jejunal vein is catheterized to permit measurement of portal pressure using a water manometer during band placement and tightening.
The polypropylene suture is tightened so as to occlude the shunt completely and measurement of the previously described physiologic parameters repeated. Elevation of the heart rate by more than 20 beats per minute, a fall in systolic arterial pressure of more than 10 mm Hg, a fall in central venous pressure of more than 1 mm Hg, or a rise in portal pressure of more than 10 cm H20 (to a maximum of 20 cm H20) all signify inability to completely occlude the shunt.
Congestion and cyanosis of the pancreas and intestines, and a substantial increase in intestinal motility are also considered indications of unacceptable portal hypertension.
In animals weighing 10 kg or less, cellophane bands between 2 and 3 mm diameter are usually placed around the shunt. A 3 mm band is placed if the shunt is not amenable to total occlusion. If mild to moderate changes in baseline hemodynamic parameters and intestinal color and motility are observed, a 2.5 mm band is placed. If no change is observed, a 2 mm band is applied. In dogs weighing 10 kg or more, the band diameter is dictated by changes in portal pressure, as for other forms of attenuation. Cellophane bands between 2 and 3 mm diameter result in substantial shunt attenuation, however, life-threatening portal hypertension necessitating removal of the cellophane band has only been seen in one small dog (a Bichon Frise in which a small thrombus embolized to the attenuation site 3 days after surgery). Wider cellophane bands may also cause complete eventual occlusion, but this has not been proven in an experimental setting.
Preparation and Placement of the Cellophane Band
Following identification and mobilization of the shunt, a strip of cellophane 1.2 cm wide and about 15 cm long is folded lengthwise to produce a 3-layered band 4 mm in width and 15 cm in length. The end of the cellophane is cut obliquely to facilitate passage around the shunt.
The cellophane band is passed gently around the shunt, incorporating as little perivascular tissue as possible (Figure 21-16A). The cellophane is easily torn when wet, so manipulation of the band should be minimized once it is in place around the vessel.
The surgeon should hold both ends of the band between thumb and forefinger and insert a stainless steel pin of appropriate diameter inside the band, next to the shunt vessel (Figure 21-16B). Hemostatic clips are then applied while the cellophane band is held tight around both the pin and the shunt (Figure 21-16C). Recent work has shown that the resistance to tensile forces of the clip-cellophane configuration increases when multiple clips are alternately applied from opposing directions.19 In practice, the forces applied to the cellophane band following implantation are low, and placement of two clips with opposing orientations should be sufficient. This results in creation of a cellophane band of the required diameter. The stainless steel pin is withdrawn, allowing the shunt to expand inside the cellophane band to the predetermined diameter (Figure 21-16D). One of the original research studies4 showed that the diameter tended not to decrease by more than 3 mm following cellophane band application, and hence it is recommended that this diameter not be exceeded in smaller patients. However, other researchers6 have shown that placement of loose bands that do not constrict the shunt may be preferable in larger patients. It should be noted, however, that the clear film used in these other reports was not cellophane, and may therefore behave differently to cellophane in clinical patients.
Haemodynamic measurements are repeated and the intestine and pancreas inspected to ensure that safe portal pressures have not been exceeded. The ends of the cellophane are cut, so as to leave 1 mm protruding beyond the surgical clip. The cellophane band is gently rotated to ensure it does not kink the shunt or adjacent vessels. The polypropylene suture is tied loosely and cut to leave 4 cm ends. This enables identification of the shunt if subsequent surgery is required due to persistent signs of hepatic dysfunction or portosystemic shunting. The polypropylene suture may be pulled tight during later surgery to check whether the original shunt is closed or patent, thus avoiding the necessity of dissecting through fibrous tissue. The polypropylene suture may be tightened if necessary without having to disturb the shunt itself. The need for a second surgery is rare following cellophane banding of portosystemic shunts.
The abdomen is lavaged with warm saline and the celiotomy wound closed routinely. Animals are monitored intensively for the first 72 hours after surgery, which is considered the high risk period for seizures and portal hypertension. A broad spectrum antibiotic is administered perioperatively. Phenobarbital is given as a premedication 30 minutes before surgery (10 mg/kg intramuscularly) and continued for 72 hours postoperatively (2 to 5 mg/ kg twice daily by injection or per os). If the animal experienced generalized motor seizures before surgery, phenobarbital is continued for approximately four weeks postoperatively and the dose then tapered. Animals are maintained on a commercially available restricted protein diet (Hills L/D) for the first 4 weeks after surgery. No other medical management is used unless animals show signs of hepatic encephalopathy (rare). If the patient is clinically normal four weeks after surgery, the owners are instructed to gradually return them to the original diet they were eating before they experienced clinical signs. If the patient shows signs of hepatic encephalopathy, medical management with restricted protein diet, lactulose syrup (0.5 ml/kg twice daily) and antibiotics is resumed. Analysis of liver function using ammonia tolerance testing, serum bile acid determination or scintigraphy is recommended two months after surgical attenuation of the shunt. Follow up of patients demonstrating continued liver dysfunction should include some form of imaging (ideally contrast-enhanced computer tomography) to differentiate the cause of persistent shunting and determine the best management plan.
Results of cellophane banding have been reported by several authors.5-8 The mortality rate is up to 5.5%, largely resulting from portal hypertension and post ligation neurological dysfunction. Liver function returned to normal postoperatively in 85% of dogs and 60% of cats. Reasons for continued liver dysfunction include failure of the shunt to close, inappropriate placement of the cellophane band, and development of acquired shunts.7,9 This was similar to reported results for a series of 127 dogs that underwent placement of ameroid constrictors in dogs7 and cats.10,11 The survival rate and resolution of hepatic dysfunction were lower in dogs with intrahepatic shunts versus those with extrahepatic shunts. Follow up of an additional 33 dogs subsequent to the cases reported above3 confirms the low mortality rate (1 dog, 3%). This dog (a Bichon Frise) was the only animal that experienced post ligation neurological disorder and was euthanatized as a result of uncontrollable seizures that commenced 70 hours after shunt attenuation. No instances of life-threatening portal hypertension were encountered. Cellophane banding continues to yield poorer results in cats than in dogs, for reasons that are not entirely clear.8
- Harari J, Lincoln J, Alexander J, et al. Lateral thoracotomy and cellophane banding of a congenital portoazygous shunt in a dog. J Sm Anim Pract 31: 571, 1990.
- Connery NA, McAllister H, Skelly C, Pawson P, Bellenger CR: Cellophane banding of congenital intrahepatic portosystemic shunts in two Irish wolfhounds. Journal of Sm Anim Pract 43: 345-349, 2002.
- Youmans KR, Hunt GB: Cellophane banding for the gradual attenuation of single extrahepatic portosystemic shunts in eleven dogs. Aust Vet J 76: 1998.
- Youmans KR, Hunt GB: Experimental evaluation of four methods of progressive venous attenuation in dogs. Vet Surg 28: 531, 1999.
- Hunt GB, Kummeling A, Tisdall PLC, et al.: Outcomes of cellophane banding for congenital portosystemic shunts in 106 dogs and 5 cats. Vet Surg 33: 25, 2004.
- Frankel D, Seim H, Macphail C, et al: Evaluation of cellophane banding with and without intraoperative attenuation for treatment of congenital extrahepatic portosystemic shunts in dogs. J Am Vet Med Assoc 228: 1355, 2006.
- Landon BP, Abraham LA, Charles JA: Use of transcolonic portal scintigraphy to evaluate efficacy of cellophane banding of congenital extrahepatic shunts in 16 dogs. Aust Vet J 86: 169, 2008.
- Cabassu J, Seim HB III, MacPhail C, et al: Outcomes of cats undergoing surgical attenuation of congenital extrahepatic portosystemic shunts through cellophane banding: 9 cases (2000-2007). J Am Vet Med Assoc 238: 89, 2011.
- Nelson NC, Neslon LL: Anatomy of extrahepatic portosystemic shunts in dogs as determined by computed tomography angiography. Vet Rad Ultrasound, 52, 498, 2011.
- Vogt J, Krahwinkel DJ, Bright RM, et al.: Gradual occlusion of extrahepatic portosystemic shunts in dogs and cats using the ameroid constrictor. Vet Surg 25: 495, 1996.
- Havig M TK: Outcome of ameroid constrictor occlusion of single extrahepatic portosystemic shunts in cats: 12 cases (1993-2000). J Am Vet Med Assoc 220: 337, 2002.
- Kyles AE HE, Mehl M, Gregory CR: Evaluation of ameroid ring constrictors for the management of single extrahepatic portosystemic shunts in cats: 23 cases (1996-2001). J Am Vet Med Assoc 220: 1341, 2002.
- Mehl ML , Kyles AE, Hardie EM, ety al: Evaluation of ameroid ring constrictors for treatment of single extrahepatic portosystemic shunts in dogs: 168 cases (1995-2001). J Amer Vet Med Assoc 226, 2020-2030, 2002.
- Falls EL, Milovancev M, Hunt GB et al: Long term outcome after surgical ameroid ring constrictor placement for treatment of single extrahepatic portosystemic shunts in dogs. Vet Surg 42: 951, 2013.
- Leveille R JS, Birchard SJ: Transvenous coil embolization of portosystemic shunt in dogs. Vet Radiol Ultrasound 44: 32, 2003.
- Sereda CW, Adin CA, Ginn PE, Farese JP: Evaluation of a percutaneously controlled hydraulic occluder in a rat model of gradual venous occlusion. Vet Surg 34: 35, 2005.
- Stone PW MR: A method for experimental production of gradual occlusion of the portal vein. Proc Soc Exp Biol Med 72: 255, 1949.
- Harley GH BL: Cellophane in surgery. Am J Surg 68: 229, 1945.
- Smith RR, Hunt GB, Garcia-Nolen TC, et al: Spectroscopic and mechanical evaluation of thin film commonly used for banding congenital portosystemic shunts in dogs. Vet Surg 42 (4), 478-87, 2013.
- McAlinden AB, Buckley CT, Kirby BM. Biomechanical evaluation of different numbers, sizes, and placement configurations of ligaclips required to secure cellophane bands. Vet Surg 39: 59, 2010.
In general, surgeons prefer to avoid the pancreas, because manipulation may incite inflammation and pancreatitis. The blood supply of the pancreas is intimately connected to that of the duodenum, which makes pancreatic resection technically challenging. However, there are some indications for surgery on the pancreas.1,2 Pancreatic biopsy is used to confirm pancreatic disease. Nodule removal or partial pancreatectomy is used to treat insulinoma, other endocrine tumors, and pancreatic carcinoma. Complete pancreatectomy has been used mainly as a research surgery to create diabetic models, but may be performed in animals with intractable chronic pancreatitis. Acute pancreatitis is not treated surgically, but may require placement of a jejunostomy tube for enteral feeding. The intimate relationship of the pancreatic duct and the bile duct as they enter the duodenum means that inflammation or scarring of pancreatic tissue may compress the bile duct, and stenting or diversion of the biliary tract may be needed in animals with pancreatitis. The pancreas can develop cysts or abscesses, and drainage or resection may be needed to resolve clinical signs related to these fluid accumulations.
The pancreas is a bilobed organ that sits in the angle between the duodenum and the greater curvature of the stomach. The portion of the gland lying along the duodenum is termed the right lobe, while the portion lying adjacent to the stomach is the left lobe. The portion where the two lobes join is the body. The right lobe lies within the duodenal mesentery. The more distal aspect of the right lobe can be separated from the duodenum, but the gland is tightly adherent to the duodenum in the region of the body. The left lobe lies within the dorsal sheet of the greater omentum. Accessory pancreatic tissue may occur in the region of the gall bladder or mesentery in the dog.3
Exocrine secretions from pancreatic tissue are carried by ducts that run along the center of each pancreatic lobe (Figure 21-17).
There is significant anatomic variation between individuals and between species in the number and location of the principal pancreatic ducts that carry pancreatic secretions to the duodenum.1,3 In most dogs, there are two ducts entering the duodenum. The pancreatic duct is in the body of the pancreas and enters the duodenum, along with the bile duct, at the major duodenal papilla. The second duct, the accessory pancreatic duct, is further distal in the right pancreatic lobe and enters the duodenum at the minor duodenal papilla. In most dogs, the accessory pancreatic duct is the larger duct and drains both lobes of the pancreas, while the pancreatic duct is small and only carries a small amount of secretions. Variations include the presence of three ducts (two opening at the minor papilla and one at the major papilla) and completely separate ducts for the right and left lobes. In the cat, the pancreatic duct is the larger duct, joining the bile duct and entering the duodenum at the major duodenal papilla. Eighty percent of cats do not have an accessory pancreatic duct or a minor duodenal papilla. Ferrets are similar to cats, but the accessory pancreatic duct is present more often.4 Pancreatic bladders, which are dilations off the pancreatic duct, have been reported in cats.3
The blood supply to the right lobe of the pancreas comes from the cranial and caudal pancreaticoduodenal arteries, which anastomose in the right lobe (Figure 21-18). The cranial pancreaticoduodenal artery is a branch of the gastroduodenal artery, while the caudal pancreaticoduodenal artery is a branch of the cranial mesenteric artery. The left lobe of the pancreas is supplied by the splenic artery and small branches off the hepatic artery. Venous blood drains to the portal vein through the pancreaticoduodenal veins and the splenic vein. Lymphatic drainage goes to the pancreaticoduodenal, hepatic, jejunal and splenic lymph nodes.3
Pancreatic biopsy is performed to diagnose or confirm pancreatic disease.1,5 Chronic low-grade pancreatitis must be differentiated from other causes of chronic gastrointestinal disease. Chronic pancreatitis may only be apparent microscopically and may be multifocal rather than diffuse, requiring several small biopsies to confirm or deny a diagnosis.6 In animals with macroscopic disease of the pancreas, biopsy is used to differentiate between diseases such as chronic pancreatitis, pancreatic carcinoma, and pythiosis. Leiomyosarcoma of the duodenal wall may invade the pancreas through the shared blood supply.
If the biopsy is being obtained from a grossly normal pancreas, it is usually taken at the distal aspect of the right lobe of the pancreas because of the ease of exposure and low risk of inciting pancreatitis. If the biopsy is obtained laparoscopically, a small piece of tissue is removed using cup biopsy forceps.7 If needed, hemorrhage is controlled with gentle pressure or a piece of Gelfoam. When the biopsy is taken as part of an exploratory laparotomy, an encircling ligature of a monofilament suture is placed around a portion of the distal lobe. The ligature is tightened and the tissue is removed. If multiple small samples of pancreatic tissue are needed, hemostatic clips can be used to occlude the vessels supplying the tissue which is then excised distal to the clip. The mutilobular nature of pancreatic tissue makes this a relatively easy procedure, but small delicate instruments and magnification are helpful when isolating a lobule. The major ducts and vessels should be avoided, thus biopsies are most safely taken at the edges of the gland opposite the duodenum and the stomach. The mesentery or omentum overlying the portion of the pancreas to be biopsied must be incised to expose the tissue.
Partial Pancreatectomy and Nodule Removal
Partial pancreatectomy is most commonly used to treat insulin secreting beta cell tumor (insulinoma), but there is confusion in the veterinary literature over the term partial pancreatectomy.2,8 The term has been used to describe neoplastic nodule removal (enucleation), nodule removal with removal of a border of normal pancreatic tissue, and removal of most of one lobe of the pancreas. The term should probably be reserved for removal of most of one lobe. In general, pancreatic neoplastic nodules should be removed with a border of normal tissue, which is most easily accomplished by removing the nodule and the lobe of the pancreas distal to the nodule. In ferrets, it has been shown that animals with beta-cell tumors treated with partial pancreatectomy survive longer than animals treated with enucleation.8 Enucleation should be reserved for animals with nodules in the body of the pancreas. If the nodule in the body is large or is in a difficult location, it may be preferable to biopsy the nodule using a needle biopsy technique and forego nodule removal in favor of medical therapy (frequent feeding, corticosteroids, diazoxide, octreotide, streptozocin).2,9,10 The risk of pancreatitis is higher when extensive or prolonged dissection of the body is performed.
The technique for partial pancreatectomy differs for the two lobes of the pancreas. For the right lobe, dissection is begun at the distal aspect of the lobe, where the pancreaticoduodenal vessels are most easily visualized. The mesentery is incised and the distal pancreas is grasped. The dissection proceeds towards the pylorus, and care is taken to protect the pancreaticoduodenal vessels. Hemoclips or bipolar cautery are used to control bleeding from small branches of the pancreaticoduodenal vessels entering the pancreas. The pancreas becomes more tightly associated with the duodenum as the dissection proceeds proximally, making isolation of the pancreaticoduodenal vessels more difficult. Blunt dissection using moistened cotton swabs or fine hemostats is used to separate the lobules from the vessels (Figure 21-19). In the dog, the right lobe can only be removed to the level of the accessory pancreatic duct, while in the ferret or the cat, the lobe can be removed to the level of the pancreatic duct. Once the desired portion of the pancreas is dissected free from its attachments, one of several techniques may be used to occlude the ducts. An encircling ligature can be placed around the organ, a stapling device can be used to compress the tissue, or fine hemostats can be used to bluntly remove glandular tissue from the vessels and ducts, which are then individually occluded with vascular clips or ligated. The distal portion of the gland is then removed. Any complete rent in the mesentery created by removal of the gland is directly repaired or is covered with an omental patch.
To gain exposure to the left lobe, the ventral leaf of the omentum is opened. The distal portion of the lobe is grasped and the relationship of the pancreas to the splenic and left gastroepiploic vessels is identified. The pancreatic arteries supplying the distal left lobe are branches off the splenic artery. The venous drainage of the left lobe of the pancreas is through two branches that enter the splenic vein. The various pancreatic vascular branches are occluded with vascular clips or ligated, while preserving the splenic vessels. If there is doubt about the integrity of the splenic vessels, splenectomy is performed. As the dissection proceeds towards the body, the branches of the hepatic artery that supply the pancreas must be ligated. Care is taken to preserve the celiac, left gastric, hepatic and gastroduodenal arteries. Once the vasculature is clipped or ligated, the pancreatic tissue is removed in a similar fashion to the right lobe.
Nodule removal is performed by bluntly dissecting the nodule from the surrounding tissue using cotton swabs or a fine hemostat. Hemorrhage from small vessels may be controlled using pressure or small vascular clips. Care is taken to preserve the major intestinal and pancreatic vessels and ducts. Ideally, a border of normal pancreatic tissue should be removed with the nodule.
If multiple pancreatic nodules are found, it may be necessary to use a combination of techniques to remove the nodules. If no nodules are found, intraoperative ultrasound may aid in identification. In dogs, injection of methylene blue has been used to help identify nodules, but the technique carries the risk of causing acute renal failure and is falling out of favor. Finally, if no nodules can be identified , pancreatic biopsy should be performed to rule out diffuse pancreatic beta cell tumor, a condition that occurs in < 5% of dogs with insulinoma.2
Most animals with insulinoma have microscopic or gross metastatic lesions present at the time of initial diagnosis. Metastasis is seen most commonly in regional lymph nodes and the liver. Since metastases are functional tumors it is important to identify and remove as many of the lesions as possible. It would be ideal if metatstatic lesions were identified before surgery, but surgical exploration is currently the most accurate method for identifying these lesions. Ultrasound, computed tomography and single photon emission computed tomography have all been used to identify primary and metastatic lesions, but no technique is superior to surgery.11 The pancreaticoduodenal, hepatic, jejunal and splenic lymph nodes are carefully examined for enlargement. Precise, careful dissection using fine vascular instruments and magnification is often needed to remove an enlarged lymph node while preserving the vasculature to the intestines. Nodules within the liver can be removed with partial hepatectomy. If removal of the metastatic lesions is likely to endanger the life of the animal, it may be preferable to treat with medical therapy.
Pancreatic tumors other than insulinomas are rare. Endocrine tumors include gastrinomas, glucagonomas and other neuroendocrine cell tumors. Surgical treatment of these tumors is similar to that of insulinoma. Pancreatic carcinomas are often extensive at the time of diagnosis and are highly metastatic. Partial pancreatectomy can provide a period of remission from clinical signs if the primary tumor is localized to one lobe.12
Complete pancreatectomy is a formidable procedure and is rarely indicated. Removal of the entire pancreas produces an animal that is diabetic and has pancreatic exocrine insufficiency. Management of these patients requires an intelligent, dedicated owner, who can follow a detailed feeding, medication and glucose monitoring regime. The technique is similar to the technique for partial pancreatectomy, except that the dissection is carried around the body of the pancreas. The dissection is most commonly performed from the left to the right side. The pancreatic branches from the hepatic and gastroduodenal arteries are ligated. Blunt dissection is used to expose and preserve the pancreaticoduodenal vessels and the branches entering the pancreas are clipped or ligated. The pancreatic ducts are transected without ligation. After removal of the pancreas, the rent in the duodenal mesentery is closed.
Surgical Treatment of Pancreatitis
A recent consensus conference on the treatment of acute pancreatitis in people confirmed that surgical treatment of acute pancreatitis is not indicated unless confirmed bacterial abscess formation is present.13 Studies in dogs have shown that animals treated with early enteral feeding rather than intravenous feeding during pancreatitis have reduced plasma endotoxin levels, decreased bacterial translocation to the portal and systemic blood, and improved measures of bowel wall health.14 Jejunal feeding tubes can be placed during celiotomy or using minimally invasive surgery techniques. Acute pancreatitis can also lead to obstruction of the bile duct secondary to inflammation. Temporary choledochal stenting (See Hepatobiliary Surgery) is used to maintain biliary tract patency.15 Animals with chronic pancreatitis can have obstruction of the bile duct secondary to scar formation and may need to be treated with a biliary diversion procedure.
Surgical Treatment of Pancreatic Cysts and Abscesses
Cystic fluid accumulations and abscesses can occur in pancreatic tissue, mainly in association with pancreatitis. Sterile abscesses may be the result of tissue necrosis. When a pancreatic fluid accumulation is observed on ultrasonic examination, needle aspiration is used to identify the fluid and may also be used to drain the accumulation. Cysts and sterile abscesses are not usually treated surgically, unless they are causing obstruction. Infected abscesses require surgical debridement and drainage.
The pancreatic region is carefully explored and the fluid accumulation is located. The wall of the cyst or abscess is removed. The region is flushed and debrided, if indicated. If available, omentum can be placed in the cavity to aid in drainage.16 A silicone closed suction wound drain or a sump drain is placed to further drain the region.
Glucose control is an important part of perioperative management of an insulinoma patient. At the time of food withdrawal, an intravenous infusion of a balanced electrolyte solution containing 2.5-5% dextrose is begun. Infusion is continued through surgery and into the postoperative period. Large doses of dextrose may cause an exaggerated insulin response and should be avoided. After surgery, glucose must be monitored closely because hyperglycemia (8-35% of canine patients) and hypoglycemia (15-26% of canine patients) have been reported. The goal is to maintain a blood glucose between 40-200 mg/dL. If hyperglycemia persists after 48-72 hrs, insulin therapy may be needed.2
Animals should be kept well hydrated to help prevent the development of pancreatitis. Oral feeding may be delayed for 24-72 hours after surgery, depending on the extent of pancreatic manipulation. When food is reintroduced, small bland meals are fed. The animal is monitored closely for the development of nausea, vomiting, cranial abdominal pain or systemic inflammatory syndrome. Postoperative pancreatitis has been reported in 10-43% of canine patients undergoing nodule removal or partial pancreatectomy.2 It is rare in ferrets.8 If extensive dissection in the body of the pancreas is performed, a jejeunostomy tube should be placed prophylactically to allow early enteral feeding after surgery. Placement of a closed silicone abdominal drain in the region of the pancreas at the conclusion of surgery allows for rapid diagnosis of postoperative pancreatitis and aids in the management of abdominal effusion associated with pancreatitis.
- Cornell KF, J. Surgery of the exocrine pancreas In: Slatter D, ed. Textbook of Small Animal Surgery, third edition. Philadelphia, PA: W.B. Saunders, 2003;p 752.
- Kyles A. Endocrine Pancreas In: Slatter D, ed. Textbook of Small Animal Surgery, third edition. Philadelphia, PA: W. B. Saunders, 2003; p1724.
- Miller ME CG, Evans HE. Anatomy of the Dog. Philadelphia: W. B. Saunders, 1964. p. 706.
- Poddar S. Gross and microscopic anatomy of the biliary tract of the ferret. Acta Anat (Basel);97:121, 1977.
- Caywood D. Surgery of the Pancreas In: Bojrab M, ed. Current Techniques in Small Animal Surgery 2nd edition. Philadelphia: Lea & Febiger, 1983; p 232.
- Newman S, Steiner J, Woosley K, et al. Localization of pancreatic inflammation and necrosis in dogs. J Vet Intern Med 18:488, 2004.
- Harmoinen J, Saari S, Rinkinen M, et al. Evaluation of pancreatic forceps biopsy by laparoscopy in healthy beagles. Vet Ther;3:31, 2002.
- Weiss CA, Williams BH, Scott MV. Insulinoma in the ferret: clinical findings and treatment comparison of 66 cases. J Am Anim Hosp Assoc;34:471, 1998.
- Moore AS, Nelson RW, Henry CJ, et al. Streptozocin for treatment of pancreatic islet cell tumors in dogs: 17 cases (1989-1999). J Am Vet Med Assoc;221:811, 2002.
- Robben JH, van den Brom WE, Mol JA, et al. Effect of octreotide on plasma concentrations of glucose, insulin, glucagon, growth hormone, and cortisol in healthy dogs and dogs with insulinoma. Res Vet Sci 2005, in press.
- Robben JH, Pollak YW, Kirpensteijn J, et al. Comparison of ultrasonography, computed tomography, and single-photon emission computed tomography for the detection and localization of canine insulinoma. J Vet Intern Med;19:15, 2005.
- Tasker S, Griffon DJ, Nuttall TJ, et al. Resolution of paraneoplastic alopecia following surgical removal of a pancreatic carcinoma in a cat. J Small Anim Pract;40:16, 1999.
- Nathens AB, Curtis JR, Beale RJ, et al. Management of the critically ill patient with severe acute pancreatitis. Crit Care Med;32:2524, 2004.
- Qin HL, Su ZD, Gao Q, et al. Early intrajejunal nutrition: bacterial translocation and gut barrier function of severe acute pancreatitis in dogs. Hepatobiliary Pancreat Dis Int;1:150, 2002.
- Mayhew PD RR, Mehler SJ, Holt DE, Weisse. Choledochal tube stenting for decompression of extrahepatic biliary obstruction in dogs. Proceedings of the American College of Veterinary Surgeons Veterinary Symposium 2004:14.
- Jerram RM, Warman CG, Davies ES, et al. Successful treatment of a pancreatic pseudocyst by omentalisation in a dog. N Z Vet J 2004;52:197, 2004.
Surgery of Pancreatic Neoplasia
James M. Fingeroth
Many veterinarians are reluctant to touch, palpate, or operate on the pancreas because of concern for inducing pancreatitis. Leakage and activation of pancreatic enzymes caused by pancreatic trauma or surgery is possible and caution is indicated but it should not inhibit pancreatic manipulation in an appropriate manner when indicated. Pancreatic palpation, biopsy, and resection can all be performed safely, and proper post-operative patient management will minimize complications postoperatively.
Pancreatic examination should be part of every routine exploratory celiotomy. The right limb of the pancreas is easily visualized by identification and elevation of the descending duodenum toward the ventral midline from right to left during ventral midline celiotomy. The left limb can then be identified by tracing the right limb towards the angle (body), and retraction of the spleen. It can be helpful to perforate the greater omentum to better visualize and palpate the left limb of the pancreas as it courses dorsally along the greater curvature of the stomach. In the area of the angle and left limb of the pancreas the surgeon should also examine the regional lymph nodes since these may be affected by metastasis in cases of pancreatic neoplasia (Figure 21-20).
Because of the lobulated nature of the pancreatic parenchyma, and the tendency for the organ to sometimes fold on itself, examination of the pancreas should be both visual and tactile (See Figure 21-20). The latter requires the surgeon to gently palpate the organ between his or her fingers along its entire course. Small, but potentially significant lesions (e.g., islet cell tumors) may be missed if the pancreas is not palpated in addition to visual inspection.
On occasion the pancreas will be explored because a large mass has been identified on pre-operative imaging, or because of medically unresponsive pancreatitis. Surgeons should be familiar with the appearance of such lesions as pancreatic pseudocysts and abscesses when examining the pancreas at the operating table. Surgeons should especially be aware that inflammatory disease of the pancreas may appear aggressive and invasive. The organ may be diffusely enlarged, irregular, have varying color, and appear to invade into surrounding omental fat. This appearance may suggest a gross diagnosis of “extensive and unresectable malignant neoplasia”, and may even prompt the surgeon to recommend immediate euthanasia. However, it is not uncommon for biopsies of aggressive appearing pancreatic lesions to reveal no evidence of neoplasia, and instead necrotizing/hemorrhagic inflammation along with local steatitis, adhesions, and fat saponification. While the diagnosis of necrotizing/hemorrhagic pancreatitis may prove to be a serious and potentially fatal diagnosis, it may still be manageable with appropriate therapy. The surgeon should not conclude that neoplasia is the diagnosis on the basis of appearance alone.
Similarly, it is common to see multifocal or diffuse small white spots in the pancreas, during exploratory celiotomy especially in older animals. These are usually not neoplastic or of any clinical significance. They usually represent areas of fibrosis. However, I have seen cases of lymphoma affecting the pancreas (albeit there are usually lesions beyond the pancreas as well in such cases), so any doubt or concern should be resolved with pancreatic biopsy.
The pancreas is coarsely lobulated with color that varies between a creamy white, to pink, to occasionally brownishred (dependent on the amount of blood in the organ).1 The right limb is molded to the duodenum with which it shares its blood supply (cranial and caudal pancreaticoduodenal artery; caudal pancreaticoduodenal vein). The “tightness” of this fit between the pancreas and duodenum varies from patient to patient. In some animals there is quite a bit of mesenteric tissue between the two organs, but even then they usually become more closely apposed at the cranial aspect of the right limb near the angle. The arteries course longitudinally between the two organs and are almost completely obscured by pancreatic parenchyma on both sides. The cranial and caudal pancreaticoduodenal arteries (the former a branch of the celiac via the hepatic; the latter a branch from the cranial mesenteric) anastomose within the organ. The left limb of the pancreas is contained within the deep leaf of the greater omentum. Its main blood supply is from the pancreatic branches of the splenic and hepatic arteries (branches of the celiac), with some contribution by the gastroduodenal artery. Thus, the blood supply to the left limb is more segmental than the right. The left and right limbs are joined at a V-shaped angle called the body. This portion of the pancreas resides caudal to the pylorus and antral region of the stomach, and is where the exocrine ducts of the pancreas enter into the duodenum.
The location of the right limb of the pancreas brings it into proximity with other abdominal structures including the right body wall/flank, sublumbar fat containing the right ureter and kidney, the caudate process of the liver, the ascending colon and cecum, and loops of jejunum. The left limb may be in contact with the caudate process of the liver, the portal vein, caudal vena cava, aorta, left adrenal gland, transverse colon, and cranial pole of the left kidney.2 These relationships may have implications for the surgeon when examining or operating on the pancreas.
The pancreas has lymphatics that drain into the mesenteric, hepatic, and splenic lymph nodes, and these nodes (along with the pyloric nodes) should be examined for metastatic disease when pancreatic neoplasia is suspected. The pancreas receives some sympathetic innervation from the nerves that emerge from the celiac plexus, while parasympathetic nerve fibers from the vagus course to the gland with the celiac and cranial mesenteric vessels. Venous drainage from the pancreas (caudal pancreaticoduodenal vein from the right limb and splenic vein from the left) empties into the portal vein.
The exocrine ducts were named based on the description in humans (pancreatic vs. accessory pancreatic) and this leads to some confusion. Although variation in ductal anatomy has been well described in dogs, the vast majority of dogs have most of their pancreatic exocrine flow into the duodenum via the accessory duct and the minor duodenal papilla. Since, with few exceptions, the left and right ducts anastomose within the body, the accessory duct carries secretion from both limbs. The smaller (in dogs) pancreatic duct enters the duodenum at the major papilla directly, or by opening into the bile duct as it joins the intestine. In cats, the ducts from left and right join to empty almost exclusively via the pancreatic duct into the bile duct at the major duodenal papilla.3
Indications for Pancreatic Surgery
Exocrine Pancreatic Disease
The pancreas may be explored because of a clinical diagnosis of exocrine pancreatic insufficiency (EPI). Dogs with EPI are expected to have a significantly reduced volume of pancreatic parenchyma compared with normal individuals. A confirmatory biopsy may be performed as described below. Assuming the entire organ is diffusely affected, the easiest and safest location to biopsy is the distal aspect of the right limb. Dogs with EPI, especially German shepherds, have a reported higher risk for mesenteric volvulus, and may also be at higher risk for gastric volvulus.4 Therefore, a dog with suspected EPI should have a prophylactic gastropexy performed as part of the surgical procedure (See Chapter 19).
Pancreatitis is treated with intense medical management and is rarely an indication for exploration of the pancreas surgically. However, if imaging studies suggest the presence of an abscess or pseudocyst then there may be benefit to surgical intervention. The goal should be to obtain appropriate samples for histopathology and culture, and to establish drainage. Drainage techniques will be dependent on the location, size, and mobility of any cavitary lesion identified. Marsupialization is probably the least practical or desirable technique. Drainage tubes may be chosen, and of these a fenestrated silastic drain attached to a closed-suction type device exited through the body wall would be best. Another excellent option to consider is omentalization. This has been described for use with a variety of intra-abdominal abscesses and involves placing a pedicle of vascularized omentum into and/or through the abscess or cystic cavity and securing it with sutures. The omentum brings a blood supply as well as lymphaticovenous drainage to the site of disease.5-12
Pancreatitis may be associated causally with or as a result of biliary disease.13,14 Because of the close anatomic association of the pancreatic and accessory pancreatic ducts with the bile duct in the proximal duodenum it is possible for disease in one system to spread to the other. Sludging of bile with extrahepatic biliary obstruction has been reported in dogs with previous episodes of acute pancreatitis.13,14 Similarly, but less commonly, a primary cholangitis/cholangiohepatitis might result in spread of micro-organisms from the biliary tree into the pancreatic ducts, inducing pancreatitis. Thus, whenever examining the pancreas in instances of exocrine disease the surgeon should also evaluate the biliary tree and liver.
Exocrine tumors of the pancreas (pancreatic adenocarcinoma) are infrequently diagnosed in the canine and feline. Clinical signs of vomiting and anorexia are non-specific, however cats may develop a cutaneous syndrome that includes lameness due to foot pad ulceration and sloughing.15-17 Clinical signs of exocrine pancreatic neoplasia may be due to the mass effect on neighboring organs if the tumor is large enough, or due to the effects of metastatic disease and/or carcinomatosis. Dogs with pancreatic adenocarcinoma usually do not have signs of either EPI or of pancreatitis. Surgical resection may be attempted depending on the extent of disease, but the prognosis is usually grim. Malignant pancreatic tumors are aggressive cancers and the absence of specific clinical signs usually results in a delay in diagnosis until late in the biological course of disease.
Endocrine Pancreatic Disease
The most common endocrine disease of the pancreas is diabetes mellitus. This disease is usually not an indication for pancreatic surgery. There are important considerations with respect to properly managing diabetic patients undergoing anesthesia and surgery for other disease processes that are addressed elsewhere.18
The most common indication for pancreatic surgery due to endocrine disease is the suspicion that the patient has a functional endocrine tumor. Several types of endocrine pancreatic neoplasia have been documented in small animals. The endocrine functions of the pancreas are located in the islet cells (of Langerhans), which are distributed randomly throughout all portions of the pancreas. These mostly neural crest-derived APUD (Amine Precursor Uptake and Decarboxylation) cells migrate into the pancreas during embryonic development. This migration can be imperfect, and as a result functional neuroendocrine cells normally associated with the pancreatic islets may be located in extra-pancreatic locations, including the gastric wall, duodenum, and elsewhere. This in turn implies that functional “pancreatic” tumors may arise ectopically, and this must be borne in mind when exploring a patient’s abdomen for a suspected endocrine tumor, especially if a primary lesion is not found in the pancreas itself.
Endocrine pancreatic neoplasia is usually named based on the predominant hormone produced by the tumor. The most common of these tumors is the insulinoma, derived chiefly from a clone of neoplastic beta cells in an islet. In older veterinary literature and in the parlance of the human literature a distinction is made between “insulinoma” (a benign proliferation of beta cells) and “functional islet cell adenocarcinoma” (the malignant variety most commonly diagnosed in dogs). However, in current veterinary clinical and pathology literature the two terms tend to be used interchangeably, so that the term “insulinoma” can describe either benign or malignant neoplasia. Other reported neuroendocrine tumors include gastrinomas (Zollinger-Ellison syndrome) arising mostly from non-pancreatic sites, but occasionally in the pancreas (putatively from delta cells), glucagonomas (alpha cells), non-specific polypeptidinomas, and somatostatinomas (delta cells). In dogs these tumors are usually malignant, and spread to local lymph nodes (Stage II disease) or liver (Stage III disease) is commonly found at the time of initial surgery. The implications for prognosis (disease-free interval and survival time) have been reported as has the use of adjuvant medical therapy.18-23 This discussion will be limited to patient management during surgery and the immediate postoperative period. The reader is directed elsewhere for a review of criteria for confirming the diagnosis of specific endocrine tumors of the pancreas.18
Pancreatic Biopsy and Partial Pancreatectomy
Incisions into the pancreas have the potential for inducing pancreatitis as a consequence of enzymatic leakage and activation of zymogens. Even gentle tissue handling may cause enzymatic activation. The safest course of action, in my opinion, is to assume that some leakage has occurred. I recommend withholding food and water for a minimum of 36 hours after pancreatic incision. Serum enzymes such as lipase and amylase may be monitored as desired, but these enzymes are notoriously insensitive and non-specific markers for acute pancreatitis. A better indication of when to resume oral intake is the clinical appearance of the patient, including such signs as rectal temperature and emesis. If the patient has not vomited for 36 hours or more, there is no fever, and there is no unusual abdominal tenderness on palpation, oral consumption of small amounts of water, followed by small amounts of bland food every few hours can be attempted, with a gradual return to normal alimentation. Oral consumption should be discontinued or delayed if the animal has signs suggestive of pancreatitis. If extensive pancreatic manipulation is required a jejunostomy feeding tube should be placed at the time of surgery (See Chapter 6). The jejunostomy tube will permit feeding the animal without stimulation of pancreatic exocrine secretion.
A generous cranial ventral midline incision is made to expose the cranial abdomen. Exposure of the pancreas is facilitated by appropriate use of retractors and moistened laparotomy pads. Self-retaining retractors such as Balfours placed on the abdominal wall and a surgical assistant using malleable ribbon retractors to retract viscera are beneficial for exposure. Warmed irrigation solution is indicated for local lavage after pancreatic surgery is completed, and suction is helpful to aspirate blood and lavage fluid.
When lesions are confined to the caudal aspect of the right limb of the pancreas, or a random biopsy is intended, the easiest method is excision of the caudal aspect of the right pancreatic limb. This can be performed with sutures, surgical stapling equipment, or the use of a hemostatic sealing device (eg. Liga SureTM). For those animals with a small pancreas it may be suitable to mass ligate the isolated portion with suture (suture-fracture technique) after dissection of the pancreas from the mesoduodenum. I recommend the use of 2-0 or 3-0 monofilament non-absorbable suture such as polypropylene. Alternatively, the duodenal serosa can be gently grasped and dissected off the pancreatic lobules; the lobules are then separated (sterile cotton swabs are useful) from the midline of the gland to expose the vessels and ducts. The vasculature and ducts can then be ligated with suture (3-0 or 4-0) or hemostatic clips and the pancreas resected distal to the ligations. Thoracoabdominal staplers are effective for single-stage ligation and resection. In most dogs the TA-30 size will be suitable, and small vascular staple cartridges (V3) are most effective (Figure 21-21) Stapling can also be performed by laparoscopy. Although the suture-fracture and stapling techniques induce some parenchymal crushing as the suture is tightened or staples are fired, no differences in complication rates have been found.24 Ligation of a pancreatic duct does not induce pancreatitis but will induce acinar atrophy in any residual pancreas distal to the ligation.
If biopsy or excision of a lesion nearer the body or in the left limb is required, surgical options include partial pancreatectomy as described above (for the left side this requires dissection of the deep leaf of the omentum for exposure), enucleation of the mass, or incisional or needle biopsy. The latter may be performed with a Tru-cut device or other biopsy needle such as Vim-Silverman needle. Enucleation refers to a local dissection of pancreatic lobules while leaving the pancreas distal to the biopsy site intact. Lobules of parenchyma are teased away from the tissue to be removed using fine hemostats and sterile cotton swabs. Hemostasis can be achieved with gentle direct pressure, fine suture (4-0 or 5-0) or fine-tipped bipolar electrocautery. However, if extensive damage to the ducts or vessels is required (depending on the size and location of the lesion), partial pancreatectomy is considered and is preferred rather than enucleation. Incisional biopsy is performed using a #15 scalpel blade to take a small wedge of tissue and a single absorbable suture is used to close the defect.
When pancreatic disease is identified during surgery, the surgeon must determine whether and how to employ the above techniques for successful excision if possible. The most difficult anatomic location to excise a lesion is in the body of the pancreas since there is a risk of disrupting both the pancreatic and accessory pancreatic ducts. There are techniques for attempting to directly anastomose the remaining pancreas and duct to the intestine, but this is technically difficult and rarely performed in veterinary clinical cases.25 In this situation, or in other situations that might call for total pancreatectomy (such as lesions causing complete obstruction to exocrine flow already, as might be seen with chronic pancreatitis or neoplasia), the surgeon must give careful consideration to the merits of attempting to resect all disease relative to the impact on the animal’s (and client’s) quality of life following surgery.
There are no indications for total removal of the pancreas in dogs other than in the research laboratory. The clinical diagnosis where total pancreatectomy might be indicated is extensive pancreatic neoplasia, but it would be unlikely to have disease confined to the pancreas in such a case. The presence of local infiltration and distant metastasis make such surgical treatment a short term palliative procedure at best. Because of the shared blood supply between duodenum and pancreas, total pancreatectomy will require duodenectomy, splenectomy, and biliary diversion. As a result of surgery the patient will be diabetic and have EPI post-operatively. To my knowledge, there are, at present, no reports of total pancreatectomy for treatment of naturally-occurring disease in dogs or cats.
Surgical Technique for Treating Pancreatic Endocrine Neoplasia
The most common indication for pancreatic exploration and partial pancreatectomy is the suspicion of a functional beta-cell tumor (insulinoma). In most cases the veterinarian should have make a diagnosis of insulinoma by demonstrating that the patient has persistent hypoglycemia not due to laboratory error, and a high level of serum insulin when the serum glucose is well below normal ranges. These findings are not exclusive to insulinoma however. There may be other causes for hyperinsulinism such as hepatic disease (usually neoplasia) that disrupts normal insulin degradative metabolism and which may also consume glucose prodigiously. Appropriate imaging studies (ultrasound, computed tomography, magnetic resonance imaging) should be able to distinguish those patients with a primary hepatic lesion. With the possible exception of CT or MRI, however, imaging studies (particularly ultrasound) are often not able to confirm the presence of a primary insulinoma in the pancreas. Thus, in most cases animals undergo celiotomy for diagnostic confirmation as well as for disease staging and treatment.
The goal of pre-operative and intra-operative patient management should be to stabilize the blood glucose in an acceptable range, ideally in the low normal range if possible. Anesthetized patients and those with a history of hypoglycemia-induced seizures are particularly vulnerable to the effects of neuroglycopenia which can cause cortical laminar necrosis and permanent brain damage. To some degree, the central nervous system (CNS) has adaptive mechanisms that permit function even at low levels of blood glucose, but the neurons are at a threshold and are intolerant of any further (especially sudden) decrease in glucose levels. Achieving and keeping blood glucose normalized and stabilized is challenging since insulinomas, although not responsive to normal negative feedback mechanisms, may still have intact positive feedback. Administering exogenous dextrose especially in high concentrations may stimulate further secretion of insulin. This may fail to raise the blood glucose level by stimulating excess insulin secretion and may cause wide variations in glucose levels. These variations, especially sudden decreases in glucose may induce more severe signs of CNS dysfunction than persistently low blood glucose, at least in conscious patients. The use of 10% to 20% glucose solutions is indicated for management of patients with persistent hypolglycemia. Hypertonic dextrose solutions are best adminstereed through a jugular catheter. A second peripheral catheter can be used for blood sampling and monitoring. In addition to dextrose, other techniques for raising and stabilizing blood glucose include constant rate infusions of glucagon,26 administration of corticosteroids, beta-blockers, and specific drugs that inhibit secretion of insulin from beta cells such as diazoxide.18-23 Blood glucose should be monitored regularly during anesthesia and modifications in treatment made as necessary to stabilize levels in the appropriate range.
Anesthetic protocols, other than for glucose homeostasis, are routine and at the discretion of the surgeon or anesthesiologist. I administer prophylactic antibiotics, typically cefazolin (22mg/kg IV, q2h) starting at induction, and pre-emptive use of analgesics should be standard. Drugs that cause blood pooling in the spleen (barbiturates, phenothiazines, certain opioids) should be avoided since retraction of an enlarged spleen may make surgical visualization and manipulation of the left limb of the pancreas more difficult.
Exploratory surgery of the pancreas for an insulinoma is preceded by complete abdominal exploration to identify related or unrelated disease. Special attention and examination for metastasis is focused on the liver and local lymph nodes. I usually reserve examination of the pancreas for last so as to not miss other lesions. The entire pancreas should be exposed, then examined visually and thoroughly palpated. Most islet cell tumors will appear as discrete, raised, firm, lobulated nodules. They range from light brown to almost violet in color. Size can range from a few millimeters in diameter to several centimeters. There is no proven site predilection within the pancreas and tumors have been reported with equal distribution in both limbs and the body of the organ. There is also no correlation between the severity/ refractoriness of pre-operative hypoglycemia and the size of the primary tumor. Tumors are usually solitary but the entire pancreas should be examined to ensure that no additional tumors are present. Once the tumor is identified the surgeon will need to determine which of the techniques for partial pancreatectomy is appropriate. In all cases, whether there are gross lesions or not, one or more regional lymph nodes should be resected and at least one liver biopsy obtained for staging purposes. Partial pancreatectomy is desirable when possible since recurrence rates may be lower with this technique compared to enucleation of the mass. All apparent neoplastic tissue including metastatic disease is resected when possible. Persisitent hypoglycemia may result if gross neoplastic disease cannot be resected.27 The local area should be lavaged with warm saline to remove bacterial contamination or pancreatic enzymes that might have leaked, and the abdominal incision closed routinely.
In rare instances, examination of the pancreas will fail to identify the tumor. This could be the consequence of missing a tumor that’s present (eg., a small tumor enveloped within surrounding exocrine parenchyma), an ectopic (extra-pancreatic) tumor, or a misdiagnosis. The first two are most likely. In this case, it can be helpful to utilize intra-operative vital staining with methylene blue, USP. Methylene blue concentrates in specific endocrine cells, notably pancreatic islet cells and parathyroid chief cells. The degree of cellular uptake (and therefore intensity of tissue staining) is correlated with the degree of function (secretion) of these cells. Thus islet cell tumors and parathyroid gland tumors will selectively stain more intensively than normal cells.28,29
|Methylene blue, USP (MB) is provided in 10 ml ampules as a 1% solution. It is approved for in vivo, intravenous administration. IT IS NOT THE SAME AS NEW METHYLENE BLUE (NMB)! The latter is a laboratory reagent, and other than for the unfortunate similarity in common names, the two products are entirely different chemically. If you choose to use this technique be certain you use the correct product. Do not use New Methylene Blue!|
The recommended protocol is to calculate a dose of 3mg/kg methylene blue and dissolve this quantity in 250 to 500 ml of 0.9% saline. This fluid can then be infused intravenously at a maintenance fluid rate of 10ml/kg/hr. Visualization of tissue staining will usually occur 15 to 20 minutes after starting the infusion, with the pancreas taking on a dusky pale blue hue. An islet cell tumor will stain a more intense blue or purplish color. Once the tumor is visualized the MB infusion can be discontinued.28,29
In addition to identifying an occult primary tumor or ectopic disease MB infusion can help determine if a lesion seen beyond the pancreas is a metastatic nodule, and help determine if it should be resected.30
Using MB infusion routinely during pancreatic exploration for endocrine tumors is not recommended because of potential negative effects. The patient may develop a pseudocyanosis that has the potential for interfering with monitoring of patient oxygenation during anesthesia. More significantly, MB can induce a Heinz-body anemia that will cause the hematocrit to decrease 1 to 2 days after MB administration. In experimental cases and limited clinical use the anemia has not required transfusion however the potential exists, especially if the patient has sustained acute blood loss from the operation. There have been reports of acute renal failure after MB infusion. I am not convinced this was a toxic effect of MB as the reported cases did not provide adequate descriptions of either the pre-operative renal status or of the use of intra-operative fluid therapy. However, caution dictates that this potentially serious adverse effect should be considered especially if the animal has preexisting renal disease. Finally, MB is excreted in the urine. This will make the urine green, and has the potential of staining flooring surfaces that urine may come in contact with.28
After the primary insulinoma has been resected the surgeon can expect a rapid rise in blood glucose levels. Fluid therapy should be modified as glucose levels change. In most dogs, the blood glucose will return to and remain in the normal range after administration of dextrose and other pro-glycemic agents has been stopped. However, in some instances the dog will become hyperglycemic and have at least a transient diabetes mellitus. This is largely explained by down-regulation of receptors on the normal beta cells. Persistent hyperglycemia may require exogenous insulin for treatment. Less commonly, but especially if incompletely excised metastatic disease in lymph nodes or liver is present, hypoglycemia may persist after removal of the primary tumor. Further surgical resection of gross disease is possible however most animals are managed with combinations of euglycemic agents such as corticosteroids, diazoxide, and dietary modification. Because almost all insulinomas in dogs are malignant, metastatic disease, even if not grossly apparent at the time of surgery, is likely to develop. Development of metastatic disease may result in illness caused by the effects of the tumor in the organ involved, or more likely, due to the recurrence of hyperinsulinism and resultant hypoglycemia. In some cases a second (or more) operation can be used to effectively debulk metastatic disease and prolong the disease-free interval and survival time.
In addition to medical therapy that specifically promotes euglycemia, cytotoxic chemotherapy can be used as adjunctive treatment. The current drug of choice is streptozotocin. This drug acts specifically to cause death of islet cells, but is also extremely nephrotoxic. Historically, the drug was not used clinically because of its nephrotoxic effects which were reported to be lethal. Interestingly, this conclusion was reached based on a report of four dogs in the literature. More recently, streptozotocin has been used with success in treating islet cell tumors when administered with an intensive diuresis protocol.31
Other Pancreatic Islet Cell Tumors
Less common than insulinoma are the other islet cell tumors of the pancreas. The principles of surgical exploration, disease staging, and partial pancreatectomy are similar to that described for insulinomas. Management of the medical syndrome induced by the specific hormome excess is dictated by the effects of that syndrome. Gastrinomas are usually associated with the Zollinger-Ellison syndrome. These tumors produce hypergastrinemia that cause pyloric mucosal hypertrophy and possible gastric outflow obstruction. Gastrin also acts synergistically with histamine and acetylcholine to increase production of hydrochloric acid by parietal cells in the stomach, this may cause gastric ulceration. Antacids such as proton-pump inhibitors, as well as H2-receptor antagonists are part of the medical management for this neuroendocrine tumor. Definitive therapy is removal of the primary tumor, however gastrinomas may be occult, ectopic, or diffuse, making identification and complete removal difficult. Although gastrin is produced by fetal islet cells (some gastrinomas have a primary pancreatic location), in adults most gastrin is derived from extra-pancreatic sites. One of the treatments for this disease is to remove the target for gastrin, ie, to perform a partial gastrectomy with gastroduodenostomy (Bilroth I) or gastrojejunostomy (Bilroth II).
Too few glucagonomas, VIPomas, pancreatic polypeptidomas or somatostatinomas have been reported in animals to reach meaningful conclusions about their biological behavior or treatment, but the principles with respect to pancreatic surgery should be similar. Glucagonomas in dogs have been associated with superficial necrolytic dermatitis and diabetes mellitus, but these conditions can arise independently of a glucagonoma, and need not occur in confirmed cases of glucagonoma.32-34
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- Westermarck E, Rimmaila-Parnanen E: Mesenteric torsion in dogs with exocrine pancreatic insufficiency: 21 cases (1978-1987). J Am Vet Med Assoc 195:1404-1406, 1989.
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- Campbell BG: Omentalization of a non-resectable uterine stump abscess in a dog. J Am Vet Med Assoc 224:1799-1803, 2004.
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- Pascal-Tenorio A, Olivry T, Gross TL, et al: Case report: paraneoplastic alopecia associated with internal malignancies in the cat. Vet Derm 8:47-52, 1997.
- Brooks DG, Campbell KL, Dennis JS, et al: Pancreatic paraneoplastic alopecia in three cats. J Am Anim Hosp Assoc 30:557-563, 1994.
- Seaman RL: Exocrine pancreatic neoplasia in the cat: A case series. J Am Anim Hosp Assoc 40:238-245, 2004.
- Fingeroth JM: Endocrine Pancreatic Disease In: Bojrab MJ (ed). Disease Mechanisms in Small Animal Surgery, 2nd ed. Philadelphia, Lea and Febiger, 1993, p589-607.
- Caywood DD, Klausner JS, O’Leary TP, et al: Pancreatic insulinsecreting neoplasms: Clinical, diagnostic, and prognostic features in 73 dogs. J Am Anim Hosp Assoc 24:577-584, 1987.
- Leifer CE, Peterson ME, Matus RE: Insulin-secreting tumor: diagnosis and medical and surgical management ion 55 dogs. J Am Vet Med Assoc 188:60-64, 1986.
- Steiner JM, Bruyette DS: Canine insulinoma. Compend Contin Educ Pract Vet 18:13-16, 1996.
- Trifonidou MA, Kirpensteijn J, Robben JH: A retrospective evaluation of 51 dogs with insulinoma. Vet Quarterly 20:S114-115, 1998.
- Tobin RL, Nelson RW, Lucroy MD, et al: Outcome of surgical versus medical treatment of dogs with beta cell neoplasia: 39 cases (1990- 1997). J Am Vet Med Assoc 215:226-230, 1999.
- Allen SW, Cornelius LM, Mahaffey EA: A comparison of two methods of partial pancreatectomy in the dog. Vet Surg 18:274-278, 1989.
- Markowitz J, Archibald J, Downie HG: Experimental surgery. Baltimore, Willams and Wikeins, 1964, p236-252.
- Fischer JR, Smith SA, Harkin KR: Glucagon constant-rate infusion: A novel strategy for the management of hyperinsulinemic-hypoglycemic crisis in the dog. J Am Anim Hosp Assoc 36:27-32, 2000.
- Melhaff-Schunk, C: Surgery of the pancreas. In: Bojrab MJ (ed) Current Techniques in Small Animal Surgery, 3rd ed. Philadelphia, Lea and Febiger, 1990, p304-308.
- Fingeroth JM, Smeak DD, Jacobs RM: Intravenous methylene blue infusion for intraoperative identification of parathyroid gland and pancreatic islet-cell tumors in dogs. Part I: Experimental determination of dose-related staining efficacy and toxicity. J Am Anim Hosp Assoc 24: 165-173, 1988.
- Fingeroth JM, Smeak DD: Intravenous methylene blue infusion for intraoperative identification of pancreatic islet-cell tumors in dogs. Part II: Clinical trials and results in four dogs. J Am Anim Hosp Assoc 24:175- 182, 1988.
- Smeak DD, Fingeroth JM, Bilbrey SA: Intravenous methylene blue as a specific stain for primary and metastatic insulinoma in a dog. J Am Anim Hosp Assoc 24:478-480, 1988.
- Moore AS, Nelson RW, Henry CJ, et al: Streptozotocin for treatment of pancreatic islet cell tumors in dogs: 17 cases (1989-1999) J Am Vet Med Assoc 221:811-818, 2002.
- Gross TL, O’Brien TD, Davies AP, et al: Glucagon-producing pancreatic endocrine tumors in two dogs with superficial necrolytic dermatitis. J Am Vet Med Assoc 197:1619-1622, 1990.
- Langer NB, Jergens AE, Miles KG: Canine glucagonoma. Compend Contin Educ Pract Vet 25:56-63, 2003.
- Feldman EC, Nelson RW: The Endocrine Pancreas. In: Feldman EC, Nelson RW: Canine and Feline Endocrinology and Reproduction, 2nd ed. Philadelphia, WB Saunders, 1996. pp. 450-452.
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