----start---- 10/29 medsurg3 washabau [after this hour we will have lectures on surgical management of the disorders we have discussed so far] diseases of the exocrine pancreas: acute/chronic pancreatitis (APN/CPN) exocrine pancreatic insufficiency (EPI) pancreatic cancer we really only have time to discuss APN and EPI. signs of CPN are similar to APN but are more chronic. Regarding pancreatic cancer - it occurs.that's all we will really say. Acute Pancreatic Necrosis (APN) aka acute pancreatitis take home points:** -it's an inflammatory disease (whereas EPI is degenerative) -clinical presentations are very variable -dx is very difficult -APN is a multisystemic disease [slide] pancreas of affected animal - lumen of duodenum is seen - fat necrosis, hemorrhagic pancreas, whole area hemorrhagic, inflamed these animals may present with mild signs of not eating, vomiting, or may come in collapsing, near death. so realize, the most fulminant form is not always the way you see it. these animals can present with mild/moderate clinical signs. we do labtests, imaging, but dx can still be really hard. and because it is a multisystemic disease, the outcome isn't' always good. the animal whose pancreas is seen here had ventricular arrhythmias, pulmonary edema, and acute tubular necrosis as well. [slide] drawing of pancreatic acinar cell, which makes zymogens. remember there are 4 ways for it to protect itself from autodigestion - making zymogens, compartmentalizing them in zymogen granules, targeting lysosomal enzymes with mannose-6-phosphate to separate granules, putting trypsin inhibitor into zymogen granules. in response to feeding, there is exocytosis, delivery of zymogens innto ducts - not activated til they get to small intestine where there is enterokinase. so these cells try hard to protect themselves. pathophysiology of APN: there is a lot of evidence that there is premature activation of zymogens within the acinar cells. 1. trypsin - broad range of proteolytic activity, now within cell - changes architecture, causes necrosis 2. kallikrein - converts kininogen to kinin - part of inflammtory cascade 3. elastase - blood vessel elastin digestion, vascular damage - this is why it gets so hemorrhagic 4. lipase, phospholipasse A - fat necrosis, membrane dissolution - if this gets to pulmonary circulation, we see pulmonary edema 5. amylase, carboxypeptidase, ribonuclease - no significant pathology now, this can extend locally throughout the region - extending to stomach, duodenum, colon; further, these substances and other vasoactive things can be distributed systemically to remote sites, causing multisystemic complications. all these things affect glomerular filtration, can contribute to ATN. so remember this process may in fact disseminate, become multisystemic, often fatal. how do they present? history and PE findings are variable. some animals have mild nnecrosis, mild pancreatitis, others have severe ATN. history: anorexia, vomiting, lethargy, diarrhea, hematochezia. why? it's inflammatory. inflammation reduces appetite, can trigger central emetic response, be associated with diarrhea b/c of local extension of inflammation into ascending or transverse colon, or duodenum. hematochezia seen with colitis. so any/all of these signs can be present. PE: fever - due to inflammation - may be mild/mod/severe. shock - multisystemic dz! abdominal pain - when present you may localize it to right upper quadrant, but it may also be diffuse and cause total guarding. bloody feces (hematochezia). tachypnea may occur due to multisystemic effects (or pain?), jaundice may occur b/c in dog, pancreatic duct is not far from major common bile duct, and inflammation may involve the bile duct, causing obstruction. in cats, we often see jaundice, because there is a shared entry pathway b/w pancreatic duct and bile duct - so jaundice is more common in cats but does also sometimes occur in dog. oliguria may occur as well - reduced urine output is a manifestation of acute tubular necrosis. so again, it's variable, inflammatory, multisystemic. what do we do to substantiate our dx? labwork. CBC/chem/ua. lab findings: WBC high - inflammatory dz - leukocytosis, often very high counts RBCs thrombocytopenia increased PT/PTT/bilirubin hyperglycemia hypercalcemia hypercholesterolemia due to biliary obstruction azotemia increased ALT/AST/SAP- we have obstructive jaundice, so expect disproportionate increase in SAP compared to ALT and AST (hepatocellular leakage enzymes) hypoxemia - evidence of multisystemic disease, pulmonary insufficiency methemalbuminemia hyperamylasemia hyperlipasemia hypertrypsinogenemia remember, there is always a small amount of enzyme secreted into circulation, so in animals with pancreatitis we expect to see increases in these enzymes in the blood. this is more true in the dog than in the cat. amylase and lipase are not remarkably changed in feline APN for some reason. but the assays are useful in the dog. if lipase is increased, 70% chance of the dog having APN. trypsinogen assays are useful for dx of EPI, for sure. also we think it is useful in dx feline APN, but aren't sure if it is useful for dx of APN in dogs. bottom line - consider amylase/lipase/trypsinogen in dog, just trypsinogen in cat. [slide] example of lab data from affected dog- inflammatory leukogram, marked increase in cholestatic enzyme (ALP), mild increase in ALT. azotemia, low urine SG, marked increase in serum total bilirubin. we are dealing with extrahepatic biliary obstruction. so bilirubin increases, cholesterol increases, and alk phos increases (is induced) other dx: rads - four major findings: in dogs, not really in cats: -increased density in right upper quadrant (58%) -left gastric displacement (55%) -right duodenal displacement (42%) -dilated, gas filled duodenum/colon (around 40%) we rely really on history and PE, then do these ancillary tests, obviously none of them are perfect. ultrasound: -loss of echodensity or echogenicity of pancreas -mass effect [slide] canine abdominal u/s - hypoechoic pancreas compared to adjacent spleen. this dog has severe inflammation, edema, necrosis of pancreas one other finding, b/c of close anatomy b/w pancreatic and biliary duct, there may be obstruction of biliary duct, you may see dilation of the duct and distension of the gall bladder. APN etiologies: most cases are idiopathic - we have no idea. true in people too, although in man alcohol consumption, gallstones are also major entities. Alexander the Great probably died after a drinking binge of APN. other etiologies - major ones we think we see are: nutrition problems - high fat diet can induce APN in some dogs, maybe cats that's not the only cause though. drugs - in dogs, L-asparaginase can cause this (?), as can azothiaprine. not a major entity, though. ischemia is probably an important cause - if an animal has some other dz, causing changes in blood flow - dehydration, heatshock, parvoviral enteritis - ischemia, poor perfusion, can lead to APN. organophosphates - occasionally in dogs and cats, exposure to OP (lawn application or whatever) will precipitate a case of APN. experimentally if you tx healthy animals with OPs some will go on to get APN. usually idiopathic. take excellent history do excellet PE labwork rads sometimes histology sometimes we can't be sure! sometimes we dx on necropsy differential diagnoses: GI foreign body nonspecific gastroenteritis hemorrhagic gastroenteritis acute renal failure adrenocortical insufficiency (anorexia, v/d, blood in diarrhea...) peritonitis/ruptured bowel disc disease colitis hepatitis RMSF don't memorize this list at this time :) treatment: usually medical tx usually symptomatic tx, critical care as needed -find and remove any underlying cause -NPO -IV fluids -supportive care -analgesics in 1998, we as vets or MDs still have no selective therapies for APN. some investigational therapies are being looked at but these aren't proven. supportive care is reaally usually it. sometimes, we have to use surgical tx if: -persistent obstructive jaundice -abscess/mass/pseudocyst (he said "if animal has developed an ass" but he meant abscess) -intestinal obstruction (due to inflammation) Feline APN: Dr Van Winkle characterized this well a few years ago.until 1993 they said this didn't exist, but it does. a few important points: if you read his paper and look at signs reported in 40 cats - most importannt signs: lethargy 100% anorexia 97% dehydration 92% vomitinng 25% abd pain 23% abd mass 15% diarrhea 20% so cats do present differently. they do not necessarily show the same signs as a dog. major signs in cats are lethargy, anorexia, dehydration. imaging findings - rads not useful. u/s - hypoechoic changes in pancreas. another key point - while APN can be distinct entity in dogs, it is associated with other things in cats. one of these is hepatic lipidosis - cats can have both hepatic lipidosis and APN. it's hard to tell these apart. cats can have one or the other or both. cats may also have cholangiohepatitis, with the other two. in many cats, these three things are all preceded by inflammtory bowel disease! if you consider pathogenesis...perhaps some cats haave IBD as initiating entity. then with recurrent bouts, pressure goes up in duodenum causing reflux into duct - inducing APN and cholangiohepatitis. so if you think you see APN in cat, look for these other things. EPI: exocrine pancreatic insufficiency -usually NOT inflammatory; is degenerative or atrophic -signs usually very straightforward -usually NOT multisystemic - just in pancreas -dx and therapy are usually straightforward signs: loss of ability to secrete zymogens and bicarb from pancreas, so: huge weight loss diarrhea/steatorrhea/smelly stool voracious appetite coprophagy "starving in the midst of plenty" dx: quantitation of trypsin like immunoreactivity aka TLI. this test is great. these dogs lose ability to secrete trypsinogen, and they are easily diagnosed. treatment: replace the enzyme. there are several types of enzymes available. best forms are the powders. sprinkle them on food to initiate digestion prior to feeding. many animals respond to this alone; other animals need a short course of abx to treat small bowel bacterial overgrowth. some treatmet failures occur b/c this isn't recognized. treatment failures also occur due to underdosage, or inactivation of enzymes by acid. ---break---- holt abdominal incisions stomach, pylorus ventral midline incision - linea alba most frequently used incision for laparotomy cranial incision: xiphoid to umbilicus, for working on stomach, liver caudal approach: umbilicus to pubis, for urinary bladder, etc slide: severely enlarged liver with white spots- LSA - this incision isn't big enough to explore the abdomen, there is a huge liver there. point: do not be afraid to extend the incision as needed linea alba: midline ventral strip of fascia from xiphoid to pubis, the insertion for body wall muscles. it narrows caudally and the dorsal sheath becomes very thin caudally. if you can't find it, go to the umbilicus to find it. remember the dorsal sheath caudally has little holding strength. falciform ligament: dorsal to linea, from umbilicus to xiphoid. this is important/useful b/c when you explore animal with hemoperitoneum, if you go straight into linea, blood goes all over and you can't see. so instead, incise through linea, to falciform fat so you see it bulge out - extend xiphoid to umbilicus, without getting blood in field, then go through with suction to remove blood. umbilical lig: from umbilicus to symphysis pubis - often have to sever this. so once you get through the skin, you have to separate fat - use your fingers or some forceps. some people will teach you to separate the fat off the linea. but, that means, you are creating dead space, and you have to then close it back up with sutures to reappose it to prevent seroma/hematoma formation. you might just make a small incision through the linea with the blade, instead of stabbing through...once you are through, you have to extend. yesterday, there was a young cat that had had a cystotomy for a urate stone indicating a possible shunt. so they wanted to look in bladder and up near liver. they went through linea at umbilicus. then, they hd to think about possible adhesions to the dorsal linea. so they should extend the incision cranially first then in area of prior surgery while looking for adhesion carefully. slides: ligating falciform fat male dog: skin incision must go around the prepuce be aware of a few things - there is a muscle running from prepuce cranially - the preputial muscle - you have to transect it. usually a wimpy saran wrap like thing. you have to reattach it when you close or the prepuce retracts caudally and the owner sees the penis protruding and it isn't good. also, there is the caudal superficial epigastric vein running to the prepuce - try to find these and ligate them before you gut them. closure: take the time to look at what you are doing - look and see what the linea looks like, especially caudally. you need to get your suture into the ventral sheath because caudally the dorsal sheath is reallly weak. subcutaneous tissue - close with 2/0 or 3/0 absorbable suture - can close with continuous suture and that is faster, but we do single interrupted here b/c it is good experience and b/c it may be more secure - if you place a continuous suture and one part pulls out, the whole thing is lost. suturing the subcu eliminates dead space. it doesn't just make the skin incision look nice. skin: single interrupted flank incisions: rarely used here, but flank spays more common in the UK - although, if anything bad goes on with the ovary/pedicle of the down side,it's hard to deal with. flannk approach exposes lateral abdomen, used for kidney, stomach, OHE - advantage is few hernias, disadvantage is limited access to the rest of abdominal cavity. Dr H uses flank incision when closing chest after esophgeal surgery, to place a stomach tube. [slide] diagram of abdominall muscles - usually you make a skin incision caudal to 13th rib, then split parallel to muscle fibers of internal oblique, and then to transverse - so your incision gets smaller. paracostal incisions: for big splenic or liver tumor - gives wide access to abdomen. if you're in via ventral midline laparotomy, and there is a huge splenic tumor, and you can't elevate the spleen, you need to do a left paracostal - transect skin, sbcu, muscle caudal to 13th rib. then you have a big body wall flap you can retract. sometimes right paracostal for liver tumor, or nasty adrenal tumor. never be afraid to give yourself more exposure retroperitoneal - rarely used. sometimes for surgery on adrenal, kidney, or ureter. allows direct approach without intrusion of abdominal viscera. if adrenal tumor is making dog cushingoid, you can use retroperitoneal approach to avoid problems with wound healing in ventral midline - but adrenal is very vascular and you have to be careful b/c there is limited exposure and if you screw up there is no extra exposure for you. esp on right where capsule is fused with adventitia of vena cava. - stomach: remember, where the esophagus enters is the cardia, then the fundus, pyloric antrum, and pylorus. blood supply: branches of the aorta - branch off celiac a b/c left gastric - supplies lesser curvature. right gastric is branch of hepatic. left and right gastroepiploic aa supply greater curvature. there used to be a thing in splenectomies where you coulldn't ligate left gastroepiploic - but you can. indication for sx: hiatal hernia gastroesophageal reflux GDV gastric bleeding delayed gastric emptying Gastric Bleeding: vomiting blood, true melena chronic renal/hepatic dz, mast cell tumors (histamine -> H2 receptors), Zollinger/Ellison syndrome (gastrinoma - hypergastrinemia), gastric neoplasia, NSAID toxicity (decreased prostaglandin production -> decreased cytoprotection, loss of mucus and bicarb production, decreased gastric blood flow, decreased mucosal cell proliferation) dx: look for underlying dz, contrast rads, endoscopy note: big ad campaign right now - COX2 inhibitors. COX1 is constitutive, it maintains mucosal barrier, renal blood flow. COX2 is induced during inflammation. you want to block COX2. Etogesic, Rimadyl, etc are supposed to be COX2 specific. there is not good evidence for these being better than other NSAIDs except aspirin and some other one. aspirin, bute, and piroxicam cause the most ulceration. etolac/etogesic and rimadyl/carprofen cause less gastric ulceration. gastric bleeding tx: H2blockers - cimetidine protectants - sucralfate antiemetics - metoclopramide coag panel/crossmatch/transfusion surgical removal of gastrin producing tumors in pancreas resection of gastric ulcers if one focal ulcer, but not if whole stomach is affected. do endoscopy first to see what is going on. gastrotomy: main indicationn is large foreign body cranial midline laparotomy pack off ventral midline of stomach with moist lap pads to catch spillage incision - b/w greater and lesser curvature closure: 2 layer - mucosa/submucosa, muscularis/serosa. any pattern you like - continuous lembert with simple interrupted lembert over it. slide: dog with lots of plastic in stomach, many pieces. place stay sutures incise b/w greater and lesser curvature, open stomach - another stay suture can pull incision open for you. make incision big enough! delayed gastric emptying: usually true vomiting of undigested food is seen,, sometimes congenital pyloric stenosis (boxer, bulldog, boston, siamese cat) or acquired chronic hypertrophic pyloric gastropathy - formerly seen a lot in smalll dogs. also caused by fb, neoplasia slide: contrast hanging out in the stomach. this is two hours post barium administration in awake animal. emptying should occur within 20-30 min. pyloromyotomy - here, you are making a lonngitudinal incisionn in the pylorus. let mucosa bulge out. this is effective in congenital stenosis, not acquired gastropathy. pyloroplasty - make longitudinal incision,, sew transversely. also only good for congenital some sort of Y something is now being drawn on the board. you cut a y shape, at the pylorus, then sew the flap down to the bottom of the Y. you're advancing it distally. Y-u pyloroplasty partial gastrectomy - "billroth" surgery. two type - billroth I and billroth II. billroth I: removes part of pylorus and antrum - usually for neoplasia or hypertrophic gastropathy thing. duodenum is then sewn to stomach. you have to oversew stomach edge until lumen size matches duodenal size. this surgery results in "dumping" of large particles and gastric acid innto duodenum. dogs do seem to compensate well with time. what if tumor is further down duodenum? be careful! bile duct and pancreatic ducts are there. billroth II - more radical. if tumor is further down duodeum, you've ligated common bile duct - sew duodenum closed, sew stomach closed, resect your tumor, then do side to side gastrojejunostomy so stomach empties into jejunum. then, you need to perform biliary diversion - hepatic ducts drain into commonn bile duct - which has a duct into gall bladder - so you take gall bladder, open it, so it to jejunum - cholecystojejunostomy. but what if the pancreatic duct is also tied off? if you can't find an accessory pancreatic duct, you have to remove pancreas and treat as diabetic EPI patient. slides: how you do all this stuff. lots of simple interrupted sutures :) gastric neoplasia in dog, except leiomyo and LSA, have poor survival time even with good resection. ----end----