---start--- medsurg3 10.30.98 holt gastric dilatation and volvulus (GDV) [slide] large dog with IV caths. standard poodle. he's standing up, panting, otherwise seems ok. [slide] drawing of a stomach [slide] GDV - this stomach is not filling whole abdomen and is not purple, so that is good. the first thing we're going to clear up right now - textbooks are confusing. they say "imagine you are in northern hemisphere, dog is pointing north, and stomach rotate right." forget that. remember -esophagus is on left, pylorus right 95% or more of these stomachs rotate such that pylorus moves either to ventral midline, to the left lateral body wall, to the dorsum. realize the esophagus is attached to the stomach. this is twisting. slide: bdly affected tomach - large part of it is dark purple/blue. this dog also has severe peritonnitis. GDV described first in 1906 which came first - bloat, or twist? answer is, who cares? this isn't one condition. this isn't "GDV" it is a range of things. they can bloat, or dilate, without twisting their stomachs, they can have dilation and volvulus, or can have chronic volvulus without dilatation. so there is a range of presentations from percute collapse to chronic flipping back and forth of stomach with no acute signs. etiology: not clear gastrin? - delays gastric emptying, increases gastroesophageal sphincter pressure - but not significantly different b/w affected and normal dogs in a study that was done. when you are sampling by the way, if gastrin is higher in GDV dog the question is, is this cause or effect? same thing with delayed gastric emptying. people thought this was a pyloric problem - dog eats large meal, can't empty stomach, bloats. but they studied this in affected dogs. so delayed gastric emptying is not thought to be a cause. people have been doing various pyloric procedures - a study by Greenfield at Illinois looked at dogs with and without pyloric procedure and found no change in bloating frequency esophageal motility - is not normal in these dogs with recurrent GDV. cause? effect? dietary factors: once daily feeding of dry food results in larger stomach size but no difference in gastric motility. a study of 600 dogs found no change in GDV incidence based on diet/exercise patterns. myoelectric dysfunction - role unclear. what do we know, then, if we don't know this stuff? slide: rad - stomach full of air gastric gas - originally thought to be from fermentation, but it isn't. it's the result of aerophgiea. these dogs are greedy eaters, swallow a lot of air. so empirically, we see they tend to be greedy eaters, and run around lots after eating. what else do you see on the slide? these dogs come in shocky a lot. why? whatshould you see in caudal thorax? lugs, mediastinum, caudal vena cava. can't see vena cava. that's why they come in shocky. stomach gets so distended it collapses vena cava, no venous return to heart. often large breed,deep chested dogs, greedy eaters, recent ingestion of large meal, often restless, noxious, salivting, with nonproductive retching. that makes you think of esophageal obstruction...but think laterally. anytime there is regurgitation a lot - think of aspiration.do not forget the possibility of aspiration pneumonia. dogs often have aabdominal distension and are progressively weak. this is nice to discuss in lecture, but in life you must consider differentials. don't come to clinics and try to shotgun dx things. PE: poor perfusion/shock. REMEMBER perfusion - this tells you what's broken and what you have to fix. pale mm, weak thready pulses. variable abdominal distension, collapse, stupor, coma, severe shock: suspect gastric rupture ddx distended abdomen: simple gastric dilation in puppies - often they get distended after meals. that's usually ok. they have more compliance to their body walls, that might be why they re ok. mesenteric volvulus - rare but occurs splenic torsion or masses lliver masses ascites peritonitis all these things cause abdominal distension pathophysiology: compression of portal vein, caudal vena cavaa decreased venous return to the heart decreased cardiac output decreased arterial blood pressure net result: poor tissue perfusion realize - portal vein and caudal vena cava get shut down - venous return is really poor. experimentally, GDV is not hard to mimic - just obstruct pylorus and LES, inflate stomach. we've documented these findings. tissue does not get perfused. so what happens: increases in circulating levels of endotoxin in many dogs prostaglandin release reperfusion injury: lipid peroxidation damages cell membranes. when tissues aren't well oxygenated and then blood flow returns, free radicals form and they hurt the tissue. cardiac arrhythmias - on presentaation or postop due to myocardial ischemia. cardiac output is low, myocardial perfusion is low. after 6-24 hr, arrhythmias occur. other things contributing to it are circulating cardioactive substances - epi, norepi...aand myocardial depressant factors released from ischemic pancreas. so CO falls more than 60%. stomach has distended and or twisted so flow to stomach gets reduced by 80%. mucosal cells are most active so suffer first. if you look inside stomach, often the mucosa is black, and will slough. mucosal necrosis is ok, will regenerate. but full thickness necrosis is bad. spleen - gets engorged - splenic vein drains to portal vein which is shut down. kidney - may see prerenal azotemia liver- decreased portal flow so, you know there is decreased CO due to poor venous return. correct circulatory collapse, then dx D or DV. decompress stomach and pexy if needed. monitor postop for complications! rapid volume expansion - shock doses - 90 ml/kg balanced electrolyte solu'n or 5 ml/kg/min hypertonic 7% saline and 6% dextran. must follow that with crystalloids. extended database: PCV/TS/AZO/Dex, Na/K, ABG EKG radiography decompress stomach slide: catheter placement - clip hair adequately, prep area. use a large enough catheter. use jugular catheter if needed. do not place caths in saphenous - venous return is blocked. you need to volume resuscitate before you decompress the stomach. our success rate is up to 85% for GDV now, and Dr Holt notes this is since his arrival. what has changed? better intensive care. dedicated ES clinicians. use of volume resuscitation prior to surgery. we use aggressive fluid replacement first. passing stomach tube - measure it first so you know how far. sedate and intubate first if needed. rads: you need a right lateral view because then, pylorus should be down on the film and full of fluid and not visible. if you do not see it, think bloat, not twist. but if you have rotation, it is full of air, and you do see it.this is called the "popeye sign" sometimes. looks like a flexed bicep :) in most cases, anyway. situation - a dog was bloated, rads looked ok, but couldn't pass stomach tube. took another view. still looked just bloated. but couldn't pass stomach tube b/c kept hitting resistance. so - what do you do? cut. why would you have a normal rad and not pass a tube? 360 degree volvulus. if in doubt, go look. remember the esophagus. do not attempt to force the tube down. now and then, they find rupture right up near diaphragm, perhaps from someone trying to force a tube. to decompress - large bore needle, clip and scrub a spot on the abdomen somewhere where the spleen is NOT, then decompress by trocharization. sometimes chest rads show air in esophagus - that's ok. let it go. not megaesophagus. occsionally, you see great detail of the bowel in abdomen - free gas, sign of ruptured stomach. surgical plan: decompress, repositio stomach, assess viability of stomach, assess spleen for thrombus, infarction, torsion, pexy stomach to body wall to prevent volvulus. usually omentum is over stomach when it twists. if not, usually just bloat. if just bloat- can trocharize or pass stomach tube. slide: omentum is over stomach. how do you derotate this? pylorus moves from dog right to dog left. so you can grab and pull with right hand, push with left hand. what if you get confused? pylorus is the landmark. how do you find it? find the duodenum with pancreas stuck on it - it will be attached to the pylorus. then pull the pylorus back to the right side of the dog. this stomach looks ok. slide: another stomch that is sort of hemorrhagic - some hemorrhagic serosa , but still ok. other procedures: slide: black, ruptured stomach tissue -requires resection. partial gastrectomy - manual or stapled. this dog had macaroni and cheese peritonitis - ruptured stomach after mac and cheese meal. oops. when you use the stapler, you should oversew - continuous lembert over top of it. splenectomy - if it looks thrombotic, remove spleen. gastric outflow enhancing procedures are contraindicated. do not do them. slide: spleen looking ok, slight hemorrhge nearby slide: black necrotic spleen pexy: not most important but usually done. incisional, nonincisional, beltloop, tube, muscle flap, etc. many times of them. they all work. the idea is you taake pyloric antrum, fix it to body wall so it can't move. you do not suture pylorus itself. you go a bit back up to antrum tube gastropexy: what he usually does. feel behind 13th rib, make skin incision, pass tube through body wall. +/- omentum wrapped around tube, pass tube into antrum, put purse string around tube. without pexy, GDV recurs >50% of the time. suture stomach to body wall - how? imagine square around tube and square on body wall - suture the corners. inflate balloon and you are set. postop - continue IV fluids 10-20 ml/kg/hr initially, recalculate as needed monitor electrolytes esp K+ and supplement colloids (hetastarch, plasma) as needed - this one dog had an albumin of 1.5 postop... antibiotics - used in cases of gastric necrosis and aspiration pneumonia. arrhythmias often do not appear til postop period. usually ventricular. some say they are prognostic. dr brockman's study says they are not. when you get a ventricular arrhythmia -do not reach for lidocaine. think what is causinng it - myocardial ischemia due to poor perfusion. think - how is the perfusion. is it ok now? reassess perfusion, electrolytes, blood gas. treat arrhythmia if associated with poor perfusion or if severe (rate > 160 associated with poor diastolic filling, R on T complexes). so increase fluids if needed, fix electrolyte derangements first. slide: EKG- ventricular arrythmias - but good pulse pressure - rate 113 - do not need to tx. R on T = fibrilliation is coming. tx lidocaine. DIC: another postop complication. death is coming, dog in cooler, dave is clinician...blood stasis, pooling, hypoxia, acidosis, endotoxemia. why does animal die? thrombosis. yes, dog is bleeding out. but the big thing to realize is the clots are going somewhere and are obstructing flow. DIC will not go away unless you tx underlying cause. almost all dogs post GDV sx had some coagulopathy, but they did fine b/c perfusion problem was fixed. tx - correct underlying cause, maintain tissue perfusion, consider heparin and plasma. still more postop complications: silent aspiration pneumonia - fever 3 days out often presenting sign. thoracic rads, transtracheal wash, abx, nebulization. gastric necrosis - peritoneal tap, lavage, immediate re-exploration recommendations to owers -this is quackery but try to feed them a few small meals a day and try to make them eat slowly. restrict exercise after meals. consider prophylactic gastropexy to prevent volvulus in high risk dogs? ---break--- dr brockman - yet another no show. that's three for me so far this quarter. wow. ok, so, dr holt again: Perineal hernia: slide: ayre's rock? never rains. place to see in australia. desert climate. Perineal hernia - swelling near anus, on one or both sides. caused by weakness in muscles of pelvic diaphragm resulting in loss of support for rectal wall and subsequent rectal dilation or deviation. some say rectum will have a diverticulum in it. that would mean mucosa protrudes into muscularis layer of rectum. so, when muscle next to rectum atrophies, rectum can curve, or sometimes it feels like there is an outpouching - not a true diverticulum. main presenting sign - tenesmus - b/c feces sit in the deviation or the pouch. why does the atrophy occur? don't know. several theories. neurogenic atrophy? EMGs were done. changes on EMGs and on path specimens were classic for neurogenic atrophy. decreased adrogen receptors in pelvic diaphragm (levator ani and coccygeus) - these dogs do have decreased receptors - do not know why. changes in concentration of relaxin? - someone took some muscle and did immunostaining for relaxin - remember, that hormone loosens pelvic symphesis allowing calf to exit a cow. why is relaxin in a male dog? who knows. but they found normal dogs had no relaxin, and affected dogs had relaxin. so, for some reason maybe their prostates made relaxin and caused this weakening. signs: tenesmus constipation bulge/swelling in perineal area which is often mistaken for neoplasm sometimes, signs of acute urinary obstruction - imagine this dog is straining to urinate due to mild cystitis or prostatomegaly - imagine then the bladder gets flipped up into perineal hernia- now, urethra is kinked 180 degrees. ureters don't change. bladder gets big. perineum swells. skin gets discolored blue, purple black... it isn't cancer... PE: most affected dogs are older. check for other diseases too. dx: via rectal exam - alway rectal your normal dog patients too. you should not be able to put finger in and turn it side to side. check for bilateral vs unilateral herniation. check for bladder or prostate in hernia. put finger next to anus - should feel muscles resisting. if muscle is atrophied, you will be able to press in really far - unless there is a feces filled rectal pouch there. then you'll feel that. bladder retroflexion: large swelling with skin discoloration azotemia, hyperkalemia, just like blocked cat decompress! you can try to pass urinary cath - it will not go. so, you have to do perineal cystocentesis. stick needle into the middle of the swelling. decompress. then reposition bladder or move it enough that you can pass urinary catheter. now, you also have to deal with illness - give insulin and glucose to drive potassium into cells if hyperkalemic. rehydrate. drawing: action potential -80 is resting membrane potential difference. if potassium is lost, potential gets more negative. if there is too much, resting potential moves closer to the threshold potential. this is bad. too much potassium causes arrhythmia and then bradycardia and cardiac arrest. when resting potential approaches threshold, repolarization can not occur. this is why the heart stops. another tx for this - calcium gluconate slow IV - it is the functional antagonist of K+ b/c it will increase the threshold potential and make the difference the same as it was before. if you give too much, you will increase the threshold potential too much and prevent depolarization. so we tx with IV cal gluconate slow IV and avoid giving more K+ you could do peritoneal dialysis but it takes too long. so - perineal cystocentesis, give fluids w/o K+, give cal gluconate ok, so ddx for perineal swelling: prostatic dz - abscess, cyst pelvic masses rectal tumors pararectal abscess ruptured anal sac anal sac adenocarcinoma which is usually in females realize when the bladder flips back to the hernia, prostate and bladder blood supply is dorsal, when it flips back it is cut off. not happy. intestine will rarely herniate bakc here too. slide: paraprostatic cyst - this can also get back there. conservative management - highly digestible, low residue diet, stool softeners, periodic enemas. this is not fixing the real problem. surgical considerations: preop bloodwork, well padded rectal stand to avoid obturator nerve damage, NO immediate preoperative enema (will make a watery, nasty mess out of dry feces), perioperative abx? if used, cefoxitin is good for gram negs and anaerobes - you re doing sx in a contaminated area, that's true. but use of abx is controversial. one small study showed no difference in infection rates w/ or w/o abx. sx: open hernia sac, put contents in normal position, try to reconstruct pelvic diaphragm. this is not so easy what's in pelvic canal? internal pudendal a,n,v. so do little dissection. free adhesions bluntly, push stuff back. coccygeus and levator ani may be sewn to external anal sphincter; internal obturator also sewn to external anal sphincter. problem is, there is a big gap and you can't really fill it in with suture. see, the levator ani and coccygeus are too far lateral from the ventral anal sphincter. there is too much pressure when you try to pull them together. you end up ripping the coccygeus or pulling open the anus. mesh repair - the problem is, what if you get an infection, and there's a foreign body there? so, there is an internal obturator flap technique; internal obturator siton floor of pelvis, runs over femur with big tendon. come in caudally, incise along th eischium, elevate the obturator muscle, and lift it up. you re incising the origin, and folding it up into the defect. this is good- it uses healthy tissue to repair the defect. when you are in there, it is hrd to see the ischium so you have to feel for the hard bone. incise caudal border of ischium with scalpel - do not incise further cranially at the muscle, you will not get strong periosteum. now, laterally, you're still attached - have to cut w/o cutting the lateral vessel. you cut all the way forward and cut the tendon. you sew part of your flap to anal sphincter, and part to coccygeal and levator ani. there is still a small defect you will fill in iwth more sutures. sutures are all preplaced. results of surgery: classic repair: 21% recurrence with experienced surgeons, 70% with less experienced surgeons flap transposition: study 1: reherniation in 1/42 dogs, study 2: 31/31 dogs improved after surgery. bilateral dz, chronic signs - more postop problems. if bladder is protruding - blood supply is damaged, nerves may also be damaged. you have to maintain a urinary catheter to keep the bladder decompressed. he's seen two cases of complete bladder ischemia and necrosis. wound infection 10-25% of cases. it's a contaminated area. infection tends to be just subcu - debride, lavage, leave it open to heal. prevention better than cure - no preop enema, avoid putting drains in this area. perioperative antibiotic benefit unclear. rectal prolapse - dogs with large rectal flexures or sacculations are at risk. mild: pursestring x 2 days severe: abdominal colopexy for infection - we aren't sure if antibiotics should be used. infection here is no surprise. remember - minimal dissection, push stuff back where it belongs. sciatic nerve damage- sutures placed cranial to the scrotuberous ligament penetrating or entrapping the sciatic nerve. remember - you are suturing stuff to an atrophied muscle. cranial to these muscles though, is the sacrotuberous ligament going from sacrum to ischial tuberosity. you can anchor your sutures here. BUT cranial and ventral to that is sciatic nerve. so you must feel the ligament and take a bite of it, not go around it. if you go around it you may catch part or all of sciatic nerve. then dog wakes up knuckling and painful. then you have to reopen, remove the suture, and give postoperative steroids. so the weak link here, btw, is external anal sphincter - suturing collagen to collagen to muscle... castration: effect on recurrence uncertain. still will decrease prostatomegaly and straining to defecate. if it recurs after obturator flap technique , refer it. if you can't refer becaue you are the referral surgeon, you can try to do a second flap technique using aa new layer of periosteum; or you can try semitendinosus flap repair - take semitendinosis which runs from ischium to tibia - sever at distal femur and ligte the vessels in midbody of muscle, and do not damage caudaal gluteals. fold muscle belly up into defect. this can also occur in cats. in both dogs and cats - do an epidural - more comfy postop. use same technique in cat. the thing in cats is - they have no sacrotuberous ligament, and they often also have concurrent megacolon. so you wonder what to fix first. if there is megacolon, fix tht first. that may be enough. ----end---