---start---- medsurg3/9003 Dr Washabau has plainly stated: THE FINAL IS NOT CUMULATIVE (Kirsten asked me to type this) Exams will be mostly multiple choice as in the past. Palmer - malabsorption syndromes- an overview/granulomatous enteritis definitions: malabsorption: failure of passage of products of digestion through intestinal mucosa, into the blood maldigestion: failure of intralumeal digestion due to an enzyme defect most common maldigestion syndromes: lactose maldigestion man is pretty much the only animal who does NOT have lactose malabsorption with aging...people are born with more lactase in the brush border than you will ever have and it is gradually lost. in most animals, it is lost at weaning age. in people, some can drink milk to old age - mainly people of northern european descent, who come from dairy farming people. these people tend to maintain lactase in brush border for life. also, there is a whole plethora of milk protein allergies only maldigestion described in large animals is a few cases of lactase deficiency. lactase isn't plentiful, is very vulneraable to disturbances of GI tract such as rotavirus infection which kills mucosal cells. then there is a period of milk intolerance which is usually transient and not worth investigating. malabsorption pathogenesis: defect in cellular phase: not grossly evident: problems that you don't see on histopath, that cause malabsorption. can be transient, secondary to GI insult. -loss of structural polarity -loss of carrier proteins -loss of brush border enzymes villus atrophy: -decreased cell production -increased cell loss -loss of functional numbers -minimal atrophy: 75% loss is required for experts to detect atrophy -clubbing and fusion: 90% loss required for joe vet to detect problem -villus atrophy: 97% loss so significant problems are possibly present but not visible. defect in delivery phase: diffusion block: -cellular absorption normal, but not delivered to blood or lymph causes: -inflammatory cells, tumor cells, amyloid - these separate the epi cell from capillary. you may have cellular defects without delivery defects, but when there are delivery defects you usually also get cellular defects because cell become malnourished. infiltrative disease prevents nutrients from diffusing into cell from blood. Malabsorption etiologies: granulomatous enteritis intestinal LSA strongylus vulgaris (rarely seen now but immature forms in mesenteric aa reduce blood flow to gut) cyathostomes (encysted forms in mucosa, inflammatory rxn) rotavirus - destroys absorptive epi cells ischemia protein malnutrition - starves enterocytes. sometimes seen w/milk replacer diet. antibiotics m.tuberculosis v.avium m. paratuberculosis histoplasmosis intestinal amyloidosis diagnosis of malabsorption: monosaccharide absorption tests: used fairly regularly -glucose absorption test -xylose absorption test dissaccharide absorption test -lactose absorption test starch absorption test mixed grain absorption test tritiated oleic acid absorption test vitamin A absorption test (tests fat absorption) to do all these tests, you feed the stuff, then look for it in the blood monosaccharide absorption test: 12-18 hr fast to get empty stomach so you don't affect results 0.5 gm/kg xylose 10% solution or 1 gm/kg glucose 20% solution give via stomach tube, no sedation which might affect results draw blood q 1/2 hr for 4 hrs glucose test - in fluoride xylose test - in heparin refrigerte no food or water during the test no washing it down with water! would change gastric emptying and sugar concentrations. should see peak at 1-2 hrs - glucose values double, xylose gets >12 abnormal results: delayed peak: most common "abnormal" finding. usually a normal absorber, though. causes: delayed gastric emptying hypertonicity of fluid excitement pain retained gastric contents * most common partial obstruction false flat curve: because of severely dellayed gastric emptying decreased blood flow to bowel hypovolemia bacterial overgrowth - bacteria eat sugar prior to absorption ascites: diffusion into fluid is faster than asorption into blood abnormal metabolism falsely high curves: decreased urine output liver dz metabolic dz pasture diet - horses on pasture have falsely high curves for some reason. Glucose absorption test: effect of fasting: 12 hr fast will decrease absorption to 80% 36 hr fast will decrease absorption to 40-50% so if animall is anorexic, curve might be flat not due to primary malabsorption, but due to fast. also if you're deciding what test to do - if you repeat tests, let animal eat b/w tests, don't do a continuous fast. choosing test: glucose v xylose: glucose is readily available, less specific, need more damage before test is positive. may miss subtle problems. more convenient test, though. xylose is poorly absorbed so more sensitive, but less available and more expensive. more difficult to run. usually do glucose then repeat w/xylose if unsure. treatment: depends on specific problem nonspecific therapy: use common sense. if animal has poor absorptive capacity, feed small, frequent meals - this takes advantage of natural remaining absorptive capacity. use easily absorbed protein source, good AA balance, good fat content - equine senior high fat, high energy feed....also remember may need to give parenteral vitamins and feed mineral supplements. classic malabsorption in horse: Granulomatous enteritis: granulomas in the bowel also in other tissues, often - lung, liver, etc young horses - 3-5 yrs, mainly standardbreds some familial tendency etiology: idiopathic - most common cyathostomes mycobacteria (avian form - only in immunosuppressed patient) histoplasmosis eosinophilic form - eosinophilic rxn common in horse allergic LSA - lots of lymphocytes present but w/granulomatous enteritis also giant cells, granulomas. LSA is common *misdiagnosis* of GE. signs: wt loss in most cases lethargy dependent edema diarrhea < 50% of cases b/c small intestine more affected chronic colic - granulomas may cause strictures, etc dermatosis - due to malnutrition or skin granulomas rectal exam: mesenteric masses colonic lymphadenopathy (nonpainful) intestinal masses thickened, friable rectum feces may be loose slide: mesenteric lymphadenopathy - big LNs, sort of soft, feel near hilus of left kidney for these fingerlike projections slide: mass attached to small intestine. may feel like fecall ball but w/rough edges slide: stricture secondary to granulomatous invasion. clinical lab: hypoproteinemia is common, is not nutritional! these horses with malabsorption are using muscle for protein. but the granulomas cause increased epi turnover and protein losing enteropathy, patient can't make protein fast enough to keep up with losses. plasma transfusions do not help - protein drains out anemia - may be nutritional leukopenia - endotoxin? abnormal absorption test dx: rectal biopsy, exploratory sx, necropsy surgery not usually recommended - these horses do not heal well - usually malnourished lesions: adhesions strictures/stenosis ulceration small or large intestinal masses LNs, pancrease, liver, spleen, bm, kideys, skin, joints - widespread histologic lesions intestine may look very rugose, won't lie flat - due to infiltration of submucosa. tx: corticosteroids - probably best tx sulfasalazine - have tried it, salicylate may decrease inflammation, mixed response. isoniazid - for mycobacterial infection metronidazole - for anaerobic infection larvicidal therapy - won't hurt, might help DMSO MSM slide: Arabian colt - thin 3 yr old wt loss 2-3 mos, variable appetite, anemia, low total protein, EIA neg, tx with larvicidal fenbendazole, no help absorption tests - xylose curve flat, glucose curve flat. big LNs pred and antimicrobial therapy tried; one week later owner stopped pred without telling anyone. horse came back in 2 mos with more wt loss and on postmortem, typical mesenteric lymphadenopathy, thickened rugose bowel ---break--- washabau - SA GI disease see the Dr. Littman handouts in the packet of handouts Esophageal disease: signs of esophageal motility disorders: these are often the signs causing animal to present to us: 1. dysphagia - difficulty in swallowing 2. odynophagia - painful swallowing - seen with inflammatory conditions as extension of neck during swallowing, or yelping in pain when swallowing 3. regurgitation * major one * passive evacuation of ingested stuff from esophagus - not vomiting - no abdominal component 4. excessive salivation - also seen with inflammation, which is a stimulus for salivation 5. avoidance of food - again, because of pain - esophagitis, etc. some animals with esophageal disease may have excellent appetite - those animals usually have something like idiopathic megaesophagus, dilation and abnormal funnction of esophagus without any inflammation. diagnostic workup: 1. PE and good history 2. oral exam 3. survey rads 4. barium fluoroscopy 5. endoscopy +/- manometry (often instead of 3, 4) so...[slide of neural regulation of esophageal motility]...this is a human, upright esophagus. our patients have horizontal ones. pharynx, OES, esophageal body, LES, stomach. there are afferent and efferent neural pathways. in all animals except dog, proximal esophageal body is striated, distal part is smooth muscle. (about 50-50). in the dog, for whatever reason, the whole thing is striated, down to the LES which is smooth muscle in all animals. This is important. it frustrates our ability to tx megaesophagus in the dog. ** important! survey rads and contrast studies: slide: barium esophagram from cat with healthy esophagus - we see material moving from proximal to distal into stomach. normal width of esophageal body. remember in cat, proximal 1/2 is striated muscle, distal 1/2 is smooth. look closely and you see there are some undullations of the mucosa highlighted by the barium - this is characteristic of smooth muscle. not in dog!*** may have to anesthetize and do endoscopy to directly visualize mucosa. slide: healthy canine esophageal mucosa - pinkish white, tends to collapse onto endoscope unless we insufflate the lumen. glistening. remember this image! slide: another example - smooth, pink slide: lower esophageal sphincter LES - closed, even during anesthesia. place endoscope there and push through to get into stomach. pale pink. slide: distal esophageal body of cat - undulations are present. Esophageal foreign bodies - relatively common slide: chest rad - there is a turkey cartilage piece in the esophagus. how do you treat this? welll, you could do a thoracotomy. you could also do endoscopic retrieval. slide: dog came in at christmas with radioopaque thing in esophagus these animals present with peracute, rapid onset of signs slide: fishhooks in esophagus - also usually seasonal. about 85% of these can be removed via endoscopy. there are also some metal sutures visible from last year's thoracotomy...and lead pellets in stomach! slide: easter egg in esophagus - intact! slide: knife in esophagus - was removed via gastrotomy 28 yrs ago... Vascular ring anomalies: these are congenital or hereditary slide: kitten, 3-4 wks postweaning, chest rads - progressive regurgitation present, failure to gain wt...chest rads show huge outpouchings of the esophagus in the thoracic cavity, and two diverticuli cranial to the heart base., in the area of a vascular ring... most important of these is PRAA (in dog and cat). at weaning, compression and obstruction of esophagus occurs. slide: VD view - dilated esophagus cranial to heart base, contrast not passing....this is a surgical condition thoracotomy and ligation of ligamentum arteriosum...but important to note, if animal presents after a few weeks, there is significant dilation of proximal esophagus, and myenteric neuronal degeneration, which may cause persistent dysfunction of proximal esophageal segment. so you have to telll the client that you don't know if surgery will make animal better. this kitten did improve and do reasonably well. with progressive obstruction and compression, there is also some fibrosis at the level of the ring, so you would also want to do a balloon dilation procedure to physically dilate that section of the esophagus, b/c of the fibrous tissue contributing to the compression at that site. if these are treated early on, prognosis is pretty good. Esophageal diverticula: these are diverticula that are not associated with vascular ring anomalies. we see barium transit droppinng down into dependent portion of thorax - congenital abnormality - herniation of esophagus into mediastinal structures. this animal had regurgitation with good appetite, failure to thrive. the only real therapy would be surgical correction, diverticulectomy. this animal had that, and significantly improved. can be congenital malformation, or if you practice in northern CA, there are foxtails which animals eat or inhale or whatever, and cause mediastinal or pulmonary abscesses that may involve esophagus. it heals, fibroses, abscesses, etc. diverticuli may form. these occur in adults. the prognosis for those is not so good, due to severe pulmonary abscessation, difficulty in dissection, infection, etc. Esophageal neoplasia: slide: barium study of upper GI tract in old cat with progressive regurgitation, dysphagia, loss of appetite, loss of body condition. survey rads not revealing. esophagram shows barium flow seeming to stop midthorax. but we do not see a discrete mass here, in mediastinum or esophageal lumen. endoscopy revealed a mass in there, though - it was an adenocarcinoma. malignancies of esophagus tend to be bad. leiomyoma/leiomyosarcoma can be resected with reasonably good px, others tend to be difficult to resect with poor px. so with esophageal neoplasia, generally, it isn't good. slide: this used to be seen around here, but not really in past 20 yrs - now mainly in SE US or mideast - older dog, dysphagia, regurgitation - mass in thorax is present - spirocerca lupi granuloma formation which sometimes transforms into sarcoma. this dog also had progressive lameness and characteristic finding of metaphyseal osteodystrophy (hypertrophic pulmonary osteopathy - proliferation of metaphyseal bone in response to primary pulmonary disease). Hiatal hernia: common cause of heartburn in dog/cat case: signalment: 4 mo old female shar pei 1 wk history excessive salivationn, vomiting, and regurgitation PE NR for shar pei survey rads: herniation of proximal stomach through esophgaeal hiatus into caudodorsal thorax. congenital. causes obstruction of flow into stomach. there is laxity in esophageal hiatus,, permitting stomach to move into thorax. contrast study: uh, uh-oh. the whole fundus/corpus is in thorax. esophagus is torturous. also he aspirated a whole bunch of barium. usually that isn't' a problem. but these animals sometimes present in acute respiraatory distress b/c of stomach preventing lung expansion. slide: endoscopic view - erythematous, hemorrhagic esophageal mucosa with fibrosis in areas. severe hiatal hernia here. types of hiatal hernia - congenital or acquired. we see the sliding type hiatal hernia in animals (type I) - movement of stomach through esophageal hiatus into thorax. instability due to incomplete fusion of hiatus during development. almost all the hiatal hernias we see are like this paraesophageal types - type II - where stomach herniates lateral to esophagus a series of cases of hiatal hernia was studied here...found to uniformly require surgical repair. 1. diaphragmatic crural apposition (don't include vagus nerves!) 2. esophagopexy to diaphragm 3. gastropexy to lateral body wall 4. gastrostomy feeding tube if there is severe esophagitis, feed this way for a few days. the surgery restores normal anatomy and cures disease Reflux esophagitis <--> hiatal hernia can be very debilitating and painful remember healthy LES we saw before - pink, whitish, tightly closed slide: LES of miniature poodle with signs of esophageal dz. severe inflammation, redness, hemorrhage visible on endoscopy how do you treat this? Tums works for Dr Washabau well, chemical diffusion barrier is important. in cats we found sucralfate will be a good diffusion barrier and will allow esophagitis lesion to heal. sucralfate/carafate is given as a liquid suspension - it fills in the eroded sites and prevents further diffusion of acid/pepsin etc into those sites. this is the mainstay of therapy. but it may not be sufficient. sometimes you have to also inhibit acid secretion. proton pump inhibitors, etc. or, third level of defense - drugs to increase tone of LES and improve gastric emptying - cisapride/Propulsid. some animals require chemical diffusion barrier, acid inhibitor, and motility promoter. Esophageal stricture - an unfortunate complication of esophagitis in some animals. also occurs secondary to ingestion of caustic substances. slide: animal that had elective OVH two weeks ago; had reflux during anesthesia, developed esophagitis, owner ignored signs of salivation and regurgitation and food avoidance, and with time stricture developed. movement of food is dependent on radius to the fourth power...small changes make a big difference. tx: balloon dilation - place catheter in to site of obstruction; progressively dilate to reach more normal size of lumen. after balloon dilation - realize animals are at risk for recurrence since esophaagus mainly heals by fibrosis. use antiinflammatory doses of steroids to prevent. ---end----