1 / 48

GI DISEASES

GI DISEASES. LAM 1 August 2005 Amy Fayette. SMALL INTESTINE. Ascarid Impaction. Clinical signs will typically mimic those of strangulating obstructions d/t severe necrosis and inflammation Signalment: weanlings Risk factors: recent administration of very effective anthelmintics CS:

naasir
Download Presentation

GI DISEASES

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. GI DISEASES LAM 1 August 2005 Amy Fayette

  2. SMALL INTESTINE

  3. Ascarid Impaction • Clinical signs will typically mimic those of strangulating obstructions d/t severe necrosis and inflammation • Signalment: weanlings • Risk factors: recent administration of very effective anthelmintics • CS: • Can get worms in gastric reflux • Toxic, shocky, moderate to severe colic • Tx • Surgical intervention

  4. Feed or Foreign body impaction • Ileal impaction is most common • Risk factors: GA, Fl, TX, and LA • Feeds w high fiber content: bermuda grass • Fine hay particles w water squeezed out to form a firm mass • CS • Rectal: SI distension, as impaction progresses gets pulled out of reach • Tx • Conservative: mineral oil, IV fluids and analgesics • Surgical intervention: post op illeus usually occurs • Prognosis: fair survival • Better if its fixed < 17 hours after starting

  5. Muscular Hypertrophy • Ileum • Primary (idiopathic) • Secondary (compensatory due to distal stenosis) • Signalment • Mature horses • Can be associated w presence of tapeworms • CS • Intermittent colic after eating • Tx • Medical if associated w tapeworms • Surgery • Prognosis: favorable after sx

  6. Abscesses • Signalment: < 5 years old • History: weight loss and/or unthriftiness • CS • Depressed, anorectic and febrile • Neutrophilia w left shift and hyperfibrinogenemia • Abdominocentesis (elevated TP and WBC) • EA: S. equi, S. zooepidemicus, R. equi, C. pseudotuberculosis • Tx • Conservative: long term AB’s, treatment of choice but guarded prognosis • Sx

  7. Adhesions • D/t inflammation in the abdomen esp peritonitis • History: recurrent bouts of colic, often secondary to previous abdominal surgery • Tx: sx • Prognosis: guarded to poor (recurrence common)

  8. Neoplasia • SCC and lymphosarcoma most common

  9. Volvulus • Twist on the long axis of the mesentery at least 180 degrees • One of the most common causes of true strangulating obstruction in the SI • Signalment: <3 years old • <1 year olds may be d/t diet change or ascarid infection • Ileum is commonly involved

  10. Strangulating Lipoma • Signalment: older horses, overweight horses • Pedunculated fat mass oin the end of a fibrovascular stalk • History: recurrent bouts of abdominal pain • Prognosis: guarded

  11. Internal Herniation • Epiploic foramen • Signalment: older horses (possibly d/t reduction in size of the liver with age) • CS: • Peritoneal fluid evaluation: abnormal in 56% of cases • Rectal exam: SI distention in ¾ of cases • Reflux in almost all cases • Tx: surgical correction can result in immediate death of horse d/t rupture of the caudal vena cava or portal vein • Gastrosplenic ligament entrapment • Mesenteric defects

  12. External Herniation • Inguinal • Indirect are present w/I the vaginal tunic • Direct are those in which the intestines lie in the SQ tissues outside the vaginal tunic • Signalment: newborn colts, breeding stallions • CS in stallion: usu indirect and unilateral (left esp) • CS in foal • Indirect: reducible, non painful, correct spontaneously • Direct: acute, painful

  13. External Herniation • Umbilical • Second most common congenital lesion in the horse • Strangulation of SI associated w this lesion is rare • Predisposing factors: manual breaking of umbilical cord, umbilical infection, excessive straining, ligation of the cord • Hernias in need of surgical correction: increase in size, firmness, warmth, edema, pain on palpation • Diaphragmatic: rare • Risk factors: trauma, increased intraabdominal pressure (parturition) • CS: resp or GI signs (episodic colic) • Prognosis: guarded

  14. Intussusception • Risk factors: higher rate during times of fecal consistency change, tapeworm infestation, previous SI sx, anthelmintic administration, ascarids etc • Signalment: <3 years (can occur in older horses) • Ileum and ileicecal junction • CS: acute colic followed by intermittent colic lasting weeks to months • peritoneal fluid change may not reflect the degree of intestinal necrosis b/c dead gut is isolated from the peritoneal cavity • Prognosis with surgery: fair to poor

  15. DPJ • Aka Anterior enteritis • Looks like strangulating disease • Signalment : all ages, mostly adults, those on an adequate to high plain of nutrition • Pathophysiology: • Accelerated transmucosal fluid movement • CS • Moderate to severe abdominal pain (subsides after decompression, most horses remain very depressed) • Lots of NG fluid • Dehydration, injected MM • Temp >101 F but not high fever

  16. DPJ • Tx: decompression and fluid administration • NSAIDS: not enough to mask signs of pain in case it is a strangulating lesion • Antiendotoxic therapy: flunixin and antiserum administered IV • Antibiotics: cover systemic effects of altered mucosa • Motility drugs: if reflux for 7 or more days • Sx if no resolution or to confirm absence of strangulating lesion • Complications: adhesions and laminitis • Prognosis • >90% survive primary insult • Usually succumb to complications

  17. CECUM

  18. Cecal tympany • 2 types • Primary- rapid gas production and decreased motility • Secondary- associated w obstruction in the large or small colon • CS: • bloated in right flank • HR > 100 bpm • Silent abdomen but right flank has high pitched pinging • Tx • Decompression percutaneously • Supportive therapy w fluids and analgesics

  19. Cecal impaction • 2 types • Dehydrated firm food mass filing cecum • Cecal dysfunction: idiopathic w ingesta of fluid conistency • Risk factors: dehydrated type associated w diet high in corn or coarse hay • History: orthopedic problems • Signalment: more common in adults • CS: • mild to moderate intermittent pain w decreased gut sounds • Cecal dysfunction type usually more severe pain and signs of endotoxemia

  20. Cecal impaction • Tx • Medical • NG intubation w DSS • IV fluids • Walking • Analgesia (xylazine and butorphanol) • Sx: if pain cannot be controlled

  21. Cecal perforation and rupture • Risk factors: tapeworms, parturition, ulceration etc • Tx: repair often imposible, removal of cecum • Prognosis: poor

  22. LARGE COLON

  23. Impaction • Often in winter d/t worse hay, and horses drink less water when its cold • Risk factors: poor dentition, foreign materia, decreased water intake, altered colonic motility, adhesions • CS: intermittent colic, pain worsens if unresolved • Tx • IV fluids • Analgesics: can be worsened by multiple doses of alpha 2 agonists • Laxatives: mineral oil or DSS • Walk frequently • Off feed until a substantial amount of manure is passed • Prognosis: good unless evidence of bowel wall compromise

  24. Sand Enteropathy • Risk factors • Feeding on ground in sand stalls or sandy pasture • CS • Similar to Lg colon impaction • Weight loss, diarrhea • Lie on side or back to relieve tension on mesentary • “sand on beach” sound may be heard in ventral abdomen • Dx • Float feces, find sand in the bottom • Rads of ventral abdomen • Tx • Psyllium (binds and removes sand • Sx may be necessary if complete obstruction, if unresponsive pain or if deterioration despite therapy

  25. Enterolithiasis • Signalment: 5-10 years (takes time to form) • Risk factors • California • Nidus of undigestible material (twine/rubber fencing) • Dietary magnesium • Spherical (often single), tetrahedral (often multiple) • CS • Recurrent colic • Rarely feel enterolith • Tx • Surgical removal • Medical dissolution doesn’t work

  26. Right Dorsal Displacement • Idiopathic • Signalment: all horses (maybe large breed) • CS: • insidious to moderate colic depending on degree of gaseous distention • Reflux occurs if duodenum is obstructed by displacement

  27. Nephrosplenic Entrapment (LDD) • Signalment: warm bloods, large horses and drafts • CS • Pain (will lie down sternal to decrease the pull on mesentary) • Dx • Rectal: The most overdiagnosed cause of colic in the horse (presence of gut in region may not be trapped) • Ultrasound of nephrosplenic space • Abdominoscentesis to look for other evidence of bowel compromise

  28. Nephrosplenic Entrapment (LDD) • Tx • Medical : phenylephrine causes splenic contraction which will release colon (do PCV and TP before and after) or try rolling horse • Surgical correction: tack edge of spleen to nephrosplenic ligament (decrease space) • Complications • Recurrence etc

  29. Large Colon Torsion • Signalment: older brood mares, can be any age and any sex • Risk Factors: 1 month prior to 1 month after parturition • Pathophysiology • Exact cause unknown • Root of mesentery is the location for constriction of the twist • If torsion > 180 degrees venous occlusion occurs • If torsion > 270 degrees arterial occlusion occurs

  30. Large Colon Torsion • CS: sudden severe pain, the most painful colic • Pulse may be normal • DOA d/t metabolic acidosis, resp compromise, endotoxemia etc • Tx: • Fast surgical correction • Possible lg colon removable • Support for endotoxemia

  31. Inflammatory Collitis • Look like strangulating disease • Often associated with typhlitis • Etiologies • Infectious: Salmonellosis, Potomac Horse Fever, Clostridiosis • Nutritional: Grain overload, blister beetle, Sand enteropathy • Parasitic: Cyathostomiasis • Plant and chemical toxins • Drug induced: NSAIDS (phenylbutazone), antibiotics

  32. Inflammatory Collitis • Pathophysiology: inciting cause leads to mucosal damage results in inflammation which leads to further mucosal necrosis • May progress to protein losing enteropathy (NSAIDs) • Diarrhea in horse = large colon disease • CS • Emergency d/t severe fluid losses and toxemia • Looks like strangulating colic • Fever, depression, shock, diarrhea

  33. Inflammatory Collitis • CS • Colic evaluation: reflux- usually none; rectal palpation- distended bowel but not usually tight • Clin Path: increased PCV and TP d/t dehydration; hypoproteinemia depends on severity and inciting cause; severe endotoxemia and stress pattern for WBC

  34. Inflammatory Collitis • Dx • Definitive dx only in 20-30% of cases • CBC, chem profile • Hct: increased TP: variable low normal • WBC: often low Total CO2: test for bicarb • Renal fnct: BUN, Creatinine d/t hypovolemia • Fecal cultures/fecal flotation • Serology • Rectal mucosal biopsies • Abdominocentesis, sand sedimentation

  35. Inflammatory Collitis • Tx • Supportive therapy • Anti-inflammatories and analgesics • NSAIDS- avoid if possible • DMSO- use at 1/10th standard dose • Analgesics : not banamine, use alpha 2 agonists or butorphanol • Antimicrobial • Not indicated in uncomplicated cases • For systemic issues in face of animal that is immunocompromised or showing signs of bacteremia etc • Use Pen w gentamicin or potentiated sulfa (TMS may cause colitis)

  36. Inflammatory Collitis • Tx • GI protectants • Impact of effect considered minimal in most cases • Mineral oil, activated charcoal, bismuth subsalicylate • Feeding • May be anorexic initially • Frequent small feedings, High quality • Good management: bedding, baths, tail wraps • ICU care

  37. Salmonellosis • Most frequently diagnosed infectious cause of diarrhea in horses • Very contagious, potentially zoonotic • Etiology • No host adapted salmonella in the horse • Epidemiology • Fecal oral transmission • Outbreaks more typical in warmer months • Asymptomatic carriers under stress can shed organisms

  38. Salmonellosis • Risk Factors • Very STRESS related disease • Risk factors: concurrent GI disease, long transport, sudden feed cahnges, antimicrobial administration d/t disturbed GI microbial population etc • Pathophysiology • Produces endotoxin, cytotoxin (cell death in colonic mucosa), and enterotoxin

  39. Salmonellosis • CS • Malodorous profuse watery diarrhea • Several syndromes • Fever w leukopenia • Colic w diarrhea • Colic w/o diarrhea • Proximal enteritis/jejunitis • Septicemia (foals and neonates) • Asymptomatic carriers

  40. Salmonellosis • Dx • Lab eval • Leukopenia, neutropenia, met acidosis, decrease Na, Cl, HCO3 • Fecal eval • Cultures: minimum 3 usually 5 sequential culture • Neg culture doesn’t mean horse is negative it indicates that the horse isn’t infective • Can also culture reflux (if presents as DPJ) or abdominocentesis fluid • Rectal mucosal biopsy/culture • Tx: same as general therapy for collitis • Prevention/control: strict isolation and disinfection

  41. Potomac Horse Fever (Equine Monocytic Ehrlichiosis) • Virtually indistinguishable from salmonellosis, can be infected with both • Etiology: neorickettsia risticii (aka E. risticii) • Epidemiology • No known horse to horse transmission • Involves a trematode vector • Pathophysiology • Obligate intracellular parasite which infects trematode • Trematode then infects snail

  42. Potomac Horse Fever (Equine Monocytic Ehrlichiosis) • CS • Very high fever (104-106) 1-2 days prior to development of other signs • High frequency of laminitis, often severe enough to warrant euthanasia • Diarrhea: cow like to watery feces, chronic diarrhea does not occur • Dx • Isolation/culture typically difficult • Paired serum samples: IFA or ELISA • Tx • Oxytetracycline • Oxytet associated with development of salmonellosis in some horses • Supportive therapy

  43. PHF VS SALMONELLA

  44. Antibiotic associated colitis • Antimicrobials can disrupt the normal flora and cause GIT disturbances • Should never be used: clindamycin, lincomycin and neomycin • Associated with colitis: tetracyclines, TMS, ceftiofur, erythromycin, pen, rifampin, metronidazole, enrofloxacin

  45. Clostridial Enterocolitis • Etiology: C perfringens, C difficile • Epidemiology • Risk factors: foals or adults in training, altered GI flora (antibiotics) high protein or carb diets • Clostridium is part of the normal flora, however those that inhabit GI are in low numbers and do not produce enterotoxins • CS • Necrotizing enterocolitis • Severe toxemia and shock • Hemorrhagic diarrhea in foals

  46. Clostridial Enterocolitis • Dx • Fecal gram stain • Fecal culture • Toxin ID (ELISA for C difficile toxin( • PCR • Necropsy: smears of GI mucosa • Tx • Frequently unsuccessful • Aggressive shock and symptomatic therapy • Foals: metronidazole if C difficile

  47. Cantharidin ToxicosisBlister Beetle Toxicosis • Risk factors • Ingestion of alfalfa hay (2nd cutting or later) • Hay cut and crimped at the same time • More frequent in hay harvested in midwest • Most contaminated bales are at outer edge of the pasture • CS • Very severe unresponsive pain • Polyuria, Pollakiuria, hematuria • Severe hypocalcemua (may see SDF) • SOME OF THE WORST COLICS YOU WILL EVER SEE

  48. Cantharidin ToxicosisBlister Beetle Toxicosis • Pathophysiology • Cantharidin (toxic principle) severely caustic • Causes erosions and ulcerations in GIT • Dx: CS associated with risk in history • Texas A+M can id toxin (antemortem: urine, post mortem: GI contents) • Tx • Unresponsive to analgesics • Supportive therapy • Most will die

More Related