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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:
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GI DISEASES LAM 1 August 2005 Amy Fayette
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
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
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
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
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)
Neoplasia • SCC and lymphosarcoma most common
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
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
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
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
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
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
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
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
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
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
Cecal impaction • Tx • Medical • NG intubation w DSS • IV fluids • Walking • Analgesia (xylazine and butorphanol) • Sx: if pain cannot be controlled
Cecal perforation and rupture • Risk factors: tapeworms, parturition, ulceration etc • Tx: repair often imposible, removal of cecum • Prognosis: poor
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
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
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
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
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
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
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
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
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
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
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
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
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)
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
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
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
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
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
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
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
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
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
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
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
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