Diseases of the Equine SI Flashcards
Gastric Impaction
Infrequent cause of colic in horses Dry feed material and decreased water intake May occur during winter when dry hay is fed and water intake is lower Diagnosed at Sx in horses with colic Endoscopic examination Tx with dioctyl sodium succinate (DSS) - 5% solution via NG tube in 4-6L fluid Lavage at Sx, resolve in 24-48h
Gastric neoplasia
Uncommon in older horses
SCC most common
- Lymphosarcoma and adenosarcoma also occur
Arises from squamous mucosa and metastasizes to the abdominal cavity and viscera and/or extends up the esophagus
CS: chronic weight loss, anemia, naso-gastric reflux, colic
Gastric neoplasia Dx and Tx
CS Endoscopy (definitive) Biopsy Abd US Necropsy Tx: none Prognosis: grave
Disorders of the SI
Anterior enteritis (proximal duodenitis-jejunitis) - Vs SI obstruction (SISO) IBD Intestinal neoplasia Lawsonia intracellularis
Anterior Enteritis basics
Proximal enteritis, proximal duodenitis/jejunitis
Exact etiology and pathogenesis is unknown
- Salmonella, Clostridium, idiopathic, pancreatitis?
- Marked inflammation of SI***
Similar CS as SISO so a prompt Dx is crucial
Adult horse on high level of nutrition
SI distension, copious reflux and edema
CS of Anterior Enteritis (AE)
Acute onset of moderate to severe colic Copious amounts of nasogastric reflux - Orange/brown with fetid odor Moderate to severe SI distension -US or rectal palpation Mild fever (101.5F - 102.5%), tachycardia - Dehydration Decreased gut motility Prolonged capillary refill time (CRT)
DDx for Anterior Enteritis (AE)
SI strangulating obstruction
- SI volvulus
- SI incarceration through a rent in the mesentery
- Epiploic foramen entrapment
Ileal impaction
May not be clear clinical demarcation between these dz and AE
Dx of Anterior Enteritis (AE)
CS Distended loops of SI on restal examination and/or abd US Improvement in CS or depression after nasogastric intubation and removal of reflux fluid Peritoneal fluid analysis: - Increased total protein (>3.0gm/dL) - WBC count <10,000 cells/uL Exploratory laparotomy Necropsy
Therapy for Anterior Enteritis (AE)
Gastric decompression via NG tube
Aggressive fluid and electrolyte replacement, IV
NSAIDs
- Flunixin meflumine, phenylbutazone
Prokinetic agents
- Yohimbine - alpha 2 antagonist
- Lidocaine - sympathoadrenal refles
. Blocks transmission through afferent nerves (group 5)
. Antiinflammatory and antiendotoxic properties
Anterior Enteritis Antimicrobials and antiendotoxins
Antimicrobials:
- Potassium Penicillin
- Gentamycin
- Metronidazole
Antiendotoxin - polymyxin B
- Binds endotoxin and prevents release of TNF
- Administered especially if horse is neutropenic
Sx: Empty jejunum into cecum +/- infuse bowel with penicillin
IBD characteristics
Granulomatous enteritis, chronic eosinophilic gastroenteritis, plasmacytic-lymphocytic enteritis
This diseases is characterized by infiltration of the small and large intestine and regional LN with inflammatory cells, including lymphocytes, plasma cells, macrophages, and eosinophils
The inflammatory condition may be limited to only a short segment of the bowel or be more diffuse
IBD CS
Weight loss Recurrent colic Hypoproteinemia Generalized skin disease Diarrhea Malabsorption PLE
IBD Dx
CS
Thickened bowel or enlarged mesenteric LN on rectal palpation
Low serum protein concentration
Intestinal or rectal biopsy
Failure to absorb oral glucose or D-xylose verifies malabsorption from the SI
Pathophysiology of IBD
Not understood
Thought to be an altered immune response to a common intestinal factor (feed, parasites, bacteria)
Treatment of IBD
Limited success with many methods Corticosteroids Dietary alterations Metronidazole Azathioprine (antimetabolite) Supportive care (frequent feeding of good quality, high energy feeds)
Intestinal Neoplasia Basics
SCC of the stomach and the alimentary form of lymphosarcoma are the most common forms of neoplasia involving the GIT in horses
Chronic weight loss may be the primary clinical sign
Chronic diarrhea and hypoalbuminemia may develop when lymphosarcoma has infiltrated the wall of the intestine
T/F: Because the incidence of GI neoplasia is high, it should be the top differential for weight loss
False; low incidence, investigate other causes first
Dx of Intestinal Neoplasia
Exclusion of other causes of weight loss and histopath
Gastroscopy if SCC in stomach (endoscope 2-3m long)
In lymphosarcoma, enlarged mesenteric LN or thickened bowel may be detected by rectal palpation or by US
Occasionally, neoplastic cells are ID by cytology of abd fluid
US
Exploratory laparotomy
Tx of Intestinal Neoplasia
Generally not attempted
Sx
Prognosis: grave
Lawsonia intracellularis
Obligate intracellular, curved, Gr - bacterium that resides freely within the apical cytoplasm of infected intestinal enterocytes
Causes proliferation of the affected enterocytes, resulting in a thickened small and sometimes large intestine
Equine proliferative enteropathy
First reported in 1982
Outbreaks on breeding farms described
Almost worldwide
Pathophysiology of equine proliferative enteropathy (EPE)
Predisposing factors: weaning stress, parasitism
Route of infection unknown (feco-oral route suspected)
Infection =/= affected
Clinical presentation of equine proliferative enteropathy (EPE)
Manifested in foals 2-8mo and is seen August-Jan in NA
Lethargy, anorexia, fever, peripheral edema of the ventrum, sheath, throatlatch, distal limbs, weight loss, colic, diarrhea (not always)
Dx of equine proliferative enteropathy (EPE)
Ante mortem challenging:
- Hypoproteinemia
- Exclusion of common enteric diseases
- Thickening of segments of the SI wall on US
- Positive serology
- Molecular detection of L. intracellularis in feces
Nonspecific blood abnormalities in foals with equine proliferative enteropathy (EPE)
Anemia or hemoconcentration Leukocytosis or neutropenia Hyperfibrinogenemia Increased activity of muscle enzymes Electrolyte abnormalities (hypocalcemia, hypochloremia, and hyponatremia)
Therapy for L. intracellularis
Erythromycin Azithromycin Clarithromycin Doxycycline Chloramphemicol
