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Chronic GIT disease in horses - Coggle Diagram
Chronic GIT disease in horses
Weight loss
= decrease in body weight, usually due to a loss of body fat
reduced feed intake
malassimilation
malutilisation
common causes
dental disease
larva cyasthostominosis
IBD
gastrointestinal neoplasia
chronic grass sickness
liver failure
PPID
chronic renal failure
protein losing enteropathies/nephropathies
Chronic D+
mild and will often have persisted for months
usually bright and alert (BAR) and remain hydrated
pathophysiological mechanisms
altered structure/permeability
altered epithelial cell transport
osmotic effect
altered motility
common causes
larval cyathostominosis
IBD
proliferative enteropathy
NSAID induced ulcerative rights dorsal colitis
sand enteropathy
gastrointestinal neoplasia
peritonitis
Recurrent colic
= abdominal discomfort that persist over several days OR repeated bouts of abdominal discomfort, separated by a period of remission
pathological mechanisms
gastrointestinal
gastric pain
intestinal stenosis e.g. partial obstruction, incomplete displacement
abnormal intestinal motility
peritoneal or mesenteric pain e.g. peritonitis, abdominal abscess
non-gastrointestinal
urogenital, hepatic, musculoskeletal pain
common causes
gastric ulcers
IBD
peritonitis
chronic grass sickness
sand enteropathy
abdominal abscess
gastrointestinal neoplasia
Diagnostic approach
History
Signalment
young horses more susceptible to parasitism and proliferative enteropathy
older horses are more likely to have neoplasia, dental disorders, renal disease adn PPID
Diet
"won't eat" vs "can't eat"
access to food
Medical history and preventative medicine
when was the horse last weighed?
when were teeth last checked?
dewormed?
are other horses affected?
D+
previous medication?
Physical examination
other clinical abnormalities
colic
nasal discharge
jugular pulses + loud murmur
faecal staining
ventral oedema
hypoproteinaemia
peripheral oedema
Body condition score
ideal score= 5
Rectal exam
rectal palpation
examine faeces
Oral exam
oral lesions
abnormal odour
dental points
wave mouth and loose or missing teeeth
Clinicopathological data
Complete blood count +/- fibrinogen/SAA
with chronic inflammation, WBC is usually elevated
horses will often have an anaemia of chronic inflammation
fibrinogen and SAA (serum amyloid A) are usually
Total protein, albumin, globulin
low albumin
PLE and PLN
effusions--> peritoneal and pleural
liver disease
high globulin
chronic inflammatory disease
Liver enzymes, creatinine and BUN
SDH, GLDH, GGT, AST and ALP +/- bile acids --> liver disease
creatinine and BUN--> renal disease
Abdominocentesis
peritoneal colour, WBC, protein + cytology
useful to rule out peritonitis
in rare cases neoplastic cell may be seen
Ultrasonography
thoracic and abdominal US useful for detecting and evaluating effusions, masses, intestinal motility, and bowel wall thickness--> suggest infiltrative or IBD
hepatic + renal disease
Gastroscopy
horse needs to be starved for at least 16hrs and water withheld for 2hrs
rule out gastric ulcers + gastric neoplasia
can also obtain duodental pinch biopsies
Oral glucose absorption test
evaluates SI malabsorption
starve overnight, administer 1g/kg glucose as a 20% solution via nasogastric tube, keep horse calm and do not sedate with alpha 2 agonists, take blood samples every 30min and submit for glucose analysis
normal: >85% increase in blood glucose conc. at 120mins
partial malabsorption 15-85% increase 120minns
complete malabsorption: <15% increase at 120mins
Rectal biopsy
helpful if there is infiltration/inflammation in large intestine which is also affect the rectum
correlation with intestinal pathology in 40% cases
Larval cyathostominosis
aka red worm
encysted L3 larvae cause colon inflammation
diagnosis based on demonstration of larvae in faeces
faecal egg counts are often negative
serological test can detect IgG(T) antibodies specific to larval cyathostomins
treatment involves larvicidal doses of fenbendazole or moxidectin +/- corticosteroids
IBD
weight loss
chronic D+ may be seen if colon is involved
chronic colic can occur due to abnormal intestinal motility +/- stenosis
hypoproteinaemia is common due to PLE and may present as ventral oedema
granulomatous enteritis, plasmacytic lymphocytic enteritis, eosinophilic enteritis, multisystemic epitheliotropic eosinophilic disease (MEED)
diagnosis based upon characteristic clinicopathological data, thickened intestinal walls on US and abnormal glucose absorption test and full thickness intestinal biopsies
rectal biopsy may indicate infiltration of inflammatory cells
treatment= corticosteroids + dietary management
palatable, easily assimilated high energy + protein source is indicated
supplement with electrolytes, minerals + vitamins
Gastrointestinal neoplasia
alimentary lymphoma + gastric squamous cell carcinoma most common
weight loss, anorexia, fever +/- chronic D+. recurrent
hypalbuminaemia evident in many cases due to PLE + peritoneal effusion
hyperfibrinogenaemia is common
rectal exam + abdominal US
peritoneal cytology may reveal abnormal cells
prognosis POOR
Proliferative enteropathy
Lawsonia intracelluris
weanling + yearlings
clinical signs: fever, lethargy, ventral oedema, chronic D+ colic, weight loss
mild anaemia, hypoalbuminemia, high fibrinogen
thickened SI
diagnosis based upon faecal PCR or serology
treatment with tetracyclines is curative in most cases
Gastric ulcers
aka EGUS, ESGD, EGGD
common cause of poor perfomance
may cause colic + contribute to weight loss due to inappetence
lesions may occur in squamous or glandular regions of stomach
managemental risk factors that increase exposure of squamous mucosa to acid
gastroscopy is used for diagnosis
treatment= management + dietary modification in conjunction with the use of acid suppressant--> omeprazole is the drug of choice
Sand enteropathy
chronic D+ +/- recurrent colic
accumulates in colon
diagnosis based on demonstration of sand in colon on radiography or using a faecal sand sedimentation test
oral administration of psyllium mucilloid and magnesium sulphate once daily for 3-5 days is curative in most cases
Ulcerative right dorsal colitis
associated with administration NSAIDs
right dorsal colon preferentially affected
clinical signs: recurrent colic, D+, weight loss + ventral oedema (due to PLE)
diagnosis based on characteristic clinical signs, history NSAID administration, hypoalbuminaemia + thickening of right dorsal colon on US
treatment = discontinuation of NSAIDs, misoprostol, dietary manipulation
Chronic grass sickness
aka Equine dysautonomia
causes neuronal degeneration in autonomic and enteric nervous systems that results in intestinal dysmotility
NE Scotland, rest of UK, Northern Europe, South America
pasture derived neurotoxin likely implicated
usually seen in spring--> particularly in dry weather after period of rain
young horses more susceptible
acute, subacute + chronic forms
acute form presents with acute colic, nasogastric reflux, small intestinal distension
subacute + chronic form presents with chronic GIT disease
may also see dysphagia, rhinitis sicca, ptosis, tachycardia, patchy sweating + trembling
greyhound appearance--> very tucked up
diagnosis based on characteristic clinical signs, 0.5% phenylephrine eyedrops and an ileal biopsy
angle of eyelashes change, which can help make diagnosis
treatment is supportive but often unrewarding