Gastric Disease Syndrome Flashcards
What are the causes of gastric disease syndrome?
Dilation
Impaction
Rupture
Equine gastric ulcer syndrome (EGUS)
Tumors (SCC)
General CS associated with gastric disease syndrome
Painful abdomen (mild to severe)
From off feed → depression and colic (laying sternal or violent rolling)
Progression → uncontrolled pain, damage/ alteration of gastric tissue, endotoxemia → death
Gastric dilation
Secondary to intestinal ileus
Backflow of gas/ fluid into stomach (reflux)
Build up of pressure not moving through GI
What is gastric dilation associated with?
CHO, feed fermentation, proximal duodenal-jejunitis
Refeeding injury or parasites (bots)
CS of gastric dilation
Anorexia, depression, or mild to moderate signs of colic
Gastric dilation dx
Endoscopy*
Rads/ US for small horses
Emptying time test
What can happen with prolonged gastric dilation?
Damage to nerves and muscle due to over stretching
Future dilations or impactions
Client education for gastric dilation
Multiple small meals, chopped/ soaked quality hay, 1-2 tbs salt, fresh water, mash of senior chow
Gradually reintroduce normal feed
Avoid lush/ spring pasture
Tx for gastric dilation
Decompress PRN
IV fluids, electrolytes replacement, analgesics, anti-inflamms
Gastric impaction
Masses of large amounts of compacted, soft to doughy or hardened material
+/- gas or fluid
Rare (1%), fast eaters, social standing, starvation
What is gastric impaction associated with?
Lack of deworming (parasites, bots, tapeworms- Anaplocephala perfoliata)
No access to water
Consumption of large amounts of feed
Eat feeds that swell (dehydrated feed)→ consumption of material that expands with water
Refeeding a starved horse
Primary causes of gastric impaction
Functional or anatomic defects:
↓ gastric emptying, acid secretion, pyloric strictures, chronic dilation
Secondary causes of gastric impaction
Poor mastication, FB, dehydration, hepatic dz, any GI disturbance resulting in ileus, refeeding injury
CS of gastric impaction
Inappetence to acute colic
Signs of shock
Duration: hours to months
DX of gastric impaction
Gastric endoscopy: finding feed after withholding food/ water for 18- 24hr*
US (smaller horses with distended stomachs)
Peritoneal tap (transudate/ exudate, fibrous matter)
Hematology (systemic inflamm)
Rectal palpation (+/-displaced spleen)
Tx for gastric impaction
Decompress PRN, IV fluids
Breakdown mass: diocytl sodium succinate
Laxatives: MgSO4 (stomach filled halfway or less)
Anti-inflamms, analgesics, abx
What broad spectrum abx are given if the gastric impaction ruptures?
Ceftiofur + gentamicin
Crystalline penicillin + gentamicin
Prognosis of gastric impaction
Guarded to poor:
Factors: overstretched muscles/ nerves, mass too dense, altered blood flow, pressure necrosis
Euthanasia
Client education on gastric impaction
Resolves: patient goes home
Multiple small meals, mash or soaked hay, hydration
Healing: 7 days for each day sick
What happens if gastric dilation/ impaction cannot be resolved?
Shock, rupture then DEATH
Gastric rupture
Loss of serosal/ muscle integrity from gastric distention, localized infarction from impaction/ dilation impairing blood flow or severe EGUS and perforation
Where does the rupture occur on the stomach
Greater curvature
CS of gastric rupture
Moderate to severe colic
Depression, toxic line
Shock
Absent gut sounds, abnormal mm, gastric reflux, gritty serosal surface (rectal)
Sweating
What are the signs of shock?
Cold extremities, weak but rapid pulse, tachycardia, shallow breathing, low absent urine output, sudden cold sweat
Full thickness GR is _________
Fatal
Primary causes of gastric rupture
Excessive intake or fermentation of ingesta
Delayed emptying (ulcers, gastroparesis)
Slow onset of symptoms
Secondary causes of gastric rupture
Intestinal obstruction aboral to stomach
Obstruction: FB, tapeworms/ bots, CHO
Enteric: ulcerative gastritis, trauma, strictures, etc
Peritoneal: ileus, peritonitis
When do horses go into SIRS (systemic inflammatory repsonse) if they have gastric ruptures?
If they fit 2 or more:
T> 101.5, HR >60, RR >30
Fibrinogen >400
WBC >12.5 10^9 or <4.5 10^9, >10% band neutrophils
Gastric rupture tx
NONE with grave prog and euthanasia
Client education for gastric ruptures
Minimum stress
Slow down greedy horse, avoid fermented feed, gradual dietary changes
Equine squamous gastric dz
Lesions in squamous region (↑ exposure to acid)
Dx: gastroscopy
Tx of Equine squamous gastric dz
Gastric protectant, promote healing, ↑ roughage, fluid PRN, reduce stressors
Equine glandular gastric dz
Lesions in the glandular region
Impaired mucosal defense
Dx: gastroscopy
Mucus- bicarbonate layer
Mucus keeps excess acid away from mucosa
Bicarb neutralizes acid near the muscosa- gradient action
Cellular restitution
Contributes to mucosal integrity via rapid cell turnover
Epidermal growth factor
Potent gastric acid inhibitors
Potent stimuli of mucosal growth
Mucosal blood flow
Supplies mucosa with O2, nutrients and takes away metabolic waste
Maintained by PG-E2
Prostaglandin E2
Directly cytoprotective
Influences blood flow, ↑ mucus- bicarb secretion and inhibits gastric acid secretion
Risk factors associated with EGUS
Stress → endogenous corticosteroids
Other dx for EGUS
Admin fluids → positive response is ulcers
Oral exam
Rectal palpation/ US (rule our right dorsal colitis and thinning/ thickening of intestinal wall)
Gastroscopy
If no response to tx and severe CS
Confirms ulcers
Finds lesions in squamous, glandular region
Grades of ulcers
0: stomach lining intact, no reddening
1:Stomach lining intact, some reddening
2: small, single or multiple ulcers
3: large single or multiple ulcers
4: extensive ulcers
What happens if ulcers go untreated?
Perforate → septic peritonitis and endotoxemia and death
Tx of EGUS
IV fluids with electrolytes
Gastric protectant: oral antacids/ sucrlafate (topical), acid inhibitors- omeprazole or ranitidine/ cimetidine (systemic)
Eat good roughage
