Ruminant Indigestion: Diagnosis and Clinical Signs

• Signalment is crucial for diagnosing ruminant indigestion, considering factors like age, use (dairy vs. beef), production stage, feeding requirements (feedlot, freshening), and concurrent diseases like hypocalcemia.
• A thorough history, particularly feeding history, is important as it affects fermentation patterns, leading to conditions like frothy bloat (low fiber, high concentrate, legumes), ruminal impaction (poor hay/straw), or ruminal acidosis (high carbohydrate, sudden access).
• Most indigestion cases aren't emergencies, except for frothy bloat or acute ruminal acidosis.
• Clinical signs are often nonspecific: hypo- or anorexia, dullness/depression, decreased productivity, and altered ruminal contractions.
• Failure to identify the underlying cause can lead to overlooking primary reticuloruminal disease.
• Malnutrition in calves leads to poor growth and a rough hair coat.
• Fever is uncommon, except in cases like TRP (Traumatic Reticuloperitonitis) or rumenitis.
• Shock is uncommon, except in severe acute bloat with respiratory/CV compromise or acute ruminal acidosis due to fluid shifts and acidosis.
• Decreased reticulorumen fill is often linked to hypomotility and anorexia in primary and secondary indigestion, especially if prolonged.
• Increased reticulorumen fill can indicate impeded forward ingesta flow (overfeeding, vagal indigestion) or fluid sequestration (acute ruminal acidosis).
• Ventral distension is associated with rumen issues (usually left, but can be right), hydrops (left dorsal), +/- left displaced abomasum, abomasal/intestinal diseases (right side leading to reflux), or generalized peritonitis/prolonged obstruction (bilateral/diffuse).
• Cranial abdominal pain suggests TRP or abomasal ulcers, evident in a painful expression, reluctance to move, short gait, kyphosis, and extended neck.
• Normal ruminal contents have fluid, a firm fiber mat, and gas layers; abnormalities like taut distension (bloat), firm fibrous material (impaction), or fiber sinking below fluid (stasis, e.g., TRP) indicate issues.
• Fluid accumulation is splashy in acidosis and occurs with vagal indigestion or abomasal outflow obstruction.
• Assess rumen contraction frequency, duration, and strength, using tests like the scootch/wither’s pinch or grunt test for cranial, ventral abdominal pain.
• Per rectal: Detect gas, rumen shape changes (L-shaped rumen), abomasal distension/impaction, and rumen lymph node enlargement (rumenitis).
• Fecal abnormalities are common but delayed; normal transit time is 1.5-4 days.
• Decreased, dry feces indicate anorexia, acute digestion, or obstructions.
• Decreased amount, dry, firm feces with increased fiber length suggest TRP, omasal transport failure, rumen impaction, dental disease, or abomasitis.
• Increased whole grain suggests ruminal acidosis.
• Greasy feces with fine particles indicate abomasal displacement/pyloric outflow failure.
• Foamy, fluid, yellow acidic feces suggest acute ruminal acidosis.
• Pasty to fluid feces with a foul odor suggest fermentative indigestions or enteritis.
• Rumenocentesis via needle is reliable for accessing ventral sac fluid, but risks abdominal contamination.
• Naso- or oro-gastric tubes can get stuck on the fiber mat or plugged; saliva contamination increases pH; specialized tubes minimize these issues, and nasal passage may reduce saliva contamination.

Bloodwork Analysis

• CBC: an inflammatory leukogram with increased fibrinogen signals TRP, rumenitis, vagal indigestion (secondary to pneumonia/TRP inflammation), or complications from bacterial translocation in ruminal acidosis.
• Hemoconcentration suggests dehydration, while anemia indicates chronic disease.
• Chemistry: anorexia leads to hypocalcemia, hypokalemia, ketonemia, and ketonuria (especially in lactating cows).
• Acidemia occurs in ruminal acidosis.
• Azotemia is a sign.
• Increased liver and muscle enzymes may indicate vagal indigestions.
• Omasal transport failure shows minimal abnormalities, while abomasal outflow failure shows significant abnormalities.

Imaging Techniques

• Ultrasound
• Peritoneum: Detects free fluid, fibrin, and abscesses.
• Reticulum: Assesses the semicircular structure, contractions, and gas contents in the cranioventral abdomen; abnormalities indicate TRP, abscesses, or fibrin.
• Rumen: Assesses the smooth, thin wall, contractions, and gas contents in the left paralumbar fossa and caudoventral abdomen; thickening indicates ruminitis, abscesses, or peritonitis.
• Radiographs: Detect TRP.

Traumatic Reticuloperitonitis (TRP) / Hardware Disease

• Pathophysiology: Wire/metallic foreign body penetrates the reticulum, causing abscess, peritonitis, pleural space issues, and pericarditis.
• The reticulum becomes inflamed, leading to motility dysfunction, ruminal stratification loss, impaired rumen outflow, and consistency changes in ingesta entering the abomasum, impairing abomasal emptying.
• Vagal indigestion may play a role.
• Severe, acute signs: fever, anorexia, ruminal hypomotility, cranial abdominal pain, decreased milk production, ketosis, regurgitation, tachycardia, reluctance to move, abducted elbows, and mild bloat.
• Over time, signs become subtle: weight loss, diarrhea, rough hair coat; involvement of the heart, liver, or spleen.
• Heart: Pericardial effusion (muffled/sloshing sounds), right-sided CHF (distended jugular veins, weak pulses), or acute death (coronary artery laceration).
• Liver or spleen abscesses may develop.
• Treatment: Medical (magnet ingestion, antibiotics, confinement) or surgical (rumenotomy).
• Prognosis: Fair to good with localized peritonitis and liver/spleen involvement if inflammation recedes; poor to guarded with pericarditis, pleuritis, or diffuse adhesions.
• Prevention: Magnets at 6-8 months and removing sharp objects from feed.

Free Gas Bloat

• Pathophysiology: A clinical sign of various indigestion causes--not a primary disease.
• Failure of eructation due to mechanical obstruction (esophageal, cardia) or motility dysfunction.
• Fermentation disorders reduce excitability of gastric centers and the reticulum, decreasing eructation.
• Reticulorumen wall distension and blockage of cardia with vagal indigestion, ruminal acidosis, or rumen impaction.
• Chronic, recurrent bloat is associated with vagal indigestion.
• Diagnosis: Left dorsal distension "ping" relieved by passing a tube.
• Treatment: Treat underlying disease; acute severe cases require emergency gas removal via oro-/nasogastric tube or trocar; chronic/recurrent cases may need temporary fistula.
• Prognosis: Depends on the underlying disease.

Frothy Bloat

• Pathophysiology: Digestion of feed results in stable froth in the rumen, causing severe distension; froth near cardia prevents relaxation, leading to obstruction.
• Legumes, lush winter wheat pasture, and grain diets can cause it. Some cattle are predisposed.
• Diagnosis: Severe distension, colic, respiratory compromise, inability to relieve gas with a tube, presence of froth on the tube.
• Treatment: Poloxalene for pasture, mineral oil/animal tallow for feedlot/grain.
• Prognosis: Pasture death losses 0.5-2.5%; feedlot incidents ~1% with 0.1% death losses.
• Prevention: Avoid high-risk pastures (difficult), supplement with poloxalene, oils, tallow, rumensin; increase fiber in grain diets, slowly introduce concentrate, use lasalocid.

Vagal Indigestion

• Classification: Failure of eructation, rumen outflow, abomasal outflow, or partial pyloric outflow/proximal intestinal obstruction.
• Pathophysiology: Hypermotility of the rumen is common, leading to accumulation of ingesta in the reticulum, creating an L or papple shape, and empty omasum/abomasum.
• Causes: TRP and other abscesses/adhesions of the reticulum, hepatic diseases, diffuse peritonitis.
• Diagnosis: Vigorous rumen contractions (especially if eructation still occurs), inappetence, mild dehydration, and electrolyte imbalance.
• Treatment: Treat underlying disease, supportive care (fluids, electrolytes), empty ingesta, resolve bloat, limit feed/water, and transfaunate.
• Prognosis: Slow response; positive indicators = normal contractions, improved appetite, weight gain, increased fecal output; negative indicators = continued distension, scant feces, poor motility, recurrent bloat.

Simple Indigestion

• Pathophysiology: An abrupt change in feed, moldy/overheated feeds, or bad silage cause imbalance in microflora and fermentation products.
• Diagnosis: Anorexia for 1-2 days, diarrhea after 24 hours, reduced ruminal activity, mild bloat, and mild pH changes.
• Treatment/Prognosis: Generally self-limiting as rumen microflora adapts.

Acute Ruminal Lactic Acidosis

• Pathophysiology: Carbohydrate-rich feed causes rapid fermentation → lactic acid → decreased ruminal pH.
• Overproduction of lactic acid, producing/using bacteria, increases rumen fluid osmolarity, pulling fluid into the rumen causing hypovolemia.
• Chemical damage to the mucosa allows toxins/bacteria to leak into the bloodstream, causing secondary infections.
• Mycotic and bacterial infections occur in the rumen wall.
• Thrombi, liver abscesses, and laminitis occur distantly.
• Hypovolemic and distributive shock (plus lactic acid leakage from the rumen) → acidosis.
• Diagnosis: Shock, ruminal distension, and splashy fluids.
• Treatment: Aggressive supportive care, rumenotomy, therapy for bacterial translocation/rumenitis, and thiamine supplementation.
• Prognosis: Depends on stabilization ability and complication severity.

Subacute Ruminal Lactic Acidosis

• Pathophysiology: Similar to the acute form, but milder and prolonged.
• Ruminal wall changes: parakeratosis, ruminitis, liver abscessation, and laminitis
• Key diagnostic findings: Herd problem, decreased appetite and ruminal hypomotility, foamy, fluid feces, and acidic pH.

Ruminal Impaction

• Pathophysiology: Ruminal microbial flora becomes inactive due to lack of nutrients, especially with poor-quality roughage deficient in protein/digestible nutrients.
• Decreased activity prevents feed breakdown, leading to large fibers causing distension.
• Diagnosis: Severe distension (papple), roughage mixed with fluid or sinking, decreased feces with long stem particles, decreased growth/production, ketosis, emaciation, and poor hair coat.

Ruminal Drinking

• Failure of esophageal groove function is caused by the type of liquid, feeding method, or age.
• Abnormal microflora results in poor nutrition
• Leads to poor performance, potbelly, altered rumen pH, enteritis/diarrhea, and acid-base/electrolyte disorders.

Ruminal Bloat (Recurrent Tympany)

• Usually gas-related.
• Occurs frequently With disease, indigestion, LDA, or lung disease.
• Sudden filling of the abomasum occurs when already filled with other feed during weaning.

Simple Obstruction of Reticulomasal Opening

• Indigestion of foreign material.
• Occurs especially in small ruminants like goats.
• Presents similarly to other reticulorumen outflow obstructions.
• Surgical removal via rumenotomy is likely to have a good prognosis.

Abomasal Disease

• Outflow obstruction, either mechanical (displacement, volvulus, impaction, pylorus obstruction, intestinal obstructions) or functional (vagal indigestion) or inflammation/ulceration.
• Signalment/History: Dairy cows in early lactation (displacement/volvulus), calves (3 weeks to 4 months), Suffolk sheep (emptying defect), wintering pregnant beef cattle (impaction), or pregnancy (vagal indigestion, pyloric outflow failure).
• Physical Exam: Shock (abomasal calculus); ping (displacements/volvulus); rumen fluid with increased chloride (internal vomiting/abomasal reflux).
• Clinical Pathology: Hypochloremic metabolic alkalosis (obstruction).

Abomasal Displacement and Volvulus

• Pathophysiology: Decreased motility → distension with gas.
• Concurrent diseases and postpartum changes implicated: ketosis, hypocalcemia, metritis, retained placenta, mastitis, fatty liver, hyperinsulinemia, diet/exercise changes.
• Can occur sporadically in calves, dairy bulls, and beef cattle.
• Abomasal ulcers, FB, and geo sediment can predispose LDA.
• Types: LDA, RDA, AV.
• Diagnosis: Drop in milk production, decreased appetite/feces, physical exam, AV tend to have more signs of systemic shock, ping (cannot differentiate RDA/AV), rectal exam and AV more common.
• Clinical Pathology: Urine ketones; AV usually have more severe electrolyte and acid-base abnormalities and CMT.
• Treatment: position correction; blind/open laparoscopy; RDA/AV emergency Sx.
• Prognosis: LDA/RDA good, AV fair to good; underlying disease is important.
• Prevention: Dietary management, slow introduction of concentrate, DCAD diet to prevent hypocalcemia.

Abomasal Impaction

• Pathogenesis: Accumulation of firm ingesta.
• Mechanical: Abnormal, dry contents, poor quality roughage, hair, placenta, sand, gravel, or mural lesions (lymphosarcoma, abscess).
• Functional: Vagal indigestion, TRP, late pregnancy, perforating abomasal ulcers, or AV.
• Diagnosis: Progressive anorexia, decreased fecal output, loss of condition, right or bilateral ventral/papple distension, ballottement of the abomasum right cranial abdomen.
• Clinical Path: Dehydration and electrolyte abnormalities over time.
• Treatment: Medical management (digestible feeds, fluids, laxatives, prokinetics) or surgical treatment.
• Prognosis: Overall poor, often caught late, surgery rarely successful; dairy cows with limited pyloric antrum involvement can have a good prognosis with medical treatment.
• Prevention: Attention to feeding, shelter, and water in severe winter conditions.

Abomasal Dilation and Emptying Defect of Suffolk Sheep

• Pathophysiology: Occurs mainly in Suffolk sheep; mechanism unknown (possible acquired dysautonomia).
• Contents similar to ventral rumen; pylorus patent, ingesta present in distal GI tract.
• Clinical Presentation: Anorexia, weight loss, watery green diarrhea or normal feces, ruminal tympany, ventral abdominal distension motility changes, ballottement of mass right cranial ventral abdomen.
• Clinical Path: Minimal changes, hypocalcemia, increased rumen chloride.
• Prognosis: Usually poor; some success with surgery and prokinetics; most die of cachexia.

Abomasal Ulcers

• Lesion that penetrates the basement membrane of abomasal mucosa, graded by depth (cattle): Type I (non-perforating), Type II (non-perforating bleeding), Type III (perforating, local peritonitis), and Type IV (perforating, generalized peritonitis).
• Incidence and predisposing factors: All ages of cattle, rarely sheep/goats/camelids (C3 glandular portion).
• Type 1: Veal calves (2-8 weeks), weanling calves, fattening cattle, high-producing dairy cows. Predisposing factors stress, changes in housing/feed, straw ingestion, infectious agents. High incidence but often subclinical.
• Type II: Lymphosarcoma-related ( 5 years, throughout lactation) or related (4 years, early lactation, concurrent postpartum disease).
• Type III/IV: Sporadic in adult cattle related to metabolic stress with concurrent disease, high concentrate and corn silage diets.
• Calves: Veal/beef calves (4-12 weeks), yearling feedlot. Perforating cases proposed factors include nutritional deficiencies, bacterial/fungal agents, abrasive agents, and stress.
• Diagnostics: Abdominocentesis, abdominal US, blood work (CBC: inflammation, anemia, hemoconcentration; Chem: stasis, hypochloremic, metabolic alkalosis, shock, acidosis), and BLV testing ( 5 y/o with Type II).
• Treatment: Correct dietary problems, reduce stress, treat concurrent disease, supportive care (transfusion), treatment of peritonitis, and medication to reduce acid in the abomasum.
• Prognosis: Good for Type I; ok for Type II and III; poor for Type IV and II due to lymphosarcoma.

Gastric Disease

• Outflow Obstruction: Mechanical (poorly digested feed, phytobezoar persimmon seeds) or functional (concurrent GI dysmotility, chronic, recurrent form) and inflammation rupture.
• Clinical Signs: Inappetence, colic, variable severity, chronic dysmotility forms may have displaced spleen on rectum.
• Treatment: Supportive care, enteral fluids and lavage, laxatives/agents to break up impaction, motility agents, and surgical access to the stomach

Equine Gastric Ulcer Syndrome (EGUS)

• Incorporates ulceration of the distal esophagus, non-glandular (squamous) and glandular stomach, and proximal duodenum.
• Equine Squamous Gastric Disease (ESGD): Exposure to irritants, gastric acids, and pepsin.
• Equine Glandular Gastric Disease (EGGD): Acid injury, compromise of protective mechanisms.
• Prevalence: ESGD (40-90% in performance horses), EGGD (8-63%), EGUS (60-70% in domestic horses, 22-30% in feral horses).
• Risk Factors: Age, gender, training, concurrent GI disease, diet, and environment.
• Factors that induce ESGD: exercise, high concentration/low roughage diet, fasting, transport, stall confinement
• Clinical Signs: Vague systemic signs, inappetence, poor BCS/weight loss, diarrhea, changes in behavior, poor performance, pain with tightening girth, stereotypic or abnormal behavior, colic; clinical signs of ESGD do not always correlate with ulcer presence/severity.
• Foal EGUS: Prevalence (25-50%), age (2-6 months), four clinical syndromes (subclinical, clinical, perforating, obstructing); signs include bruxism, drooling, diarrhea, colic, lethargy, interrupted nursing, and tongue rolling.
• Diagnosis: Endoscopy is definitive.
• Treatment: Management changes (modify exercise, increase pasture turnout, eliminate bolus feeding, increase forage/fiber, decrease CHO intake, preventative medication doses), pharmacotherapy (acid reduction, coating ulcers, antacids, PGE2 analogue, prokinetics).

Pyloric Stenosis in Foals

• Clinical signs Colic, reflux, regurgitation, unthrifty, pot-bellied.
• Diagnosis Endoscopy contrast radiography
• Treatment Nutritional, gastric decompression, supportive care, Sx

Gastric Rupture

• Acute septic peritonitis often colicky and the acute sweating.
• Diagnosis US and Abdominocentesis
• Treatment Surgery

Constipation Terminology

• Constipation - Infrequent or difficult fecal elimination
• Obstipation - Intractable constipation
• Tenesmus - Ineffectual and painful straining at defecation
• Dyschezia - Difficult or painful defecation that aries exclusively from disease of the anal and perianal tissues