Bovine Abomasal Disease Study Guide

Overview and Clinical Importance

Abomasal diseases are among the most economically significant gastrointestinal disorders affecting dairy cattle worldwide. The abomasum, or "true stomach," is susceptible to displacement, ulceration, and volvulus, with conditions occurring most frequently in high-producing dairy cattle during the periparturient period. Understanding the pathophysiology, clinical presentation, and management of these conditions is essential for the NAVLE examination and clinical practice.

The four-compartment ruminant stomach places the abomasum in a vulnerable position. Suspended loosely by the greater and lesser omentum, the abomasum can shift from its normal ventral position on the abdominal floor to either the left side (LDA) or right side (RDA), and may undergo life-threatening volvulus.

Section 1: Abomasal Displacement

Etiology and Risk Factors

The etiology of abomasal displacement is multifactorial, with decreased abomasal motility and gas accumulation playing central roles. The loosely suspended abomasum becomes displaced when hypomotility allows gas to accumulate, causing the organ to "float" dorsally.

Key Risk Factors

Left Displaced Abomasum (LDA)

LDA accounts for 80-90% of all abomasal displacements and represents the most common surgical condition in dairy cattle. The gas-filled abomasum floats dorsally along the left abdominal wall, becoming trapped between the rumen and body wall.

Pathophysiology

Abomasal hypomotility leads to gas accumulation (primarily carbon dioxide from fermentation). The partially gas-distended abomasum buoys upward along the left abdominal wall. The corpus and greater curvature displace first, followed by the pylorus and proximal duodenum. This creates partial obstruction of abomasal outflow, leading to fluid sequestration and metabolic alkalosis.

Clinical Signs

• Anorexia: Typically selective - decreased appetite for grain with relatively preserved appetite for roughage
• Milk production: Notable decrease (less dramatic than with peritonitis)
• Vital parameters: Usually normal temperature, heart rate, and respiratory rate
• Rumen motility: Reduced frequency and strength of contractions
• Feces: Reduced quantity, may be more fluid than normal
• Abdominal contour: "Sprung" appearance of left rib cage; "papple-shaped" abdomen when viewed from behind (Type III vagal indigestion)
• Ketosis: Frequently concurrent - check urine/milk for ketones

Diagnostic Findings

The pathognomonic finding is the "ping" detected during simultaneous auscultation and percussion of the left abdomen between ribs 9-13, along a line from the elbow to the tuber coxae.

Right Displaced Abomasum (RDA)

RDA is less common than LDA (ratio approximately 1:30) but carries significantly higher risk because it can rapidly progress to abomasal volvulus. The abomasum displaces from the ventral abdomen into the craniodorsal right abdominal cavity.

Clinical Signs

Clinical signs are similar to LDA but generally more pronounced. The critical distinction is that RDA can progress to volvulus at any time, making it a surgical emergency.

• Complete anorexia more common than with LDA
• Ping detected on the RIGHT side from the paralumbar fossa extending cranially
• May palpate distended abomasum per rectum
• Cannot clinically differentiate RDA from early abomasal volvulus without surgery

Abomasal Volvulus

Abomasal volvulus is a life-threatening emergency that typically develops from an RDA. The abomasum rotates on its mesenteric axis (usually counterclockwise when viewed from the right), causing complete obstruction, vascular compromise, and ischemic necrosis.

Pathophysiology

Rotation typically occurs counterclockwise as viewed from the rear and right side. The volvulus may involve the abomasum alone (AV), the omasum and abomasum (AVO), or the reticulum, omasum, and abomasum (AVOR). Vascular occlusion leads to ischemic necrosis, endotoxemia, and cardiovascular collapse. Up to 50 liters of chloride-rich fluid may sequester in the abomasum.

Clinical Differentiation from RDA

Treatment of Abomasal Displacement

Conservative Management (LDA only)

Rolling: The cow is cast into right lateral recumbency, rolled to dorsal recumbency while agitating the abdomen, then to left lateral recumbency before standing. Success rate is approximately 93% initially, but recurrence rate is 50-57%. Only appropriate for early, uncomplicated LDA.

Surgical Options

Abomasal Volvulus Treatment

Abomasal volvulus requires EMERGENCY surgical correction via right flank approach. Pre-operative stabilization with aggressive IV fluid therapy (20-40L isotonic saline with KCl supplementation), calcium borogluconate if hypocalcemic, and dextrose if ketotic.

Surgical procedure: Right flank laparotomy allows access to decompress the abomasum (abomasotomy may be required with up to 15-40L fluid drainage), assess tissue viability, de-rotate the volvulus, and perform omentopexy. If the abomasal wall is gangrenous or will not hold sutures, euthanasia is indicated.

Prognosis

• LDA: Excellent with surgical correction; 85-95% short-term success rate regardless of technique
• RDA: Good with prompt surgery (approximately 81% return to production)
• Abomasal Volvulus: Guarded to poor; approximately 67% return to production; many cows never regain normal abomasal motility

Section 2: Abomasal Ulcers

Abomasal ulcers represent erosions or excavations of the abomasal mucosa penetrating through to the muscularis mucosae. They are caused by breakdown of the gastric mucosal barrier, permitting back-diffusion of hydrogen ions. Ulcers are classified into four types based on severity and complications.

Classification of Abomasal Ulcers

Risk Factors for Abomasal Ulcers

Like abomasal displacement, ulcers are most common within 6 weeks of lactation. Stress increases cortisol, pepsin, and gastric acid secretion while decreasing protective prostaglandin secretion.

• NSAIDs: Inhibit prostaglandin synthesis; particularly phenylbutazone; risk increases with dehydration
• Concurrent disease: Mastitis, metritis, ketosis, abomasal displacement
• Dietary factors: High starch diets, rapid diet changes
• Stress: Transport, commingling, heat stress
• In calves: Hairballs/trichobezoars, tube feeding (vs. nursing), low feeding frequency, weaning transition
• Lymphosarcoma: Infiltrative neoplasia of abomasal wall

Clinical Presentation by Ulcer Type

Type 2 (Bleeding) Ulcers

Melena is the hallmark sign - dark, tarry, malodorous feces resulting from digested blood. However, melena requires at least 8 hours to develop after hemorrhage begins. In South American camelids (SACs), detecting melena is more difficult due to normally dark, dry feces.

Signs of blood loss include: tachycardia (100-140 bpm), pale mucous membranes, weak pulse, cool extremities, shallow breathing, tachypnea. Sudden death may occur with massive hemorrhage.

Types 3 and 4 (Perforating) Ulcers

Signs of peritonitis predominate: complete anorexia, abnormal demeanor, abdominal guarding, grunting with respiration, positive foreign body tests, fever (early) progressing to hypothermia, tachycardia, tachypnea, ruminal stasis. Type 4 ulcers show more severe and rapid progression.

Diagnosis of Abomasal Ulcers

Definitive antemortem diagnosis is challenging. The combination of clinical signs, laboratory findings, and imaging provides a presumptive diagnosis.

Treatment of Abomasal Ulcers

Treatment focuses on supportive care, addressing underlying causes, and preventing progression.

Prevention of Abomasal Disease

Prevention focuses on proper nutrition and management during the transition period.

• Adequate effective fiber: 5-10 cm particle size; avoid excessive grinding of feed
• Gradual diet transitions: Especially around calving
• Minimize concentrate overload: Balance concentrate:forage ratio
• Prevent hypocalcemia: Proper dry cow nutrition; anionic salts
• Early disease detection: Prompt treatment of mastitis, metritis, ketosis
• Minimize stress: Avoid commingling, overcrowding, transport stress
• Judicious NSAID use: Ensure adequate hydration; proper dosing

LDA Memory Aid - "LEFT = L-E-F-T"

• L = Lactating dairy cow (within 4 weeks post-calving)
• E = Eating poorly (selective anorexia for grain)
• F = Flank ping on LEFT side
• T = Treatment is surgical

RDA/Volvulus Memory Aid - "Right = Emergency"

Never let the sun set on a right-sided ping! RDA can rapidly progress to volvulus.

Ulcer Classification - "1-2-3-4 = None-Bleed-Local-More"

• Type 1 = None (minimal bleeding, subclinical)
• Type 2 = Bleed (severe hemorrhage, MELENA)
• Type 3 = Local (localized peritonitis)
• Type 4 = More (diffuse peritonitis, fatal)

Metabolic Alkalosis - "KLOR-ida trapped in the abomasum"

Chloride-rich HCl is sequestered, leading to hypochloremic, hypokalemic metabolic alkalosis with paradoxical aciduria.