Equine Malnutrition Study Guide

Overview and Clinical Importance

Malnutrition in horses encompasses a spectrum of nutritional disorders ranging from simple energy deficits to complex vitamin and mineral imbalances. Understanding equine malnutrition is essential for the NAVLE because it represents a common clinical presentation with potentially life-threatening complications, particularly during rehabilitation. This topic integrates knowledge of equine physiology, nutrition, metabolism, and emergency medicine.

Malnutrition may result from inadequate feed intake, poor-quality feed, malabsorption syndromes, chronic disease states, dental abnormalities, parasitism, or neglect. The multisystemic nature of malnutrition affects virtually every organ system, making it a high-yield topic for board examinations.

Body Condition Scoring: The Henneke System

The Henneke Body Condition Scoring (BCS) system is the standardized method for assessing equine body fat. Developed by Don Henneke at Texas A&M University in 1983, this system uses a 1-9 scale based on visual appraisal and palpation of fat deposits at six anatomical locations: neck, withers, behind the shoulder, ribs, loin, and tailhead.

Henneke Body Condition Score Descriptions

Etiology and Pathophysiology of Malnutrition

Primary Causes of Equine Malnutrition

Malnutrition in horses occurs when nutrient intake fails to meet metabolic demands. This may result from:

• Inadequate feed quantity or quality: Insufficient calories, protein, or essential nutrients
• Dental disease: Sharp enamel points, wave mouth, missing teeth impair mastication
• Parasitism: Heavy burdens of strongyles, ascarids, or tapeworms compete for nutrients
• Chronic disease: PPID (Cushing's disease), neoplasia, chronic infections increase metabolic demands
• Malabsorption: Inflammatory bowel disease, lymphosarcoma, chronic enteritis
• Social hierarchy: Subordinate horses in group housing may not access adequate feed

Metabolic Adaptations During Starvation

During starvation, the horse undergoes predictable metabolic changes:

• Glycogen depletion (0-24 hours): Hepatic and muscle glycogen stores are exhausted first
• Lipolysis (1-7 days): Fat mobilization provides fatty acids for energy; ketone body production increases
• Proteolysis (greater than 7 days): Skeletal muscle protein catabolism provides gluconeogenic substrates
• Metabolic rate reduction: Resting metabolic rate decreases up to 20% to conserve energy

Clinical Signs of Malnutrition

Refeeding Syndrome: A Critical Emergency

Refeeding syndrome is a potentially fatal metabolic complication that occurs when a chronically starved horse is fed too aggressively. It typically develops within 3-5 days of initiating refeeding and is characterized by severe electrolyte shifts, particularly hypophosphatemia, which is the hallmark finding.

Pathophysiology of Refeeding Syndrome

During starvation, intracellular phosphorus, potassium, and magnesium become depleted, but serum levels often remain normal or only mildly decreased. When carbohydrates are reintroduced:

• Insulin release is stimulated by rising blood glucose
• Insulin drives glucose AND electrolytes (phosphorus, potassium, magnesium) into cells
• Serum electrolyte levels plummet (especially phosphorus)
• Hypophosphatemia impairs ATP production and oxygen delivery by red blood cells
• Multi-organ failure ensues (cardiac, respiratory, renal)

Clinical Signs of Refeeding Syndrome

• Weakness and recumbency
• Ventral edema (pectoral, limbs, ventral abdomen)
• Tachycardia, arrhythmias, cardiac failure
• Respiratory distress, tachypnea
• Neurologic signs (tremors, seizures, ataxia)
• Hemolytic anemia (phosphorus-dependent)
• Diarrhea and colic

Safe Refeeding Protocol for Starved Horses

The UC Davis refeeding protocol is widely accepted as the standard of care:

Memory Aid - Refeeding: "SLOW" S = Start with water and electrolytes first L = Low nonstructural carbohydrates (alfalfa, not grain) O = Only 50% of energy needs initially W = Wait 10+ days before adding concentrates

Specific Nutritional Diseases

White Muscle Disease (Nutritional Myodegeneration)

Etiology: Caused by dietary deficiency of selenium and/or vitamin E. Most commonly affects newborn foals born to dams on selenium-deficient diets during gestation. Geographic areas with selenium-deficient soils (Pacific Northwest, Great Lakes, Northeast US) are high-risk.

Pathophysiology: Selenium is a component of glutathione peroxidase, which destroys damaging peroxides. Vitamin E scavenges free radicals within cell membranes. Together, they prevent oxidative damage to muscle cells. Deficiency leads to myodegeneration of skeletal and cardiac muscle.

Clinical Signs (Foals): Two presentations exist:

• Fulminant (cardiac) form: Sudden death due to myocardial necrosis
• Subacute (skeletal) form: Muscle stiffness, trembling, weakness, difficulty rising, dysphagia, aspiration pneumonia risk

Diagnosis: Elevated serum CK and AST (muscle enzymes); whole blood selenium less than 0.07 mcg/mL; serum vitamin E less than 2 mcg/mL

Treatment: Injectable selenium (0.055-0.067 mg/kg IM once) and vitamin E (0.5-1.5 IU/kg); supportive care including antimicrobials for aspiration pneumonia, fluid therapy, nasogastric tube feeding

Prevention: Supplement pregnant mares in endemic areas; parenteral vitamin E/selenium injection to foals at birth in high-risk regions

Nutritional Secondary Hyperparathyroidism (Big Head Disease)

Etiology: Caused by chronic calcium deficiency, excess phosphorus intake, inverted Ca:P ratio (less than 1:1), or high dietary oxalates that bind calcium and prevent absorption.

Common Risk Factors:

• Diets high in wheat bran or rice bran (high phosphorus, low calcium)
• Grazing tropical/subtropical grasses high in oxalates: buffel grass, kikuyu, setaria, pangola, green panic
• Grain-heavy diets without calcium supplementation

Pathophysiology: Low blood calcium stimulates parathyroid hormone (PTH) release. PTH causes calcium and phosphorus resorption from bone. Over time, bone mineral is replaced with fibrous connective tissue, particularly in the facial bones (hence "big head").

Clinical Signs: Shifting leg lameness (early); enlarged facial bones (maxilla, mandible); loose teeth; difficulty eating; respiratory stridor (if nasal passages narrowed); pathological fractures

Diagnosis: Serum calcium may be normal (compensated by PTH); serum phosphorus often elevated; elevated PTH; dietary history evaluation; radiographs showing demineralization

Treatment: Correct diet to appropriate Ca:P ratio (1.5-2:1); supplement with calcium carbonate (limestone) or alfalfa hay (high calcium); NSAIDs for pain; recovery may take 9-12 months; bone changes may be irreversible in severe cases

Summary of Common Nutrient Deficiencies

Diagnostic Approach to the Malnourished Horse

Initial Assessment

• Body Condition Score: Document BCS using Henneke system; photograph for records
• Weight estimation: Weight tape or scale; note that weight tapes may overestimate in emaciated horses
• Complete physical examination: Assess hydration, mucous membranes, heart rate, gut sounds
• Dental examination: Rule out dental disease as cause of poor intake

Laboratory Evaluation

Exam Focus: Blood calcium levels do NOT accurately reflect dietary calcium intake due to PTH compensation. Similarly, pre-refeeding electrolyte levels may be falsely normal - the dangerous shifts occur AFTER refeeding begins. Monitor electrolytes daily during the first week of refeeding.

Prognosis and Recovery Timeline

• Horses recumbent for greater than 72 hours have poor prognosis
• Horses that lose greater than 45-50% of body weight are unlikely to survive
• With proper refeeding, expect approximately 1 BCS improvement per month
• Full recovery may take 3-10 months depending on severity
• Behavioral abnormalities (pica, aggression) may persist even after physical recovery