Equine Peripheral Vascular Disease Study Guide

Overview and Clinical Importance

Peripheral vascular disease (PVD) in horses encompasses a spectrum of conditions affecting arteries, veins, and lymphatic vessels outside the heart. These conditions range from life-threatening emergencies like aorto-iliac thrombosis to common iatrogenic complications such as jugular thrombophlebitis. Understanding the pathophysiology, clinical presentation, and management of PVD is essential for equine practitioners and represents a specific NAVLE competency domain under Equine Cardiovascular Disease.

Peripheral vascular disease significantly impacts equine health across multiple disciplines, from performance horses developing exercise-induced hindlimb lameness to hospitalized patients with catheter-related complications. Early recognition and appropriate intervention are critical for successful outcomes.

Arterial Disease

Aorto-Iliac Thrombosis (AIT)

Definition and Pathophysiology

Aorto-iliac thrombosis (AIT) is a progressive vascular disease characterized by thrombus formation in the terminal aorta or iliac arteries, causing partial or complete occlusion of blood flow to the hindlimbs. The condition is analogous to "intermittent claudication" in humans and "saddle thrombus" in cats.

Proposed etiologies include: mechanical damage to the aortic intima during locomotion at the aortic quadrifurcation, organization of Strongylus vulgaris-related thromboemboli, spontaneous degenerative intimal plaques, systemic infections (strangles, influenza), trauma, and hypercoagulable states. The pathogenesis involves endothelial injury leading to platelet aggregation, fibrin deposition, and progressive thrombus enlargement.

Clinical Signs of Aorto-Iliac Thrombosis

Diagnosis

Rectal palpation: The terminal aorta and iliac arteries can be palpated per rectum. Thrombosed vessels feel enlarged, firm, and may have reduced or absent pulsation. Compare pulse quality between left and right iliac arteries.

Transrectal ultrasonography: Gold standard for diagnosis. Use a 5-MHz linear or sector probe. Normal vessels appear anechoic with thin walls. Thrombi appear as echogenic intraluminal masses. Doppler can assess blood flow velocity and turbulence.

Metatarsal artery palpation: Assess pulse quality immediately post-exercise. Reduced or absent metatarsal pulse indicates significant proximal arterial occlusion.

Nuclear scintigraphy: Can demonstrate reduced perfusion to affected limb. Useful when ultrasound findings are equivocal.

Treatment Options for AIT

Verminous Arteritis (Strongylus vulgaris)

Pathophysiology

Strongylus vulgaris is the most pathogenic equine strongyle. Fourth-stage larvae (L4) migrate through the intestinal wall into arterial branches and travel proximally to the cranial mesenteric artery (CMA) and its root at the aorta, where they remain for approximately 3-4 months. This migration causes endarteritis, thrombosis, aneurysmal dilation, and potential thromboembolism. The prepatent period is approximately 6 months.

Clinical consequences include: Thromboembolic colic from intestinal infarction, mild recurrent colic, weight loss, intermittent fever, and rarely, aberrant migration to cerebral, renal, or coronary arteries. Despite widespread anthelmintic use, recent studies indicate verminous arteritis remains prevalent (6-17% in some populations) and should be considered a re-emerging disease.

Diagnosis and Clinical Features

Fecal egg counts are NOT diagnostic for migrating larvae since eggs are only shed by adult worms in the intestinal lumen. Larval culture can identify adult S. vulgaris but takes 14 days. Transrectal ultrasound can measure CMA dimensions and detect thrombi. An ELISA for larval-specific antigens (SvSXP) is available for prepatent diagnosis. Post-mortem examination remains the definitive diagnostic method.

Venous Disease

Jugular Thrombophlebitis

Definition and Etiology

Jugular thrombophlebitis (JVT) is inflammation of the jugular vein with concurrent thrombus formation. It is the most common iatrogenic vascular complication in hospitalized horses, occurring in 1-50% of indwelling catheters depending on the underlying disease. The condition develops when Virchow's triad converges: endothelial injury (catheter trauma, irritating drugs), venous stasis, and hypercoagulability.

Risk Factors for Jugular Thrombophlebitis

Clinical Signs

Early signs: Subtle thickening of the vein wall at catheter site, heat, mild pain on palpation, change in filling pattern when vein occluded distally.

Established thrombosis: Firm, cord-like jugular vein, non-compressible distention, visible distension of proximal vein and superficial head vessels, may have soft tissue swelling around jugular groove.

Septic thrombophlebitis: Fever, depression, neck stiffness, local abscessation, cavitation visible on ultrasound. May see gas echoes (anaerobic infection). Risk of bacteremia, endocarditis, pulmonary thromboembolism, and pleuropneumonia.

Bilateral thrombosis: Head and facial edema (especially during grazing or exercise), laryngeal/pharyngeal swelling potentially requiring tracheostomy, impaired thermoregulation.

Diagnostic Approach

Ultrasonography (7.5-10 MHz linear probe): Gold standard. Thrombus appears as echogenic intraluminal material adhered to vessel wall. Assess: thrombus extent, degree of occlusion, wall thickening, perivenous edema/abscessation, gas echoes (septic). Doppler can detect residual or collateral flow. Saline contrast ultrasonography can confirm complete occlusion.

Culture: Aspirate thrombus with 22-gauge needle under ultrasound guidance, or culture catheter tip if recently removed. Common isolates include Staphylococcus spp., Streptococcus spp., E. coli, and anaerobes.

Treatment of Jugular Thrombophlebitis

Vasculitis and Immune-Mediated Disease

Purpura Hemorrhagica

Definition and Pathophysiology

Purpura hemorrhagica (PH) is an acute, aseptic, necrotizing vasculitis caused by a Type III hypersensitivity reaction. It is characterized by immune complex deposition in small blood vessel walls, leading to complement activation, neutrophil infiltration, endothelial damage, and increased vascular permeability. The result is widespread edema, petechial/ecchymotic hemorrhages, and potentially tissue infarction.

The most common trigger is Streptococcus equi subspecies equi (strangles). PH typically develops 1-4 weeks after recovery from strangles or following vaccination in horses with pre-existing high antibody titers. The immune complexes contain IgA and streptococcal M protein (SeM) antigen. Other triggers include Corynebacterium pseudotuberculosis, Rhodococcus equi, equine influenza, and EHV-1.

Clinical Signs of Purpura Hemorrhagica

Pathognomonic features: Acute onset of well-demarcated, pitting subcutaneous edema primarily affecting the distal limbs, ventral abdomen, and head. The edema has sharply defined borders and does not "feather" into surrounding tissue.

Mucosal hemorrhages: Petechiae and ecchymoses on gingival, nasal, and conjunctival mucous membranes. Thrombocyte count is typically NORMAL (unlike DIC).

Systemic signs: Fever (often greater than 103°F/39.5°C), depression, anorexia, reluctance to move due to limb edema and pain.

Severe cases: Serum oozing through taut skin, skin necrosis and sloughing, secondary cellulitis, colic from GI tract infarction, laryngeal obstruction (may require tracheostomy), laminitis, renal compromise from glomerulonephritis.

Diagnosis

Clinical presentation: History of recent respiratory infection or vaccination + characteristic edema pattern + petechiae is highly suggestive.

Serology: SeM-specific ELISA titer greater than or equal to 1:12,800 supports diagnosis of S. equi-associated PH. Also useful for identifying horses at risk before vaccination.

Skin biopsy: Histopathology shows leukocytoclastic vasculitis with fibrinoid necrosis of small dermal vessel walls, neutrophilic infiltration, and hemorrhage. Confirms diagnosis.

CBC: Neutrophilia with left shift, hyperfibrinogenemia. Platelet count is typically normal (important to distinguish from DIC).

Treatment of Purpura Hemorrhagica

Exam Focus: PH case fatality rate is approximately 10% with appropriate treatment. Poor prognostic indicators include severe skin necrosis, renal involvement, and GI infarction. Supportive care including hydrotherapy, gentle exercise when tolerated, and monitoring for secondary complications (laminitis, pneumonia) is essential.

Other Forms of Equine Vasculitis

Pastern Leukocytoclastic Vasculitis (PCLV)

Also called pastern and cannon leukocytoclastic vasculitis. Primarily affects non-pigmented skin of the distal limbs, particularly pasterns. Characterized by crusting, ulceration, and erythema with lesions often worsening in summer (suspected photosensitization component). Histopathology shows leukocytoclastic vasculitis in dermal vessels. May be associated with dermatophytosis, bacterial infection, or chorioptic mange. Treatment includes corticosteroids, keeping limbs clean and dry, and protecting from UV exposure.

Equine Viral Arteritis (EVA)

Caused by equine arteritis virus (Arterivirus). Systemic viral infection with tropism for vascular endothelium. Causes fibrinoid necrosis of small muscular arteries, edema, abortion in pregnant mares, and respiratory disease. Subclinical infection is common in Standardbreds. Stallions can become persistent carriers and shed virus in semen. Notifiable disease. Supportive treatment; modified live vaccine available. Reportable disease in many jurisdictions.

Lymphatic Disease

Sporadic Lymphangitis (Big Leg Disease)

Definition and Pathophysiology

Lymphangitis is inflammation of the lymphatic vessels, most commonly affecting the hindlimbs. It is distinct from cellulitis (infection of subcutaneous tissues) and stocking up (simple fluid accumulation). Lymphangitis involves direct damage to lymphatic vessels, which cannot regenerate like blood vessels. Once scarred, lymphatic channels remain permanently compromised, predisposing to recurrence.

Common pathogens: Staphylococcus aureus, Streptococcus spp. (especially S. zooepidemicus), E. coli. Corynebacterium pseudotuberculosis causes ulcerative lymphangitis with nodule/abscess formation. Entry typically occurs through a wound or skin abrasion.

Comparison: Stocking Up vs Cellulitis vs Lymphangitis

Treatment of Lymphangitis

Antibiotics: Broad-spectrum coverage targeting Staphylococcus. Enrofloxacin 7.5 mg/kg IV q24h (preferred for acute cases), TMS 20-30 mg/kg PO q12h, or Penicillin G 22,000 IU/kg + Gentamicin 6.6 mg/kg IV. Continue for 10-14 days minimum.

NSAIDs: Phenylbutazone 4.4 mg/kg IV/PO q12h or Flunixin 1.1 mg/kg IV q12h for inflammation and pain.

Hydrotherapy: Cold hosing in acute phase. Alternating warm/cold water helps move lymphatic fluid. Aggressive hydrotherapy is critical in first 24-48 hours to prevent permanent lymphatic damage.

Exercise: KEY INTERVENTION. Hand-walking 10-15 minutes 4-6 times daily. Muscle contractions pump lymphatic fluid. Stall rest is COUNTERPRODUCTIVE.

Pentoxifylline: 10 mg/kg PO q12h improves microcirculation in severely swollen limbs.