Aortic-iliac thrombosis in horses.

This study describes blood clots and fibrous blockages at the point where the main body artery splits to supply the hindlimbs in horses, causing exercise intolerance and hind-leg lameness. The authors reviewed 15 clinical cases (10 confirmed post mortem), detailed the lesion structure and locations, discussed likely causes, and recommended routine checks to detect silent disease.

What the researchers did and who was affected

• Identified 15 horses with clinically diagnosed vascular obstruction to the hindlimbs (manifesting as poor performance and hindlimb lameness).
• Characterized the vascular lesions at necropsy in 8 of those 15 horses; in addition, found the condition incidentally at post mortem in 2 more horses (total necropsy confirmations: 10).
• Focused on the terminal aorta and its branches to the hindlimbs—especially the aortic quadrifurcation (where the aorta divides into the left and right external and internal iliac arteries) and more distal segments.

Key clinical signs and presentation

• Progressive exercise intolerance: horses fatigued sooner than expected and could not sustain previous levels of work.
• Hind-leg lameness: may be intermittent or progressive, consistent with reduced blood flow (ischemia) to hindlimb muscles.
• Clinical course suggested a chronic, evolving process rather than an acute catastrophic event in most cases.

Where the lesions were and what they looked like (gross and microscopic pathology)

• Primary locations:
  • Aortic quadrifurcation (terminal aorta as it divides into internal and external iliac arteries).
  • Distal parts of the femoral arteries and internal iliac arteries.
• Nature of the obstructive material:
  • Well-organized, well-vascularized fibrous tissue forming plaques or masses that partially or completely blocked the vessel lumen—indicating chronicity.
  • Occasional foci of hemorrhage or degeneration within these organized masses.
  • Large, unorganized (fresh) thrombi often located upstream (proximal) to the organized occlusions—consistent with flow disturbance and thrombus propagation.
• Vessel wall changes:
  • Tunica intima largely obliterated at the site of organized masses; however, the internal elastic lamina usually remained intact, helping distinguish this from classic atherosclerosis.
  • Tunica media generally preserved, but showed ischemic necrosis where arteries were markedly distended or beneath very thick plaques.

Proposed pathogenesis (how and why these lesions may form)

• Unresolved cause: the study could not definitively identify a single mechanism.
• Two main hypotheses:
  • Organization of strongyle-related thromboemboli: larval migration and verminous arteritis from equine strongyles (classically Strongylus spp.) could seed emboli that become organized into fibrous occlusions downstream.
  • Progressive enlargement and organization of spontaneously developing fibrous intimal plaques: non-parasitic intimal proliferation leading to luminal narrowing and secondary thrombosis.
• Contributory factors:
  • Hypercoagulability: noted in one mare with nephrotic syndrome, suggesting systemic prothrombotic states can exacerbate or precipitate thrombosis.
  • Hemodynamic factors: high-flow bifurcation/quadrifurcation geometry and turbulent flow may promote intimal injury and thrombus formation.

Clinical implications: diagnosis, differentials, and management

• Clinical suspicion:
  • Progressive exercise intolerance and hindlimb lameness without obvious musculoskeletal cause.
  • Possible coldness of distal limbs, diminished arterial pulses, or post-exercise muscle pain in hindquarters.
• Ante-mortem evaluation (practical approaches in horses):
  • Doppler ultrasonography of the terminal aorta and iliac/femoral arteries (via transrectal or transabdominal approach) to detect narrowed lumens, reduced flow velocities, or post-stenotic turbulence.
  • Angiography (where available) for definitive vascular mapping and identification of occlusions/stenoses.
  • Rule-out testing for systemic prothrombotic conditions (e.g., protein-losing nephropathy) if suspected.
• Management considerations (based on lesion chronicity described):
  • Medical therapy is often limited because organized, fibrous occlusions are not readily reversed by anticoagulants or thrombolytics.
  • Antiplatelet/anticoagulant strategies may help prevent propagation of fresh proximal thrombi but are unlikely to restore lumen where fibrous organization is advanced.
  • Address underlying contributors:
    • Strategic anthelmintic control to reduce strongyle exposure and verminous arteritis risk.
    • Treat systemic diseases causing hypercoagulability (e.g., nephrotic syndrome).
  • Surgical or endovascular options are rarely performed in horses and carry substantial risk; case selection is crucial and prognosis guarded.
  • Workload modification may alleviate clinical signs but does not correct the underlying obstructive disease.
• Differential diagnoses to consider:
  • Primary musculoskeletal hindlimb lameness, exertional rhabdomyolysis, neurologic disease (e.g., EPM), or orthopedic causes of poor performance.
• Prognosis:
  • Guarded to poor for return to previous athletic function when significant organized occlusion is present.

Why routine examination of the aortic quadrifurcation is recommended

• Subclinical disease is possible: two horses had incidental post-mortem findings without recognized clinical signs.
• Systematic necropsy checks can:
  • Improve detection of early or silent lesions.
  • Clarify lesion distribution and evolution (natural history).
  • Support better epidemiologic understanding and prevention strategies (e.g., parasite control efficacy).

Strengths, limitations, and unanswered questions

• Strengths:
  • Combines clinical observations with necropsy confirmation, providing anatomical-pathological correlation.
• Limitations:
  • Small case series; not designed to quantify risk factors or treatment outcomes.
  • Pathogenesis remains speculative; causality (parasite-associated vs spontaneous intimal plaques) is unresolved.
• Future directions:
  • Prospective studies linking antemortem imaging, parasitological status, coagulation profiles, and outcomes.
  • Standardized diagnostic criteria and screening protocols for poor-performance horses.
  • Evaluation of preventive strategies (parasite management, coagulation control) and feasibility of interventional therapies in selected cases.