Thrombotic Arteriovenous Graft (AVG) Causes and Management

Primary Mechanism: Venous Stenosis

Venous outflow stenosis is the predominant precipitator of AVG thrombosis, causing increased intra-access pressure and decreased blood flow that ultimately leads to clot formation if untreated 1, 3
Unrecognized stenosis is the primary determinant of graft thrombosis rates, with baseline rates of 0.5-0.8 episodes/graft-year that can be reduced by 43-67% through surveillance programs 1
Hemodynamically significant stenosis is defined as ≥50% reduction in vessel diameter accompanied by clinical or physiologic abnormalities 4, 3

Diabetes mellitus significantly decreases prosthetic graft survival, even within the first 30 days 1, 7
Increasing age adversely affects graft patency in non-diabetic patients 1, 7
Hypertension and vascular disease contribute to access dysfunction 1
Patients with chronic kidney disease exhibit a prothrombotic state through multiple mechanisms including elevated fibrinogen, D-dimer, plasminogen activator inhibitor-1, and inflammatory markers 5, 6

Primary failure within 30 days reflects surgical construction problems or inappropriate vessel selection rather than stenosis 1, 7
Inadequate pre-operative vascular assessment leads to suboptimal graft placement 7
Premature cannulation and hematoma formation can precipitate early thrombosis 1, 7

Absence of bruit or thrill is highly predictive of thrombosis or severe stenosis 4
A palpable thrill indicates flow ≥450 mL/min; its absence warrants immediate evaluation 4
Arm swelling suggests venous outflow obstruction 4

Thrombectomy must be performed within 48 hours for optimal outcomes when thrombosis occurs 4
Identification and treatment of ALL significant stenoses during thrombectomy is essential for long-term patency 2
After percutaneous thrombectomy, 3-month primary patency rates are only 30-40%, compared to 40-50% for preemptive PTA of non-thrombosed grafts 1, 2
Preemptive treatment of stenosis before thrombosis occurs yields superior outcomes: 71-85% of grafts remain intervention-free versus only 33-63% after thrombectomy 1

Delaying evaluation of access dysfunction leads to thrombosis rather than allowing preemptive stenosis correction 3
Inadequate correction of stenosis during thrombectomy procedures results in rapid re-thrombosis 2
Not implementing systematic surveillance programs to detect stenosis before thrombosis occurs 1