What is a thrombus and what are the recommended management steps for arterial and venous thrombi?

What is a Thrombus?

A thrombus is a blood clot composed of fibrin and blood cells that forms within the cardiovascular system, with arterial thrombi being platelet-rich "white clots" forming under high flow conditions, while venous thrombi are red blood cell-rich "red clots" forming in areas of stasis. 1

Structural Composition

Arterial Thrombi

• Form under high-flow conditions and consist primarily of platelet aggregates bound together by thin fibrin strands 1, 2
• Develop at sites of ruptured atherosclerotic plaques where thrombogenic subendothelium becomes exposed to platelets and coagulation proteins 1
• May incorporate into the vessel wall when nonocclusive, accelerating atherosclerotic plaque growth 1
• When flow slows or stenosis becomes severe, platelet-rich thrombi can propagate as red stasis thrombi 1

Venous Thrombi

• Form in areas of blood stasis and are predominantly composed of red blood cells with large amounts of interspersed fibrin and relatively few platelets 1, 2
• Develop through coagulation activation as the critical mechanism rather than platelet aggregation 2
• Contain essentially the same blood-borne cells as arterial thrombi (red blood cells, leukocytes, platelets), but in different relative proportions 3

Mixed Thrombi

• Form in regions of slow to moderate flow 1
• Composed of a mixture of red cells, platelets, and fibrin 1

Natural Evolution of Thrombi

• Leukocytes become attracted by chemotactic factors from aggregated platelets and incorporate into thrombi 1
• Aggregated platelets swell, disintegrate, and are gradually replaced by fibrin 1
• Eventually, fibrin clots are digested by fibrinolytic enzymes released from endothelial cells and leukocytes 1

Clinical Consequences

Arterial Thrombosis

• Produces tissue ischemia through vessel obstruction or distal embolization into the microcirculation 1, 2
• Causes stroke, myocardial infarction, or limb ischemia depending on location 1, 2
• In patients with cardiac shunts, can result in paradoxical embolization to systemic circulation 1

Venous Thrombosis

• Leads to pulmonary embolism, which represents a leading cause of death 2
• Can cause local vessel obstruction preventing essential vascular access 1
• In specialized populations (e.g., Fontan circulation), may cause circulatory failure or death 1

Universal Complications

• Local vessel obstruction 1
• Distant embolism of thrombotic material 1
• Consumption of hemostatic elements (less common) 1

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Management of Arterial Thrombi

Pharmacologic Strategy

Both anticoagulants and antiplatelet drugs are effective for prevention and treatment of arterial thrombosis because both platelet activation and blood coagulation contribute to pathogenesis 1, 2

Acute Arterial Thrombosis

• Initiate anticoagulation with heparin (50-100 U/kg bolus) for acute occlusive events 1
• Increase systemic blood pressure with phenylephrine to maximize perfusion pressure distal to occlusion 1
• Consider epinephrine (10 μg/kg) as alternative if phenylephrine unavailable 1

Specific Scenarios

Left Ventricular Apical Thrombus

• Initiate warfarin immediately (target INR 2.0-3.0) combined with low-dose aspirin (100 mg daily) for minimum 3 months 4
• Bridge with unfractionated heparin IV or low molecular weight heparin until INR reaches 2.0-3.0 4
• Continue anticoagulation beyond 6 months if persistent apical akinesia, ejection fraction <25%, or prior systemic embolization occurred 4
• Perform serial echocardiography at 2 weeks, 1 month, 3 months, and 6 months to confirm thrombus resolution 4
• Never discontinue anticoagulation based solely on symptom improvement—imaging confirmation of thrombus resolution is mandatory 4

Systemic-to-Pulmonary Artery Shunt Occlusion

• Recognize as medical emergency requiring immediate heparin anticoagulation (50-100 U/kg) 1
• Increase systemic blood pressure with phenylephrine 1
• Provide controlled ventilation to maximize oxygen delivery 1
• Consider emergent catheterization for thrombus removal or emergent sternotomy for thrombectomy 1
• Prepare for ECMO if initial maneuvers unsuccessful 1

Mechanical Interventions

Thrombolytic Therapy

• Consider for life-threatening situations where thrombus causes hemodynamic obstruction, valve dysfunction, or high embolic risk 4
• Perform immediate neuroimaging to exclude hemorrhage before thrombolytic administration if systemic embolization suspected 4

Surgical Thrombectomy

• Reserved for critically ill patients with obstructive thrombosis causing hemodynamic compromise 4
• May require urgent valve replacement if thrombus causes valve dysfunction 4

Critical Pitfalls to Avoid

• Never delay anticoagulation once arterial thrombus is confirmed—this is the single most important intervention to prevent embolic complications 4
• Do not assume dual antiplatelet therapy alone is sufficient for left ventricular thrombus—therapeutic anticoagulation is required 4
• Do not stop anticoagulation prematurely as thrombus recurrence occurs when discontinued despite persistent wall motion abnormalities 4

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Management of Venous Thrombi

Pharmacologic Strategy

Anticoagulants are very effective for prevention and treatment of venous thromboembolism 2

Acute Venous Thrombosis

Pulmonary Embolism

• Treat incidental pulmonary embolism with therapeutic anticoagulation if it involves segmental or more proximal branches, multiple subsegmental vessels, or single subsegmental vessel with proven DVT 5
• For isolated subsegmental pulmonary embolism, decide treatment case-by-case considering benefits versus bleeding risks 5
• Target INR 2.0-3.0 for pulmonary embolism arising from right atrium or venous circulation 1
• Consider indefinite anticoagulation in most patients with pulmonary embolism 1

Deep Vein Thrombosis

• Treat incidental DVT with therapeutic anticoagulation identical to symptomatic DVT 5
• Perform serial imaging at 3-6 months to assess for recanalization 5

Cancer-Associated Thrombosis

• Use low molecular weight heparin as preferred option for first 6 months 5
• Provide minimum 6 months of anticoagulation, with consideration of indefinite treatment until cancer is cured 5
• Consider edoxaban or rivaroxaban as alternatives to LMWH in patients without gastrointestinal cancer 5
• Monitor for bleeding complications (12.4% cumulative incidence of major bleeding at 1 year) 5

Non-Cancer Associated Thrombosis

• Use direct oral anticoagulants (DOACs) or vitamin K antagonists as appropriate options 5

Catheter-Related Venous Thrombosis

Intraluminal Thrombolytic Administration

• Administer alteplase 1-2 mg intraluminally with 30-60 minute dwell time for dysfunctional central venous catheters 1
• Treatment success (blood flow ≥300 mL/min) achieved in 95% after single dose of alteplase 1 mg 1
• Tenecteplase 2 mg with 1-hour dwell time achieves 22% success rate versus 5% with placebo 1

Conservative Maneuvers Before Thrombolysis

• Reposition patient to Trendelenburg position 1
• Use rapid saline flushes to dislodge possible thrombus 1
• Reverse catheter lumens to provide temporary function 1

Mechanical Interventions

• Consider fibrin sheath disruption, catheter exchange, or catheter removal with replacement if thrombolytic therapy fails 1

Monitoring and Follow-up

• Perform serial imaging to assess thrombus resolution at 3-6 months 5
• Consider follow-up imaging if symptoms persist or worsen 5
• Monitor INR weekly during warfarin initiation, then monthly once stable, maintaining time in therapeutic range >70% 4

Assessment Before Treatment

• Determine location and extent of thrombus (segmental, subsegmental, proximal, or multiple vessels) 5
• Assess for overlooked symptoms that may have been attributed to other causes 5
• Evaluate for underlying risk factors, particularly malignancy 5
• Check for contraindications to anticoagulation: active bleeding, severe thrombocytopenia, recent surgery 5