Thrombophlebitis

Introduction

Thrombophlebitis is the inflammation of a vein associated with thrombus formation, typically affecting the superficial veins of the extremities. It can cause pain, redness, and swelling, and in certain cases, lead to serious complications such as deep vein thrombosis and pulmonary embolism. Early recognition and management are essential to prevent progression and long-term sequelae.

Anatomy and Physiology Relevant to Thrombophlebitis

Venous System Overview

The venous system is composed of superficial and deep veins that return deoxygenated blood to the heart. Superficial veins lie close to the skin and are more prone to thrombophlebitis, while deep veins are located within muscle compartments and are associated with higher-risk thrombotic events.

• Superficial veins: Include the great and small saphenous veins, commonly affected in superficial thrombophlebitis.
• Deep veins: Include femoral, popliteal, and iliac veins, where thrombosis carries a higher risk of embolization.

Venous Valves and Their Function

Venous valves prevent retrograde flow and maintain unidirectional circulation toward the heart. Dysfunctional valves or valve damage can contribute to stasis, increasing the risk of thrombus formation.

Blood Flow Dynamics and Factors Influencing Stasis

Normal venous return relies on muscle contractions and competent valves. Factors such as prolonged immobility, venous compression, or varicose veins can impair flow, promoting thrombosis and inflammation.

• Stasis: Reduced blood flow increases clotting risk.
• Endothelial injury: Damage to vein walls triggers inflammation and thrombus formation.
• Hypercoagulability: Altered blood constituents can predispose to clotting.

Etiology and Risk Factors

Primary Causes

Primary thrombophlebitis occurs spontaneously without an identifiable precipitating event, often involving superficial veins.

• Spontaneous venous inflammation: Inflammation of the vein wall without trauma or catheterization.
• Idiopathic thrombosis: Clot formation with no apparent underlying cause, sometimes related to undiagnosed hypercoagulable states.

Secondary Causes

Secondary thrombophlebitis results from identifiable triggers or underlying conditions that increase clotting or inflammation.

• Trauma or intravenous catheterization: Direct injury to the vein wall can initiate thrombus formation.
• Prolonged immobilization: Extended bed rest or sedentary behavior slows venous return, promoting stasis.
• Malignancy: Cancer-related hypercoagulability increases the risk of thrombus formation.
• Pregnancy and postpartum period: Hormonal changes and increased venous pressure predispose to thrombosis.
• Hypercoagulable states: Genetic or acquired disorders such as Factor V Leiden or antiphospholipid syndrome.

Predisposing Factors

Certain patient characteristics and lifestyle factors increase susceptibility to thrombophlebitis.

• Age and sex: Older adults and females may have a higher risk in specific contexts.
• Obesity: Excess weight contributes to venous stasis.
• History of thrombophlebitis or deep vein thrombosis: Previous events increase recurrence risk.
• Varicose veins: Impaired venous function predisposes to inflammation and clot formation.
• Smoking: Promotes endothelial damage and hypercoagulability.

Pathophysiology

Thrombophlebitis develops due to the interplay of vascular injury, blood flow abnormalities, and hypercoagulable states.

• Virchow’s triad: The three primary mechanisms leading to thrombus formation are stasis, endothelial injury, and hypercoagulability.
• Mechanisms of thrombus formation: Platelet aggregation and fibrin deposition within the inflamed vein initiate clot development.
• Inflammatory response in the vein wall: Inflammation leads to pain, redness, and localized swelling.
• Propagation and complications of thrombus: Clots may extend into deep veins or fragment, causing pulmonary embolism or chronic venous insufficiency.

Classification

Thrombophlebitis can be classified based on the location, severity, and presence of infection, which influences management and prognosis.

• Superficial thrombophlebitis: Involves veins close to the skin surface, commonly affecting the lower extremities.
• Deep vein thrombosis (DVT): Involves deep veins, carries a higher risk of complications such as pulmonary embolism.
• Septic vs. non-septic thrombophlebitis: Infection within the thrombus can lead to systemic illness and requires antimicrobial therapy.
• Upper extremity vs. lower extremity involvement: Upper limb cases are often catheter-related, whereas lower limb cases are more commonly spontaneous or associated with immobility.

Clinical Presentation

Symptoms

Patients with thrombophlebitis often present with localized and systemic symptoms depending on the severity and vein involved.

• Pain and tenderness along the affected vein
• Redness and warmth over the inflamed area
• Swelling or edema of the limb
• Fever and malaise in cases of septic thrombophlebitis

Signs

Physical examination can reveal characteristic findings that aid in diagnosis.

• Palpable cord-like vein indicating thrombosis
• Calf tenderness and positive Homan’s sign suggestive of deep vein involvement
• Skin discoloration or ulceration in chronic or recurrent cases

Diagnostic Evaluation

Laboratory Tests

Laboratory investigations help identify inflammation, coagulopathy, and infection in patients with thrombophlebitis.

• Complete blood count and inflammatory markers: Elevated white blood cells or C-reactive protein indicate inflammation or infection.
• D-dimer assay: Useful for detecting thrombus formation, particularly in deep vein involvement.
• Blood cultures in septic cases: Identify causative pathogens and guide antibiotic therapy.

Imaging

Imaging studies are essential for confirming the diagnosis and assessing the extent of thrombosis.

• Duplex ultrasonography: First-line imaging modality to visualize thrombus and assess blood flow.
• CT or MR venography: Provides detailed evaluation of deep veins and pelvic or abdominal involvement.
• Venography: Invasive imaging reserved for complex or unclear cases.

Management

Conservative Treatment

Most superficial thrombophlebitis can be managed with non-invasive measures aimed at symptom relief and prevention of progression.

• Rest and elevation of the affected limb
• Warm compresses and local care to reduce inflammation
• Non-steroidal anti-inflammatory drugs (NSAIDs) for pain and swelling
• Compression stockings to improve venous return and reduce edema

Pharmacological Therapy

Medication is used to prevent thrombus extension, treat underlying infection, and reduce complications.

• Anticoagulation: Heparin, warfarin, or direct oral anticoagulants (DOACs) for deep vein involvement or high-risk superficial thrombophlebitis.
• Antibiotics: Indicated for septic thrombophlebitis to eliminate infection and prevent systemic spread.

Surgical and Interventional Management

In selected cases, invasive procedures may be necessary to remove or isolate thrombi.

• Vein ligation or excision: Surgical removal of the affected vein to prevent propagation.
• Thrombectomy or catheter-directed thrombolysis: Minimally invasive techniques for extensive or high-risk clots.

Complications

Thrombophlebitis can lead to several local and systemic complications if not promptly diagnosed and managed.

• Extension to deep veins: Superficial thrombophlebitis may progress to deep vein thrombosis, increasing the risk of pulmonary embolism.
• Recurrent thrombophlebitis: Patients may experience repeated episodes, especially if underlying risk factors persist.
• Chronic venous insufficiency: Damage to venous valves from repeated thrombosis can lead to long-term edema, skin changes, and ulceration.
• Sepsis in infected cases: Septic thrombophlebitis can cause systemic infection and life-threatening complications if untreated.

Prevention

Preventive measures aim to reduce the risk of thrombosis, particularly in high-risk populations.

• Prophylactic anticoagulation in high-risk patients: Used in hospitalized or post-surgical individuals to prevent clot formation.
• Early mobilization and exercise: Encourages venous return and reduces stasis during prolonged immobility.
• Proper catheter care and avoidance of vein trauma: Reduces the incidence of catheter-related thrombophlebitis.
• Lifestyle modifications: Weight control, smoking cessation, and regular activity help maintain vascular health.

Prognosis and Outcomes

The prognosis of thrombophlebitis depends on the location, extent, and underlying cause of the thrombus. Early diagnosis and appropriate management generally result in favorable outcomes, particularly for superficial thrombophlebitis.

• Natural course of superficial vs. deep thrombophlebitis: Superficial cases often resolve with conservative treatment, while deep vein involvement carries higher risk for complications.
• Factors affecting recovery and recurrence: Age, comorbidities, presence of varicose veins, and adherence to treatment influence outcomes.
• Long-term vascular health implications: Chronic venous insufficiency, post-thrombotic syndrome, and recurrent thrombosis can affect quality of life.

References

1. Callam MJ. Epidemiology of varicose veins. Br J Surg. 1994;81(2):167-173.
2. O’Donnell TF, Passman MA, Marston WA, et al. Management of superficial venous thrombophlebitis: clinical practice guidelines of the Society for Vascular Surgery and the American Venous Forum. J Vasc Surg. 2018;68(1):3S-21S.
3. Prandoni P, Polistena P, Bernardi E, et al. Upper extremity thrombophlebitis: a prospective cohort study. Blood. 1997;90(5):1970-1974.
4. Büller HR, Agnelli G, Hull RD, et al. Antithrombotic therapy for venous thromboembolic disease: American College of Chest Physicians evidence-based clinical practice guidelines. Chest. 2012;141(2_suppl):e419S-e494S.
5. Goldhaber SZ. Superficial thrombophlebitis. N Engl J Med. 1998;339(4):232-238.
6. Decousus H, Quéré I, Presles E, et al. Superficial venous thrombosis and risk of pulmonary embolism. J Thromb Haemost. 2005;3(11):1999-2004.
7. O’Donnell TF, Passman MA. Superficial vein thrombosis: epidemiology, pathophysiology, and clinical management. Semin Vasc Surg. 2007;20(1):13-18.
8. Kearon C, Akl EA, Ornelas J, et al. Antithrombotic therapy for VTE disease: CHEST guideline and expert panel report. Chest. 2016;149(2):315-352.
9. Weitz JI, Fredenburgh JC, Eikelboom JW. A review of venous thromboembolism: epidemiology, pathophysiology, and prevention. Thromb Haemost. 2017;117(1):1-14.
10. Schwab RJ, Hill RB. Upper extremity thrombophlebitis: clinical presentation and management. Vasc Med. 2010;15(3):221-227.