Thrombophlebitis

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Chapter 58 Thrombophlebitis

INTRODUCTION

Description: Thrombophlebitis is an inflammatory condition of the veins with secondary thrombosis. This may occur in two forms: aseptic or suppurative (septic). The vessels may be either superficial or deep. Risk factors may be present, or the onset may be idiopathic. Risk varies with location and cause.
Prevalence: Two million cases per year in the United States, 10% of nosocomial infections, intravascular (venous or arterial) catheter-related—88 of 100,000.
Predominant Age: Septic—childhood; aseptic—age 20 to 30 years; superficial—older than 40 years.
Genetics: Uncommon—antithrombin III, proteins C and S, and factor XII deficiencies (autosomal dominant with variable penetrance), factor V Leiden or prothrombin C-20210-a genes.

ETIOLOGY AND PATHOGENESIS

Causes: Sepsis (Staphylococcus aureus [65% to 75%], multiple organisms [14%]), hypercoagulable states (congenital deficiencies, malignancy, pregnancy, high-dose oral contraceptives, Behçets syndrome, Buerger’s disease, factor V Leiden deficiency), venous stasis (varicose veins), injury to vessel wall. Septic thrombophlebitis may be caused by Candida albicans in unusual cases. (Virchow triad: intimal damage [trauma, infection, or inflammation], stasis, or changes in the blood constituents [changes in coagulability].)
Risk Factors: Trauma (general or vascular), prolonged immobility (hospitalization, prolonged air travel), advanced age, obesity, pregnancy or puerperium, recent surgery, intravascular catheters, steroid or high-dose estrogen therapy (high-dose oral contraceptives), high altitude, hemoglobinopathies, malignancy, nephrotic syndrome, homocystinuria, congenital abnormality.

CLINICAL CHARACTERISTICS

Signs and Symptoms

• Asymptomatic
• Generalized limb pain or swelling
• Swelling, tenderness, redness along the course of the vein
• Fever (70% of patients)
• Warmth, erythema, tenderness, or lymphangitis (32%)
• Systemic sepsis (84% in suppurative cases)
• Red, tender cord
• Swelling of collateral veins

DIAGNOSTIC APPROACH

Differential Diagnosis

• Cellulitis
• Erythema nodosa
• Cutaneous polyarteritis nodosa
• Sarcoid
• Kaposi’s sarcoma
• Ruptured synovial cyst (Baker’s cyst)
• Lymphedema
• Muscle tear, sprain, strain
• Venous obstruction (secondary to tumor, lymph node enlargement)

Associated Conditions: Budd-Chiari syndrome (hepatic vein thrombosis), renal vein thrombosis, homocystinuria, hypercoagulability states (antiphospholipid antibody syndrome), Behçets syndrome, and varicose veins.

Workup and Evaluation

Laboratory: Complete blood count, blood culture (positive in 80% to 90% of superficial cases), D-dimer assay, coagulation profiles (antithrombin III levels are suppressed during the acute event—evaluations for abnormal levels should await completion of therapy), activated partial thromboplastin time (APTT) and prothrombin time (PT) to monitor anticoagulant therapy. For patients with septic thrombosis—periodic white blood cell counts.
Imaging: Contrast venography is the “gold standard” for diagnosis. Doppler studies of vascular flow may be effective for some deep vessels. Chest radiography or spiral computed tomography if embolism is suspected.
Special Tests: Impedance plethysmography, I125-fibrinogen scans (not widely available and requires 41 hours), bone or gallium scans for associated periosteal sepsis, ventilation/perfusion scans of the lungs if an embolism is suspected. Duplex ultrasound evaluation is becoming the diagnostic study of choice to search for venous thrombosis.
Diagnostic Procedures: History, physical examination, imaging or other diagnostic study (impedance plethysmography, 125I-fibrinogen scans).

Pathologic Findings

Clot is attached to vessel wall with variable degrees of inflammation present in the vessel wall. Enlargement of the vessel with thickening is common. Perivascular suppuration or hemorrhage may be seen.

MANAGEMENT AND THERAPY

Nonpharmacologic

General Measures: For superficial aseptic conditions—heat, elevation, observation. For deep or septic thrombophlebitis—hospitalization, anticoagulation, bed rest for 1 to 5 days with progressive return to normal activity. Patients with deep vein thrombosis confined to the calf (distal to the popliteal system) may be managed as outpatients.
Specific Measures: Heparin anticoagulation initially followed by oral maintenance therapy (warfarin) for 3 to 6 months for first episodes or 12 months for recurrent episodes. Filtering devices (“umbrellas”) should be considered for those who cannot receive anticoagulation therapy or those with evidence of emboli. Surgical excision of involved superficial veins (and tributaries) may be required.

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Diet: No specific dietary changes indicated.
Activity: Initially, bed rest for deep or extensive thrombosis with gradual return to activity in 1 to 5 days. No restriction once acute episode is resolved.
Patient Education: Patients who have had an episode of thrombosis should be instructed in risk reduction and warning signs that require reevaluation.

Drug(s) of Choice

Heparin 5000 to 10,000 U IV bolus followed by 1000 U per hour IV (may also use bolus of 80 U/kg, followed by 18 U/kg/hour). Dosage must be titrated based on APTT: target >2 times control. Low molecular weight heparin (LMWH) may also be used.
Maintenance with warfarin (Coumadin) starting at 1 to 5 days. Initial dose 5 to 10 mg PO daily, adjusted based on PT: target >1.3 to 1.5 times control (international normalized ratio [INR] of 2.0 to 3.0). (Intermittent subcutaneous heparin therapy with 15,000 U twice a day may also be used.)
Antibiotic therapy should be added for any patient suspected of sepsis (nafcillin 2 g IV every 6 hours, gentamicin 1 to 1.7 mg/kg IV).
Contraindications: Acute bleeding, recent neurosurgical procedure, known adverse reaction. Warfarin is contraindicated in pregnancy—these patients must continue heparin therapy. Relative contraindications—recent hemorrhage or surgery, peptic ulcer disease (severe), recent nonembolic stroke.
Precautions: Patients should continue to receive heparin until the target PT level is reached. Heparin therapy may cause thrombocytopenia. Intramuscular injections should be avoided while patients are receiving anticoagulant therapy. Warfarin therapy may be associated with necrotic skin lesions in a small number of patients (warfarin necrosis). Desogestrel-containing oral contraceptives are associated with a higher incidence of thromboembolism than other oral contraceptive formulations. This difference is small (20 to 30 of 100,000 versus 10 to 15 of 100,000 for levonorgestrel and 4 of 100,000 for nonpregnant women).
Interactions: Agents that prolong or intensify the action of anticoagulants—alcohol, allopurinol, amiodarone, steroids, androgens, many antimicrobials, cimetidine, chloral hydrate, disulfiram, all nonsteroidal antiinflammatory agents, sulfinpyrazone, tamoxifen, thyroid hormone, vitamin E, ranitidine, salicylates. Agents such as aminoglutethimide, antacids, barbiturates, carbamazepine, cholestyramine, diuretics, griseofulvin, rifampin, and oral contraceptives reduce the efficacy of oral anticoagulants.

Alternative Drugs

Thrombolytic agents (urokinase, streptokinase, tissue plasminogen activator) are effective in dissolving clots but remain investigational for the treatment of thrombosis. For mild superficial clots, nonsteroidal antiinflammatory agents may be used.

FOLLOW-UP

Patient Monitoring: Patients must be carefully monitored for embolization or further thrombosis. At the start of heparin therapy, the APTT must be monitored several times daily until the dose has been stabilized. The dose of warfarin must be monitored with periodic evaluation of the PT. Monitoring should be done daily until the target has been achieved, weekly for several weeks, and then monthly during maintenance therapy. Periodic checks should be made for hematuria and fecal occult blood.
Prevention/Avoidance: Avoid prolonged immobilization. Active prophylaxis (e.g., for patients after surgery) using low-dose subcutaneous heparin, low molecular weight heparin (enoxaparin), mechanical leg compression, and early ambulation. Changing intravenous sites every 48 hours reduces the risk of infection and inflammation.
Possible Complications: Pulmonary embolism (fatal in up to 20% of patients), phlegmasia cerulens dolens (rare). Hematuria or gastrointestinal bleeding may occur while patients are receiving anticoagulants. Any bleeding must be investigated and not presumed to be related to therapy; therapy may unmask an underlying condition such as cancer or ulcer disease. After thrombophlebitis, persistent pain and swelling of the limb may occur. Septic thrombophlebitis is associated with bacteremia (85%), septic emboli (45%), or abscess formation or pneumonia (45%).
Expected Outcome: Superficial thrombophlebitis and distal deep disease generally respond to prompt therapy with eventual resolution of symptoms. Up to 20% of proximal thrombosis may lead to embolization.

MISCELLANEOUS

Pregnancy Considerations: The use of warfarin is contraindicated. Patients who must receive anticoagulant therapy should be given heparin or low molecular weight heparin (intermittent subcutaneous therapy). Pregnancy causes a 49-fold increase in the incidence of phlebitis. Risk is increased with increased maternal age, multiparity, multiple pregnancy, hypertension, and preeclampsia.
ICD-9-CM Codes: Based on location and type.

REFERENCES

Level I

Agnelli G, Piovella F, Buoncristiani P, et al. Enoxaparin plus compression stockings compared with compression stockings alone in the prevention of venous thromboembolism after elective neurosurgery. N Engl J Med. 1998;339:80.

Pinede L, Ninet J, Duhaut P, et alInvestigators of the “Duree Optimale du Traitement AntiVitamines K” (DOTAVK) Study. Comparison of 3 and 6 months of oral anticoagulant therapy after a first episode of proximal deep vein thrombosis or pulmonary embolism and comparison of 6 and 12 weeks of therapy after isolated calf deep vein thrombosis. Circulation. 2001;103:2453.

Prandoni P, Tormene D, Pesavento R, Vesalio Investigators Group. High vs. low doses of low-molecular-weight heparin for the treatment of superficial vein thrombosis of the legs: a double-blind, randomized trial. J Thromb Haemost. 2005;3:1152.

Scurr JH, Machin SJ, Bailey-King S, et al. Frequency and prevention of symptomless deep-vein thrombosis in long-haul flights: a randomised trial. Lancet. 2001;357:1485.

Superficial Thrombophlebitis Treated by Enoxaparin Study Group. A pilot randomized double-blind comparison of a low-molecular-weight heparin, a nonsteroidal anti-inflammatory agent, and placebo in the treatment of superficial vein thrombosis. Arch Intern Med. 2003;163:1657.

Level II

Anonymous. Low-molecular-weight heparin in the treatment of patients with venous thromboembolism. The Columbus Investigators. N Engl J Med. 1997;337:657.

Anonymous. Prevention of pulmonary embolism and deep vein thrombosis with low dose aspirin: Pulmonary Embolism Prevention (PEP) trial. Lancet. 2000;355:1295.

Daniel KR, Jackson RE, Kline JA. Utility of lower extremity venous ultrasound scanning in the diagnosis and exclusion of pulmonary embolism in outpatients. Ann Emerg Med. 2000;35:547.

Grady D, Sawaya G. Postmenopausal hormone therapy increases risk of deep vein thrombosis and pulmonary embolism. Am J Med. 1998;105:41.

Joffe HV, Kucher N, Tapson VF, Goldhaber SZ, Deep Vein Thrombosis (DVT) FREE Steering Committee. Upper-extremity deep vein thrombosis: a prospective registry of 592 patients. Circulation. 2004;110:1605. Epub 2004 Sep 7

Kamran SI, Downey D, Ruff RL. Pneumatic sequential compression reduces the risk of deep vein thrombosis in stroke patients. Neurology. 1998;50:1683-1688.

Lepercq J, Conard J, Borel-Derlon A, et al. Venous thromboembolism during pregnancy: a retrospective study of enoxaparin safety in 624 pregnancies. BJOG. 2001;108:1134.

Lutter KS, Kerr TM, Roedersheimer LR. Superficial thrombophlebitis diagnosed by duplex scanning. Surgery. 1991;110:42.

Tagalakis V, Kahn SR, Libman M, Blostein M. The epidemiology of peripheral vein infusion thrombophlebitis: a critical review. Am J Med. 2002;113:146.

Level III

American College of Obstetricians and Gynecologists. Thromboembolism in pregnancy. ACOG Practice Bulletin 19. Washington, DC: ACOG, 2000.

American College of Obstetricians and Gynecologists. Prevention of deep vein thrombosis and pulmonary embolism. ACOG Practice Bulletin 20. Washington, DC: ACOG, 2000.

American College of Obstetricians and Gynecologists. Air travel during pregnancy. ACOG Committee Opinion 261. Washington, DC: ACOG, 2001.

American College of Obstetricians and Gynecologists. Safety of Lovenox in pregnancy. ACOG Committee Opinion 276. Washington, DC: ACOG, 2002.

Katz VL. Postoperative counseling and management. In: Katz VL, Lentz GM, Lobo RA, Gershenson DM, editors. Comprehensive Gynecology. 5th ed. Philadelphia: Mosby/Elsevier; 2007:672.

Samlaskie CP, James WD. Superficial thrombophlebitis. I. Primary hypercoagulable states. J Am Acad Dermatol. 1990;22:975.

Samlaskie CP, James WD. Superficial thrombophlebitis. II. Secondary hypercoagulable states. J Am Acad Dermatol. 1990;23:1.

Vandenbroucke JP, Helmerhorst FM, Bloemenkamp KW, Rosendaal FR. Third-generation oral contraceptive and deep venous thrombosis: from epidemiologic controversy to new insight in coagulation. Am J Obstet Gynecol. 1997;177:887.

Weinman EE, Salzman EW. Deep-vein thrombosis. N Engl J Med. 1994;331:1630.

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