eMedicine Specialties > Emergency Medicine > Cardiovascular

Deep Venous Thrombosis and Thrombophlebitis: Follow-up

Author: Donald Schreiber, MD, CM, Associate Professor of Surgery (Emergency Medicine), Stanford University School of Medicine
Contributor Information and Disclosures

Updated: Aug 5, 2009

Follow-up

Further Inpatient Care

  • Admitted patients may be treated with a LMWH, fondaparinux, or unfractionated heparin. Warfarin 5 mg PO daily is initiated and overlapped for about 5 days until the INR is therapeutic >2 for at least 24 hours.
  • If inpatient treatment is necessary, LMWH or fondaparinux is effective and obviates the need for intravenous infusions or serial monitoring of the aPTT.
  • With the introduction of LMWH or fondaparinux, selected patients qualify for outpatient treatment only if adequate home care and close medical follow-up can be arranged. As discussed, subcutaneous unfractionated heparin may be substituted for LMWH or fondaparinux if insurance issues are a limiting factor. Outpatient therapy with unfractionated heparin carries a higher risk of heparin-induced thrombocytopenia and remains a second-line drug.
  • At some centers, patients with isolated calf vein DVT are treated with full anticoagulant therapy for 3 months.
  • For admitted patients treated with unfractionated heparin, the aPTT or heparin activity level must be monitored every 6 hours while the patient is taking intravenous heparin until the dose is stabilized in the therapeutic range. Patients treated with LMWH or fondaparinux do not require monitoring of the aPTT.
  • Platelets should be monitored. Heparin or LMWH should be discontinued if the platelet count falls below 75,000. Fondaparinux is not associated with HIT.
  • While the patient is initiating therapy with warfarin, the prothrombin time (PT, INR) must be monitored closely (daily or alternate days) until the target is achieved, then weekly for several weeks. When the patient is stable, monitor monthly. Inability to monitor INR precludes outpatient treatment of DVT.
  • For the first episode of DVT, patients should be treated for 3-6 months. Recurrent episodes should be treated for at least 1 year.
  • Significant bleeding (ie, hematemesis, hematuria, gastrointestinal hemorrhage) should be thoroughly investigated because anticoagulant therapy may unmask a preexisting disease (eg, cancer, peptic ulcer disease, arteriovenous malformation).

Further Outpatient Care

  • Most patients with confirmed proximal vein DVT may be safely treated on an outpatient basis. Exclusion criteria for outpatient management are as follows:
    • Suspected or proven concomitant PE
    • Significant cardiovascular or pulmonary comorbidity
    • Ileofemoral DVT
    • Contraindications to anticoagulation
    • Familial or inherited disorder of coagulation - ATIII deficiency, prothrombin 20210A, protein C or protein S deficiency, or factor V Leiden
    • Familial bleeding disorder
    • Pregnancy
    • Morbid obesity >150 kg
    • Renal failure (creatinine >2 mg%)
    • Unavailable or unable to arrange close follow-up care
    • Unable to follow instructions
    • Homeless
    • No contact telephone
    • Geographic—too far from hospital
    • Patient/family resistant to outpatient therapy
  • Treatment of isolated calf vein DVT is best individualized, taking into account local preferences, patient reliability, the availability of follow-up care, and an assessment of ongoing risk factors.
  • Patients with suspected or diagnosed isolated calf vein DVT may be discharged safely on a nonsteroidal anti-inflammatory drug (NSAID) or aspirin with close follow-up care and repeat diagnostic studies (ie, ultrasonography) in 7 days to evaluate for proximal extension.
  • At certain centers, patients with isolated calf vein DVT are treated with full anticoagulant therapy.
  • Patients with suspected DVT but with negative initial noninvasive study results need to be reassessed by their primary care provider within 7 days.
  • Patients with ongoing risk factors need to be reevaluated at 1 week to detect proximal extension because of the limited accuracy of noninvasive tests for calf vein DVT.
  • Prandoni et al found that the use of ultrasonography to determine the duration of anticoagulation can reduce recurrences of venous thromboembolism after a first episode of acute proximal deep venous thrombosis (DVT). In the study, 538 consecutive outpatients who had completed an uneventful 3-month period of anticoagulation were randomized to receive either fixed-duration anticoagulation (up to 9 months for secondary DVT and up to 21 months for unprovoked thrombosis) or flexible-duration anticoagulation, with treatment discontinued once ultrasound showed recanalization of the affected veins. Recurrent venous thromboembolism developed in 17.2% of the patients allocated to fixed-duration anticoagulation and 11.9% of the patients allocated to flexible-duration anticoagulation; no significant difference was noted in the rate of major bleeding.25

Transfer

  • Transfer may be necessary for patients with special concerns such as inherited coagulation disorders.
  • Transfer may be required depending on local expertise for thrombolytic therapy or insertion of a venocaval filter.

Deterrence/Prevention

  • Prophylaxis for DVT is required in all patients with risk factors. DVT prophylaxis for patients scheduled to undergo major surgery is well recognized.
  • Recently, a large multicenter double-blind placebo-controlled trial showed that a single subcutaneous 40-mg daily dose of enoxaparin achieved a 63% reduction in the incidence of DVT/PE in general medical patients admitted to the hospital.26
  • In the Women's Health Study, supplementation with vitamin E (alpha-tocopherol, 600 IU every other day) reduced the risk of venous thromboembolism in women, especially those with a prior history or genetic predisposition.27
  • High-risk patients should also be prescribed a single prophylactic subcutaneous 40 mg dose of enoxaparin prior to a long plane trip (>6 h).

Complications

  • Acute PE may still occur despite adequate anticoagulation.
  • Hemorrhagic complications are the most common adverse effects of anticoagulant therapy. The risk of major hemorrhage while taking heparin is approximately 5%.
  • The treatment of hemorrhage while taking heparin depends on the severity of the bleeding and the extent to which the aPTT is elevated above the therapeutic range. Patients who hemorrhage while receiving heparin are best treated by discontinuing the drug. The half-life is relatively short, and the aPTT usually returns to the reference range within a few hours. Treatment with fresh frozen plasma or platelet infusions is ineffective. For severe hemorrhage, such as intracranial or massive gastrointestinal bleeding, heparin may be neutralized by protamine at a dose of 1 mg for every 100 units. Protamine should be administered at the same time that the infusion is stopped.
  • The treatment of major hemorrhage associated with LMWH is similar to heparin. However, the half-life of these agents is longer (4-6 h). As with heparin, fresh frozen plasma or platelet transfusions are ineffective. Protamine may be used, but it only reverses 60% of the drug's effects.
  • The risk of bleeding on warfarin is not linearly related to the elevation of the INR. The risk is conditioned by other factors, including poor follow-up, drug interactions, age, and preexisting disorders that predispose to bleeding.
  • Patients who hemorrhage while receiving oral warfarin are treated by withholding the drug and administering vitamin K. Severe life-threatening hemorrhage is managed with fresh frozen plasma in addition to vitamin K. Recombinant factor VIIa is another option especially for CNS hemorrhage.
  • Additional complications include the following:
    • Systemic embolism
    • Chronic venous insufficiency
    • Postphlebitic syndrome (ie, pain and edema in the affected limb without new clot formation)
    • Soft tissue ischemia associated with massive clot and very high venous pressures - Phlegmasia cerulea dolens

Prognosis

  • All patients with proximal vein DVT are at long-term risk of chronic venous insufficiency.
  • Approximately 20% of untreated proximal (above the calf) DVTs progress to pulmonary emboli, and 10-20% of these are fatal. With anticoagulant therapy, the mortality rate is decreased 5- to 10-fold.

Patient Education

Miscellaneous

Medicolegal Pitfalls

  • Failure to consider the diagnosis in patients with risk factors
  • Failure to recommend repeat noninvasive studies and reassessment in high-risk patients with negative findings on initial evaluations

Special Concerns

  • Superficial thrombophlebitis
    • Superficial thrombophlebitis is often associated with DVT in 2 specific settings. The following high-risk groups require further evaluation for DVT:
      • Superficial thrombophlebitis in the absence of coexisting venous varices and no other obvious etiology
      • Involvement of the greater saphenous vein above the knee, especially if it extends to the saphenofemoral junction: These latter patients should be treated as having proximal vein DVT and treated with full anticoagulant therapy.
    • Uncomplicated superficial thrombophlebitis may be treated symptomatically with heat, NSAIDs, and compression hose. Bed rest is not recommended.
    • Some centers recommend full anticoagulation for high-risk patients with isolated superficial thrombophlebitis. Some physicians may anticoagulate high-risk patients with negative initial study results until follow-up surveillance studies are completed. An alternative approach involves symptomatic care alone with close follow-up and repeated noninvasive testing in 1 week. Full anticoagulation is then reserved only for those patients with proven proximal vein DVT.
  • Axillary/subclavian vein thrombosis
    • This was first described by Paget in 1875 and von Schrötter in 1884 and is sometimes referred to as Paget–von Schrötter syndrome. The pathophysiology is similar to that of DVT, and the etiologies overlap. The incidence is lower than that of lower extremity DVT because of decreased hydrostatic pressure, fewer venous valves, higher rates of blood flow, and less frequent immobility of the upper arm.
    • Thoracic outlet compression from cervical ribs or congenital webs may precipitate axillary/subclavian venous thrombosis. Catheter-induced thrombosis is increasingly a common cause of this condition. The increased use of subclavian catheters for chemotherapy and parenteral nutrition has resulted in a dramatic increased incidence of proven thrombosis.
    • Similarly, pulmonary artery catheters are associated with a high incidence of internal jugular and subclavian vein thrombosis. Pulmonary embolism (PE) occurs in approximately 10% of patients. Fatal or massive PE is extremely rare.
    • Ultrasonography and venography are the diagnostic tests of choice. Ultrasonographic findings may be falsely negative because of collateral blood flow. Duplex ultrasonography is accurate for the evaluation of the internal jugular vein and its junction with the subclavian vein where the innominate vein begins.
    • Thrombolytic therapy is the treatment of choice for axillary/subclavian venous thrombosis. Restoration of venous patency is more critical for the prevention of chronic venous insufficiency in the upper extremity. Thrombolysis is best accomplished with local administration of the thrombolytic agent directly at the thrombus. After completion of a venographic study, a catheter is floated up to the site of the clot, and the thrombolytic agent is administered as a direct infusion. Venographic assessment for clot lysis is repeated every 4-6 hours until venous patency is restored. Heparin is usually given concurrently to prevent rethrombosis.
    • In the presence of anatomic abnormalities, surgical therapy is recommended to minimize long-term morbidity and recurrence. Catheter-induced thrombosis may require removal of the device. Locally infused thrombolytic agents have been used successfully and are currently the treatment of choice.
 


More on Deep Venous Thrombosis and Thrombophlebitis

Overview: Deep Venous Thrombosis and Thrombophlebitis
Differential Diagnoses & Workup: Deep Venous Thrombosis and Thrombophlebitis
Treatment & Medication: Deep Venous Thrombosis and Thrombophlebitis
Follow-up: Deep Venous Thrombosis and Thrombophlebitis
Multimedia: Deep Venous Thrombosis and Thrombophlebitis
References
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Further Reading

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Contributor Information and Disclosures

Author

Donald Schreiber, MD, CM, Associate Professor of Surgery (Emergency Medicine), Stanford University School of Medicine
Donald Schreiber, MD, CM is a member of the following medical societies: American College of Emergency Physicians
Disclosure: Abbott Point of Care Inc Research Grant and Speaker''''''''''''''''s Bureau Speaking and teaching; Bristol-Myers Squibb Inc Honoraria Speaking and teaching; Sanofi-Aventis, Inc Honoraria Speaking and teaching; Nanosphere Inc Grant/research funds Research; Singulex Inc Grant/research funds Research

Medical Editor

Francis Counselman, MD, Program Director, Chair, Professor, Department of Emergency Medicine, Eastern Virginia Medical School
Francis Counselman, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Emergency Physicians, Association of Academic Chairs of Emergency Medicine (AACEM), Norfolk Academy of Medicine, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

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Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Gary Setnik, MD, Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School
Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine
Disclosure: SironaHealth Salary Management position; South Middlesex EMS Consortium Salary Management position

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Barry E Brenner, MD, PhD, FACEP, Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, University Hospitals, Case Medical Center
Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

 
 
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