eMedicine Specialties > Emergency Medicine > Cardiovascular
Thrombophlebitis, Superficial: Treatment & Medication
Updated: Sep 28, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
Treatment
Emergency Department Care
Current treatment options are aimed at resolving symptoms and preventing extension to the deep-venous system. The following treatment options are based on the Cochrane Database of Systematic Reviews article published in 2007 that showed that nonsteroidal anti-inflammatory drugs (NSAIDs) and low-molecular weight heparin (LMWH) are the first options.7
- NSAIDs
- NSAIDs have similar efficacy as low-molecular weight heparin (LMHW) in reducing the risk of extension of superficial thrombophlebitis into the deep venous system and are often more practical and more easily administered than LMHW.
- One NSAID has not been shown to be superior in the treatment of superficial thrombophlebitis.
- LMWH
- The Cochrane Database of Systematic Reviews article suggested that anticoagulation with LMWH is better in reducing local signs and symptoms, along with reducing propagation to a DVT.7
- In addition, LMWH is useful in preventing the progression of thrombosis and is recommended when there is evidence for deep venous thrombosis.
- Antibiotics
- Antibiotics are not routinely indicated for treatment of superficial thrombophlebitis, as the erythema and tenderness is a local inflammatory reaction, not an allergic reaction. However, if suppurative thrombophlebitis could be present, then antibiotics should cover both skin flora and anaerobic organisms, especially if an abscess is present.
- One should also consider MRSA coverage with vancomycin if their local population warrants this.
- Local thrombolytics: No adequate studies have been performed on use of local thrombolytics, and they were excluded from the Cochrane Database of Systematic Reviews article. Therefore, at this time, their use is not recommended.
Adjunctive therapy
- Surgery: Data suggest that surgery may be beneficial with regard to local recurrence and extension of thrombosis, allowing for superior symptomatic relief from pain. It should be reserved for those who are poor candidates for NSAID and LMWH therapy or for those who have recurrent thrombophlebitis.8
- Continued ambulation: Ambulation is important to limit venous stasis and reduce the progression of thrombosis. Recognized causes of venous stasis, such as air travel or extended bed rest, are not recommended in patients with phlebitis of any type.
- Warm compresses: This is indicated for symptomatic relief. Care should be taken to avoid hot compresses that can lead to skin burning.
- Compression stockings: Gradient compression stockings are an often-overlooked adjunctive therapy that is both benign and effective. Gradient compression hose are highly elastic stockings that provide a gradient of compression that is highest at the toes (at least 30-40 mm Hg) and gradually decreases to the level of the thigh. This amount of compression reduces capacitive venous volume by approximately 70% and increases the measured velocity of blood flow in the deep veins by a factor of 5 or more. Gradient compression hose also have been shown to increase local and regional intrinsic fibrinolytic activity.
Consultations
- An emergency physician with training and experience in vascular ultrasonography may perform duplex ultrasonography, but, most often, it is carried out in the vascular laboratory or the radiology department.
Medication
The goals of therapy for superficial phlebitis are to prevent progression into the deep venous system and to hasten the resolution of the inflammatory and thrombotic processes in areas already involved.
Nonsteroidal Anti-inflammatory Drugs
Along with LMWHs, NSAIDS are considered first options to resolve symptoms and prevent extension of thromboembolism.
Ibuprofen (Motrin, Ibuprin)
Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.
Adult
400-800 mg PO q8h, not to exceed 3200 mg daily (proper dose guidelines for CPH not established)
Pediatric
<12 years: Not recommended
>12 years: Administer as in adults
Coadministration with aspirin increases risk of inducing serious NSAID-related side effects; simultaneous administration with low-dose aspirin may decrease aspirin's cardioprotective and stroke preventive effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, beta-blockers, and diuretic effect of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; may increase phenytoin or lithium serum levels
Documented hypersensitivity; peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency, or high risk of bleeding (concomitant or recent use of anticoagulants; hemorrhagic conditions); renal or hepatic impairment
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in coagulation abnormalities or during anticoagulant therapy
Indomethacin (Indocin)
Rapidly absorbed; metabolism occurs in liver by demethylation, deacetylation, and glucuronide conjugation; inhibits prostaglandin synthesis. Available as immediate-release preparation, sustained-release preparation, suppository, and oral suspension.
Adult
Immediate-release: 25-50 mg PO tid
Sustained-release: 75 mg PO qd/bid; not to exceed 200 mg/d
Suppository: 50 mg PR
Pediatric
<14 years: Not recommended except for neonates with patent ductus arteriosus
>14 years: Administer as in adults
Coadministration with aspirin increases risk of inducing serious NSAID-related side effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently; may increase serum concentration and prolong digoxin half-life
Documented hypersensitivity; active GI bleeding or history of recurrent GI lesions; renal insufficiency; syndrome of nasal polyps; angioedema or bronchospastic reaction to aspirin and other NSAIDs; pulmonary hemorrhage; simultaneous use of lithium (may result in lithium toxicity)
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Acute renal insufficiency (ie, serum creatinine >2 mg/dL), hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; reversible leukopenia may occur (discontinue if there is persistent leukopenia, granulocytopenia, or thrombocytopenia)
Caution with hepatic dysfunction, bleeding disorders (ie, platelets <75,000/mm3), parkinsonism, depression, epilepsy, psychiatric disturbances (may cause worsening of symptoms); can mask usual signs and symptoms of infection; fluid retention and peripheral edema have been reported in a few patients
Naproxen (Aleve, Anaprox, Naprelan, Naprosyn)
Inhibits inflammatory reactions and pain by decreasing activity of cyclooxygenase, which results in decrease of prostaglandin synthesis.
Adult
275 mg PO tid or 550 mg bid (proper dose guidelines for CPH not established)
Pediatric
<12 years: Not recommended
>12 years: Administer as in adults
Coadministration with aspirin increases risk of inducing serious NSAID-related side effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; concomitant or recent use of anticoagulants; hemorrhagic conditions; renal or hepatic impairment
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of drug
Anticoagulants
Heparin is essential for patients with superficial thrombophlebitis that is progressive and for those with particular risk factors for progression or recurrence. Heparin should always be used when thrombophlebitis involves the greater saphenous vein. Heparin is the mainstay of treatment when deep system involvement is suggested, but anticoagulation alone does not guarantee a successful outcome. The disease may progress despite full and effective heparin anticoagulation.
Heparin works by activating antithrombin III to slow or prevent the progression of venous thrombosis. Heparin does not dissolve existing clot.
Fractionated LMWHs have largely replaced unfractionated heparin in the treatment of superficial phlebitis. LMWHs offer several distinct advantages over unfractionated heparin: they may be used in the outpatient setting, they do not require measurement of the aPTT, they produce more reliable anticoagulation, and they are associated with a lower risk of bleeding.
When unfractionated heparin is used, an aPTT of at least 1.5 times the control value is necessary for a therapeutic effect. To achieve this, unfractionated heparin must be given intravenously in adequate doses. Low-dose subcutaneous unfractionated heparin should not be used, as it is not an effective therapy for thrombophlebitis and it is not an effective prophylaxis against progression of the disease.
Warfarin should not be used in the acute treatment of superficial phlebitis, because the early risk of increased thrombogenesis outweighs any convenience of oral therapy.
Enoxaparin (Lovenox)
First LMWH released in US. Only LMWH now approved by FDA for both treatment and prophylaxis of DVT.
Widely used in pregnancy, although clinical trials not yet available to demonstrate that it is as safe as unfractionated heparin.
No utility in checking aPTT (drug has wide therapeutic window and aPTT does not correlate with anticoagulant effect).
Adult
Thrombosis: 1 mg/kg SC q12h
Prophylaxis: 30 mg SC q12h
Pediatric
Not established; suggested dose is 1.6 mg/kg SC bid if <2 months and 1 mg/kg/dose SC bid if > 2 months
Platelet inhibitors or oral anticoagulants such as dipyridamole, salicylates, aspirin, NSAIDs, sulfinpyrazone, and ticlopidine may increase risk of bleeding
Documented hypersensitivity; major bleeding; thrombocytopenia
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
If thromboembolic event occurs despite LMWH prophylaxis, discontinue drug and initiate alternate therapy; elevation of hepatic transaminases may occur but is reversible; heparin-associated thrombocytopenia may occur with fractionated LMWHs; 1 mg of protamine sulfate reverses effect of approximately 1 mg of enoxaparin if significant bleeding complications develop
Heparin
Initial bolus used for patients with inflammatory or septic thrombosis lower than that needed for spontaneous deep vein thrombosis and pulmonary embolism, because most patients with inflammatory or septic thrombophlebitis do not have underlying hypercoagulability. Patients with DVT and PE require more aggressive therapy because DVT is manifestation of active hypercoagulable state.
Do not check aPTT until 6 h after initial bolus, as extremely high or low value during this time should not provoke any action.
Adult
60 U/kg (max 4000 U) IV bolus, followed by 12 U/kg/h (max 1000 U/h) maintenance IV infusion
After bolus, check aPTT q6h until stable, and adjust heparin dosing as follows: If APTT low (<1.5 times control value), rebolus with 4000 U and increase drip by 10%; if aPTT high (>2.5 times control value), decrease drip 10%; If aPTT extremely high (>100 sec), hold heparin drip for 1 h and decrease drip 10%
Pediatric
Administer as in adults
Digoxin, nicotine, tetracycline, and antihistamines may decrease effects; NSAIDs, aspirin, dextran, dipyridamole, and hydroxychloroquine may increase toxicity
Documented hypersensitivity; subacute bacterial endocarditis; active bleeding; history of heparin-induced thrombocytopenia
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Thromboembolism may occur due to inadequate dosing; may cause hemorrhagic complications and can trigger immune thrombotic thrombocytopenia 1-2 wk after beginning treatment; platelet-consuming disseminated thrombosis refractory to traditional treatment can be fatal if not recognized quickly and managed appropriately; if significant bleeding develops, 15 mg of protamine (infused over 3 min) usually reverses anticoagulant effect; in neonates, preservative-free heparin recommended to avoid possible toxicity (ie, gasping syndrome) by benzyl alcohol, which is used as preservative; caution in severe hypotension and shock
Antibiotics
These agents are not routinely useful in nonseptic superficial phlebitis. Antibiotics are indicated whenever infection is suspected to play a role and whenever phlebitis of the greater saphenous vein above the knee threatens to approach the saphenofemoral junction. The choice of antibiotics should be guided by blood culture results whenever possible, but empiric therapy should at a minimum provide coverage for group A streptococci and for Staphylococcus aureus.
Superficial phlebitis must not be confused with septic phlebitis, which can be life threatening. If septic phlebitis is suspected, the selection of antibiotics is critically important and depends upon the clinical setting. Antibiotics for septic phlebitis are discussed in the article Thrombophlebitis, Septic.
Ceftriaxone (Rocephin)
Third-generation cephalosporin with broad-spectrum, gram-negative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms. Arrests bacterial growth by binding to one or more penicillin-binding proteins. When used for treatment of phlebitis, should be administered IV rather than IM.
Effective in superficial phlebitis and bacterial septicemia caused by S aureus, Staphylococcus epidermidis, Streptococcus pyogenes, Viridans group streptococci, E coli, Enterobacter cloacae, Streptococcus pneumoniae, Haemophilus influenzae, Klebsiella oxytoca, Klebsiella pneumoniae, Proteus mirabilis, Pseudomonas aeruginosa, Morganella morganii, Serratia marcescens, Acinetobacter calcoaceticus, Bacteroides fragilis, and various Peptostreptococcus species.
Adult
1-2 g IV qd or divided bid; not to exceed 4 g/d
Pediatric
50-75 mg/kg/d IV divided q12h; not to exceed 2 g/d
Probenecid may increase levels; ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity
Documented hypersensitivity
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Adjust dose in renal impairment; caution in breastfeeding women and allergy to penicillin
Cephalexin (Keflex, Biocef, Keftab)
First-generation cephalosporin that may be used as adjunctive therapy in superficial phlebitis where infection is possible but unlikely, and where only likely organisms would be skin flora, including staphylococci and streptococci.
Adult
250-1000 mg PO q6h for 10-14 d; not to exceed 4 g/d
Pediatric
25-50 mg/kg/d PO q6h; not to exceed 3 g/d
Aminoglycosides increase nephrotoxic potential
Documented hypersensitivity
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Adjust dose in renal impairment; may cause nephrotoxicity or cholestatic jaundice
More on Thrombophlebitis, Superficial |
| Overview: Thrombophlebitis, Superficial |
| Differential Diagnoses & Workup: Thrombophlebitis, Superficial |
 Treatment & Medication: Thrombophlebitis, Superficial |
| Follow-up: Thrombophlebitis, Superficial |
| References |
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References
Verlato F, Zucchetta P, Prandoni P, et al. An unexpectedly high rate of pulmonary embolism in patients with superficial thrombophlebitis of the thigh. J Vasc Surg. Dec 1999;30(6):1113-5. [Medline].
Wichers IM, Di Nisio M, Buller HR, Middeldorp S. Treatment of superficial vein thrombosis to prevent deep vein thrombosis and pulmonary embolism: a systematic review. Haematologica. May 2005;90(5):672-7. [Medline].
Rosendaal FR, Helmerhorst FM, Vandenbroucke JP. Oral contraceptives, hormone replacement therapy and thrombosis. Thromb Haemost. Jul 2001;86(1):112-23. [Medline].
Kim J, Richards S, Kent PJ. Clinical examination of varicose veins--a validation study. Ann R Coll Surg Engl. May 2000;82(3):171-5. [Medline].
Gillet JL, Ffrench P, Hanss M, Allaert FA, Chleir F. [Predictive value of D-dimer assay in superficial thrombophlebitis of the lower limbs]. J Mal Vasc. Apr 2007;32(2):90-5. [Medline].
Bergqvist D, Jaroszewski H. Deep vein thrombosis in patients with superficial thrombophlebitis of the leg. Br Med J (Clin Res Ed). Mar 8 1986;292(6521):658-9. [Medline].
Di Nisio M, Wichers IM, Middeldorp S. Treatment for superficial thrombophlebitis of the leg. Cochrane Database Syst Rev. Apr 18 2007;CD004982. [Medline].
Quenet S, Laporte S, Decousus H, Leizorovicz A, Epinat M, Mismetti P. Factors predictive of venous thrombotic complications in patients with isolated superficial vein thrombosis. J Vasc Surg. Nov 2003;38(5):944-9. [Medline].
Ascher E, Hanson JN, Salles-Cunha S, Hingorani A. Lesser saphenous vein thrombophlebitis: its natural history and implications for management. Vasc Endovascular Surg. Nov-Dec 2003;37(6):421-7. [Medline].
de Godoy JM, Braile DM. Protein S deficiency in repetitive superficial thrombophlebitis. Clin Appl Thromb Hemost. Jan 2003;9(1):61-2. [Medline].
De Maeseneer MG. Superficial thrombophlebitis of the lower limb: practical recommendations for diagnosis and treatment. Acta Chir Belg. Apr 2005;105(2):145-7. [Medline].
Feied CF. Pulmonary chest pain, cor pulmonale and pulmonary embolism. In: Gibler, Aufderheide, eds. Emergency Cardiac Care. Vol 1. ed. Mosby-Year Book; 1994:243-303.
Feied CF. Pulmonary embolism. In: Rosen P, Barkin RM, eds. Emergency Medicine Principles and Practice. 4th ed. Mosby-Year Book; 1998:3.
Feied CF. Peripheral venous disease. In: Rosen P, Barkin RM, eds. Emergency Medicine Principles and Practice. 4th ed. Mosby-Year Book; 1998:3.
Schonauer V, Kyrle PA, Weltermann A, et al. Superficial thrombophlebitis and risk for recurrent venous thromboembolism. J Vasc Surg. Apr 2003;37(4):834-8. [Medline].
Unno N, Mitsuoka H, Uchiyama T, et al. Superficial thrombophlebitis of the lower limbs in patients with varicose veins. Surg Today. 2002;32(5):397-401. [Medline].
Further Reading
Keywords
superficial thrombophlebitis, superficial thrombophlebitis causes, superficial thrombophlebitis treatment, superficial venous thrombosis, superficial vein thrombophlebitis, blood clot, deep vein thrombosis, DVT, pulmonary embolism, phlebitis, deep vein thrombophlebitis, superficial phlebitis
