eMedicine Specialties > Emergency Medicine > Cardiovascular

Thrombophlebitis, Superficial

Adam J Rosh, MD, MS, Assistant Professor, Department of Emergency Medicine, Wayne State University/Detroit Receiving Hospital

Updated: Sep 28, 2009

Introduction

Background

Superficial vein thrombophlebitis is a common inflammatory-thrombotic process that may occur spontaneously or as a complication of medical or surgical interventions. Sterile thrombophlebitis limited to the superficial veins rarely is life threatening, but a thorough diagnostic evaluation is mandatory because many patients with superficial phlebitis also have occult deep vein thrombosis (DVT), which carries high rates of morbidity and mortality.

Superficial phlebitis with infection, such as phlebitis originating at an intravenous catheter site, is referred to as septic thrombophlebitis. This clinical entity requires special diagnostic and therapeutic approaches that are different from those applicable to sterile phlebitis. Septic thrombophlebitis is discussed in a separate article (see Thrombophlebitis, Septic).

Superficial vein thrombophlebitis and deep vein thrombosis share the same pathophysiology, pathogenesis, and risk factors. Although not common, superficial thrombophlebitis can progress through perforating veins to involve adjacent deep veins. Therefore, it is not surprising that in people with a diagnosis of superficial thrombophlebitis, the incidence of associated DVT and pulmonary embolism (PE) is high.¹

Superficial thrombophlebitis is a clinical diagnosis. The clinician can identify tender and inflamed superficial veins. However, ruling out a DVT in this clinical setting is difficult and often further testing is required to evaluate for a DVT.

Treatment is aimed at patient comfort and preventing superficial phlebitis from progressing to involve the deep veins, because damage to deep vein valves leads to chronic deep venous insufficiency (often referred to as postphlebitic syndrome) as well as to recurrent pulmonary embolism and an increased risk of death.

Pathophysiology

Microscopic thrombosis is a normal part of the dynamic balance of hemostasis. In 1846, the German pathologist Virchow recognized that if this dynamic balance is altered by venous stasis, abnormal coagulability, or vessel wall injuries, microthrombi could propagate to form macroscopic thrombi.

In the absence of a triggering event, neither venous stasis nor abnormal coagulability alone causes clinically important thrombosis, but vascular endothelial injury does reliably cause thrombus formation. The initiating injury triggers an inflammatory response that results in immediate platelet adhesion at the site of injury. Further platelet aggregation is mediated by thromboxane A2 and by thrombin.

Platelet aggregation due to thromboxane A2 is inhibited reversibly by nonsteroidal anti-inflammatory agents and irreversibly by aspirin, but thrombin-mediated platelet aggregation is unaffected by aspirin and nonsteroidals. This is why aspirin and nonsteroidal anti-inflammatories are somewhat effective in preventing arterial thrombosis, as seen in stroke and myocardial infarction, but they are not very effective in preventing or treating venous thrombophlebitis.

Frequency

International

Superficial thrombophlebitis is so common that it is difficult to obtain valid estimates of its frequency.

Mortality/Morbidity

Adverse outcomes from thrombophlebitis are uncommon. However, when the process extends to involve the deep venous system, an increased risk of pulmonary embolism (PE) exists.² Also, the recanalization of thrombosed veins can result in a valveless channel, leading to a prolonged venous circulation time and often to chronically elevated ambulatory venous pressure within the legs. This often leads to a clinical postphlebitic syndrome of chronic pain, edema, hyperpigmentation, ulceration, and an increased risk of recurrent thrombophlebitis.

Sex

• Pregnancy and the puerperium are recognized risk factors for phlebitis. High-dose estrogen therapy is also a risk factor, but no intrinsic sex-linked preferential risk exists for the disease.
• The likelihood of thrombophlebitis is increased through most of pregnancy and for approximately 6 weeks after delivery. This is partly due to increased platelet stickiness and partly due to reduced fibrinolytic activity.
• Case-controlled and cohort studies based on clinical signs and symptoms of thrombosis suggest that, by taking high-estrogen oral contraceptives, a woman may increase her risk of thrombosis by a factor of 3-12 times, although the absolute risk remains low. Newer low-dose oral contraceptives are associated with a much lower risk of thrombophlebitis, although the absolute risk has not been well quantified.³

Age

Age is not an independent risk factor for phlebitis, but the incidence of other recognized risk factors increases with age, leading to an overall increased risk with increasing age.

Clinical

History

Patients with superficial thrombophlebitis often give a history of a gradual onset of localized tenderness, followed by the appearance of an area of erythema along the path of a superficial vein. A history of local trauma, prior similar episodes, varicose veins, prolonged travel, hormone use, tobacco use, family history of blood coagulopathies, or enforced stasis may be given. Asking about these risk factors for hypercoagulability should be done, but the absence of identifiable risk factors has no prognostic value.

• Traumatic thrombophlebitis: Ask about trauma, needlesticks, indwelling IV catheters, drug (eg, phenytoin) or hypertonic (10% calcium chloride) solution infusion and sclerotherapy.
• Thrombosed varicose veins: Ask about history of varicose veins, previous history of thrombosed varices, and any injury to the leg with the varices. One should ascertain whether there was a thrombosed vein and timing of erythema and pain.
• Thrombosed hemorrhoids: History, as in varicose veins, should focus on previous history of thromboses, surgical intervention, and timing of symptoms.
• Other, migratory thrombophlebitis: Also known as Trousseau’s sign of malignancy, this is described as thrombophlebitis that travels, often one leg to another. It has a strong association of adenocarcinoma of the pancreas and lung, and, therefore, history should be directed toward finding malignancy.

Physical

• Inspection: Visual appearance is not a reliable guide to a peripheral venous condition, because the clinical findings of venous disease (erythema, edema, and pain) are common to many other entities. Swelling may result from acute venous obstruction (as in deep vein thrombosis) or from deep or superficial venous reflux, or it may be caused by an unrelated disease condition such as hepatic insufficiency, renal failure, cardiac decompensation, infection, trauma, or environmental effects. Lymphedema may be primary or it may be secondary to overproduction of lymph due to severe venous hypertension.
  • Normal veins are distended visibly at the foot, ankle, and occasionally in the popliteal fossa, but not in the rest of the leg. Normal veins may be visible as a blue subdermal reticular pattern, but dilated superficial leg veins above the ankle usually are evidence of venous pathology.
  • Darkened, discolored, stained skin or nonhealing ulcers are typical signs of chronic venous stasis, particularly along the medial ankle and the medial lower leg. Chronic varicosities or telangiectasias also may be observed.
• Palpation: Palpation of a painful or tender area may reveal a firm, thickened, thrombosed vein. Palpable thrombosed vessels are virtually always superficial.
• Percussion
  • Perthes percussive test is a classic maneuver with high sensitivity (97%) but low specificity (20%)⁴ that tests if venous segments are interconnected. With the patient in a standing position, a vein segment is tapped at one location while an examining hand feels for a pulse wave at another location. Propagation of a palpable pulse wave suggests that a fluid-filled vessel with open or incompetent valves connects the two locations.
    • A pulse wave may be propagated after prolonged standing in the absence of true pathology, because prolonged standing causes even normal veins to become distended and normal valves to float open.
    • Perthes test is most valuable when a bulging varicosity in the lower leg has no obvious connection with a varicosity in the upper thigh. A palpable pulse wave propagation between the two vessels is proof positive of the existence of an unseen connection.
  • Trendelenburg test: The Trendelenburg test is a classic physical examination maneuver that helps to distinguish superficial venous reflux from incompetence of the deep vein valves.
    • The leg is elevated until all superficial veins have collapsed, and the point of suspected reflux from the deep system is occluded by manual compression or by a tourniquet. The patient is then asked to stand, and the distal varicosity is observed for refilling. If the distal varicosity remains mostly empty, the reflux pathway is principally through the peripheral varicosity that has been occluded.
    • Inability to prevent rapid filling of the varicosity despite manual occlusion of the suspected high point of reflux suggests that another reflux pathway is involved.
    • Rapid refilling of calf varices despite occlusion of the proximal trunk suggests deep system reflux or failure of the valves of multiple perforating veins.

Causes

The most important clinically identifiable risk factors for thrombophlebitis are a prior history of superficial phlebitis, deep vein thrombosis, and pulmonary embolism. Some common risk markers include recent surgery or pregnancy, prolonged immobilization, and underlying malignancy. Other recognized markers of risk for venous thromboembolic disease are listed here.

• AIDS (lupus anticoagulant)
• Antithrombin III deficiency
• Behçet disease
• Blood type A
• Burns
• Catheters (indwelling venous infusion catheters)
• Chemotherapy
• Congestive heart failure
• Drug abuse (intravenous [IV] drugs)
• Drug-induced lupus anticoagulant
• DVT in the past
• Estrogen replacements (high dose only)
• Fibrinogen abnormality
• Fractures
• Hemolytic anemias
• Heparin-associated thrombocytopenia
• Homocysteinemia
• Homocystinuria
• Hyperlipidemias
• Immobilization
• Malignancy
• Myocardial infarction
• Obesity
• Old age
• Oral contraceptives
• PE in the past
• Phenothiazines
• Plasminogen abnormality
• Plasminogen activator abnormality
• Polycythemia
• Postoperative
• Postpartum period
• Pregnancy
• Protein C deficiency
• Protein S deficiency
• Resistance to activated protein C
• Systemic lupus erythematosus
• Thrombocytosis
• Trauma
• Ulcerative colitis
• Varicose veins
• Venography
• Venous pacemakers
• Venous stasis
• Warfarin (first few days of therapy)

Differential Diagnoses

Workup

Laboratory Studies

• Blood tests rarely are helpful in the diagnosis of thrombophlebitis, except in those patients at risk for an underlying hypercoagulable state.
• Several common hypercoagulable states can be identified through laboratory studies. Some of these states include the following:
  • Resistance to activated protein C (most often due to factor V Leiden)
  • Protein C deficiency
  • Protein S deficiency
  • Antithrombin III deficiency
  • Antiphospholipid antibodies
  • Prothrombin gene 2010-a mutation (factor II mutation)
• The prothrombin time (PT) and activated partial thromboplastin time (aPTT) are not useful in the diagnostic evaluation of patients with suspected superficial or deep thrombophlebitis. Most patients with thrombophlebitis have a normal PT and aPTT, and active thrombophlebitis is not uncommon in patients with a therapeutically elevated INR due to warfarin therapy.
• A low white blood cell (WBC) count lowers the likelihood of an infectious process and raises the likelihood of phlebitis. An elevated WBC count is nonspecific because both normal and elevated WBC counts are common in patients with thrombophlebitis. Chronic venous insufficiency (venous congestion due to reflux) and superficial or deep vein thrombosis can mimic leg cellulitis very closely, and true cellulitis (with an elevated WBC count) is a frequent complication of both diseases.
• D-dimer is a unique degradation product produced by plasmin-mediated proteolysis of cross-linked fibrin that is often measured in the evaluation for DVT and PE. However, its use in detecting thrombophlebitis is of little clinical use.⁵
• In patients with migratory thrombophlebitis, a malignancy workup is appropriate.

Imaging Studies

• Proper diagnosis of venous system disease often requires both functional and anatomic information about the venous circulation. 
  • The functional tests (discussed below) are extremely useful as measures of whole-leg or regional venous function, but functional tests can detect only regionally significant reflux or a significant impediment to venous outflow.
  • Anatomic imaging of the venous system can detect small amounts of local and regional reflux as well as obstructing and nonobstructing thrombus. Unfortunately, anatomic imaging often fails to identify important functional deficits.
  • A combination of functional and semi-anatomic or anatomic techniques allows a complete understanding of most venous system pathology.
• All patients with superficial thrombophlebitis above the knee should undergo duplex ultrasonography as the initial diagnostic modality of choice to rule out DVT.
• When the patient has superficial thrombophlebitis below the knee, duplex ultrasonography is only indicated for signs and symptoms consistent with a DVT (eg, asymmetrical swelling, erythema, and pain). Superficial thrombophlebitis in lower extremity varicose veins have an extremely low incidence of DVT.⁶  
• The diagnostic evaluation of patients with potential septic thrombophlebitis, such as phlebitis associated with an intravenous catheter site, is discussed in the article Thrombophlebitis, Septic.
• Magnetic resonance venography (MRV) is a noninvasive test that probably is more sensitive and more specific than ultrasonography in the detection of deep venous thrombophlebitis; however, this is not readily available and is not practical at most institutions.
• Invasive contrast venography, once the criterion standard for evaluation of the venous system, has fallen out of favor due to its invasiveness, use of ionizing radiation, and use of intravenous contrast. In addition, it can lead to venous scarring and thrombophlebitis.
• CT venography is a reasonable alternative to duplex ultrasonography to evaluate the iliac and pelvis venous systems.

Procedures

• Local incision and evacuation
  • A painful section of a superficial vein containing a palpable intravascular coagulum may be treated by puncture incision with an 18-gauge needle and evacuation of the clot after local anesthesia. This procedure often produces marked rapid relief and rapid resolution of the inflammation.
  • Puncture and evacuation is less effective in the first week after the onset of symptoms because the vessel wall is thickened and the coagulum itself is more cohesive during the early phase of a phlebitis.

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.

Dosing

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

Interactions

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

Contraindications

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

Precautions

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.

Dosing

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

Interactions

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

Contraindications

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)

Precautions

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.

Dosing

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

Interactions

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

Contraindications

Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; concomitant or recent use of anticoagulants; hemorrhagic conditions; renal or hepatic impairment

Precautions

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).

Dosing

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

Interactions

Platelet inhibitors or oral anticoagulants such as dipyridamole, salicylates, aspirin, NSAIDs, sulfinpyrazone, and ticlopidine may increase risk of bleeding

Contraindications

Documented hypersensitivity; major bleeding; thrombocytopenia

Precautions

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.

Dosing

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

Interactions

Digoxin, nicotine, tetracycline, and antihistamines may decrease effects; NSAIDs, aspirin, dextran, dipyridamole, and hydroxychloroquine may increase toxicity

Contraindications

Documented hypersensitivity; subacute bacterial endocarditis; active bleeding; history of heparin-induced thrombocytopenia

Precautions

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.

Dosing

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

Interactions

Probenecid may increase levels; ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity

Contraindications

Documented hypersensitivity

Precautions

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.

Dosing

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

Interactions

Aminoglycosides increase nephrotoxic potential

Contraindications

Documented hypersensitivity

Precautions

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

Follow-up

Patients should follow-up with their primary care physician or vascular surgeon in 2-3 days to ensure that the disease process is improving.

Complications

• Extension into deep venous system
• Conversion to suppurative thrombophlebitis
  • Septicemia
  • Septic emboli
• Persistence of nodule

Prognosis

• The prognosis for superficial thrombophlebitis is generally good.

Patient Education

For excellent patient education resources, visit eMedicine's Circulatory Problems Center. Also, see eMedicine's patient education articles Varicose Veins, Blood Clot in the Legs, and Phlebitis.

Miscellaneous

Medicolegal Pitfalls

• Patients who present with clinical evidence of superficial phlebitis often have deep system involvement that is clinically occult. Those who lack deep system involvement often progress to develop deep vein thrombosis (DVT) over time. The incidence of fatal PE in these patients is not insignificant. Any chest symptoms, no matter how minor, should be considered extremely worrisome in a patient with superficial thrombophlebitis, as pulmonary embolism (PE) is extremely common and can be difficult to diagnose.
• Phlebitis that has progressed to involve any other deep veins (anterior or posterior tibial veins, proximal peroneal vein, popliteal vein, or femoral vein at any level) is a life-threatening condition that must not be confused with superficial venous thrombophlebitis.
• The principal deep vein of the thigh often is referred to incorrectly as the "superficial femoral vein." Do not be misled by this nomenclature. A thrombus in the superficial femoral vein is the most serious type of DVT.
• A small number of often-repeated mistakes in diagnosis and treatment are responsible for a large proportion of the bad outcomes with serious legal repercussions.
  • Failure to pursue a definitive workup, attempting instead to diagnose superficial thrombophlebitis and to rule out DVT on clinical grounds that are known to be unreliable.
  • Failure to warn the patient that superficial phlebitis can progress to the deep veins and that any change in symptoms warrants immediate reevaluation.
  • Failure to begin a workup for pulmonary embolism when a patient has chest symptoms in the presence of leg symptoms
  • Failure to start anticoagulation immediately upon the diagnosis of DVT or at suspicion of pulmonary embolism.

Special Concerns

• Venous thrombophlebitis and PE are common during all trimesters of pregnancy and for 6-12 weeks after delivery.
• Superficial varicosities and superficial phlebitis are common during pregnancy, and associated DVT is also common because of a pregnancy-related reduction in intrinsic plasminogen activator activity.
  • The diagnostic approach should be exactly the same in a pregnant patient as in a nonpregnant one.
  • Duplex scanning is safe in pregnancy.
  • If indicated, a nuclear perfusion lung scan may be performed safely in pregnancy.
  • If indicated, heparin may be used in pregnancy.
  • If indicated, fibrinolytics may be used in pregnancy.
  • Failure to treat the mother properly is the most common cause of fetal demise.

References

1. 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].

2. 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].

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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

Contributor Information and Disclosures

Author

Adam J Rosh, MD, MS, Assistant Professor, Department of Emergency Medicine, Wayne State University/Detroit Receiving Hospital
Adam J Rosh, MD, MS is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Samuel M Keim, MD, Associate Professor, Department of Emergency Medicine, University of Arizona College of Medicine
Samuel M Keim, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Public Health Association, and Society for Academic Emergency Medicine
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Eddy Lang, MDCM, CCFP (EM), CSPQ, Assistant Professor, Department of Family Medicine, McGill University; Consulting Staff, Department of Emergency Medicine, The Sir Mortimer B Davis-Jewish General Hospital
Eddy Lang, MDCM, CCFP (EM), CSPQ is a member of the following medical societies: American College of Emergency Physicians
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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
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Chief Editor

David FM Brown, MD, Assistant Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital
David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine
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The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors, Craig F Feied, MD, and Jonathan A Handler, MD, to the development and writing of this article.

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