Superficial Thrombophlebitis – Causes, Symptoms, Diagnosis, Treatment and Ongoing care



  • Superficial thrombophlebitis is an inflammatory condition of the veins with secondary thrombosis.
  • Septic (suppurative) thrombophlebitis types:
    • Iatrogenic
    • Infectious, mainly syphilis and psittacosis
  • Aseptic thrombophlebitis types:
    • Primary hypercoagulable states: Disorders with measurable defects in the proteins of the coagulation and/or fibrinolytic systems
    • Secondary hypercoagulable states: Clinical conditions with a risk of thrombosis
  • System(s) affected: Cardiovascular
  • Synonym(s): Phlebitis; Phlebothrombosis

Geriatric Considerations

Septic thrombophlebitis is more common; prognosis is poorer.

Pediatric Considerations

Subperiosteal abscesses of adjacent long bone may complicate the disorder.

Pregnancy Considerations

  • Associated with increased risk of aseptic superficial thrombophlebitis
  • Warfarin and nonsteroidal anti-inflammatory drugs (NSAIDs) are contraindicated.


  • Predominant age:
    • Septic: More common in childhood
    • Aseptic primary hypercoagulable state:
      • Antithrombin III and heparin cofactor II deficiency: Neonatal period, but 1st episode usually at age 20–30 years
      • Proteins C and S: <30 years of age
    • Aseptic secondary hypercoagulable state:
      • Mondor disease: Women, ages 21–55 years
      • Thromboangiitis obliterans onset: Ages 20–50 years
  • Predominant sex:
    • Suppurative: Male = Female.
    • Aseptic:
      • Mondor: Female > Male (2:1)
      • Thromboangiitis obliterans: Female > Male (1–19% of clinical cases)


  • Septic:
    • Up to 10% of all nosocomial infections
    • Incidence of catheter-related thrombophlebitis is 88/100,000 persons.
    • Develops in 4–8% if cutdown is performed
  • Aseptic primary hypercoagulable state: Antithrombin III and heparin cofactor II deficiency incidence is 50/100,000 persons.
  • Aseptic secondary hypercoagulable state:
    • Trousseau syndrome (migratory venous thrombosis associated with occult malignancy)
    • Trousseau syndrome incidence in malignancy is 5–15%.
    • Trousseau syndrome incidence in pancreatic carcinoma is 50%.
    • In pregnancy, 49-fold increased incidence of phlebitis
    • Superficial migratory thrombophlebitis in 27% of patients with thromboangiitis obliterans


  • Superficial thrombophlebitis is common.
  • One-third of patients in a medical ICU develop thrombophlebitis that eventually progresses to the deep veins.

Risk Factors

  • Nonspecific:
    • Immobilization
    • Obesity
    • Advanced age
    • Postoperative states
  • Septic:
    • IV catheter (68% of cannulas have been left in place for 2 days)
    • Incidence is 40× higher with plastic cannulas (8%) than with steel or scalp cannulas (0.2%).
    • Lower extremity IV catheter
    • Cutdowns
    • Cancer, debilitating diseases
    • Steroid
    • Thrombosis
    • Dermal infection
    • Burned patients
    • IV antibiotics
    • AIDS
    • Varicose veins
  • Antithrombin II and heparin cofactor II deficiency:
    • Pregnancy
    • Oral contraceptives
    • Surgery, trauma, infection
  • In pregnancy:
    • Increased age
    • Hypertension
    • Eclampsia
    • Increased parity
  • Thromboangiitis obliterans: Persistent smoking
  • Mondor disease:
    • Breast abscess
    • Antecedent breast surgery
    • Breast augmentation
    • Reduction mammoplasty
  • Superficial thrombophlebitis may occur spontaneously or as a complication of medical or surgical interventions.


  • Septic: No known genetic pattern
  • Antithrombin III deficiencies: Autosomal dominant
  • Proteins C and S deficiency: Autosomal dominant with variable penetrance
  • Disorders of fibrinolytic system: Congenital defects inheritance variable
  • Dysfibrinogenemia: Autosomal dominant
  • Factor XII deficiency: Autosomal recessive

General Prevention

  • Use of scalp vein cannulas
  • Avoidance of lower extremity cannulations
  • Insertion under aseptic conditions
  • Secure anchoring of the cannulas
  • Replacement of cannulas, connecting tubing, and IV fluid every 48–72 h
  • Antibacterial ointment in cutdown


  • Microscopic thrombosis is a normal part of the dynamic balance of hemostasis.
  • In the absence of a triggering event, neither venous stasis nor abnormal coagulability alone causes clinically important thrombosis.
  • 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.
  • Platelet aggregation owing to thromboxane A2 is inhibited reversibly by NSAIDs and irreversibly by aspirin, but thrombin-mediated platelet aggregation is unaffected by aspirin and NSAIDs.


  • Septic:
    • Staphylococcus aureus in 65–78%
    • Enterobacteriaceae, especially Klebsiella
    • Multiple organisms in 14%
    • Anaerobic isolate rare
    • Candida sp.
    • Cytomegalovirus (CMV) in AIDS patients
  • Aseptic primary hypercoagulable state:
    • Antithrombin III and heparin II deficiency
    • Protein C and protein S deficiency
    • Disorder of tissue plasminogen activator
    • Abnormal plasminogen and coplasminogen
    • Dysfibrinogenemia
    • Factor XII deficiency
    • Lupus anticoagulant and anticardiolipin antibody syndrome
  • Aseptic secondary hypercoagulable states:
    • Malignancy (Trousseau syndrome: Recurrent migratory thrombophlebitis): Most commonly seen in metastatic mucin or adenocarcinomas of the GI tract (pancreas, stomach, colon, and gallbladder), lung, prostate, and ovary
    • Pregnancy
    • Oral contraceptives
    • Infusion of prothrombin complex concentrates
    • Behçet disease
    • Buerger disease
    • Mondor disease



Pain along the course of a vein

Physical Exam

  • Swelling, tenderness, redness along the course of a vein or veins
  • May look like cellulitis or erythema nodosa
  • Fever in 70% of patients
  • Warmth, erythema, tenderness, or lymphangitis in 32%
  • Sign of systemic sepsis in 84% of suppurative

Diagnostic Tests & Interpretation


  • If septic concern:
    • Blood cultures (bacteremia in 80–90%)
    • Culture of IV fluid bag
    • Complete blood count (CBC) demonstrates leukocytosis.
  • Aseptic: Evaluation for coagulopathy if recurrent (e.g., protein C, protein S, lupus anticoagulant, anticardiolipin antibody, factor analysis)


Septic and aseptic:

  • None needed if below the knee and no risk factors for deep vein thrombosis (DVT)
  • Evaluation of complications (DVT and others):
    • CXR: Multiple peripheral densities or a pleural effusion consistent with pulmonary embolism, abscess, or empyema
    • Bone and gallium scan: For associated subperiosteal abscess in septic thrombophlebitis

Diagnostic Procedures/Surgery

Skin biopsy if not responding to therapy as expected

Pathological Findings

  • The affected vein is enlarged, tortuous, and thickened.
  • Associated perivascular suppuration and/or hemorrhage
  • Vein lumen may contain pus and thrombus.
  • Endothelial damage, fibrinoid necrosis, and thickening of the vein wall

Differential Diagnosis

Support's development and hosting
  • Cellulitis
  • Erythema nodosa
  • Cutaneous polyarteritis nodosa
  • Sarcoid
  • Kaposi sarcoma
  • Hyperalgesic pseudothrombophlebitis



First Line

  • Septic:
    • Initially: Semisynthetic penicillin (e.g., nafcillin 2 g IV q6h) plus an aminoglycoside (e.g., gentamicin, 1.0–1.7 mg/kg IV)
    • Duration of therapy is empirical.
    • If due to Candida albicans, consider a short course of amphotericin B, ∼200-mg cumulative dose
    • If osteomyelitis is documented, antibiotic therapy × 6 weeks at least
  • Aseptic, general:
    • For those with coagulopathy:
      • NSAIDs
      • Removal of catheter, if placed
      • Oral anticoagulant warfarin
      • Systemic anticoagulant heparin
      • Low-molecular-weight heparin
    • Antithrombin III and heparin cofactor II deficiency: IV heparin
    • Antithrombin III concentrate: Prophylaxis: Warfarin, oxymetholone
  • Proteins C and S: Long-term warfarin, lower dose, no loading
  • Disorder of tissue plasminogen activator:
    • Phenformin and ethylestrenol
    • Stanozolol and phenformin
    • Stanozolol alone
    • Ethylestrenol alone
  • Dysfibrinogenemia:
    • Acute attack: Anticoagulation
    • Prophylaxis: Stanozolol
  • Abnormal plasminogen and plasminogenemia:
    • Acute attack: Anticoagulation
    • Prophylaxis: Warfarin
  • Factor XII deficiency: Standard therapy
  • Lupus anticardiolipin: Prophylaxis: Warfarin
  • Trousseau syndrome: Heparin
  • For pregnancy: Heparin
  • Behçet disease:
    • Phenformin
    • Ethylestrenol
    • Stanozolol
  • Thromboangiitis obliterans:
    • Stop smoking.
    • Pentoxifylline
  • Contraindications: Refer to the manufacturer’s literature for each drug.
  • Precautions: Refer to the manufacturer’s literature for each drug.
  • Significant possible interactions: Refer to the manufacturer’s literature for each drug.

Second Line

  • Factor XII deficiency: Streptokinase or alteplase (tissue plasminogen activator [tPA])
  • Behçet: Oral anticoagulants plus cyclosporine
  • Thromboangiitis obliterans: Corticosteroid, antiplatelets, and vasodilating drugs

Additional Treatment

General Measures

  • Heat application
  • Extremity elevation

Surgery/Other Procedures

  • Septic:
    • Excision of the involved vein segment and all involved tributaries if failed conservative treatment
    • Excision from ankle to groin may be required in some burn patients.
    • If systemic symptoms persist after vein excision, reexploration is necessary, with removal of all involved veins.
    • Drainage of contiguous abscesses
    • Remove all cannulas.
  • Aseptic: Management of underlying conditions

In-Patient Considerations

Initial Stabilization

  • Septic: Inpatient
  • Aseptic: Outpatient

Ongoing Care

Follow-Up Recommendations

Bed rest

Patient Monitoring

  • Septic:
    • Routine white blood cell (WBC) count and differential and culture
    • Repeat culture from the phlebitic vein
  • Aseptic:
    • Clinical follow-up to rule out secondary complications
    • Repeat of blood studies for fibrinolytic system, platelets, and factors


No restrictions

Patient Education

  • Avoid trauma.
  • Be alert to change in skin color.
  • Be alert to tenderness over extremities.


  • Septic: High mortality (50%) if untreated
  • Aseptic:
    • Usually benign course; recovery in 7–10 days
    • Antithrombin III and heparin cofactor deficiency: Recurrence rate 60%
    • Proteins C and S: Recurrence rate 70%
    • Prognosis depends on development of DVT and early detection of complications.
    • Aseptic thrombophlebitis can be isolated, recurrent, or migratory.


  • Septic: Systemic sepsis, bacteremia (84%), septic pulmonary emboli (44%), metastatic abscess formation, pneumonia (44%), subperiosteal abscess of adjacent long bones in children
  • Aseptic: DVT, thromboembolic phenomena

Additional Reading

1. Di Nisio M, Wichers IM, Middeldorp S. Treatment for superficial thrombophlebitis of the leg. Cochrane Database Syst Rev. 2007;CD004982.

2. Gillet JL, French P, Hanss M, et al. Predictive value of D-dimer assay in superficial thrombophlebitis of the lower limbs. J Mal Vasc. 2007.

3. Samlaska CP, James WD. Superficial thrombophlebitis. II. Secondary hypercoagulable states. J Am Acad Dermatol. 1990;23:1–18.

4. Samlaska CP, James WD. Superficial thrombophlebitis. I. Primary hypercoagulable states. J Am Acad Dermatol. 1990;22:975–89.

See Also (Topic, Algorithm, Electronic Media Element)

Thrombosis, Deep Vein



  • 451.0 Phlebitis and thrombophlebitis of superficial vessels of lower extremities
  • 451.9 Phlebitis and thrombophlebitis of unspecified site
  • 451.82 Phlebitis and thrombophlebitis of superficial veins of upper extremities
  • 289.81 Primary hypercoagulable state
  • 289.82 Secondary hypercoagulable state


  • 2477008 superficial thrombophlebitis (disorder)
  • 40283005 thrombophlebitis of superficial veins of lower extremity (disorder)
  • 95451004 thrombophlebitis of superficial veins of upper extremities (disorder)
  • 76612001 hypercoagulability state (finding)

Clinical Pearls

  • The disease can develop while on a plane.
  • The best modality to prevent the disease during air travel is to exercise and drink a lot of water.

About the author

Many tips are based on recent research, while others were known in ancient times. But they have all been proven to be effective. So keep this website close at hand and make the advice it offers a part of your daily life.