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

Basics

Description

  • 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.

Epidemiology

  • 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)

Incidence

  • 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

Prevalence

  • 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.

Genetics

  • 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

Pathophysiology

  • 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.

Etiology

  • 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

Diagnosis

History

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

Lab

  • 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)

Imaging

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

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  • Cellulitis
  • Erythema nodosa
  • Cutaneous polyarteritis nodosa
  • Sarcoid
  • Kaposi sarcoma
  • Hyperalgesic pseudothrombophlebitis

Treatment

Medication

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

Diet

No restrictions

Patient Education

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

Prognosis

  • 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.

Complications

  • 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

Codes

ICD9

  • 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

Snomed

  • 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.

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