eMedicine Specialties > Dermatology > Diseases of the Vessels

Mondor Disease

Robert A Schwartz, MD, MPH, Professor and Head of Dermatology, Professor of Medicine, Professor of Pediatrics, Professor of Pathology, Professor of Preventive Medicine and Community Health, UMDNJ-New Jersey Medical School
Matthew J Trovato, MD, Staff Physician, Department of Dermatology, UMDNJ-New Jersey Medical School

Updated: Apr 30, 2008

Introduction

Background

First described in detail by Henri Mondor in 1939, this condition is a rare entity characterized by a sclerosing thrombophlebitis of the subcutaneous veins of the anterior chest wall. The sudden appearance of a subcutaneous cord, which is initially red and tender and subsequently becomes a painless, tough, fibrous band that is accompanied by tension and skin retraction, is characteristic. The condition, though benign and self-limited, has been associated with breast cancer. It requires only symptomatic therapy. However, the physician must be aware of its existence to properly diagnose it and to rule out the presence of systemic disorders, especially breast cancer.¹

Subcutaneous penile vein thrombosis (penile Mondor disease) has also been described.² Its pathogenesis is unknown. It appears suddenly as almost painless indurations on the penile dorsal surface.

A related eMedicine article is Superficial Thrombophlebitis.

Pathophysiology

Mondor disease may only involve 1 or more of 3 venous channels: the thoracoepigastric vein, the lateral thoracic vein, and the superior epigastric vein. The upper, inner portions of the breast are never involved.

Race

No racial or ethnic predilection is evident.

Sex

Mondor disease is 3 times more common in women than in men.⁴

Age

The disease can occur in persons of any age, but most patients are aged 30-60 years.⁴

Clinical

History

• No systemic symptoms are present.
• Ask the patient about the following:
  • Recent breast surgery: In one report, 7 of 15 patients had a radical mastectomy prior to the onset of Mondor thrombophlebitis on the ipsilateral side.⁵ Mondor disease may occur after breast reduction surgery.⁶
  • Possibly, physical strain⁷
  • Tight dressings and tight-fitting bras⁸
  • Axillary shaving⁹
  • Blood dyscrasia¹⁰
• Subcutaneous penile vein thrombosis (penile Mondor disease) has also been described.² It is first evident as sudden and almost painless indurations on the penile dorsal surface.

Physical

• Mondor disease has a characteristic clinical picture of a sudden appearance of a linear, cordlike, thrombosed vein.
• At first, this vein is red and tender, and then, it subsequently changes into a painless, tough, fibrous band.
• The cord is accentuated by traction, elevation of the breast, or abduction of the ipsilateral arm.
• If the patient does not seek medical attention upon the initial presentation, the tenderness gradually subsides, while the thrombus organizes and recanalizes, leaving a nontender, hard, ropelike band. This band remains for varying periods up to several weeks.³

Causes

See Pathophysiology.

Differential Diagnoses

Cellulitis
Erythema Nodosum
Lymphangiectasia
Lymphangioma
Metastatic Carcinoma of the Skin

Other Problems to Be Considered

Mondor disease may be distinguished from inflammatory cancer of the breast by the presence of sudden pain, early skin adherence, and progressive improvement. These symptoms are not commonly associated with carcinoma of the breast.

The distinction from a breast abscess is made by discerning the quality of tenderness. Mondor disease is ascribed to a soreness, while an abscess presents with an exquisite tenderness.

Mondor disease may mimic a strangulated spigelian hernia.¹¹ Mondor disease may be evident in the spigelian hernia belt and cause diagnostic confusion.

Workup

Laboratory Studies

• No laboratory studies are necessary for diagnosis.
• With Mondor disease of the penis, an uncommon condition usually involving the superficial dorsal veins, ultrasound and Doppler ultrasonography examination is not useful for diagnosis but may help the clinician show the patient that the disease is a benign condition.¹²

Imaging Studies

• Mammography results are always negative. This finding helps to differentiate Mondor disease from lesions, such as cancer, cysts, and fibroadenomata, which have positive radiography shadows.¹³

Histologic Findings

From histologic studies, 4 phases of the disease have been delineated: thrombus formation; thrombus organization; recanalization; and residual, thick-walled fibrosis.¹⁴

Treatment

Medical Care

Treatment is entirely symptomatic.

• Hot, wet dressings and anodynes may be used for pain relief.
• The use of modalities such as enzymes, corticosteroids, antibiotics, vaccines, and anticoagulants has been studied, although none has been proven to hasten the resolution of the pathologic process.
• The major benefit that the physician can provide is reassurance.

Surgical Care

Treatment is symptomatic because, to date, the disease has proved to be benign and self-limited.

Medication

Nonsteroidal anti-inflammatory agents (NSAIDs) are used for symptomatic relief. Indomethacin is a good choice.

Nonsteroidal anti-inflammatory drugs

These agents have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but they may inhibit cyclo-oxygenase activity and prostaglandin synthesis. Other mechanisms may include inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions.

Indomethacin (Indocin)

Potent inhibitor of cyclo-oxygenase, which may decrease the local production of arachidonic acid–derived chemotactic factors for eosinophils present in sebum.

Dosing

Adult

50 mg PO tid pc; taper as symptoms resolve

Pediatric

<14 years: Not established
>14 years: Administer as in adults

Interactions

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse 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 patient is taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of MTX toxicity; phenytoin levels may be increased when administered concurrently

Contraindications

Documented hypersensitivity; GI bleeding; renal insufficiency

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Category D in third trimester of pregnancy (may cause closure of ductus arteriosus during the third trimester of pregnancy); may mask signs of infection; may cause fluid retention, peripheral edema, and deterioration of circulatory hemodynamics; can inhibit platelet aggregation and prolong bleeding time; liver and kidney damage may occur (rare)

Aspirin (Anacin, Ascriptin, Bayer Aspirin, Bayer Buffered Aspirin)

Treats mild to moderate pain. Inhibits prostaglandin synthesis, which prevents formation of platelet-aggregating thromboxane A2.

Dosing

Adult

325-650 mg PO q4-6h; not to exceed 4 g/d

Pediatric

10-15 mg/kg/dose PO q4-6h; not to exceed 60-80 mg/kg/d

Interactions

Effects may decrease with antacids and urinary alkalinizers; corticosteroids decrease salicylate serum levels; additive hypoprothrombinemic effects and increased bleeding time may occur with coadministration of anticoagulants; may antagonize uricosuric effects of probenecid and increase toxicity of phenytoin and valproic acid; doses >2 g/d may potentiate glucose-lowering effect of sulfonylurea drugs

Contraindications

Documented hypersensitivity; liver damage; hypoprothrombinemia; vitamin K deficiency; bleeding disorders; asthma; because of association of aspirin with Reye syndrome, do not use in children (<16 y) with flu

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

Precautions

Category D in third trimester of pregnancy; may cause transient decrease in renal function and aggravate chronic kidney disease; avoid use in patients with severe anemia, in those with a history of blood coagulation defects, or in those taking anticoagulants

Follow-up

Further Outpatient Care

• The natural course of Mondor disease is 3 weeks to 6 months. Reassurance during follow-up outpatient visits is most beneficial.

Complications

• Mondor phlebitis is not migratory and does not recur.

Prognosis

• Mondor disease has proven to be self-limited and benign. Its significance lies in the clinician's recognition and differentiation of it from primary, recurrent, or metastatic carcinoma, or an abscess of the breast. As are other forms of migratory thrombophlebitis, Mondor disease may be an indication of an occult carcinoma elsewhere in the body. Patients with this condition should continue to be observed.

Patient Education

• Explaining to the patient that no instance of Mondor disease has reportedly preceded or eventuated in breast cancer may be beneficial. However, patients with a history of Mondor disease should have periodic breast examinations, mammography, and additional tests searching for cancer elsewhere.
• For excellent patient education resources, visit eMedicine's Circulatory Problems Center and Cancer and Tumors Center. Also, see eMedicine's patient education articles Phlebitis, Breast Cancer, and Breast Self-Exam.

Miscellaneous

Medicolegal Pitfalls

• Misdiagnosis of mammary carcinoma or an abscess as Mondor thrombophlebitis is a pitfall.

Multimedia

Media file 1: Illustration of the venous channels involved in Mondor disease. A is superior epigastric vein. B is thoracoepigastric vein. C is lateral thoracic vein.

References

1. Thalhammer C, Aschwanden M. [Mondor's disease]. Dtsch Med Wochenschr. Feb 16 2007;132(7):325-6. [Medline].

2. Al-Mwalad M, Loertzer H, Wicht A, Fornara P. Subcutaneous penile vein thrombosis (Penile Mondor's Disease): pathogenesis, diagnosis, and therapy. Urology. Mar 2006;67(3):586-8. [Medline].

3. Hogan GF. Mondor's disease. Arch Intern Med. Jun 1964;113:881-5. [Medline].

4. Weinstein EC. Mondor's disease. West J Med. Jul 1975;123(1):56-7. [Medline].

5. Herrmann JB. Thrombophlebitis of breast and contiguous thoracicoabdominal wall (Mondor's disease). N Y State J Med. Dec 15 1966;66(24):3146-52. [Medline].

6. Loos B, Horch RE. Mondor's disease after breast reduction surgery. Plast Reconstr Surg. Jun 2006;117(7):129e-132e. [Medline].

7. Talhari C, Mang R, Megahed M, Ruzicka T, Stege H. Mondor disease associated with physical strain: report of 2 cases. Arch Dermatol. Jun 2005;141(6):800-1. [Medline].

8. Oldfield MC. Mondor's disease. A superficial phlebitis of the breast. Lancet. May 12 1962;1:994-6. [Medline].

9. Feller N. [Mondor's disease.]. Dapim Refuiim. Aug 1962;21:423-5. [Medline].

10. Bauer-Hack K. [Contribution to Mondor's disease.]. Med Welt. Oct 13 1962;41:2152-6. [Medline].

11. Losanoff JE, Basson MD, Salwen WA, Sochaki P. Mondor's disease mimicking a Spigelian hernia. Hernia. Jan 9 2008;[Medline].

12. Dicuio M, Pomara G, Ales V, Fabris FM, Dahlstrand C, Morelli G. Doppler ultrasonography in a young patient with penile Mondor's disease. Arch Ital Urol Androl. Mar 2005;77(1):58-9. [Medline].

13. Bircher J, Schirger A, Clagett OT, Harrison EG Jr. Mondor's disease: a vascular rarity. Mayo Clin Proc. Nov 21 1962;37:651-6. [Medline].

14. Guerri G. [Histopathology and significance of cord formations on the anterolateral chest wall (Mondor's disease and syndrome).]. Arch De Vecchi Anat Patol. Oct 1960;33:829-57. [Medline].

15. Holle-Robatsch S, Fink AM, Schubert C, Steiner A, Partsch H. [Mondor phlebitis associated with hepatitis C]. Vasa. Nov 2001;30(4):297-8. [Medline].

16. Luis Rodríguez-Peralto J, Carrillo R, Rosales B, Rodríguez-Gil Y. Superficial thrombophlebitis. Semin Cutan Med Surg. Jun 2007;26(2):71-6. [Medline].

17. Mayor M, Buron I, de Mora JC, Lazaro TE, Hernandez-Cano N, Rubio FA, et al. Mondor's disease. Int J Dermatol. Dec 2000;39(12):922-5. [Medline].

Keywords

Mondor's disease, Mondor phlebitis, superficial thrombophlebitis of the chest wall

Contributor Information and Disclosures

Author

Robert A Schwartz, MD, MPH, Professor and Head of Dermatology, Professor of Medicine, Professor of Pediatrics, Professor of Pathology, Professor of Preventive Medicine and Community Health, UMDNJ-New Jersey Medical School
Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi
Disclosure: Nothing to disclose.

Coauthor(s)

Matthew J Trovato, MD, Staff Physician, Department of Dermatology, UMDNJ-New Jersey Medical School
Matthew J Trovato, MD is a member of the following medical societies: Alpha Omega Alpha
Disclosure: Nothing to disclose.

Medical Editor

Julie C Harper, MD, Assistant Program Director, Assistant Professor, Department of Dermatology, University of Alabama at Birmingham
Julie C Harper, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

Pharmacy Editor

David F Butler, MD, Professor of Dermatology, Texas A&M University College of Medicine; Director, Division of Dermatology, Scott and White Clinic; Director Dermatology Residency Training Program, Scott and White Clinic
David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa
Disclosure: 3M Pharmaceutical Grant/research funds Other; Graceway Pharmaceuticals Grant/research funds Other

Managing Editor

Christen M Mowad, MD, Associate Professor, Department of Dermatology, Geisinger Medical Center
Christen M Mowad, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, and Phi Beta Kappa
Disclosure: Nothing to disclose.

CME Editor

Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University
Catherine Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology
Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

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