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Varicose Veins and Spider Veins Clinical Presentation

  • Author: Robert Weiss, MD; Chief Editor: William D James, MD  more...
 
Updated: Dec 08, 2015
 

History

Patients with varicose veins may present with acute varicose complications, including variceal bleeding, new onset of dermatitis, thrombophlebitis, cellulitis, and ulceration. Patients may also consult a physician because of worsening chronic symptoms or for a variety of other reasons. Some are seeking advice on the medical implications of varicose veins. Others have purely aesthetic concerns.

A careful history exposes the patient's underlying concerns and guides further workup and treatment planning. Treatment that does not properly address the patient's primary concerns cannot result in a satisfactory overall outcome.

Patients who have become acclimatized to their chronic disease may not volunteer information about symptoms. Common symptoms that should be elicited include leg heaviness, exercise intolerance, pain or tenderness along the course of a vein, pruritus, burning sensations, restless legs, night cramps, edema, skin changes, and paresthesias.

Subjective symptoms usually are more severe early in the progression of disease, less severe in the middle phases, and worse again with advancing age. Symptoms do not correlate with the size or extent of visible varices or with the volume of reflux.

Not all symptomatic patients are aware of their symptoms because the onset may be extremely gradual. After treatment, patients are often surprised to realize how much chronic discomfort they had accepted as normal.

Common symptoms of telangiectasia include burning, swelling, throbbing, cramping, and leg fatigue. Pain associated with larger varicose veins usually is a dull ache that is worse after prolonged standing.

Pain caused by venous insufficiency is often improved by walking or by elevating the legs in contrast to the pain of arterial insufficiency, which is worse with ambulation and elevation.

Pain and other symptoms may worsen with the menstrual cycle, with pregnancy, and in response to exogenous hormonal therapy (eg, oral contraceptives). A small number of women regularly experience pain associated with their varicose veins after sexual intercourse.

The venous history should also include the following elements:

  • History of venous insufficiency (eg, date of onset of visible abnormal vessels, date of onset of any symptoms, any known prior venous diagnoses, any history of pregnancy-related varices)
  • Presence or absence of predisposing factors (eg, heredity, trauma to the legs, occupational prolonged standing, sports participation)
  • History of edema (eg, date of onset, predisposing factors, site, intensity, hardness, modification after a night's rest)
  • History of any prior evaluation of or treatment for venous disease (eg, medications, injections, surgery, compression)
  • History of superficial or deep thrombophlebitis (eg, date of onset, site, predisposing factors, sequelae)
  • History of any other vascular disease (eg, peripheral arterial disease, coronary artery disease, lymphedema, lymphangitis)
  • Family history of vascular disease of any type
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Physical

The physical examination of the venous system is fraught with difficulty. In most areas of the body, the deep venous system cannot be inspected, palpated, ausculted, or percussed. Examination of the superficial venous system must serve as an indirect guide to the deep system.

Veins and their connections become gradually better defined through inspection, palpation, percussion, and hand-held Doppler examination to form a venous map that later guides treatment. The courses of all the dilated veins that are identified may be marked along the leg with a pen and later transcribed into the medical record as a map of all known areas of superficial reflux.

Inspection

Inspection is performed in an organized manner, usually progressing from distal to proximal and from front to back. The perineal region, pubic region, and abdominal wall must also be inspected.

Inspection may reveal such findings as ulceration, telangiectasias, atrophie blanche, interdigital mycosis, acrocyanosis, eczematous lesions, microulcers, stasis dermatitis, flat angiomata, prominent varicose veins, scars from a prior surgical operation, or evidence of previous sclerosant injections. Measuring and photographing lesions is recommended because patients undergoing treatment for varicose and spider veins often forget the original appearance of their legs and feet and may report that preexisting lesions were caused by treatment.

Normal veins typically are visibly distended at the foot and ankle and occasionally in the popliteal fossa. For other regions of the leg, visible distension of superficial veins usually implies disease. Translucent skin may allow normal veins to be visible as bluish subdermal reticular pattern, but dilated veins above the ankle usually are evidence of venous pathology.

Discolored skin often is a sign of chronic venous stasis, particularly if it is localized along the medial ankle and the medial aspect of the lower leg. Nonhealing ulcers in this area are most likely due to underlying venous stasis. Skin changes or ulcerations that are localized only to the lateral aspect of the ankle are more likely to be related to prior trauma or to arterial insufficiency than to pure venous insufficiency.

Palpation

The entire surface of the skin is lightly palpated with the fingertips because dilated veins may be palpable even where they are not readily observed. Palpation helps to locate both normal and abnormal veins. After light palpation to identify superficial vascular abnormalities, deeper palpation helps to elucidate the causes and sources of the superficial problems.

Palpation begins with the anteromedial surface of the lower limb (the territory of the long saphenous vein), proceeds to the lateral surface (collateral varicose veins of large trunks and nonsaphenous varicose veins), and finally focuses on the posterior surface (territory of the short saphenous vein) of both lower limbs. The location, size, shape, and course of all varicosities are noted, and the diameter of the largest vessel is measured as accurately as possible.

Both distal and proximal arterial pulses should be palpated. An ankle-brachial index is useful if any suspicion of arterial insufficiency exists.

The arch of the long saphenous vein may be palpable in some patients who do not have varicose veins, but it is particularly well appreciated in patients with truncal reflux at the saphenofemoral junction. It is best palpated 2 fingerbreadths below the inguinal ligament and just medial to the femoral artery. If reflux is present, a forced coughing maneuver may produce a palpable thrill or sudden expansion at this level.

The short saphenous vein may be palpable in the popliteal fossa in some slender patients. Other normal superficial veins above the foot usually are not palpable even after prolonged standing.

Palpation of an area of leg pain or tenderness may reveal a firm, thickened, thrombosed vein. These palpable thrombosed vessels are superficial veins, but an associated deep vein thrombosis may exist in up to 40% of patients with superficial phlebitis. When completely thrombosed, the popliteal vein (a continuation of the femoral vein as it passes behind the knee and into the calf) may sometimes be palpated in the popliteal fossa, and the same is true of the common femoral vein at the groin. Palpation for deep thrombosis is not reliable because the vast majority of cases of deep vein thrombosis do not produce any palpable abnormality.

Varices of recent onset are easily distinguished from chronic varices by palpation. Newly dilated vessels sit on the surface of the muscle or bone; chronic varices erode into underlying muscle or bone, creating deep boggy or spongy pockets in the calf muscle and deep palpable bony notches, especially over the anterior tibia.

Palpation often reveals fascial defects in the calf along the course of an abnormal vein at sites where superficial tributaries emerge through openings in the superficial fascia. Incompetent perforating veins may connect the superficial and deep venous systems though these fascial defects, but the finding is neither sensitive nor specific for perforator incompetence.

Percussion

Venous percussion is useful to determine whether different venous segments are directly interconnected. Percussion can be used to trace the course of veins already detected on palpation, to discover varicose veins that could not be palpated, and to assess the relationships between the various varicose vein networks.

With the patient in a standing position, a vein segment is percussed at one position while an examining hand feels for a pulse wave at another position. The propagation of a palpable pulse wave demonstrates a patent superficial venous segment with open or incompetent valves connecting the 2 positions. The examination findings can be misleading because prolonged standing causes even a normal vein to become distended. If valves have floated open, a pulse wave may be propagated even in a normal vein. The technique is most valuable when a bulging venous cluster in the lower leg has no obvious connection with veins in the upper thigh, yet a palpable pulse wave demonstrates the existence of an unseen connection.

Percussion can be used to elucidate the course of any significant superficial vein. With the patient standing, the lowest portion of the vein is percussed while the opposite hand searches above for a percussion wave. The procedure is repeated along the entire course of the vein and then along every identifiable superficial vein until a clear anatomic picture has been elucidated.

Perthes maneuver

The Perthes maneuver is a traditional technique intended to distinguish antegrade flow from retrograde flow in superficial varices. Antegrade flow in a variceal system indicates that the system is a bypass pathway around deep venous obstruction. This is critically important because, if deep veins are not patent, superficial varices are an important pathway for venous return and must not be sclerosed or surgically removed.

To perform the Perthes maneuver, a Penrose tourniquet is placed over the proximal part of the varicose leg in such a way as to compress superficial varicose veins but not the deep veins. The patient walks or performs toe-stands to activate the calf muscle pump. The calf muscle pump normally causes varicose veins to be emptied, but if deep system obstruction exists, then the varicose veins paradoxically become more congested.

If the result of the Perthes maneuver is positive (ie, distal varices have become engorged), then the patient is placed supine with the tourniquet in place and the leg elevated (Linton test). If varices distal to the tourniquet do not drain after a few seconds, deep venous obstruction must be suspected. These maneuvers are not consistently reliable and are of primarily historical interest.

Trendelenburg test

The Trendelenburg test can often be used to distinguish patients with superficial venous reflux from those with incompetent deep venous valves.

The leg is elevated until the congested superficial veins have all collapsed. An examining hand is used to occlude a varicose vein just below the saphenofemoral junction or at another point of suspected reflux from the deep system into the superficial varicosity. The patient stands with the occlusion still in place.

If the distal varicosity remains empty or fills very slowly, the principal entry point of high pressure into the superficial system has been identified. Rapid filling despite manual occlusion of the suspected high point of reflux means that some other reflux pathway is involved.

Doppler auscultation

The physical examination as described thus far cannot differentiate dilated veins of normal function from true varicosities that carry venous blood in a retrograde direction. Doppler examination is an adjunct to the physical examination that can directly show whether flow in a suspect vein is antegrade, retrograde, or to-and-fro.

When used as part of the physical examination, a Doppler transducer is positioned along the axis of a vein with the probe at an angle of 45° to the skin. Gentle tapping on the underlying vessel produces a strong Doppler signal and confirms the correct positioning of the transducer.

An augmentation maneuver is performed by compressing and then releasing the underlying veins and muscles below the level of the probe. Compression causes forward flow in the direction of the valves. Release of compression causes backward flow through incompetent valves, but no Doppler signal is noted if the valves are competent and the blood cannot flow backwards.

These compression-decompression maneuvers are repeated while gradually ascending the limb to a level where the reflux can no longer be appreciated.

Each superficially visible or palpable is investigated in this way. If no visible or palpable dilated varices exist, the presence or absence of retrograde flow is documented at the top, middle, and bottom of long and short saphenous veins on each leg.

Doppler flow assessment adds a great deal of information to the physical examination findings, but patients with significant varicosities should also be evaluated by duplex ultrasonography, which combines Doppler flow detection with 2-dimensional ultrasound imaging.

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Causes

Intrinsic pathological conditions and extrinsic environmental factors combine to produce a wide spectrum of varicose disease.

Most varicose disease is due to elevated superficial venous pressures, but some people have an inborn weakness of vein walls and can develop varicosities even in the absence of elevated venous pressures. Some patients with varicose veins of the legs also have abnormally distensible veins in the forearm and hand veins.

Heredity is important in determining susceptibility to primary valvular failure, but the specific genetic factors responsible for varicosities have not yet been elucidated. Reflux at the saphenofemoral junction (where the superficial greater saphenous vein joins the deep common femoral vein) is twice as likely when a parent had a similar condition. Monozygotic twins are concordant with regard to varicose veins in 75% of cases. The prevalence of varicose veins is 43% in female relatives of patients with varicose veins but is only 19% in male relatives.

Prolonged standing leads to increased hydrostatic pressures that can cause chronic venous distention and secondary valvular incompetence anywhere within the superficial venous system. If proximal junctional valves become incompetent, high pressure passes from the deep veins into the superficial veins and the condition rapidly progresses to become irreversible. Women are particularly susceptible to this type of varicose problem because vein walls and valves periodically become more distensible under the influence of cyclic increases in progesterone.

Pregnancy is a common cause of varicosities. During pregnancy, circulating hormonal factors increase the distensibility of vein walls and soften valve leaflets. At the same time, the veins must accommodate a greatly expanded circulating blood volume. Late in pregnancy, the enlarged uterus compresses the inferior vena cava, causing further venous hypertension and secondary distension of leg veins. Depending on the relative contributions of these mechanisms, varicose veins of pregnancy may or may not spontaneously regress after delivery. Treatment of existing varicose veins prior to pregnancy has been shown to prevent the progression of disease and reduce the recruitment of other veins during pregnancy.

Age is an independent risk factor for varicosities. With advancing age, the elastic lamina of the vein becomes atrophic and the smooth muscle layer begins to degenerate, leaving a weakened vein that is more susceptible to dilatation.

Wherever a venous outflow obstruction exists, varicose veins may arise as a bypass pathway. Such veins are an important pathway for venous return and must not be ablated.

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Contributor Information and Disclosures
Author

Robert Weiss, MD Associate Professor, Department of Dermatology, Johns Hopkins University School of Medicine

Robert Weiss, MD is a member of the following medical societies: American Academy of Cosmetic Surgery, American Academy of Dermatology, American College of Phlebology, American Society for Dermatologic Surgery, American Society for Laser Medicine and Surgery, MedChi The Maryland State Medical Society

Disclosure: Received honoraria from Angiodynamics for speaking and teaching; Received intellectual property rights from CoolTouch Corp for consulting; Received grant/research funds from Cynosure for independent contractor; Received grant/research funds from Palomar for independent contractor.

Specialty Editor Board

David F Butler, MD Section Chief of Dermatology, Central Texas Veterans Healthcare System; Professor of Dermatology, Texas A&M University College of Medicine; Founding Chair, Department of Dermatology, Scott and White Clinic

David F Butler, MD is a member of the following medical societies: American Medical Association, Alpha Omega Alpha, Association of Military Dermatologists, American Academy of Dermatology, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Phi Beta Kappa

Disclosure: Nothing to disclose.

John G Albertini, MD Private Practice, The Skin Surgery Center; Clinical Associate Professor (Volunteer), Department of Plastic and Reconstructive Surgery, Wake Forest University School of Medicine; President-Elect, American College of Mohs Surgery

John G Albertini, MD is a member of the following medical societies: American Academy of Dermatology, American College of Mohs Surgery

Disclosure: Received grant/research funds from Genentech for investigator.

Chief Editor

William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Kelly M Cordoro, MD Assistant Professor of Clinical Dermatology and Pediatrics, Department of Dermatology, University of California, San Francisco School of Medicine

Kelly M Cordoro, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, Medical Society of Virginia, Society for Pediatric Dermatology, Women's Dermatologic Society, Association of Professors of Dermatology, National Psoriasis Foundation, Dermatology Foundation

Disclosure: Nothing to disclose.

Acknowledgements

Craig F Feied, MD, FACEP, FAAEM, FACPh Professor of Emergency Medicine, Georgetown University School of Medicine; General Manager, Microsoft Enterprise Health Solutions Group

Craig F Feied, MD, FACEP, FAAEM, FACPh is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Phlebology, American College of Physicians, American Medical Association, American Medical Informatics Association, American Venous Forum, Medical Society of the District of Columbia, Society for Academic Emergency Medicine, and Undersea and Hyperbaric Medical Society

Disclosure: Nothing to disclose.

References
  1. Goldman MP, Guex JJ, Weiss RA. Sclerotherapy: Treatment of Varicose and Telangiectatic Leg Veins. 5th ed. Philadelphia: Saunders; 2011. 1-416.

  2. Piazza G. Varicose veins. Circulation. 2014 Aug 12. 130 (7):582-7. [Medline].

  3. Chiesa R, Marone EM, Limoni C, Volonte M, Schaefer E, Petrini O. Chronic venous insufficiency in Italy: the 24-cities cohort study. Eur J Vasc Endovasc Surg. 2005 Oct. 30(4):422-9. [Medline].

  4. Racette S, Sauvageau A. Unusual sudden death: two case reports of hemorrhage by rupture of varicose veins. Am J Forensic Med Pathol. 2005 Sep. 26(3):294-6. [Medline].

  5. Cho ES, Kim JH, Kim S, et al. Computed tomographic venography for varicose veins of the lower extremities: prospective comparison of 80-kVp and conventional 120-kVp protocols. J Comput Assist Tomogr. 2012 Sep. 36(5):583-90. [Medline].

  6. Carradice D, Leung C, Chetter I. Laser; best practice techniques and evidence. Phlebology. 2015 Nov. 30 (2 Suppl):36-41. [Medline].

  7. Nael R, Rathbun S. Treatment of varicose veins. Curr Treat Options Cardiovasc Med. 2009 Apr. 11(2):91-103. [Medline].

  8. Nijsten T, van den Bos RR, Goldman MP, et al. Minimally invasive techniques in the treatment of saphenous varicose veins. J Am Acad Dermatol. 2009 Jan. 60(1):110-9. [Medline].

  9. Bruijninckx CM. Fatal pulmonary embolism following ultrasound-guided foam sclerotherapy combined with multiple microphlebectomies. Phlebology. 2015 Sep 2. [Medline].

  10. Muller-Buhl U, Leutgeb R, Engeser P, Achankeng EN, Szecsenyi J, Laux G. Varicose veins are a risk factor for deep venous thrombosis in general practice patients. Vasa. 2012 Sep. 41(5):360-5. [Medline].

  11. Rao J, Wildemore JK, Goldman MP. Double-blind prospective comparative trial between foamed and liquid polidocanol and sodium tetradecyl sulfate in the treatment of varicose and telangiectatic leg veins. Dermatol Surg. 2005 Jun. 31(6):631-5; discussion 635. [Medline].

  12. Brooks M. FDA OKs New Minimally Invasive Treatment for Varicose Veins. Available at http://www.medscape.com/viewarticle/815039. Accessed: December 3, 2013.

  13. Alder G, Lees T. Foam sclerotherapy. Phlebology. 2015 Nov. 30 (2 Suppl):18-23. [Medline].

  14. Dudelzak J, Hussain M, Goldberg DJ. Vascular-specific laser wavelength for the treatment of facial telangiectasias. J Drugs Dermatol. 2009 Mar. 8(3):227-9. [Medline].

  15. Mao J, Zhang C, Wang Z, Gan S, Li K. A retrospective study comparing endovenous laser ablation and microwave ablation for great saphenous varicose veins. Eur Rev Med Pharmacol Sci. 2012 Jul. 16(7):873-7. [Medline].

  16. Goodyear SJ, Nyamekye IK. Radiofrequency ablation of varicose veins: Best practice techniques and evidence. Phlebology. 2015 Nov. 30 (2 Suppl):9-17. [Medline].

  17. O'Hare JL, Stephens J, Parkin D, Earnshaw JJ. Randomized clinical trial of different bandage regimens after foam sclerotherapy for varicose veins. Br J Surg. 2010 May. 97(5):650-6. [Medline].

  18. Cesarone MR, Belcaro G, Ricci A, et al. Prevention of edema and flight microangiopathy with Venoruton (HR), (0-[beta-hydroxyethyl]-rutosides) in patients with varicose veins. Angiology. 2005 May-Jun. 56(3):289-93. [Medline].

  19. Weiss RA, Feied CF, Weiss MA. Vein Diagnosis & Treatment: A Comprehensive Approach. 1st ed. New York, NY: McGraw-Hill; 2001. 1-304.

 
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Patient with large tortuous varicose veins, high-volume venous reflux, and early stasis changes of the medial ankle.
Typical chronic medial leg ulceration associated with long-standing venous insufficiency. The ulcer had been present for 12 years and was refractory to every treatment approach until treatment of the refluxing superficial varices was performed. Treatment consists of endovenous ablation, foam sclerotherapy, or ambulatory phlebectomy.
 
 
 
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