Investigação clínica de úlceras provenientes de IVP

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Investigação clínica de úlceras provenientes de IVP

Mensagem  Convidad em Ter Jul 16, 2013 2:06 am

APPROACH TO THE PATIENT — The diagnosis of chronic lower extremity venous disease is predominantly clinical. Initial evaluation consists of a thorough history and physical examination, with clinical classification of disease severity according to the Clinical-Etiology-Anatomy-Pathophysiology (CEAP) criteria (table 1) [2]. The CEAP classification is helpful in documenting venous disease severity both at initial presentation as well as in documenting changes over time. The CEAP clinical classification is discussed in detail elsewhere. (See "Classification of lower extremity chronic venous disorders" and 'Clinical signs by CEAP category' below.)

Because the presence of dilated veins is a common incidental finding on routine physical examination, many individuals are already aware that they have a vein problem. Up to one half of patients, even some with very large varicosities, have no specific complaints [9]. Symptomatic patients may or may not correlate certain lower extremity symptoms with the presence of abnormal veins; alternatively, the patient may erroneously attribute symptoms that are more consistent with orthopedic or arterial vascular disease to their visible veins.

The major goal in the clinical diagnosis of lower extremity chronic venous disease is a full clinical assessment of the lower extremities with correct interpretation of the patient's complaints and correlation with physical signs. Inconsistencies between symptoms and clinical signs may require additional diagnostic evaluation.

Risk factors for venous disease — The patient is often very interested in knowing why he or she has developed a vein problem. To help the patient better understand his or her disorder, the patient should be questioned specifically for risk factors known to contribute to the development of chronic venous disease. The most common risk factors include advancing age, family history of venous disease, increased body mass index, smoking, a history of lower extremity trauma, prior venous thrombosis and, in women, pregnancy. A more complete review of risk factors is discussed elsewhere. (See "Overview and management of lower extremity chronic venous disease", section on 'Risk factors'.)

Particular attention should be paid to identifying risk factors that can be modified (eg, obesity, lifestyle).

The patient who has no identifiable risk factors may have suffered a remote lower extremity trauma they do not recall, or an undiagnosed deep vein thrombosis (DVT). Duplex ultrasound in these patients may identify valvular insufficiency, chronic vein wall thickening, or chronic thrombosis indicative of post-thrombotic syndrome [10-12]. (See "Post-thrombotic (postphlebitic) syndrome".)

Medical history — Patients with more severe clinical manifestations (ie, edema, inflammation, ulcer) are typically older and may have significant associated medical conditions (eg, peripheral artery disease [PAD], heart failure, diabetes, arthritis).

Chronic venous disease and arterial vascular disease have some common risk factors (eg, smoking, obesity) and pathophysiologic processes [13]. The presence of varicose veins has been associated with arterial disease in two studies [14,15]. One of these, a cross-sectional study, documented a 36 percent increase in the risk of developing coronary artery disease for men with varicose veins [14].

Because of these associations, a complete medical history with particular attention to cardiovascular disease and risk factors should be obtained since co-morbidities may impact diagnostic evaluation or management choices. (See "Overview and management of lower extremity chronic venous disease".)

Quality of life — Health related quality of life outcome measures are increasingly being considered in the evaluation of the outcomes of treatment for chronic venous disease [16-19]. Patients should be specifically questioned regarding the impact of symptoms on their daily activities, especially with respect to employment. The venous clinical severity score (VCSS) (calculator 1) and venous disability score (VDS) may aid with initial and follow up assessment. (See "Classification of lower extremity chronic venous disorders", section on 'Measures of clinical severity'.)

Individuals with varicose veins can have a lower perception of their general health compared to individuals without varicose veins, especially if clinical manifestations are more significant (eg, edema, skin changes) [16]. Quality of life measures improve with management of their superficial venous disease [20]. (See "Overview and management of lower extremity chronic venous disease", section on 'Management by CEAP clinical category'.)

Patients with severe skin changes or venous ulceration also have reductions in quality of life measures that are further reduced coincident with the need for chronic wound management [17,18,21]. Ulcer healing, however, may not always result in perceived improvements in quality of life [22]. (See "Medical management of lower extremity chronic venous disease", section on 'Ulcer care'.)

SYMPTOMS — The clinical presentation of symptoms varies widely. The onset of these symptoms relative to the appearance of visibly dilated veins, skin changes, or ulceration should be ascertained and correlated with any positive risk factors. (See 'Risk factors for venous disease' above.)

The most common symptoms reported by patients with chronic venous disease are limb discomfort (ie, tired, heavy legs), pain, and limb swelling. Pain and limb discomfort were reported as a significant symptom for each of the six CEAP clinical categories in at least 50 percent of individuals surveyed in one large cross sectional study [9]. Pain may be generalized (ie, aching), or localized to specific veins, areas of lipodermatosclerosis, or ulceration. When pain accompanies more severe clinical manifestations, ambulation may become difficult or even impossible.

Pain associated with venous disease is typically worse when standing, or when seated with the feet dependent for prolonged periods of time and improves with limb elevation and walking. These features distinguish chronic venous disease from typical symptoms associated with lower extremity occlusive peripheral artery disease. Patients with mild to moderate lower extremity PAD (ie, claudication) complain of pain with walking that is relieved by rest while those with more severe PAD may complain of more pain when the limb is elevated. (See "Clinical features, diagnosis, and natural history of lower extremity peripheral artery disease".)

The pain associated with venous disease is typically directly associated with the affected veins, skin changes or ulceration; it does not radiate as with radiculopathies, and is not exacerbated by joint movement as in arthritis. (See "Lumbosacral radiculopathy: Pathophysiology, clinical features, and diagnosis".)

Extremity swelling is reported by 25 to 75 percent of patients, and correlates with increasing clinical severity (ie, increasing CEAP category). Swelling is generally worse with prolonged standing and improves with leg elevation and walking. In women, exacerbation of symptoms can occur with the menses or pregnancy, due to increased fluid volume and/or higher circulating levels of estrogen.

Other complaints include limb aching or generalized fatigue, skin discoloration or redness, muscle cramping, numbness, tingling, or itching. Numbness and tingling due to chronic venous disease can become chronic and may be difficult to distinguish from other causes of peripheral neuropathy that affect the lower extremity [23-25]. (See "Approach to the patient with sensory loss", section on 'Stocking-glove sensory loss'.)

Some patients with chronic venous disease may seek medical attention for the first time due to chronic ulcers, or bleeding that can be spontaneous (varicose vein hemorrhage) or related to a wound. The prevalence of nonhealing venous ulcers for more than a year has been reported in 55 to 60 percent of patients with chronic venous disease [26-29].

Patients should be asked about the number and location of prior ulcerations, as well as the nature of any treatments used to aid in wound care. A history of a previous venous ulcer is the strongest predictor of recurrent ulceration [26].

PHYSICAL ASSESSMENT — The goal of physical assessment is to correlate the patient's symptoms with the clinical signs of venous disease. It is important to keep in mind that a subset of patients may have typical symptoms but no visible clinical signs, while other patients may have lower extremity symptoms that are not consistent with venous disease and more likely attributable to another process. Therefore, the patient should undergo a complete physical examination with a detailed lower extremity examination that includes assessment of clinical signs of venous disease, pulse examination, and neurologic assessment. (See "The detailed neurologic examination in adults".)

The femoral and pedal pulses (ie, dorsalis pedis and posterior tibial pulses) are usually palpable in younger patients. In older patients, a hand held Doppler ultrasound may be necessary to assess pedal arterial flow. If there are any indications of arterial ischemia (ie, cool extremity, pulselessness, forefoot or digital ulceration), further noninvasive arterial evaluation should be undertaken. (See "Clinical manifestations and evaluation of chronic critical limb ischemia".)


No clinical signs — About 20 percent of patients with clinical symptoms consistent with a chronic venous disorder have no visible clinical signs [9]. Duplex examination identifies functional disease (ie, venous reflux) in approximately 20 percent of these patients. (See "Overview and management of lower extremity chronic venous disease", section on 'Management by CEAP clinical category'.)

Telangiectasia/reticular veins — The most frequently encountered manifestation of venous disease is mild venous dilation. Telangiectasias are a confluence of dilated intradermal venules less than one millimeter in diameter (picture 1). Telangiectasias are more common in women [9]. Reticular veins are dilated, bluish subdermal veins, one to three millimeters in diameter, and are usually tortuous.

Varicose veins — Varicose veins are subcutaneous dilated, tortuous veins greater than three millimeters in diameter (picture 2). They may involve the saphenous veins, saphenous tributaries, or non-saphenous superficial leg veins (figure 1A-B). (See "Classification of lower extremity chronic venous disorders", section on 'Anatomy'.)

Edema — Longstanding venous disease associated with venous reflux is characterized by the development of dependent ankle edema (picture 3) which may progress over time to include the calf region. In the early stages of chronic venous insufficiency, edema may be present only at the end of the day; however, with time it can become persistent throughout the day.

The presence of edema is not a specific finding. It occurs when the hydrostatic pressure gradient is substantially increased (eg, congestive heart failure, renal failure, or locally with venous thrombosis or insufficiency), the oncotic pressure gradient is substantially reduced (marked hypoalbuminemia), vascular (capillary) permeability is increased, or lymphatic flow is obstructed (table 2). Other etiologies may also lead to lower extremity edema. (See "Pathophysiology and etiology of edema in adults" and "Clinical manifestations and diagnosis of lymphedema" and "Popliteal (Baker's) cyst".)

The following clues point to venous insufficiency as the cause of lower extremity edema:

The edema is limited to the lower extremities and is often unilateral (particularly early) and is accompanied by venous abnormalities (telangiectasias, reticular veins, varicose veins), hyperpigmentation, or other signs of venous disease. By contrast, the edema in generalized edematous states is usually bilateral and is often not limited to the legs.
The edema typically subsides with recumbency. While many other edematous states also improve in this setting, this finding distinguishes venous insufficiency from chronic lymphatic obstruction, which is often unilateral and may not subside with recumbency. (See "Clinical manifestations and diagnosis of lymphedema".)
The central venous pressure is normal, a finding that excludes heart failure as a cause for the edema. This distinction is more difficult when both heart failure and venous disease are present.
Patients who have been given diuretics will have a poor response, and can develop signs of hypoperfusion. (See "Medical management of lower extremity chronic venous disease", section on 'Systemic agents'.)
Skin pigmentation changes/dermatitis — Pigmentation changes are initially most prominent at the medial ankle, but subsequently may encroach upon the foot and lower leg (picture 4). Brown and blue-grey hyperpigmentation on the anterior lower leg is a common finding. The pigmentation is due to hemosiderin deposition which derives from the breakdown of red blood cells that have extravasated through damaged capillaries into the dermis.

Individuals with functional venous disease due to venous reflux are prone to develop stasis dermatitis which is one of the most common and earliest dermatologic signs of chronic venous insufficiency. Stasis dermatitis is an inflammatory process that presents as an eczematous rash characterized by itching, erythema, scaling, weeping, erosions, and crusting (picture 5).

The pruritus associated with the dry, scaly skin can be difficult to relieve; excoriations are often present secondary to scratching, and can be a source of skin infection. Rashes mimicking the dermatitis on the legs can appear as eczematous patches on other body sites, or can present as a generalized body rash, an auto eczematous or "id" reaction (picture 6).

Atrophie blanche manifests as atrophic, hypopigmented patches with focal red punctate dots or telangiectasias, surrounded by hyperpigmentation. These are most often seen on the medial distal leg near the malleolus, or can occur within lipodermatosclerotic skin, where they correspond to points of avascular fibrosis (picture 7). These areas do not represent healed venous ulcers, but they are vulnerable to future ulceration because of poor perfusion. (See "Livedoid vasculopathy" and 'Venous ulceration' below.)

Lipodermatosclerosis — Chronic venous insufficiency of sufficient severity (eg, following severe cases of deep venous thrombosis or that associated with lymphatic compromise) may lead to the development of lipodermatosclerosis, a fibrosing panniculitis of the subcutaneous tissue. This disorder is characterized by a firm area of induration which is initially located at the medial ankle (picture Cool. As the process progresses, the entire leg can become circumferentially involved with extension up to the mid leg in more advanced cases (picture 9).

The skin overlying the panniculitis is typically heavily pigmented and bound down to the subcutaneous tissues. The fibrosis may be so extensive and constrictive as to girdle and strangle the lower leg, further impeding lymphatic and venous flow. Brawny edema above the fibrotic area and on the foot below is seen in advanced cased of lipodermatosclerosis. The limb now resembles an inverted champagne bottle; the bulbous cork represents the lymphedematous foot, the fibrosed area the neck of the bottle, and edematous leg the body of the bottle (picture 10).

Patients with lipodermatosclerosis are particularly prone to repeated bouts of cellulitis, usually caused by Staphylococcal or Streptococcal organisms (picture 11). (See "Cellulitis and erysipelas".)

Venous ulceration — Chronic venous disease is the most common cause of lower extremity ulcers [26-29]. They are usually located low on the medial ankle over a perforating vein, or along the course of the great or small saphenous veins (figure 1A-B); they can occur more proximally on the leg if precipitated by trauma, but never in the forefoot or above the level of the knee. The ulcers may be multiple or single, and are exquisitely tender, shallow, exudative and have a granulation base (picture 12). The ulcer borders are usually irregular but not undermined. They can extend circumferentially around the leg if left untreated [3] .

These characteristic findings often allow distinction between venous ulcers and the following types of ulcers that also appear on the lower extremities (table 3):

Arterial ulcers are typically painful, and punched out or stellate in appearance. The surrounding skin is red and taut. Some arterial ulcers are pale; others may have a black or yellow eschar. On the leg, they are more often associated with trauma and commonly occur on the foot over pressure points. In addition, the leg and/or foot may display other signs of arterial insufficiency including thin atrophic and hairless skin, poor or absent pedal pulses, diminished capillary refill, or hypertrophic deformed nails. (See "Clinical features, diagnosis, and natural history of lower extremity peripheral artery disease".)
Neuropathic foot ulcers, including diabetic ulcers, most commonly occur at areas of increased pressure at sites of bony prominences, such as over the metatarsal heads. They typically are surrounded by a thick hyperkeratosis and the ulcer often has undermined borders (picture 13). The extremity and the ulcer are usually insensitive. (See "Evaluation of the diabetic foot".)
Other possible causes of ulcers include rheumatoid arthritis and other connective tissue diseases with associated vasculitis, hemoglobinopathies (eg, sickle cell disease), pyoderma gangrenosum, and tumors, especially squamous cell carcinoma and basal cell carcinoma. It may be necessary to have the ulcer biopsied in order to rule out these uncommon causes of lower extremity ulcers.

Patrick C Alguire; et al. Clinical manifestations of lower extremity chronic venous disease. UptoDate, Abr 30, 2013.


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