VENOUS DISEASES
Anatomy of the venous system of the lower extremities
Functional Aspects of Chronic Venous Disease
Deep Venous Reflux
Pathogenesis of Venous Evaluation,
Deep Vein Thrombosis: The Disease
New biomarkers in deep vein thrombosis
venous thromboembolic disease,
Arrival
lower extremity ulceration,
lymphoedema
Treatment Options in Lymphedema
Anatomy of Venous Structure
The venous system is the vein system in our body. The genetic development of the venous network of the lower extremities explains the main variations of the venous network superficial veins, perforating veins and deep venous system. The number of so-called primitive chronic venous disease is likely to be explained by the underlying unknown anatomical abnormalities.
Functional Aspects of Chronic Venous Insufficiency Disease
The functional aspect of chronic venous disease differs significantly from arterial insufficiency. Often, the concepts in the arterial system are inappropriately applied to venous pathology. There are four domains of chronic venous disease.
Measuring saphenous reflux,
Identification of critical venous stenosis,
Grading of the severity of venous stenosis in the abdomen (iliac vein)
Function of venous lateral branches and venous bypass.
Deep Venous Insufficiency
Chronic venous insufficiency (CVI) encompasses a wide range of clinical manifestations, from swelling of the feet to non-healing ulcers. Causes of insufficiency in the deep venous system;
reflux,
Venous stenosis or occlusion
It includes a combination of the two.
Of these, reflux alone or in combination with stenosis is the contributing factor in the overwhelming majority (70-90%) of cases. Although the cause is unknown, which we usually call primary, it can also develop after any obstruction.
A developmental etiology has also been recognized because of symptoms before the actual age of presentation, often as early as the teenage years. Trauma has also been presented as a cause. Degeneration of the fibroelastic tissue of the valve over time is accepted as the most plausible cause in most patients.
Deep Vein Thrombosis
Deep vein thrombosis (DVT) is a complex set of diseases. Nowhere else in the vascular network does such a challenging ‘easy-to-find and hard-to-treat’ situation occur. The large-volume low-flow venous system in humans is affected by gravity in upright posture, and the blood in the entire system responds differently to various stimuli according to flow mechanics, physiological stress, hormonal influences, and genetic predisposition.
Venous thromboembolism (VTE) is a thrombus formation in a vein that can dislodge from its original location and travel to a distant site (embolism). The most common site for thrombus formation is the deep veins of the leg, hence the term deep vein thrombosis (DVT). The embolism can travel to the lungs and settle in the pulmonary vessels, causing Pulmonary Embolism [Pulmonary Embolism (PE)].
It is estimated that around 25,000 people die annually from preventable hospital-acquired VTE in the UK. This was highlighted by a recent UK study suggesting that 71% of patients at moderate or high risk of developing DVT did not receive any thromboprophylaxis treatment.
Non-fatal clotting is also important as it causes long-term illness that causes swelling in the foot, called post-phlebitic syndrome, skin sores. Deep vein thrombosis (DVT) typically begins in the calf veins and presents with pain, swelling and redness. There may be tenderness in the thigh or calf, there may be unilateral soft edema, and the patient may experience mild fever. However, DVT symptoms can be vague and other differential diagnoses should also be considered.
Deep veins and arteries run together in the lower extremity, and the normal vein appears as an echo-free channel on ultrasound and is usually larger than the accompanying artery. The reliability of venous ultrasound in the diagnosis of DVT is high, but its reliability is slightly lower in the calf area. About 40% of DVTs resolve spontaneously, 40% organize, and 20% diffuse.
Magnetic resonance (MRI) is useful in the examination of the intracranial venous system, especially in the evaluation of suspected dural venous sinus thrombosis.
Pathophysiology:
Rudolf Virchow (1821-1902) identified a number of factors that were largely responsible for the formation of thrombosis. These
slowing of blood flow (stasis),
Changes in blood components (hypercoagulability)
Damage to the vein wall (venous injury).
These factors are still responsible for DVT (Deep Vein Occlusion) in modern practice. Stasis may result from the patient’s inactivity.
Differential diagnosis of DVT:
calf muscle damage
acute lipodermatosclerosis
Superficial thrombophlebitis
lymphatic insufficiency/lymphedema
Torn bone (Baker’s) cyst
Leg swelling in a paralyzed extremity
Cellulite
Knee joint pathology
Broken
Reperfusion injury/compartment syndrome
Risk factors for venous thromboembolism:
Acquired disorders can be examined under two main headings as hereditary/congenital disorders.
Inherited Disorders:
Antithrombin deficiency
Protein C deficiency
Protein S deficiency
Factor V Leiden mutation
prothrombin gene mutation
Dysfibrinogenemias
Factor VII deficiency
Age XII deficiency
Antiphospholipid syndrome
Acquired Disorders
malignant tumors
Surgery, especially orthopedic surgery
Presence of central venous catheter
Trauma
Pregnancy,
HRT, birth control pills
prolonged immobility
not getting enough fluids
>60 years
Obesity (BMI>30)
previous VTE
Congestive cardiac/respiratory failure
Myeloproliferative disorders
diabetes mellitus
Hyperviscosity syndromes (myeloma)
inflammatory bowel disease
Varicose veins associated with Behçet’s disease Associated phlebitis.
Diagnosis of DVT The clinical diagnosis of DVT is not sufficient to make a full diagnosis and Homans’ finding is used in the diagnosis. The most important laboratory research is the D-dimer test. The D-dimer value has a high negative indicator value and therefore can be used to exclude the diagnosis of DVT if it does not rise. However, a high value is nonspecific and may occur in cancer, pregnancy, recent surgery or trauma.
Venography is the ‘gold standard’ diagnostic tool for DVT; However, its use is limited because it is an invasive procedure and uses contrast material. Venous Doppler ultrasonography is the preferred investigation nowadays. It is non-invasive, inexpensive, painless and easily accessible. It has approximately 97% sensitivity and specificity in the diagnosis of proximal DVT. Computed tomography (CT), magnetic resonance imaging (MRI), and impedance plethysmography may also be used. In order to avoid unnecessary research, the diagnostic method that includes clinical, laboratory and radiological interventions is used.
Varicose Veins:
Varicose veins are common and affect about a third of the adult population in the developed world. It varies clinically from cosmetic problems to severe extremity threatening wounds. Most patients with uncomplicated varicose veins never progress to develop skin changes or ulceration and can be appropriately reassured.
He recommends endovenous ablation as first-line therapy for complicated varicose veins, followed by surgery followed by foam sclerotherapy. All patients with skin changes and interventions should first be evaluated with color Doppler ultrasonography.
Varicose veins are almost always caused by superficial venous reflux venous valve mechanism incompetence. There is evidence to suggest that patients with varicose veins do indeed have a natural decrease in vessel wall elasticity. This partly explains why recurrence of varicose veins is so common after treatment. It is also suggested to have an inherited component of varicose veins.
There are other risk factors for the development of varicose veins, such as female gender, prolonged standing, increased height, obesity (via venous hypertension), increasing age, and multiple births. More rarely, varicose veins are the result of deep vein thrombosis, tumor, or vascular anomaly.
Large varicose veins do not have to have valve insufficiency in one of the trunk veins; Where varicose veins develop due to local insufficiency, the veins are sometimes referred to as ‘reticular’.
The CEAP (clinical, etiologic, anatomical, and pathophysiologic) classification is now the worldwide standard to describe in detail the clinical features of chronic venous disease. Varicose veins are often cited as responsible for a variety of symptoms including heaviness, burning, cramping, itching, tingling, and a feeling of pain. These symptoms are equally attributable to other vascular and non-vascular conditions. There is no doubt that varicose veins can be responsible for significant changes in the skin of the lower leg, and this is usually best shown on the ankle. The skin changes are thought to be the result of abnormal pressures in the venous system induced by reflux, followed by extravasation of blood into the tissues. Although skin changes are due to abnormalities in venous hemodynamics, other complications of varicose veins are related to the veins themselves. For example, when bleeding does occur, it is most commonly caused by varicose veins in the ankle and can be profuse. Thrombophlebitis is inflammation of the vein wall secondary to thrombosis and is an often recurrent phenomenon.
The examination has three purposes:
To search for a possible cause of venous insufficiency,
To study the state of the peripheral arterial system
To examine the varicose veins themselves.
An abdominal examination should be performed to look for masses that may be causing venous obstruction, to determine the contribution of peripheral vascular disease to the patient’s symptoms, and to rule out significant arterial insufficiency that may complicate future treatment options. Examination of varicose veins is best done in a warm room with the patient standing. In addition to assessing the distribution of varicose veins, traces of previous varicose vein interventions can also be sought. Although Doppler can reliably identify the site of regurgitation in most cases of varicose veins, it is limited in patients with recurrent varicose veins and where there is more than one zone of regurgitation. For those with confirmed reflux of the main veins with a history of symptomatic varicose veins, skin changes, thrombophlebitis, or venous ulceration, endothermal ablation with phlebectomies should be offered as first-line therapy, provided the patient’s venous anatomy is suitable.
Lower Extremity Ulceration
The etiological factors that can cause leg ulcers are diverse, but most patients have a genetic venous disease. Chronic venous insufficiency is ten times more common than arterial ulcers. Diabetic leg ulcers and ulcers with an inflammatory margin and skin necrosis are often associated with chronic inflammatory diseases such as ulcerative colitis or rheumatoid arthritis. Leg ulcers can also occur in patients with Klinefelter syndrome; Slow-healing ulcers may occur in these patients with hypogonadism and testosterone deficiency, with or without chronic venous disease. There is some evidence that abnormal platelet aggregation or high plasminogen activator inhibitor-1 activity may play an important role in fibrinolysis? The most important differential diagnosis of leg ulcers is ulcerations caused by malignant or semi-malignant diseases in which ulcerating tumors such as basal cell carcinoma or melanoma can mimic venous ulcerations.
For the correct treatment of venous ulcers we need to have the most accurate diagnosis possible and in some cases the diagnosis is not 100% accurate. The single most useful confirmatory test is the Doppler examination; diagnosis should evaluate not only the great saphenous vein (GSF), but also all superficial, deep and perforating venous systems. In cases where there are only venous problems, we need to find the sources of reflux (uniquely mixed).
One percent of the general population suffers from lower extremity ulceration, and this frequency increases with age (3% of those over 65 are affected), and non-healing ulceration increases the risk of lower extremity amputation. Therefore, chronic persistence and frequent ulcer recurrence also have a significant impact on patients’ quality of life: ulcers can be painful, foul-smelling and require long-term bandaging treatment.
Such a structured, evidence-based approach to management is imperative, as the etiology of lower extremity ulceration encompasses a range of pathologies and will therefore present in varying guises in primary care. However, after initial evaluation and diagnosis, most leg ulcers can be managed later in the primary care setting. Clinical evaluation of lower extremity ulceration Evaluation of the underlying cause of ulceration is the key to continued treatment.
Smoking is a known cause of peripheral vascular disease. Occupation can also contribute, especially those who stand for long periods of the workday. Elderly people with reduced mobility, likely to spend most of the day sitting in a chair with edematous dependent legs, will have reduced calf muscle pump function and be at risk for ulceration. Muscle pump stasis also occurs as a result of morbid obesity, which has implications when considering treatment options. Poorly controlled diabetes not only causes neuropathy, but also results in increased prevalence of lower extremity infection and poor wound healing.
Postthrombotic venous insufficiency DVT can lead to venous valve damage, resulting in valve regurgitation. A combination of deep vein reflux and unresolved thrombus-induced venous obstruction leads to post-thrombotic venous insufficiency (also known as post-phlebitic syndrome).
lymphedema
Lymphedema of the extremities characteristically refers to an increase in extremity volume caused by the accumulation of tissue fluid, proliferation of fat cells, and excessive collagen production. There is also an increase in infiltration into the immune cell mass. Bacterial colonization occurs as a result of the inability to lymphatic transport of microbes penetrating the skin of the feet and palms. Under physiological conditions, the capillary filtrate tissue fluid flows into the lymphatics and is transported into the blood circulation through the collected lymphatic bodies. Obliteration of the transport lymphatic channels and sinuses of the regional lymph nodes causes stagnation of intercellular water, proteins, and migrating immune cells. Tissue changes are accumulation of tissue fluid/lymph under the epidermis with hyperkeratosis, fibrosis and occasional lymphorrhea.
The most common complication of tissue fluid stasis is bacterial dermato-lymphangia-adenitis (DLA).
Lymphedema is swelling of tissues as a result of failure of lymphatic drainage. When it first develops, swelling is mainly due to fluid buildup, but over time fibrosis occurs and fatty tissue builds up. In the past, lymphedema was thought to be rare and incurable. Lymphedema/chronic edema Factors causing increased capillary filtration
Increased venous pressure, eg venous disease, deep vein thrombosis, heart failure, immobility
Increased capillary pressure due to arteriolar dilatation, eg angioedema and drugs, eg nifedipine
Decreased plasma oncotic pressure, eg in hypoalbuminemia Factors causing decreased lymphatic drainage
Structural damage to lymphatic vessels, eg surgery and/or radiotherapy
Developmental abnormality of lymphatic vessels, eg hypoplasia in Milroy’s disease
Decreased ‘muscle pump’ activity on inactivity For example, in venous disease, capillary filtration increases as a result of increased venous pressure.
This leads to an increase in lymphatic drainage to match it. When the carrying capacity of the lymphatic system is exceeded, capillary filtration exceeds the lymphatic drainage and edema develops (high outflow of lymphatics in venous edema). However, over time, the increased flow in the lymphatics decreases, possibly as a result of vessel damage, and further deterioration of lymphatic drainage develops (lymphedema).
In immobile patients, a chronic ‘addictive’ edema of the lower extremities is often observed (armpits). This is due to the failure of the muscle pump in the legs to push both blood and lymph through the veins and lymphatic vessels, respectively. Thus, venous pressure and thus capillary filtration increase and lymphatic flow decreases, resulting in edema.
In pure lymphedema, lymphatic insufficiency is of two types:
Primary Lymphedema: This is due to a genetic abnormality of the lymphatic system.
Secondary lymphedema. This is due to an external process that damages a normal lymphatic system, for example surgery, trauma, radiotherapy or infection (cellulitis and filariasis).
There is a wide variety of reported incidences of edema associated with cancer treatment. This is partly a result of the difficulty in defining what constitutes a significant edema. Breast cancer, Gynecological cancers, Genitourinary cancers, Malignant melanoma of the leg.
Treatment Options in Lymphedema
Lymphedema treatment The main treatment for lymphedema (and some other chronic oedema) is a combination of physical therapies. There is evidence that these combined therapies are effective in reducing both limb volume and the incidence of cellulite, but the relative contribution of each component and whether all elements are needed in all patients is unclear.
Patients may need two phases of treatment:
An intense phase in which the compression bandage is applied and renewed, usually for an average of 2 weeks daily. Manual lymphatic drainage can be used as part of this phase.
A lifelong care phase, both daily, that includes wearing a compression garment and skin care with the application of moisturizer. Simple lymphatic drainage may form part of this phase.
Some patients with mild edema can only be treated with the ‘maintenance phase’ approach.