Varicose Veins

History of the Procedure

The description of varicose veins as a clinical entity can be traced back as early as the fifth century BC. Forefathers of medicine including Hippocrates and Galen described the disease and treatment modalities, which are still used today.Throughout the centuries, surgical treatments have evolved from large, open surgeries to minimally invasive approaches.

Problem

Varicose veins represent a significant clinical problem and are not just a “cosmetic” issue because of their unsightly nature. The problem arises from the fact that varicose veins actually represent underlying chronic venous insufficiency with ensuing venous hypertension. This venous hypertension leads to a broad spectrum of clinical manifestations, ranging from symptoms to cutaneous findings like varicose veins, reticular veins, telangiectasias, swelling, skin discoloration, and ulcerations .Varicose veins and even chronic venous insufficiency can be managed conservatively with stockings and compression. More aggressive management can be pursued for cosmesis, worsening cutaneous findings or symptoms despite conservative management, or if the patients prefer surgical management. Most procedures to treat varicose veins can be elective, and emergent treatment and workup is usually reserved for bleeding varicosities or if deep venous thrombosis is suspected.

Frequency

The incidence and prevalence of varicose veins has been studied in a number of cross-sectional studies. In 1973, the United States Tecumseh community health study estimated that about 40 million persons (26 million females) in the US were affected. In 1994, a review by Callam found half of the adult population have minor stigmata of venous disease (women 50-55%; men 40-50%) and fewer than half have visible varicose veins (women 20-25%; men 10-15%). In 2004, these finding were also seen in a French cross-sectional study that found the odds ratio per year for varicose veins were 1.04 for women and 1.05 for men. Age and gender have been the only consistently identified risk factors for varicose veins.

Etiology

The cause of primary varicose veins is incompetent venous valves that result in venous hypertension. Secondary varicose veins result from deep venous thrombosis and its sequelae or congenital anatomic abnormalities. The etiology of these varicose veins can be classified into the following three groups:

• Primary: Valvular insufficiency of the superficial veins, most commonly at the saphenofemoral junction.
• Secondary 

1.  Mainly caused by deep vein thrombosis (DVT) that leads to chronic deep venous obstruction or valvular insufficiency. Long-term clinical sequelae from this have been called the postthrombotic syndrome.
2. Catheter-associated DVTs are also included.
3. Pregnancy-induced and progesterone-induced venous wall and valve weakness worsened by expanded circulating blood volume and enlarged uterus compresses the inferior vena cava and venous return from the lower extremities.
4. Trauma

• Congenital: This includes any venous malformations. A few examples are listed as follows: 

1. Klippel-Trenaunay variants
2. Avalvulia

Pathophysiology

Varicose veins are simply dilated, tortuous veins of the subcutaneous/superficial venous system. However, the pathophysiology behind their formation is complicated and involves the concept of ambulatory venous hypertension. To understand this, the anatomy of the lower extremity venous system must be briefly discussed. Two venous systems are found in the lower extremity, the deep and superficial .The deep system ultimately leads backs to the inferior vena cava, then to the heart. The superficial system is found above the deep fascia of the lower extremity, within the subcutaneous tissue. Many superficial veins exist, but they all drain into the 2 largest, the greater saphenous vein (GSV) and the short saphenous vein (SSV), formerly called the lesser saphenous vein.
 
The superficial venous system is connected to the deep system at a number of the following locations:

• Perforator veins: These veins transverse the deep fascia of the lower extremity. A number of named perforators are found at the thigh, knee,  and leg
• Saphenofemoral junction (SFJ): This is located proximally at the groin where the GSV meets the femoral vein
• Saphenopopliteal junction (SPJ): This is located behind the knee where the SSV joins with the popliteal vein

In healthy veins, the flow of venous blood is through the superficial system into the deep and up the leg and toward the heart. One-way venous valves are found in both systems and the perforating veins. Incompetence in any of these valves can lead to a disruption in the unidirectional flow of blood toward the heart and result in ambulatory venous hypertension .Furthermore, incompetence in one system can often lead to incompetence in another. In a study by Shami et al, the limbs of 59 patients with venous ulceration were assessed by color duplex ultrasound scanning.5 In 53% of patients only superficial venous reflux was found, in 15% isolated deep venous reflux was found, and in 32% a combination of deep and superficial venous reflux was found.
 
Incompetence in the superficial venous system alone usually results from failure at valves located at the SFJ and SPJ. The gravitational weight of the column of blood along the length of the vein creates hydrostatic pressure, which is worse at the more distal aspect of the length of vein .

 Incompetence of the perforating veins leads to hydrodynamic pressure. The calf pump mechanism helps to empty the deep venous system, but if perforating vein valves fail, then the pressure generated in the deep venous system by the calf pump mechanism are transmitted into the superficial system via the incompetent perforating veins 

 
Once venous hypertension is present, the venous dysfunction continues to worsen through a vicious cycle. Pooled blood and venous hypertension leads to venous dilatation, which then causes greater valvular insufficiency. Over time, with more local dilatation, other adjacent valves sequentially fail, and after a series of valves has failed, the entire superficial venous system is incompetent. As mentioned before, this can then cause subsequent perforator and deep venous valvular dysfunction. 
 
The inciting etiology of superficial valvular insufficiency is often difficult to determine because the clinical manifestations of venous hypertension are delayed. The original cause can be classified as primary, secondary, and congenital as previously described.
 
The clinical finding of varicose veins, reticular veins, and telangiectasias are due to the hypertension in the superficial venous system that spreads to collateral veins and tributary veins, causing dilated tortuous structures. Treatment modalities are geared towards correcting the superficial venous hypertension.

 
At times, the degree or venous hypertension does not correlate to the clinical findings. The presence and size of visible varicosities are not reliable indicators of the volume or pressure of venous reflux. A vein that is confined within fascial planes or is buried beneath subcutaneous tissue can carry massive amounts of high-pressure reflux without being visible at all. Conversely, even a small increase in pressure can eventually produce massive dilatation of an otherwise normal superficial vein that carries very little flow. In contrast to the superficial veins, the deep veins do not become excessively distended. They can withstand the increased pressure because of their construction and the confining fascia.

Clinical

Subjective symptoms
 
Patients may have a host of symptoms, but they are usually caused by venous hypertension rather than the varicose veins themselves.  Often, symptoms are purely aesthetic, and patients desire treatment of the unsightly nature of the tortuous, dilated varicosities. Complaints of pain, soreness, burning, aching, throbbing, heavy legs, cramping,muscle fatigue, pruritus, night cramps, and “restless legs” are usually secondary to the venous hypertension.  Pain and other symptoms may worsen with the menstrual cycle, with pregnancy, and in response to exogenous hormonal therapy (eg, oral contraceptives).

Also, pain associated with venous hypertension is usually a dull ache that worsens after prolonged standing, and improves by walking or by elevating the legs. This is in contrast to the pain of arterial insufficiency, which is worse with ambulation and elevation. Subjective symptoms are usually more severe early in the progression of disease, less severe in the middle phases, and more severe again with advancing age. Patients who have become acclimatized to their chronic disease may not volunteer information about symptoms. After treatment, patients are often surprised to realize how much chronic discomfort they had accepted as “normal.”

Venous history

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

Physical Examination Findings

The physical examination of the venous system is fraught with difficulty. As mentioned earlier, the severity of symptoms does not necessarily correlate with the size or extent of visible varices or with the volume of reflux. Furthermore, most of the deep venous system cannot be directly inspected, palpated, auscultated, or percussed. In most areas of the body, examination of the superficial venous system must serve as an indirect guide to the deep system.
 
Inspection

Inspection should be 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. The following items should be noted:

• Surgical scars from prior intervention
• Pigmentations and skin changes (ie, brownish darkening of the skin, resulting from extravasated blood that causes lipodermatosclerosis. This usually occurs in medial ankle region but may extend to leg and foot.)
• Varicose veins – Visible, palpable veins in the subcutaneous skin greater than 3 mm
• Reticular veins (also called blue veins, subdermal varices, and venulectasias) – Visible, dilated bluish subdermal, nonpalpable veins 1-3 mm
  Telangiectases (also called spider veins, hyphen webs, and thread veins) – Dilated intradermal venules greater than 1 mm in diameter
• Eczema – Erythematous dermatitis, which may progress to blistering, weeping, or scaling eruption of the skin of the leg.
• Atrophie blanche (white atrophy) – Localized, often circular whitish and atrophic skin areas surrounded by dilated capillaries and sometimes hyperpigmentation. (Scars of healed ulceration are excluded from this definition.)
• Corona phlebectatica (also called malleolar flare and ankle flare) – Fan-shaped pattern of numerous small intradermal veins on the medial or lateral aspects of the ankle and foot
• Ulcers of the medial ankle – Most likely the result of underlying venous insufficiency. (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 palpated lightly with the fingertips because dilated veins may be palpable even where they are not visible. Distal and proximal arterial pulses are also palpated. An ankle-brachial index is useful if arterial insufficiency is suggested.

• The anteromedial surface of the lower limb is the territory of the greater saphenous vein (GSV). The arch of the vein may be palpated in some patients with healthy veins, but this segment of the vein is particularly well appreciated in patients with truncal reflux at the saphenofemoral junction (SFJ). 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 posterior surface of the calf is the territory of the short saphenous vein. This may be palpable in the popliteal fossa in some slender patients. Normal superficial veins above the foot are usually 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 DVT may exist in as many as 40% of patients with superficial phlebitis.
• 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 superficialtributaries emerge through openings in the superficial fascia. Incompetent perforating veins may connect the superficial and deep venous systems through these fascial defects, but the finding is neither sensitive nor specific for perforator incompetence.

Percussion

This technique is useful in determining whether 2 venous segments are directly interconnected. 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. Percussion can be used to trace out the course of veins already detected by palpation, to discover varicose veins that could not be palpated, and to assess the relationships between the various varicose vein networks. Valsalva or cough with the examiners hand over the medial aspect of the knee can often elicit a palpable pulse wave with florid saphenofemoral junction incompetence.

Renal Vein Thrombosis

Background

Although renal vein thrombosis (RVT) has numerous etiologies, it occurs most commonly in patients with nephrotic syndrome ( g/d protein loss in the urine, hypoalbuminemia, hypercholesterolemia, edema).The syndrome is responsible for a hypercoagulable state. The excessive urinary protein loss is associated with decreased antithrombin III, a relative excess of fibrinogen, and changes in other clotting factors; all lead to a propensity to clot. Numerous studies have demonstrated a direct relationship between nephrotic syndrome and both arterial and venous thromboses. Why the renal vein is susceptible to thrombosis is unclear.The renal vein also may contain thrombus after invasion by renal cell cancer. Other less common causes include renal transplantation, Behçet syndrome, hypercoagulable states, and antiphospholipid antibody syndrome.

Pathophysiology

Hypercoagulability is the etiology for both arterial and venous thromboses. In the setting of malignant invasion of the vein by cancer, the presence of the tumor cells elicits thrombosis of the renal vein only.

Frequency

United States
Prevalence of RVT has been difficult to establish. Studies have shown a high degree of variability in the presence of RVT among patients with nephrotic syndrome, with reported rates of 5-62%.

Mortality/Morbidity

The morbidity and mortality of RVT usually is secondary to the effects of nephrotic syndrome (including arterial thrombosis), renal dysfunction and/or failure, or the complications resulting from thromboembolism. If the etiology of the RVT is malignancy, morbidity and mortality are a result of either thromboembolism or the cancer itself. In the setting of transplantation, RVT may lead to loss of the graft. If the RVT eventuates from the other causes discussed, thromboembolism is the source of complications.

Race

No race predilection exists.

Sex

No specific numbers are available. However, theoretically, membranous nephropathy, the most commonly associated disease for RVT, has a male-to-female ratio of 2:1. Therefore, a male preponderance may exist.

Age

Age is a factor in RVT only as associated with any age-related risk of glomerular disease. For example, membranous nephropathy, the lesion most associated with RVT, is the most common cause of nephrotic syndrome in adults, but itis rare in children. Membranous nephropathy peaks in the fourth through sixth decade, thus making RVT more likely in this specific age group. However, exact incidence or prevalence is not available.RVT from renal cell carcinoma occurs in older age groups.

History

The presentation of RVT is variable, and patients may be asymptomatic. When RVT occurs as a result of malignancy, the signs of the renal malignancy (eg, hematuria, weight loss) predominate.

• The more common chronic form of RVT generally is covert.
• The less frequent acute form usually occurs in younger patients, with flank pain and macroscopic hematuria.
• Patients may present with thrombosis and/or embolism.
• Physical Observe for signs of nephrotic syndrome (edema or anasarca).

Causes

• In patients who are nephrotic, the most common underlying nephropathy associated with RVT is membranous nephropathy. For a renal biopsy of membranous nephropathy. The tumor association for RVT is renal cell carcinoma. However, most cases of membranous nephropathy are idiopathic.
• RVT also may be the result of nephrotic syndrome from membranoproliferative glomerulonephritis, minimal change disease, rapidly progressive glomerulonephritis, amyloid, focal sclerosis, or lupus nephritis. RVT is more common in patients with primary rather than secondary nephropathy.
• Findings relative to the causative disease may be present (eg, systemic lupus erythematosus [SLE]/antiphospholipid antibody syndrome, cancer).
• Theories for the putative relationship between nephrotic syndrome and RVT have evolved. Initially, nephrotic syndrome was believed to be a consequence of RVT. However, this presumed sequence was incorrect.

1.  Experimentally induced RVT causes only mild proteinuria.
2. RVT in the absence of nephrotic syndrome has been reported in the surgical literature.
3. Nephrotic patients with RVT who have undergone histologic evaluation show evidence of an identifiable glomerulopathy.
4. RVT is known to occur after the onset of nephrotic syndrome. Thus, nephrotic syndrome is not a direct result of RVT but rather leads to RVT.

• SLE also has been associated with RVT.

1. In general, patients with lupus and documented RVT have membranous lupus nephritis (World Heath Organization class V).
2. Generally, thrombophlebitis and circulating anticoagulants (anticardiolipin antibodies) are believed to be much less important than nephrotic syndrome as predisposing factors of RVT in SLE.

• RVT is an uncommon but definite problem in neonates. A possible association exists between RVT and the factor V Leiden mutation in this age group.
• Other diseases or situations that have been associated with RVT include antithrombin III deficiency, protein C or S deficiency, antiphospholipid antibody syndrome, pregnancy or estrogen therapy (all hypercoagulable states), renal vein invasion by malignant cells, post–renal transplantation, Behçet syndrome, and extrinsic compression (eg, lymph nodes, tumor, retroperitoneal fibrosis, aortic aneurysm). Other than renal cell cancer, the other associations are uncommon.
• Trauma, ingestion of oral contraceptive agents, dehydration (infants), and steroid administration also have been associated with RVT.

Cholesterol Embolism

Background

Cholesterol embolism syndrome should be suspected in a patient who develops worsening renal function, hypertension, distal ischemia, or acute multisystem dysfunction after an invasive arterial procedure. Atheroemboli may also occur spontaneously. The protean manifestations of this syndrome make the diagnosis challenging. As the population ages, the incidence of cholesterol embolism syndrome will increase.

Pathophysiology

Any organ system, with the exception of the lungs, may be directly affected. Cholesterol embolism syndrome has 2 mechanisms of action.In the first, cholesterol crystals spontaneously break off from severely atherosclerotic plaques and shower into downstream organs, occluding arterioles 100-200 micrometers in diameter. The crystals induce an inflammatory body reaction and adventitial fibrosis, which eventually obliterate the vessel lumen. Local vasospastic mediators compound tissue ischemia and produce progressive, irreversible organ damage.With the second mechanism, larger cholesterol plaques break off and occlude larger arteries, causing tissue infarction with acute organ dysfunction. This can occur after local trauma to the atherosclerotic plaque, such as that caused by angiography or aortic trauma, or it can occur after destabilization of the protective clot overlying the plaque, which can occur as a result of anticoagulation.Cholesterol crystal embolization occurs from the arterial system, and crystals are trapped in the arterioles where they either immediately occlude the vessels or induce an intense inflammatory response that leads to tissue ischemia. Crystals do not travel to the lungs; however, inflammatory mediators released by ischemic tissue may result in acute lung injury.

Frequency

International

Estimates of the incidence of cholesterol embolic disease are usually based on autopsy data. Tissue sections from patients with the following diseases or indicate the incidence of atheroembolic events: aortic aneurysms (31%), abdominal aortic aneurysm repair (up to 77%), severe aortic disease (13-16%), and mild aortic disease (1-2%). Of patients undergoing angiography, 25-30% may have atheroembolic events, while 2.5-3% of patients who receive percutaneous coronary transluminal angioplasty vein grafts and 1.4-3% of patients undergoing renal artery angioplasty or cardiac catheterization have been reported to have clinical signs of atheroemboli.

Mortality/Morbidity

The mortality rate of acute multisystem organ failure resulting from cholesterol embolism syndrome is 58-90%. Jucgla found an overall incidence of 58% at 15 months, increasing to 65% if visceral organs were involved. Pre-existing chronic renal insufficiency had a relative risk of death of 4.54.
The mortality rate of severe cholesterol embolism is 90% at 3 months.Mild cases with renal dysfunction with or without skin findings had a mortality of 16%.

Sex

Men have a higher risk than women.

Age

Cholesterol embolism is a disease of persons ranging from middle-aged to elderly, with a minimum age of 50 years.

History

The diagnosis of cholesterol embolism must be considered in patients older than 50 years who have atherosclerotic disease presenting with multisystem dysfunction after undergoing an invasive vascular procedure or receiving an anticoagulant or thrombolytic agent within the past several months. All patients with the classic triad of livedo reticularis, acute renal failure, and eosinophilia should be evaluated for cholesterol embolism, including a funduscopic examination.

Physical

Constitutional

• Fever
• Weight loss
• Hypermetabolic state

Cardiovascular

• Tachycardia
• Uncontrolled or accelerating hypertension
• Congestive heart failure
• Myocardial infarction
• Intact peripheral pulses with livedo reticularis and tissue ischemia: These findings suggest small-vessel occlusion, such as cholesterol embolization, in a patient at risk.
  

Neurologic

• Hollenhorst plaques in retinal arteries
• Hemispheric ischemic stroke
• Paraplegia
• Confusion
• Delirium
• Renal – Oliguria, acute renal failure
• Dermatologic
• Gangrene, nodules, purpura, cyanosis, ulcerations (in 35-90% of patients)
• Livedo reticularis
• Infarction of perineal area
• Ischemic patches involving lower extremities more often than upper
• Blue toe syndrome and splinter hemorrhages
  

Geostrointestinal

• Minor or major bleeding
• Abdominal pain
• Bowel infarction
• Pancreatitis
• Acalculous cholecystitis
• Musculoskeletal – Myalgias
• Endocrine – Adrenal insufficiency
• Pulmonary – Acute respiratory distress syndrome (ARDS)

Causes

Any risk factor for atherosclerotic disease is a risk factor for cholesterol embolism.

Preoperative risk factors for cholesterol embolism syndrome after coronary artery bypass surgery include being older than 60 years, hypertension, cerebrovascular disease, aortoiliac disease, and mitral annular calcification. Although the other factors are well known, the association between mitral annular calcification and aortic atherosclerosis was identified only recently.

Identifying patients at risk and making efforts to minimize aortic wall trauma help reduce the chance of cholesterol embolism. The risk for a patient developing cholesterol embolism may be reduced by using a brachial or axillary approach in patients known to have severely ulcerated aortic plaque, using soft flexible catheters, and avoiding high-pressure jets of contrast material.

Chronic Venous Insufficiency

Chronic venous insufficiency (CVI) is a common condition affecting 2-5% of Americans. Historically, CVI was known as postphlebitic syndrome and postthrombotic syndrome, both of which refer to the etiology of most cases. However, these names have been abandoned because they fail to recognize another common cause of the disease, the congenital absence of venous valves.

History of the Procedure

In 1914, Homans postulated that the relative hypoxia of static venous blood decreases the amount of oxygen reaching the skin, causing skin changes and ulcers characteristic of CVI.In 1930, Landis et al demonstrated the direct relationship between venous hypertension in the legs and increased capillary intraluminal pressures.In 1953, Piulacks et al theorized that arteriovenous fistulas in the skin of the lower extremities cause hypoxia, resulting in changes to the skin and tissues.In 1982, Burnand et al presented the fibrin cuff hypothesis, which describes the primary problem as venous hypertension in the lower extremities causing leakage of plasma proteins, particularly fibrinogen. A fibrin cuff encircles affected capillaries, decreasing oxygen diffusion to surrounding tissues.In 1988, Coleridge-Smith et al described the white-cell trapping theory, which hypothesizes that venous hypertension and resultant increased capillary pressures trap white blood cells in the capillaries, where they become activated and damage capillary beds. Increased capillary permeability allows seepage of plasma proteins and fibrinogen into the interstitium, where a fibrin cuff forms, thus decreasing oxygen diffusion to surrounding tissues.

Problem

In addition to poor cosmesis, CVI can lead to chronic life-threatening infections of the lower extremities. Pain, especially after ambulating, is a hallmark of the disease. CVI causes characteristic changes, called lipodermatosclerosis, to the skin of the lower extremities, which lead to eventual skin ulceration.

Frequency

CVI is a significant public health problem in the United States. Of all Americans, estimates indicate that 2-5% have some changes associated with CVI.Approximately 24 million Americans have varicose veins. Approximately 6 million Americans have skin changes associated with CVI. Venous stasis ulcers affect approximately 500,000 people.The mean incidence for hospital admission for CVI is 92 per 100,000 admissions.

Epidemiology

Peak incidence occurs in women aged 40-49 years and in men aged 70-79 years.

Etiology

Congenital absence of or damage to venous valves in the superficial and communicating systems can cause CVI. Venous incompetence due to thrombi and formation of thrombi favored by the Virchow triad (venous stasis, hypercoagulability, endothelial trauma) also can cause CVI (see Image 1). Varicose veins rarely are associated with the development of CVI.

Risk factors associated with chronic venous insufficiency

Age: Incidence of CVI rises substantially with age.
Family history: History of deep vein thrombosis (DVT), which renders venous valves incompetent, causing backflow and increased venous pressure, is a risk factor.
Lifestyle: A sedentary lifestyle minimizes the pump action of calf muscles on venous return, causing higher venous pressure. CVI occurs more frequently in women who are obese. Vocations that involve standing for long periods predispose individuals to increased venous pressure in dependent lower extremities. A higher incidence of CVI is observed in men who smoke.

Pathophysiology

Two major mechanisms in the body prevent venous hypertension. First, bicuspid valves in the veins prevent backflow and venous pooling. DVTs commonly occur at these valves, causing irreversible damage to the valve. Second, during normal ambulation, calf muscles decrease venous pressures by approximately 70% in the lower extremities. With rest, pressures return to normal in approximately 30 seconds. In diseased veins, ambulation decreases venous pressures by only 20%. When ambulation is stopped, pressure in the vein lumen increases slowly, returning to normal over a period of minutes .

Venous hypertension in diseased veins is thought to cause CVI by the following sequence of events. Increased venous pressure transcends the venules to the capillaries, impeding flow. Low-flow states within the capillaries cause leukocyte trapping. Trapped leukocytes release proteolytic enzymes and oxygen free radicals, which damage capillary basement membranes. Plasma proteins, such as fibrinogen, leak into the surrounding tissues, forming a fibrin cuff. Interstitial fibrin and resultant edema decrease oxygen delivery to the tissues, resulting in local hypoxia. Inflammation and tissue loss result.

Clinical

Clinical manifestations include the following:

• Varicose veins: In addition to poor cosmesis, varicose veins serve as indicators of venous hypertension, the most common reason for patient complaints regarding CVI.
• Leg discomfort: Venous hypertension in muscles and fascial compartments of the lower leg from exercise and prolonged standing results in the characteristic ache of CVI. The discomfort is described as pain, pressure, burning, itching, dull ache, or heaviness in affected calves or legs.
• Nonhealing ulcers: Typically, these lesions occur around the medial malleolus, where venous pressure is maximal due to the presence of large perforating veins.
  Leg edema: Damage done to capillary basement membranes by white blood cells results in leg edema.
• Lipodermatosclerosis: These characteristic skin changes in the lower extremities include capillary proliferation, fat necrosis, and fibrosis of skin and subcutaneous tissues. Skin becomes reddish or brown because of the deposition of hemosiderin from red blood cells .

Infrainguinal Occlusive Disease

Problem

Although most patients with infrainguinal disease are treated nonoperatively, over 100,000 vascular reconstructive procedures are performed yearly in the United States alone. Unfortunately, intervention fails in up to 50% of cases within 5 years.Of the symptomatic patients under medical care, within 5 years, approximately 25% develop progressive symptoms, 5-10% require surgical intervention, and 1-2% undergo major amputation.The vast majority of patients with intermittent claudication remain stable or improve with noninvasive management. According to  Baumgartner, Schainfeld, and Graziani, 25% of patients with claudication will eventually require revascularization and only 5% will develop critical limb ischemia. Within the first year after the initial diagnosis, 6-9% of patients require intervention. Subsequently 2-3% of patients per year require intervention.Because lower extremity atherosclerosis is a marker for systemic atherosclerotic disease, these patients have significant systemic morbidities. Thirty percent of patients with peripheral artery disease die within 5 years and 40% die within 10 years.Feringa etal observed a cohort of 2,642 patients having ankle-brachial indices less than or equal to 0.9.6 They discovered that the major factors associated with mortality in this group of patientsincluded renal dysfunction, heart failure, ST-segment changes, age greater than 65 years, hypercholesterolemia, ankle-brachial index lower than 0.60, Q-waves, diabetes, cerebrovascular disease, and pulmonary disease. They also found that the use of statins, aspirin, and beta-blockers correlated with reduced 10-year mortality.

Frequency

Chronic atherosclerotic lower extremity disease is present in 20% of the population older than 55 years.Most affected persons are asymptomatic. In fact, estimates indicate that only approximately 20% of people with atherosclerotic lower extremity disease present to a physician because of symptoms. Another 20% are symptomatic but do not seek medical attention.

Etiology

Commonly accepted risk factors for both the occurrence and progression of atherosclerotic vascular disease include abnormal glucose tolerance, cigarette smoking, advanced age, hyperlipidemia, and hypertension.Certain biochemical factors have also been shown to be independent risk factors for atherosclerotic peripheral vascular disease. Such factors include increased plasma fibrinogen levels,hyperhomocysteinemia,and high-sensitivity C-reactive protein.These factors may also increase the risk of bypass graft stenosis and reocclusion.When more than one risk factor is present, the cumulative risk is often greater than individual risk factorscombined. This is especially true of cigarette smoking, which, when accompanied by another risk factor (such as hypertension or hyperlipidemia)  increases the disease risk to more than twice the sum of the individual risks.

Pathophysiology

Atherosclerotic occlusive disease With atherosclerotic occlusion of a major lower extremity artery, the limb is perfused via collateral pathways. Although this alternate pathway may be adequate at rest, it becomes inadequate as the oxygen demands of the leg musculature increase with activity. This results in calf muscle pain or fatigue, a symptom known as intermittent claudication. As the degree of atherosclerotic occlusion worsens, blood flow, even at rest, may become impaired. This may cause ischemic pain at rest, ischemic ulceration, and gangrene.

Acute arterial occlusion

Acute occlusion of peripheral arteries commonly involves the infrainguinal segment. Underlying atherosclerotic disease may result in intraluminal strictures that impair blood flow and cause acute thrombosis. Emboli typically lodge at bifurcations and, hence, tend to occlude the distal common femoral artery (the most common site, comprising 34% of all arterial emboli) or distal popliteal artery (14%). Popliteal artery aneurysms may thrombose as a result of turbulent blood flow. The clinical indications of acute occlusion of lower extremity arteries are the following :

• Paresthesias
• Pain
• Poikilothermia (coolness)
• Pallor
• Pulselessness
• Paralysis
  The anatomic level at which pulse loss occurs helps identify the location of the occlusion

Clinical

Most people harboring atherosclerotic disease of the lower extremities are asymptomatic; others develop ischemic symptoms. Some patients attribute ambulatory difficulties to “old age,” unaware of the existence of a potentially correctible problem. Symptomatic patients may present with intermittent claudication, ischemic pain at rest, nonhealing ulceration of the foot  or frank ischemia of the foot.Cramping or fatigue of major muscle groups in one or both lower extremities that is reproducible upon walking a specific distance suggests intermittent claudication. This symptom increases during ambulation until walking is no longer possible, and it is relieved by several minutes of rest. The onset of claudication may occur sooner with more rapid walking or when walking uphill or up stairs. The claudication of infrainguinal occlusive disease typically involves the calf muscles, while symptoms that occur in the buttocks or thighs suggest aortoiliac occlusive disease.

Physical

Physical examination discloses absent or diminished peripheral pulses below a certain level. Although diminished common femoral artery pulsation is characteristic of aortoiliac disease, infrainguinal disease alone is characterized by normal femoral pulses at the level of the inguinal ligament and diminished or absent pulses distally.Specifically, loss of the femoral pulse just below the inguinal ligament occurs with a proximal superficial femoral artery occlusion. Loss of the popliteal artery pulse suggests superficial femoral artery occlusion, typically in the adductor canal. Loss of pedal pulses is characteristic of disease involving the distal popliteal artery or its trifurcation.Importantly however, be aware that absence of the dorsalis pedis pulse may be a normal anatomic variant, noted in approximately 10% of the population. On the other hand, the posterior tibial pulse is present in 99.8% of persons aged 0-19 years. Hence, absence of both pedal pulses is a more specific indicator of peripheral arterial disease.Other findings suggestive of atherosclerotic disease include a bruit heard overlying the iliac or femoral arteries, skin atrophy, loss of pedal hair growth, cyanosis of the toes, ulceration or ischemic necrosis, and, after 1-2 minutes of elevation above heart level, pallor of the involved foot followed by dependent rubor.

Differential diagnoses

Pseudoclaudication

Although ischemic findings in the face of absent pulses clearly pinpoint arterial insufficiency as the culprit, intermittent claudication, even when associated with absent pulses, is not always due to arterial insufficiency.If symptoms are not always reproducible (ie, the patient sometimes has “good days” when ambulation is not limited by claudication) or if the symptoms are associated with low back pain or radiculopathy, the clinician should consider the possibility of pseudoclaudication, which occurs as a result of spinal stenosis or cauda equina syndrome.In that case, the pulse deficit may be an incidental finding of asymptomatic atherosclerosis. Noninvasive vascular

laboratory testing , lumbosacral imaging, and neurologic evaluation all may contribute to distinguishing between these possibilities.Two rather unusual conditions, venous claudication due to extensive iliofemoral venous thrombosis and chronic compartment syndrome due to calf muscle hypertrophy in athletes, result in a bursting type of pain in the calf with ambulation, which subsides slowly with elevation. In each case, the etiology is impaired venous outflow.

Atheroembolism

Patchy areas of ischemia involving the feet, especially in the presence of palpable pedal pulses, suggest the possibility of atheroembolism of plaque fragments from ulcerated, although nonocclusive, proximal atherosclerotic plaques or from thrombus lining the wall of an infrarenal aortic aneurysm.

Buerger disease

Severe ischemia of the toes with absent pedal pulses but normal proximal pulses in a man aged 35-50 years who smokes cigarettes may be the result of Buerger disease (thromboangiitis obliterans). Ischemia of the fingers may also be present. The digits are cool, moist, mottled, and sometimes have tender shallow ulcers. Migratory superficial phlebitis may occur.Collagen-vascular disease must be excluded. See the eMedicine article Buerger Disease (Thromboangiitis Obliterans).

Angiography reveals pathognomonic findings of “corkscrew” arteries. Treatment is discontinuation of smoking and good local wound care. Vascular surgery is rarely possible because of the poor quality of the distal arteries.

Complex regional pain syndromes (eg, posttraumatic pain syndromes, causalgia, mimocausalgia, Sudeck atrophy, reflex sympathetic dystrophy)

Complex regional pain syndromes (CRPSs) have been classified by the World Health Organization as CRPS II (ie, causalgia), which is associated with a demonstrable nerve injury, and as CRPS I (ie, mimocausalgia, reflex sympathetic dystrophy, Sudeck atrophy), which includes the remainder. Causalgia (ie, causos, heat; algos, pain) was first described in patients with arterial and nerve injuries sustained during the American Civil War. Both variants remain poorly understood and often misdiagnosed.

Although the exact pathophysiology is elusive, the sympathetic nervous system clearly plays a focal role. Therefore, surgical sympathectomy—perfected decades ago by vascular surgeons to manage nonreconstructible arterial disease (a common situation at the time)—was once the mainstay for treatment of the CRPSs.Although surgical sympathectomy is now mostly notable only for historic purposes, sympathetic blockade is quite effective and is commonly performed for the CRPSs. Hence, currently the treatment of CRPSs is performed mainly by pain management specialists. Nonetheless, because the vascular surgeon has always been primarily responsible for the diagnosis of extremity symptoms, it is not uncommon for patients with CRPS to report to a vascular surgeon because of extremity pain.Such pain may occur after extremity trauma but may seem disproportionate to the degree of injury.Pain may also manifest after delayed revascularization of an acutely ischemic extremity. The diagnosis is often one of exclusion and thus requires a high index of clinical suspicion. The diagnosis should be considered more strongly if severe superficial burning pain and agonizing hypersensitivity are present and are associated with vasomotor abnormalities such as edema, erythema, and hyperhidrosis. Radiographic studies may demonstrate relative and patchy osteopenia in the involved extremity.In addition to symptomatic relief, management of the CRPSs requires sympathetic blockade. This is best performed during the early, acute stage when the clinical course may be reversible. As the disease progresses, the erythema gives way to cyanotic mottling, the acute edema transforms to brawny edema, and the pain becomes unrelenting and disabling. These findings occur at approximately the third month and represent the second, or dystrophic, stage. At this point, both plain radiographs and bone scans tend to demonstrate indicative findings.Over time, disuse leads to atrophy, soft tissue fibrosis, and joint contractures. Radiographs confirm ankylosis and severe osteoporosis. This signals the third, or atrophic, stage. Note that atrophy can also occur because of intentional disuse for anticipated secondary gain. Such patients reportedly do not respond to treatment until litigation has concluded.Typically, the clinician does not even consider the diagnosis of a CRPS until the second stage. At that point, a dramatic clinical response to sympathetic blockade may confirm the diagnosis. Unfortunately, too much damage may have already occurred for sympathetic ablation to be effective and to break the vicious cycle of pain, sympathetic overactivity, and pain; the progression of the CRPS may be inexorable and irreversible.One other caveat is that in the face of coexisting arterial disease, the vascular surgeon who may attribute the Symptoms to ischemia and thereby may consider bypass should be aware that a surgical incision tends to exacerbate the pain in an extremity afflicted with a CRPS.

Intermittent claudication occurring in younger persons (from the teens to approximately age 45 y), particularly males, raises the possibility of popliteal artery entrapment syndrome.In this unusual condition, the artery follows an aberrant course around the gastrocnemius muscle, usually medial to the medial head instead of between the 2 heads of this muscle. Ambulation causes the muscle to compress the artery and results in transient loss of distal blood flow. Over time, the artery may thrombose or become aneurysmal.Prior to complete thrombosis, this condition can sometimes be confirmed clinically by noting loss of the pedal pulse upon active plantar flexion or passive dorsiflexion of the foot. CT scanning or MRI can reveal the muscular abnormality, and angiography with stress views can confirm the diagnosis.Treatment entails sectioning the aberrant muscle fibers. Bypass grafting is needed if the occlusion is chronic in nature. Assessing the contralateral side is important because one third of cases are bilateral.

Cystic adventitial disease of the popliteal artery

Intermittent claudication of abrupt onset occurring in a relatively young male also may be the result of cystic adventitial disease of the popliteal artery.This rare congenital anomaly is the result of ganglionlike cysts, perhaps from an adjacent synovium, compressing the artery. This compression may eventually lead to thrombosis of the artery.Prior to occlusion, pedal pulses may be found to disappear with flexion of the knee joint. Ultrasonography, CT scanning, or MRI may demonstrate the cyst, while angiography may demonstrate a characteristic hourglass deformity, which has been termed the scimitar sign.Cystic adventitial disease of the popliteal artery is treated surgically by removing the cyst. Vascular bypass is required if occlusion has occurred.

Fat Embolism

Background

In 1862, Zenker first described this syndrome at autopsy. In 1873, von Bergmann clinically diagnosed fat embolism syndrome for the first time.

Pathophysiology

Two theories about the syndrome exist. First, the mechanical theory states that large fat droplets are released into the venous system. These droplets are deposited in the pulmonary capillary beds and travel through arteriovenous shunts to the brain. Microvascular lodging of droplets produces local ischemia and inflammation, with concomitant release of inflammatory mediators, platelet aggregation, and vasoactive amines. Second, the biochemical theory states that hormonal changes caused by trauma and/or sepsis induce systemic release of free fatty acids as chylomicrons. Acute-phase reactants, such as C-reactive proteins, cause chylomicrons to coalesce and create the physiologic reactions described above. The biochemical theory helps explain nontraumatic forms of fat embolism syndrome.

Frequency

United States
Frequency is estimated to be 3-4%. Fat embolism is a clinical diagnosis. Many patients are likely to have a missed diagnosis because of subclinical illness or confounding injury or illness.

Mortality/Morbidity

The mortality rate is 10-20%.
Patients with increased age, multiple underlying medical problems, and/or decreased physiologic reserves have worse outcomes than other patients.

History

• Trauma to long bone or pelvis, including orthopedic procedures
• Parenteral lipid infusion
• Recent corticosteroid administration

Physical

Respiratory symptoms, signs or radiologic disease; cerebral signs without other etiologies; and petechial rash are the major criteria. A pulse that is over 110 beats/min, fever over 38.5ºC, retinal changes of fat globules or petechiae, renal dysfunction, jaundice, acute drop in hemoglobin and/or platelets, and elevated sedimentation rate are the minor criteria. One major and 4 minor criteria, plus fat microglobulinemia, must be present to formally diagnose fat embolism syndrome.

• Cardiopulmonary

1. Early persistent tachycardia may herald the onset of the syndrome.
2. Patients become tachypneic, dyspneic, and hypoxic due to ventilation-perfusion abnormalities 12-72 hours after injury.
3. Patients become febrile with high-spiking temperatures.

• Dermatologic

1. Alert clinicians may notice reddish-brown nonpalpable petechiae developing over the upper body, particularly in the axillae, within 24-36 hours of insult or injury.
2. These petechiae occur in only 20-50% of patients and resolve quickly, but they are virtually diagnostic in the right clinical setting.Subconjunctival and oral hemorrhages and petechiae also appear.

• Neurologic

1. Central nervous system dysfunction initially manifests as agitated delirium but may progress to stupor, seizures, or coma and frequently is unresponsive to correction of hypoxia.
2. Retinal hemorrhages with intra-arterial fat globules are visible upon funduscopic examination.

Causes

• Blunt trauma (associated with 90% of all cases)
• Acute pancreatitis
• Diabetes mellitus
• Burns
• Joint reconstruction
• Liposuction
• Cardiopulmonary bypass
• Decompression sickness
• Parenteral lipid infusion
• Sickle cell crisis
• Pathologic fractures

Extremity Vascular Trauma

Patients with extremity vascular traumas present daily in emergency departments (EDs) and trauma centers worldwide. While much of the current state-of-the-art information is the result of wartime observations, the incidence of civilian extremity vascular trauma is significant. A basic understanding of both blunt and penetrating injuries to the extremities and the resultant vascular abnormalities that occur with these injuries helps minimize mortality and morbidity in these patients.

History of the Procedure

Extremity vascular injuries have been documented during episodes of armed conflict as far back as the Greek and Roman civilizations and undoubtedly occurred before those eras. Extremity amputations were the most common procedure performed by military surgeons in the US Civil War and World War II. DeBakey and Simeone calculated the amputation rate from vascular injuries in World War II as greater than 40%. Amputation was primarily a means of saving the life of the soldier in an era with no antibiotics, limited surgical technology, and no critical care.

With the advance of general medical and surgical science and a concomitant improvement in military technology, the amputation rate from vascular injury in the Korean War and the Vietnam War dropped to approximately 15%. Rich and colleagues collected the vascular database information that has provided modern surgeons with an invaluable source of data that sets the standard for management of extremity vascular injury.

Problem

Civilian extremity vascular injury, as with the wartime experience, is most prevalent in cases of penetrating trauma; however, unlike the military experience, this penetrating trauma is usually due to knife wounds or low-velocity handgun injuries. Fortunately, high-velocity assault weapon injuries and explosive injuries are rare in the United States.

In many parts of the world, regional conflicts in which antipersonnel mines are used has given rise to a large population of children and civilian adults with extremity vascular and soft tissue injuries resulting in amputations. Civilian trauma surgeons expecting to render aid and services in these areas can refer to references such as Husum and colleagues’ War Surgery Field Manual to augment their knowledge of civilian wartime injuries.

Frequency

The actual frequency of extremity vascular injuries worldwide is difficult to quantify.

In the United States, it is possible to separate iatrogenic vascular injury from traumatic injury and to reference hospital discharge data for the frequency of diagnosis codes. However, this method may significantly underestimate the actual frequency based on the method used to code the diagnosis and the importance and ranking attached to the diagnosis. In many cases, government report forms only record the top 3 discharge diagnostic codes, enough to potentially miss codes due to iatrogenic injury.

With the increased interest in the United States, more precise incidence numbers may be observed in the next few years. Mattox et al and Feliciano et al have shown an increasing number of iatrogenic vascular injuries occurring in Houston over the last few decades, an observation that is probably mirrored nationwide.

Data on blunt and penetrating injury are somewhat easier to derive. In wartime circumstances, the number of injuries may be extreme. Sherif reported 224 extremity vascular injuries in 18 months during the Afghanistan War, roughly 150 per year. Fason et al reported 94 patients in 3 months (ie, approximately 376/y) on the Thailand-Cambodia border. In both studies, antipersonnel mines caused the majority of civilian extremity vascular injuries.

At a university teaching hospital in Australia, Tobin reported 10 cases per year of extremity vascular injuries; in Tbilisi, Georgia, Razmadze reported 10.5 cases per year; in Sweden, Kjellstrom and Risburg reported 8.2 cases per year; and in Oxford, United Kingdom, Magee et al reported 4.7 cases per year. Penetrating injuries, both violent and nonviolent, predominated as the causes of vascular injuries in these reviews.

In the United States, the situation is similar, although numbers are generally higher. Humphrey et al reported 12.4 extremity vascular injuries per year at a rural trauma center in Missouri; Feliciano et al reported approximately 55 lower extremity vascular injuries per year at Ben Taub General Hospital (a high-volume urban trauma center) in Houston, Tex. In both extremes, the predominant cause of injury, especially in isolated vascular injury, was due to penetrating causes. Mattox et al and Feliciano et al have also pointed out that the number of iatrogenic vascular injuries has significantly increased since 1958 as more and varied physician specialties access the vascular tree. (See Caps’ excellent article on the epidemiology of vascular injuries in Seminars in Vascular Surgery [1998] and Mattox and colleagues’ paper on epidemiological evolution of these injuries in Annals of Surgery [1989]).

Etiology

Extremity vascular injury may result from penetrating injury (eg, gunshot wounds, knife injuries), but not all penetrating injuries are violent in nature. Many penetrating extremity injuries reported in the literature are from industrial accidents (eg, nail guns) or are iatrogenic complications of vascular access procedures for other medical problems.

Blunt injuries causing vascular injury typically result from motor vehicle accidents but may include falls, assaults, and crush injuries. Fractured long bones or dislocated joints frequently increase the overall risk of vascular injury, but certain injuries (eg, posterior knee dislocation) are more likely to cause vascular injury than other injuries (eg, a Colles fracture of the wrist, which rarely results in radial or ulnar artery injury).

The worldwide increase in explosive-type injuries constitutes an emerging third modality that combines the pathology of both blunt and penetrating injury to the extremities. Terrorist bombings, civilian land mine injuries, and combat-related injuries are becoming more common, and all physicians will undoubtedly encounter these patients sometime in their career.

Pathophysiology

As noted by the preponderance of penetrating injury in the published medical literature, the vascular tree, both arterial and venous, appears to have some limited natural protection from stretching and bending, which results in fewer blunt injuries to the extremity vasculature following trauma. The smooth muscle of the arterial media protects the patient from both stretch-type injuries and minor puncture wounds, which heal spontaneously in most cases. The smooth muscle layer also offers mild protection from death due to ongoing hemorrhage.

When the arterial vessel is transected, vascular spasm coupled with low systemic blood pressure appears to promote clotting at the site of injury and to preserve vital organ perfusion better than that which occurs with ongoing uncontrolled hemorrhage. This partially explains the prehospital finding that, in the subset of penetrating trauma, limited or no fluid resuscitation until arrival at the hospital may improve patient survival and outcome.

Clinical

Worldwide, patients with extremity vascular injuries most frequently present after a penetrating injury to an extremity. In the United States, high-speed motor vehicle accidents, often with fractures or dislocations, result in the next largest group of patients. In patients with large lacerations or open wounds, persisting or increasing hemorrhage with resuscitation is an early indication of vascular injury requiring operative exploration.

Vascular injuries can be classified clinically into hard signs and soft signs of injury based on examination. Classic so-called hard signs of vascular injury include the following:

• Observed pulsatile bleeding
• Arterial thrill (ie, vibration) by manual palpation
• Bruit over or near the artery by auscultation
• Signs of distal ischemia
• Visible expanding hematoma

These signs are used to identify patients requiring surgical intervention. A finding of cool, cold, and pulseless extremities may be attributable to a low systemic blood pressure, but isolated pulse abnormalities and significant variation in pulse quality from side to side are strong indicators of underlying proximal vascular injury. Neurologic deficit, delayed capillary refill, and bony abnormalities should increase the suspicion of extremity vascular injury and the need for emergent arteriography or surgical exploration and repair.

Soft signs of vascular injury include the following:

• Significant hemorrhage found on history
• Decreased pulse compared to the contralateral extremity
• Bony injury or proximity penetrating wound
• Neurologic abnormality

Clinical examination and reexamination remain the mainstays for identifying and treating these wounds. Clinical examination and findings should determine the need for adjunctive studies such as noninvasive Doppler ultrasound and arteriography. The physical examination may be augmented by measurement of the ankle-brachial index (ABI), also referred to as the arterial pressure index in the literature. Measurement of the ABI is a standard component in the evaluation of atherosclerotic peripheral vascular disease, and its value extends to the identification of penetrating injuries to extremity vessels. Both hard and soft signs help direct the physician to the best diagnostic and treatment options for an individual patient.

Diabetic Ulcers

Background

Diabetic foot ulcers occur as a result of various factors. Such factors include mechanical changes in conformation of the bony architecture of the foot, peripheral neuropathy, and atherosclerotic peripheral arterial disease, all of which occur with higher frequency and intensity in the diabetic population. Nonenzymatic glycosylation predisposes ligaments to stiffness. Neuropathy causes loss of protective sensation and loss of coordination ofmuscle groups in the foot and leg, both of which increase mechanical stresses during ambulation.

Pathophysiology

Diabetic persons, like people who are not diabetic, may develop atherosclerotic disease of large-sized and medium-sized arteries, such as aortoiliac and femoropopliteal atherosclerosis. However, significant atherosclerotic disease of the infrapopliteal segments is particularly common in the diabetic population. Underlying digital artery disease, when compounded by an infected ulcer in close proximity, may result in complete loss of digital collaterals and precipitate gangrene. The reason for the prevalence of this form of arterial disease in diabetic persons is thought to result from a number of metabolic abnormalities, including high low-density lipoprotein (LDL) and very-low-density lipoprotein (VLDL) levels, elevated plasma von Willebrand factor, inhibition of prostacyclin synthesis, elevated plasma fibrinogen levels, and increased platelet adhesiveness. Overall, people with diabetes have a higher incidence of atherosclerosis, thickening of capillary basement membranes, arteriolar hyalinosis, and endothelial proliferation. Calcification and thickening of the arterial media (Mönckeberg sclerosis) are also noted with higher frequency in the diabetic population, although whether these factors have any impact on the circulatory status is unclear.

The pathophysiology of diabetic peripheral neuropathy is multifactorial and is thought to result from vascular disease occluding the vasa nervorum; endothelial dysfunction; deficiency of myoinositol-altering myelin synthesis and diminishing sodium-potassium adenine triphosphatase (ATPase) activity; chronic hyperosmolarity, causing edema of nerve trunks; and effects of increased sorbitol and fructose.1The result of loss of sensation in the foot is repetitive stress; unnoticed injuries and fractures; structural foot deformity, such as hammertoes, bunions, metatarsal deformities, or Charcot foot;further stress; and eventual tissue breakdown. Unnoticed excessive heat or cold, pressure from a poorly fitting shoe, or damage from a blunt or sharp object inadvertently left in the shoe may cause blistering and ulceration. These factors, combined with poor arterial inflow, confer a high risk of limb loss on the patient with diabetes.

Frequency

According to The National Institute of Diabetes and Digestive and Kidney Diseases, “an estimated 16 million Americans are known to have diabetes, and millions more are considered to be at risk for developing the disease.” Diabetic foot lesions are responsible for more hospitalizations than any other complication of diabetes. Among patients with diabetes, 15% develop a foot ulcer, and 12-24% of individuals with a foot ulcer require amputation. Indeed, diabetes is the leading cause of nontraumatic lower extremity amputations in the United States. “In fact, every year approximately 5% of diabetics develop foot ulcers and 1% require amputation.” Diabetic peripheral neuropathy, present in 60% of diabetic persons and 80% of diabetic persons with foot ulcers, confers the greatest risk of foot ulceration; microvascular disease and suboptimal glycemic control contribute. Even after successful management resulting in ulcer healing, the recurrence rate in that patient population is 66% and the amputation rate rises to 12%. Half of all nontraumatic amputations are a result of diabetic foot complications, and the 5-year risk of needing a contralateral amputation is 50%.2

Mortality/Morbidity

Limb loss: Unfortunately, limb loss is a significant risk in patients with diabetic foot ulcers, particularly if treatment has been delayed.

Charcot foot: Sensory neuropathy involving the feet may lead to unrecognized episodes of trauma due to ill-fitting shoes. Motor neuropathy, causing intrinsic muscle weakness and splaying of the foot on weight bearing, compounds this trauma. The result is a convex foot with a rocker-bottom appearance. Multiple fractures are unnoticed until bone and joint deformities become marked. This is termed a Charcot foot (neuropathic osteoarthropathy) and most commonly is observed in diabetes mellitus, affecting about 2% of diabetic persons. If neglected, ulceration may occur at pressure points, particularly the medial aspect of the navicular bone and the inferior aspect of the cuboid bone. Sinus tracts progress from the ulcerations into the deeper planes of the foot and into the bone. Charcot change can also affect the ankle, causing displacement of the ankle mortise and ulceration, which can lead to the need for amputation.
Mortality: Mortality in people with diabetes and foot ulcers is often the result of associated large vessel arteriosclerotic disease involving the coronary or renal arteries.

Race

The issue of diabetic foot disease is of particular concern in the Latino communities of the Eastern United States, African Americans4, and in Native Americans, who tend to have the highest prevalence of diabetes in the world.

Age

Diabetes occurs in 3-6% of Americans. Of these, 10% have type 1 diabetes and are usually diagnosed when they are younger than 40 years. Among Medicare-aged adults, the prevalence of diabetes is about 10% (of these, 90% have type 2 diabetes). Diabetic neuropathy tends to occur about 10 years after the onset of diabetes, and, therefore, diabetic foot deformity and ulceration occur sometime thereafter.

History

Peripheral neuropathy:

The symptoms of peripheral neuropathy include the following:

• Hypesthesia
• Hyperesthesia
• Paresthesia
• Dysesthesia
• Radicular pain
• Anhydrosis
• Peripheral arterial insufficiency

Most people harboring atherosclerotic disease of the lower extremities are asymptomatic;

others develop ischemic symptoms. Some patients attribute ambulatory difficulties to old age and are unaware of the existence of a potentially correctible problem.Patients who are symptomatic may present with intermittent claudication, ischemic pain at rest, nonhealing ulceration of the foot, or frank ischemia of the foot.

Cramping or fatigue of major muscle groups in one or both lower extremities that is reproducible upon walking a specific distance suggests intermittent claudication. This symptom increases with ambulation until walking is no longer possible, and it is relieved by resting for several minutes. The onset of claudication may occur sooner with more rapid walking or walking uphill or up stairs. The claudication of infrainguinal occlusive disease typically involves the calf muscles, while symptoms that occur in the buttocks or thighs suggest aortoiliac occlusive disease.Discomfort, cramping, or weakness in the calves or feet is particularly common in the diabetic population because they tend to have tibioperoneal atherosclerotic occlusions. Calf muscle atrophy may also occur. Rest pain is less common in the diabetic population. In some cases, a fissure, ulcer, or other break in the integrity of the skin envelope is the first sign that loss of perfusion has occurred. When a diabetic patient presents with gangrene it is often the result of infection.

Physical

Physical examination of the extremity having a diabetic ulcer can be divided into 3 broad categories:
  (1) examination of the ulcer and general condition of the extremity .
  (2) assessment of the possibility of vascular insufficiency.
  (3) assessment for the possibility of peripheral neuropathy. Remember that diabetes is a systemic disease. Hence, a comprehensive physical examination of the entire patient is also vital.

Extremity examination

Diabetic ulcers tend to occur in the following areas: 

Areas most subjected to weight bearing, such as the heel, plantar metatarsal head areas, the tips of the most prominent toes (usually the first or second), and the tips of hammer toes (Ulcers also occur over the malleoli because these areas commonly are subjected to trauma.)
Areas most subjected to stress, such as the dorsal portion of hammer toes
Other physical findings include the following:

• Hypertrophic calluses
• Brittle nails
• Hammer toes
• Tissues
• Peripheral arterial insufficiency

Physical examination discloses absent or diminished peripheral pulses below a certain level.
Although diminished common femoral artery pulsation is characteristic of aortoiliac disease, infrainguinal disease alone is characterized by normal femoral pulses at the level of the inguinal ligament and diminished or absent pulses distally.
Specifically, loss of the femoral pulse just below the inguinal ligament occurs with a proximal superficial femoral artery occlusion. Loss of the popliteal artery pulse suggests superficial femoral artery occlusion, typically in the adductor canal. Loss of pedal pulses is characteristic of disease of the distal popliteal artery or its trifurcation.However, be aware that absence of the dorsalis pedis pulse may be a normal anatomic variant that is noted in about 10% of the pediatric population. On the other hand, the posterior tibial pulse is present in 99.8% of persons aged 0-19 years. Hence, absence of both pedal pulses is a more specific indicator of peripheral arterial disease.
Other findings suggestive of atherosclerotic disease include a bruit heard overlying the iliac or femoral arteries, skin atrophy, loss of pedal hair growth, cyanosis of the toes, ulceration or ischemic necrosis, and pallor of the involved foot followed by dependent rubor after 1-2 minutes of elevation above heart level.

Signs of peripheral neuropathy include loss of vibratory and position sense, loss of deep tendon reflexes (especially loss of the ankle jerk), trophic ulceration, foot drop, muscle atrophy, and excessive callous formation, especially overlying pressure points such as the heel.
The nylon monofilament test helps diagnose the presence of sensory neuropathy.6 A 10-gauge monofilament nylon is pressed against each specific site of the foot just enough to bend the wire. If the patient does not feel the wire at 4 or more of these 10 sites, the test is positive for neuropathy.

Causes

The etiologies of diabetic ulceration include neuropathy, arterial disease, pressure, and foot deformity.

Aortoiliac Occlusive Disease

In patients with peripheral arterial disease, obstructing plaques caused by atherosclerotic occlusive disease commonly occur in the infrarenal aorta and iliac arteries. Atherosclerotic plaques may induce symptoms either by obstructing blood flow or by breaking apart and embolizing atherosclerotic and/or thrombotic debris to more distal blood vessels. If the plaques are large enough to impinge on the arterial lumen, reduction of blood flow to the extremities occurs. Several risk factors exist for development of the arterial lesions, and recognition of these factors enables physicians to prescribe nonoperative treatment that may alleviate symptoms as well as prolong life.Surgical treatment of aortoiliac occlusive disease (AIOD) has been well standardized for many years, and the outcomes are quite good. However, the additional techniques of percutaneous transluminal angioplasty (PTA) and stenting have offered more alternatives to open surgery and offer successful techniques to patients who may have been considered at an unacceptably high risk for conventional open surgical repairs. Catheter-based endovascular treatments for aortoiliac occlusive disease (AIOD) offer the advantages of less morbidity, faster recovery, and shorter hospital stays. In fact, most endovascular interventions today are simply performed as outpatient procedures. This chapter reviews the risk factors for development of atherosclerotic occlusive disease of the aorta and iliac arteries and describes the natural history, diagnosis, and treatment of the disease.

History of the Procedure

Before prosthetic grafts for aortic bypasses became available, the first direct surgical reconstructions on the aorta were performed using the technique of thromboendarterectomy (TEA), first described by Dos Santos of Lisbon in 1947.

• The initial procedure was performed on a patient with superficial femoral artery (SFA) obstruction, and Dos Santos termed the procedure disobliteration. Edwin J. Wylie, MD, adapted this technique to the aortoiliac region and, in 1951, performed the first aortoiliac endarterectomy in the United States.
•  With the discovery of suitable prosthetic graft materials for aortic replacement in the 1960s, surgical treatment of aortoiliac occlusive disease (AIOD) became available to even more patients.In 1964, Dotter first performed percutaneous iliac angioplasty using a coaxial system of metal dilators.
•  This procedure proved to have limited application due to the cumbersome nature of the device. However, Dotter’s early work paved the way for Grüntzig, who, in 1974, developed a catheter with an inflatable polyvinyl chloride balloon that could be passed over a guidewire.
•  This device became the cornerstone for the percutaneous treatment of arterial occlusive lesions today. In 1985, Julio Palmaz introduced the first stent that helped to improve the results of angioplasty for arterial occlusive disease.5 Since the advent of angioplasty and stenting, the technology has evolved at an astronomical rate. The design and quality of endovascular devices, as well as the ease and accuracy of performing the procedures, have improved. These improvements have led to improved patient outcomes following endovascular interventions for aortoiliac occlusive disease (AIOD).

Problem

Aortoiliac occlusive disease (AIOD) occurs commonly in patients with peripheral arterial disease (PAD). Significant lesions in the aortoiliac arterial segment are exposed easily by palpation of the femoral pulses. Any diminution of the palpable femoral pulse indicates that a more proximal obstruction exists. Obstructive lesions may be present in the infrarenal aorta, common iliac, internal iliac (hypogastric), external iliac, or combinations of any or all of these vessels. Occasionally, degenerated nonstenotic atheromatous disease exists in these vessels and may manifest by atheroembolism to the foot, the “blue toe” or “trash foot” syndrome.

Frequency

At least half of patients with peripheral arterial disease (PAD) have no symptoms, and, therefore, the exact incidence and prevalence of the condition is unknown. However, the incidence of PAD is known to increase with advancing age so that, by age 70 years, as many as 25% of the US population is affected. Occlusive disease involving the aortoiliac arterial segment occurs commonly in patients with peripheral arterial disease (PAD) and is second only to occlusive disease of the SFA in frequency.

Etiology

Atherosclerosis is the most common etiology of occlusive plaques in the aorta and iliac arteries. Several risk factors exist for the development of atherosclerotic plaques in the aortoiliac arterial segment. Cigarette smoking and hypercholesterolemia are observed more commonly in patients with aortoiliac occlusive disease (AIOD) as compared with infrainguinal occlusive disease. In addition, patients with aortoiliac occlusive disease (AIOD) tend to be younger and less likely to have diabetes.

An uncommon cause of aortic obstruction is Takayasu disease, a nonspecific arteritis that may cause obstruction of the abdominal aorta and its branches. The etiology of Takayasu disease is not known. For the purpose of this chapter, only occlusive lesions caused by atherosclerosis are considered.

Pathophysiology

Atherosclerosis is an extraordinarily complex degenerative disease with no known single cause. However, many variables are known to contribute to the development of atherosclerotic lesions. One popular theory emphasizes that atherosclerosis occurs as a response to arterial injury. Factors that are known to be injurious to the arterial wall include mechanical factors such as hypertension and low wall shear stress, as well as chemical factors such as nicotine, hyperlipidemia, hyperglycemia, and homocysteine.Lipid accumulation begins in the smooth muscle cells and macrophages that occur as an inflammatory response to endothelial injury, and the “fatty streak” begins to form in the arterial wall. The atheroma consists of differing compositions of cholesterol, cholesterol esters, and triglycerides. Some plaques are unstable, and fissures occur on the surface of the plaque that expose the circulating platelets to the inner elements of the atheroma. Platelet aggregation then is stimulated. Platelets bind to fibrin through activation of the glycoprotein (Gp) IIb/IIIa receptor on the platelets, and a fresh blood clot forms in the area of plaque breakdown. These unstable plaques are prone to atheromatous embolization and/or propagation of clot that eventually can occlude the arterial lumen.

If the atheroma enlarges enough to occupy at least 50% of the arterial lumen, the flow velocity of blood through that stenosis can significantly increase. The oxygen requirements of the lower extremity at rest are low enough that even with a moderate proximal stenosis, no increase in blood flow velocity occurs. During exercise, however, the oxygen debt that occurs in ischemic muscle cannot be relieved because of the proximal obstruction of blood flow; this results in claudication symptoms. In more advanced cases, critical tissue ischemia occurs, and neuropathic rest pain or tissue loss ensues. However, critical limb ischemia is seldom, if ever, caused by aortoiliac occlusive disease (AIOD) alone. Commonly, in patients with critical limb ischemia, multiple arterial segments are involved in the occlusive atherosclerotic process.

Clinical

The most common symptom of patients with hemodynamically significant aortoiliac disease is claudication. The word claudication stems from the Latin word claudicatio, to limp. The symptom complex of claudication is defined as muscle cramps in the leg(s) that occur following exercise and are relieved by resting. In any individual patient, the exercise distance at which claudication occurs is quite constant. Claudication usually occurs first in the calf muscles, although thigh, hip, and buttocks muscles also can be affected when more extensive proximal lesions are present. Location of the muscle pain (ie, calf vs thigh) does not necessarily correlate with the level of arterial obstruction. However, more proximal symptoms (ie, buttocks or thigh claudication) are generally associated with severe aortoiliac occlusive disease. Symptoms of buttock claudication can occur in association with erectile dysfunction in patients with absent femoral pulses. This constellation of symptoms is termed Leriche syndrome, named for the surgeon who described the condition in 1923. Leriche syndrome occurs when either preocclusive stenosis or complete occlusion of the infrarenal aorta is present due to severe aortic atherosclerosis. Due to the chronic nature of the occlusive process leading to development of rich collateral vessels that supply the lower extremity, limb-threatening ischemia seldom occurs.

How to Become a Vascular Surgeon

How to Become a Vascular Surgeon

There was a time when a general surgeon could perform most surgical procedures indicated in a patient’s care. Now, the field of general surgery has been greatly subdivided into a number of subspecialties. One of these is vascular surgery–surgery on blood vessels. Because blood vessels are often injured in auto accidents and gunshot wounds, vascular surgeons are often involved in the care of patients with significant trauma. Vascular surgeons deal with some of medicine’s highest drama.

Instructions

•  Maintain a high grade point average in high school. 
•  Apply to a college with a history of placing its graduates in medical school. Once accepted, maintain an even higher grade point than you did in high school. Take the Medical College Admissions Test (MCAT).
•  Begin to select medical schools to which you want to apply in your junior year of college. Apply to at least three.
•  Begin looking at general surgery residencies towards the end of your third year in medical school.
•  ”Match” with a general surgery residency. Complete the 5 year training program in general surgery. Become board certified in general surgery through the examination process of the American Board of Surgery. Apply to vascular surgery training programs.
•  Match with a vascular surgery training program through the National Resident Matching Program. Finish your one year fellowship in vascular surgery. If your fellowship does not have a second year that includes training in the newer procedures like endoscopic procedures, apply a second time for a second year of fellowship.
•  Finish your fellowship. Do another year of research if you are headed to academic medicine. Sit for the boards in vascular surgery that are offered by the American Board of Surgery.

Tips & Warnings

The process of “matching” is how medical school graduates are placed in residencies or specialists are placed in sub-specialty fellowships. An applicant applies to a number of programs and then ranks the programs according to preference. The programs do likewise with applicants. Preferences are then “matched.”Since this program of training is a minimum of 7 years after medical school, there is some discussion of shortening it–for example not requiring that a vascular surgeon be double boarded in general surgery and vascular surgery.