Health Articles

Dilated, tortuous superficial veins associated with incompetent venous valves.
Many elderly people have moderate to large varicose veins. Often the varicosities involve only superficial veins, dilated because of incompetent valves. Valvular incompetence can be secondary to chronic venous insufficiency but typically results from primary valvular degeneration, which has a strong hereditary predisposition.
Diagnosis
Primary varicose veins must be distinguished from secondary varicose veins so that the secondary causes (eg, chronic venous insufficiency ol’the deep veins) can be addressed. Primary varicose veins lack signs of stasis and have evidence of deep and communicating vein incompetence on a tourniquet test. In this test, venous filling time is recorded when the patient rises from Trendelenburg’s to a standing position. The measurement is then repeated with a tourniquet placed at various levels on the leg. All varicose veins fill rapidly in retrograde fashion. However, when the deep and communicating veins are competent (as occurs with secondary varicose veins), compression of the superficial veins impedes retrograde filling. If the deep veins are totally competent, complete venous filling after tourniquet application requires at least 45 sec.
Treatment
Primary varicose veins represent no danger, although they may lead to superficial phlebitis and may bleed easily if traumatized. Venous ligation and stripping procedures have almost no role in the care of the elderly. Surgery for primary varicose veins is only cosmetic, and recurrence is common. Elastic support is the only treatment necessary.
In secondary varicose veins, the cause rather than the varicose veins must be treated. For example, for varicose veins secondary to chronic venous insufficiency, stripping is useless because the pathogenesis of the venous insufficiency is related to hypertension in the deep venous system.

A syndrome occurring after thrombosis, involving destruction of the deep and communicating venous valves of the teg and obliteration of the thrombosed veins.
Chronic deep venous insufficiency is almost always the result of previous symptomatic or asymptomatic deep venous thrombosis, although most patients cannot recall having had episodes consistent wilh lhal disorder. Rarely, arteriovenous fistula in the leg causes chronic venous stasis, leading to chronic venous hypertension and eventual valvular incompetence. The fistula is usually caused by trauma in !he inguinal area, which may be accidental or iatrogenic (eg, after cardiac catheterization or angioplasty via the femoral vein). Since fistulas arc associated with continuous bruits, the inguinal and upper femoral areas should be auscultated in patients with chronic venous insufficiency, especially if the findings are unilateral.
Symptoms and Signs
Chronic venous insufficiency rarely causes pain. The symptoms and signs of stasis are chronic edema, which is generally worse at the end of the day; hyperpigmentation around the medial malleolus and just above it; stasis dermatitis (scaling and pruritus) and hyperemic ulcers in Ihc same area; and varicose veins.
If edema is severe and persistent, fibrosis leads to secondary lymphedema and trapped fluid. The calf becomes permanently enlarged and hard. Ulcers then occur more often and arc more difficult to heal.
Prevention and Treatment
The vicious circle of increasing edema and ulceration can be prevented by elastic support. Since elderly people often find it difficult lo bandage their legs each day, elastic stockings should be prescribed. A slocking that exerts 30 mm Hg pressure from the toes lo just below the knee is usually sufficient, especially since significant edema of the thighs is rare. Patients should elevate their legs intermittently during the day and avoid standing still for extended periods. Ambulation should not be limited. If significant swelling persists overnight, patients should sleep with Ihcir legs elevated 3 to 4 inches above heart level.
For severe edema, pumps can reduce swelling. Older models exert a uniform pressure in rhythmic fashion to the edematous leg through an encircling sheath. More advanced models exert ihc pressure in a distal-to-proximal direction, providing more efficienl venous return.
Ulcerations arc also treated by elastic support and leg elevation. Topical antimicrobial therapy (eg. povidonc-iodine) and warm soaks are indicated for infected lesions. A plaster boot oflen aids healing of large, clear ulcers. Although the boot has to be changed every I to 2 wk, this is preferable to limiting ambulation, especially in the elderly. A boot should nol be applied if the ulcer shows signs of infection.
SUPERFICIAL THROMBOPHLEBITIS
Inflammation associated with a thrombosed superficial vein.
Etiology
In > 90% of cases, superficial thrombophlebitis occurs in varicose veins (see VARICDSF VKINS, below). Stasis within Ihcsc incompelenl veins leads to dolling, which can be prevented with elastic bandages or slockings.
In some cases, phlebitis occurs without varicose veins or is recurrent and migratory. A potential harbinger of inlernal disease, this occurrence should prompt assessment for occult neoplasm, especially pan-crealic cancer; thrombocytosis or polycythemia: anlilhrombin Ml deficiency: collagen-vascular disease: presence of cryoprotein or lupus inhibitor; and protein C or S deficiency.
Symptoms, Signs, and Diagnosis
Superficial phlebitis is a more inflammatory process than is deep venous thrombosis. The usual presenting symptom is pain. Physical examination reveals an area of erythema, warmth, and tenderness overlying a palpable venous cord. The cord represents the thrombosed vein and is easily felt superficially. Often, many areas of thrombosis occur alone the course of a superficial vein, usually along a segment of the great saphenous vein at the media! aspect of the leg or at the small saphenous vein in the posterior calf.
Superficial phlebitis rarely leads to pulmonary embolism. However, pulmonary embolism can occur when a clot propagates into the femoral vein, as a result of phlebitis of the great saphenous vein propagating up Ihe thigh toward the inguinal area.
Treatment
For superficial phlebitis below the knee, treatment consists of warm soaks, decreased ambulation, and a nonsteroidal anti-inflammatory drug. The process is self-limited, and signs of inflammation usually fade within 5 to 10 days. There may be no residual findings, or Ihe patient may have a nontender cord, which represents a permanently thrombosed vein. The cord may calcify months or even years later.
For superficial phlebitis in the lower thigh, a short course of heparin is advisable. Treatment can be discontinued as soon as signs of inflammation are gone, if further propagation is not evident. If the cord reaches the upper thigh, the great saphenous vein should be ligaled at its most proximal point. This minor procedure can be performed under local anesthesia.

The presence of a thrombus in a deep vein.
Etiology
The mechanisms behind venous clotting can be classified under Virchow’s triad: factors involving the movement of blood, ihe blood itself, and the vessel wall. Since no propelling cardiac force moves venous blood, the emptying of veins in the extremities depends entirely on skeletal muscles that pump and on one-way valves in the lumen that inhibit retrograde flow. Thus, immobilization or even a relatively sedentary exislence favors venous stasis and predisposes to thrombosis. Since incompetent venous valves lead to deep venous thrombosis, which itself damages the valves, deep venous thrombosis tends to be a recurring phenomenon. Any factor that increases hematocrit leads to greater blood viscosity and a higher incidence of clotting.
Symptoms and Signs
The hallmark of deep venous thrombosis is ihe rapid onset of unilateral leg swelling with dependent edema. Generally, swelling is first noted upon awakening. An ambulatory patient has maximal swelling at the ankle and lower leg, usually occurring over 1 or 2 days. Pain maybe present but is usually not severe. Physical examination often reveals pitting edema and a mild to moderate increase in skin temperature over the calf or thigh. In patients with heart failure and deep venous thrombosis, both legs are swollen but the phlebitic one more so.
A gap always occurs between the level of thrombosis and the location of edema. With popliteal and lower femoral venous occlusion, edema involves only the lower leg and ankle. With the clot at the midfemoral vein area, most or all of the leg is swollen. With upper femoral and external iliac vein involvement, the thigh is also swollen. If present, tenderness occurs in the calf for Icmoropopl ileal and in the medial thigh for iliofemoral venous thrombosis.
Calf vein thrombosis may be asymptomatic or may involve mild tenderness and lillle or no edema. There are four (o six deep calf veins (anterior tibial, posterior tibial, and peroneal); because all of them drain into the popliteal vein, occlusion of one or two is unlikely to impair venous drainage.
Phlegmasia cerulea dolens, a serious form of iliofemoral venous thrombosis, is characterized by massive thigh and calf edema and a cold, mottled foot. Pedal pulses are usually absent, and the leg is quite tender. Findings are secondary to proximal iliac vein thrombosis and associated arteriospasm. The danger of massive pulmonary embolism is great, even if the patient is receiving anticoagulation therapy. Foot gangrene also occurs but less often. Phlegmasia cerulea dolens may be mistaken for arterial embolism, bul misdiagnosis can be avoided by keeping in mind that acute arterial occlusion does not cause edema. Phlegmasia cerulea dolens often indicates occult malignancy.
Diagnosis
The sudden onset of lower leg swelling in a gravitational distribution without trauma and a precipitating factor suggests a diagnosis of deep venous thrombosis. However, laboratory confirmation is needed if ihc onset of swelling is not clearly acute and the findings are not entirely typical.
Risk factors: In a patient with deep venous thrombosis, risk factors should be identified; the major ones arc immobilization and decreased physical activity, venous damage, obesity, heart failure, polycythemia, thrombocytosis, dehydration, malignancy, fractured hip, and estrogen use (see TABLE 42-2).
If a risk factor is obvious (eg, bed confinement or heart failure), no further evaluation is necessary for I’emoropopliteal and tibial vein thromboses. However, all patients wilh iliofemoral venous thrombosis should have an abdominal diagnostic study (ultrasonography is usually adequate) to rule out extrinsic compression by tumor and clot in the inferior vena cava. Right iliofemoral venous thrombosis is of particular concern if no local problem exisls in the right lower extremity. Because Ihc inferior vena cava is located on the right, iliofemoral venous compression related to an abdominal tumor must be suspected when thrombosis occurs on that side. The left common iliac vein, on Ihe other hand, is normally compressed by the right iliac artery and is more likely to become (hrombosed from reasons olher than tumor compression.
If a risk factor is nol obvious, especially in patients with recurrent and migratory deep venous thrombosis, other tests are indicated to look for hypercoagulable states and tumors. These generally include stool tests for occult blood; platelet count; tests for antinuclcar antibody, cryoproleins, lupus inhibitor, antithrombin III deficiency, and occasionally, protein C and protein S deficiency; abdominal ultrasonography or CT scanning; and rectal, pelvic, and breast examinations.
One clue to antithrombin III deficiency is relative resistance to heparin. Heparin acts primarily as an antithrombin by forming complexes with anlithrombin 111. When levels of antithrombin 111 are reduced, heparin’s prolongation of the partial thromboplastin time is also reduced.
Protein C is a vitamin K-dcpendent anticoagulant; patients with protein C deficiency typically develop venous thromboembolism if warfarin therapy is initiated without heparin. Vitamin K procoagulant factors need time to be reduced.
Diagnostic tests: If no swelling is present and the patient is ambulatory, deep venous thrombosis can usually be ruled out by using a tape measure to compare the circumference of the legs at several levels. The most important measurement is just above the ankles. Calf vein thrombosis without swelling is common only in sedentary or bedridden patients and is, therefore, an important consideration in Ihe nonambulatory elderly. This diagnosis can be made only through laboratory evaluation.
Although radiocontrast venography is rarely needed, it is the gold standard for confirmation of deep venous thrombosis. It provides an anatomic map of the deep venous system, from tibial veins to the common iliac vein. To ensure that the contrast material is directed into the deep rather than superficial veins, this material is injected through a dorsal foot vein with the leg in the dependent position or with a tourniquet above the ankle. Venous occlusion can be seen as a cutoff of flow or as a filling delect in the vessel, with contrast material streaming around it. In the tibial area, a sparsity of visible veins is diagnostic. Radiocontrast venography should be avoided in patients with significant renal failure (creatinine level > 3 mg/dL) and used with caution in those with mild azotemia. Passage of contrast material through the renal tubules can exacerbate preexisting renal disease. It is important to maintain good hydration, both before and 6 to 8 h after the dye study.
Impedance plethysmography can indirectly demonstrate venous thrombi by detecting changes in venous volume when a thigh tourniquet is applied and removed. If a proximal vein is occluded, the usual rapid and large increase in venous volume is likely lo be dampened when occlusive pressure is applied. Changes in venous volume are detected by applying a very low amperage eurrenl to the calf. Since blood is a good conductor, an increase in venous volume should decrease electrical impedance and, therefore, the voltage necessary lo sustain it. Failure h> decrease impedance with pressure applied by a tourniquet indicates venous thrombosis.
Plethysmography is reliable only for occlusions above the knee and those of recent onset. If a week or more has elapsed, venous return through collateral circulation leads to a false-negative result. Although controversial, the sensitivity and specificity of impedance plethysmography arc probably about 75% Tor thrombi above the knee.
Real-time ultrasonography with color Doppleris now the technique of choice for diagnosing deep venous thrombosis above the knee. The femoral vein in the inguinal area and the popliteal vein can easily be imaged. The major signs of acute thrombosis are lack of venous compressibility and a visible filling defect in the lumen. If the clot is chronic, (he vein is usually compressible and flow is seen around a partially lysed clot. This method has sensitivity and specificity rates of 95%- In general, if ultrasonography fails to reveal any clot, venous thrombosis above the knee is very unlikely.
Radionuclide venography can be performed even in patients with severe azotemia or allergy to contrast material. Macroaggregalcd albumin lagged with technetium is injected into a dorsal fool vein to outline the venous tree, and special equipment can detect filling defects. Although the tibial veins are not visualized, thrombi in the inferior vena cava can be detected. Kalse-negalive results are common, but positive results are generally accurate. Although they do not provide as much detail as conventional venography, radionuclide studies have the advantage of allowing for perfusion lung scanning and venography with one injection.
Isotopes injected IV for diagnosis of small vein thrombi, used mainly in research, have greatly increased understanding of venous thrombosis. Fibrinogen tagged with iodine 125 accumulates in areas of active clotting, indicating a hot spot in the calf. Us long half-life allows for scanning a week after a single injection. The lest is accurate only in nonedematous limbs, where the fibrinogen can follow a small clot in the soleal sinusoids until it reaches the upper tibial area. The test is cumbersome and expensive because it requires tagging the patient’s own fibrinogen to eliminate risk of viral hepatitis. It is also overly sensitive, detecting thrombi that will never become clinically significant. More recently, platelets labeled with indium 111 have been similarly used.
Differential Diagnosis
Other conditions, such as trauma, can mimic deep venous thrombosis. Traumatic edema should be suspected if the patient noted its onset during or shortly after walking. Forcefully dorsiflexing the foot on sudden downward movement can rupture the plantar tendon or injure the gastrocnemius muscle. The swelling lends to be asymmetric and confined, occurs above the ankle, is very tender, and is often associated with visible ecchymosis.
Palpation of the popliteal fossa is also important. A popliteal cyst, by extension into the calf, can cause upper leg swelling and later can compress the popliteal vein. Again, this diagnosis should be suspected if the edema develops initially during physical activity. A sonogram can easily confirm or eliminate this possibility.
Treatment
The objective is to prevent pulmonary embolism and chronic venous insufficiency.
Anticoagulation therapy: The mainstay of treatment is anticoagulation therapy, beginning with heparin and continuing with warfarin. Heparin is given s.c. q6h,IVt|4h,orby continuous IV infusion. If the continuous IV route is used, the patient must first receive a rapid infusion (bolus) of 5,000 lo IO.0(K) u. The initial infusion rate is usually 1000 u./h; thereafter, the rate is adjusted according Lo the partial thromboplastin lime, which should be kepi between 1.5 and 2.0 limes the normal control value. The partial thromboplastin time must be measured daily, since the necessary flow rate may change.
Conlinuous IV infusion offers the most flexibility in adjusting dose. Accurate infusion is critical; inadvertent increases in rate can lead to severe bleeding, and temporary interruptions of ihe infusion can lead lo inadequate anticoagulation within I h. When an IV infusion is restarted, a rapid infusion (bolus) of 5000 u. must generally be given. Recently, IV heparin 10,000 to 12,000 u. q 12 h has been found to be as effective as continuous IV The duration of heparinization is debatable, but one recommendation is 4 days for femoropopliteal thrombosis and 5 to 7 days for iliofemoral thrombosis.
Periodic platelet counts should be obtained in patients receiving heparin therapy, usually after 5 days of therapy. Heparin therapy should be discontinued if the patient develops thrombocytopenia, which occurs in about \% of patients. A small proportion of them develop arterial and venous thrombi called Ihe syndrome of paradoxical thrombosis. Although the exact mechanism of this syndrome is not clear, heparin-dependenl platelet antibodies and abnormal amounts of immunoglobulin may deposit on endothelial cells. In the laboratory, the rale at which normal platelets release serotonin increases when they are exposed lo heparinized plasma from these patients.
To avoid discontinuity in anticoagulation therapy, warfarin should be started 4 days before heparin is stopped. Factor VII, which is not involved in the intrinsic clotting pathway, is the only clotting factor significantly depressed during the first 2 days of warfarin administration. The prothrombin time should be adjusted lo a level 1.2 to 1.4 limes the normal control value (INK of 1.6 to 2.4). For uncomplicated venous thrombosis, at least .3 mo of therapy is usually recommended, bill patients at high risk for recurrent thrombosis may need extended therapy.
Patients > 70 yr (especially women) receiving warfarin therapy area! high risk for severe hemorrhage and its consequences. Vascular integrity is impaired, and even a small head injury can lead to intracranial bleeding- A small Gl hemorrhage in a patient with atherosclerosis can trigger a myocardial infarction or a stroke. Since many older people with arthritic and neurologic problems fall frequently, warfarin should generally be avoided in patients > 80 yr and frail persons > 70 yr.
Because many drugs either potentiate or inhibit warfarin, the known effects of all drugs should be reviewed before any drugs are prescribed. Fatienls should be advised to clear use of all new drugs, including OTCs, with their primary care doctor.
Inferior vena cava filter (umbrella): Patients who need an alternative to warfarin either could receive short-term heparin treatment only or after heparin therapy could have a filter (umbrella) inserted into the inferior vena cava. Umbrella insertion provides long-term protection agains! pulmonary emboli. Other reasons for umbrella insertion include (1) hemorrhage while receiving anticoagulation therapy. (2) bleeding diatheses that prevent anticoagulation. (3) phlegmasia cerulea dolens. (4) survival after massive pulmonary embolism, and (5) recurrent pulmonary embolism in an adequately anticoagulated patient.
The- umbrella is usually inserted through the external jugular vein, passed through the right atrium, and placed in the inferior vena cava just below the renal veins. If this is technically difficult or the patient already has a transvenous cardiac pacemaker, the umbrella can be inserted through a femoral vein. The umbrella acts as a plication device, preventing large pulmonary emboli. The complication rate is low. although occasionally an umbrella can loosen and migrate into another vein or even into a pulmonary artery. Although pulmonary embolism from thrombi in the legs after umbrella insertion is uncommon, it can occur after a few months when emboli travel through collateral veins.
The decision to use an umbrella depends on the likelihood of recurrence of deep venous thrombosis, the presence of pulmonary emboli, and the location of the venous clot. Tibial vein thromboses rarely em-bolize and can remain untreated in patients at high risk for hemorrhage. Iliofemoral thrombi embolize often, and an umbrella is strongly indicated if the patient cannot be placed on warfarin.
Thrombolytic therapy: Kxtcnsive clotting leads to permanent venous valvular damage and residual venous occlusion. Patients with severe iliofemoral venous thrombosis and massive edema are at particularly high risk for chronic venous insufficiency and should be considered for thrombolytic therapy (eg, streptokinase, urokinase, or tissue plasminogen activator). Although heparin prevents further clotting, it does not lyse preformed thrombi.
Since the risk of bleeding is higher with these agents, contraindications to their use (eg, a coagulopathy, recent GI bleeding, recent stroke.
history of cerebral hemorrhage, uremia, or surgical procedures within the preceding 7 days) must be considered. The older the patient, the greater the risk of hemorrhage. The risks of severe bleeding must be weighed against the morbidity of chronic, severe leg edema. Thrombolytic therapy is advisable in a small number of elderly patients. It is unlikely to be effective for clots more than 3 days old.
Streptokinase and urokinase differ. Streptokinase forms a complex with plasminogen activator, whereas urokinase directly lyses the clot. Streptokinase is occasionally associated with allergic reactions. Although urokinase can be given repeatedly, streptokinase cannot he repeated for 6 mo because it induces antibodies that cause drug resistance and increase the chance of a serious allergic reaction. Streptokinase may be ineffective following streptococcal infections.
Before starting thrombolytic therapy, heparin’s effect must be allowed to abate. The average dose of streptokinase is 100,000 u./h administered for 12 h, after a loading dose of 250,000 u. in the first hour. The patient should be monitored closely during infusion, and a hematocrit value should be obtained q 3 to 4 h. Urokinase is also administered lor 12 h, whereas tissue plasminogen activator is given for 2 h.
Serial thrombin times are used to monitor the drug’s action. Elevation of I he thrombin lime to a! least twice normal is necessary with streptokinase or urokinase. On the other hand, tissue plasminogen activator acts only within the clot and does not raise thrombin lime. If the thrombin time cannot be raised, thrombolytic therapy should be stopped and heparin restarted for two reasons: (I) No rise in thrombin time means that no fibrin split products are being formed, which means that no clot lysis is occurring. (2) Without an elevation in thrombin time, the patient is not anticoagulated and is at high risk for pulmonary embolism.
Prophylaxis
Because of the high incidence of deep venous thrombosis (usually asymptomatic) in certain clinical situations, prophylaxis is of considerable interest. Studies with fibrinogen I 125 show a 20% to 25% rate of deep venous thrombosis in routine postoperative patients > 40 yr. Similar rates are found in immobilized patients with myocardial infarction or heart failure. After hip surgery, the incidence of deep venous thrombosis approaches 50%. Several methods of prophylaxis are available for high-risk patients.
Low-dose heparin is the most widely used. The usual dose is 5000 u. s.c. q 8 to 12 h. Significant bleeding is rare at this dosage. Controlled studies show the risk of both deep venous thrombosis and pulmonary embolism is significantly decreased in surgical patients > 40 yr. Heparin is conimindicated in patients who undergo ophthalmologic or neurosurgical procedures. Low-dose heparin is of limited prophylactic value in patients who undergo orthopedic procedures involving the extremities. Full-dose heparin or warfarin is effective in these cases, although each carries a significant risk of hemorrhage.
Oscillating boots applied to the calves are another, even safer, method of prophylaxis. A pump rhythmically inflates the boot to between 30 and 40 mm Hg and then deflates it, thus keeping the peripheral veins drained. Results are comparable to those of low-dose heparin but without risk of bleeding. Galvanic stimulation of calf muscles, begun intraoperalively and continued until the patient is ambulatory, is also quite effective.
Low-molecular-weight dextran may be used in some high-risk patients to prevent venous thrombosis. Us strong antiplatelet effects decrease both aggregation and adhesiveness. However, it is also a volume expander, and expansion can lead to fluid overload in patients with borderline cardiac or renal status. Dextran is also associated wilh acute renal failure and allergic reactions. Thus, il does not seem suitable for general use.
Even when other prophylactic measures arc taken, appropriate mobilization must be accomplished. Patients should be mobilized as quickly as possible and encouraged to move their legs frequently while in bed. Prolonged bed rest poses many risks in addition to deep venous thrombosis and pulmonary embolism.

Venous diseases include deep venous thrombosis, chronic deep venous insufficiency, superficial thrombophlebitis, and varicose veins.

Cutaneous ischemia or local areas of cyanosis or necrosis in a hand or fool with generally adequate circulation.
Ischemia in a foot or hand with palpable pulses suggests a number of diagnosiic possibilities in the elderly: cryoglobulinemia, cryofibrino-genemia. disseminated intravascular coagulation, essential thrombo-cylosis, polycythemia, vasculitis secondary to drug-induced systemic lupus erythematosus, presence of the lupus anticoagulant, scleroderma, or emboli from an arterial aneurysm, the heart, or atheromatous plaques.
Symptoms, Signs, and Diagnosis
Patients usually present with a cyanotic or gangrenous digit and may have many small lesions on several extremities. Occasionally, an entire fool or hand is cyanotic or exhibits dependent rubor. Patients with peripheral atherosclerosis and pulseless limbs must also be evaluated for small-vessel syndrome if cutaneous ischemia suddenly and inexplicably worsens or if they develop local areas of cyanosis or necrosis but the rest of the foot or hand is adequately perfused. This evaluation is particularly important when a hand is involved because severe ischemia is uncommon in the upper extremities, even if atherosclerosis is advanced.
A thorough history is important. Drug use (eg, procainamide, hydralazine, and phenytoin) may induce systemic lupus erythematosus; other findings may include arthralgias and pleural effusion. Weight loss and other symploms of anorexia may suggest a malignancy responsible for eryofibrinogenemia or disseminated intravascular coagulation. Back pain may point to multiple myeloma responsible for cryoglobulinemia. Acute gangrene with fever may suggesl septicemia, leading to cryofibrinogenemia or disseminated intravascular coagulation. Splenomegaly may point to essential thrombocytosis, a megakaryocyte myeloproliferative disease generally characterized by digital or cerebral ischemia but sometimes involving abnormal bleeding. A history of myocardial infarction should prompt suspicion of a ventricular aneurysm.
Physical examination should include a search for abdominal, femoropopliteal, and subclavian aneurysms (see Ch. 43). Popliteal aneurysms are most notorious for shedding small emboli and should be considered if ischemia is confined to one foot. Atrial fibrillation and a dyskinetic lefl ventricular impulse suggest the heart as a possible source of emboli.
Laboratory evaluation should include a CBC wilh platelet count, a coagulation screen, and tests for cryoproteins, antinuclear antibodies, and the lupus inhibitor. Lupus inhibitor is a misnomer; most patients wilh this protein do not have systemic lupus erythematosus, although the lupus inhibitor is found in about 10% of patienls with the disease. The protein, an immunoglobulin that interferes wilh phospholipid-dependent coagulation tests, binds to phospholipids that accelerate the activation of prothrombin to thrombin by factor Xa. Administering normal plasma does not correct the defect. Venous and small arterial thrombi occur in 27% of patients with tr.e lupus inhibitor. The mechanism of thrombosis is unknown, but inhibition of prostacyclin synthesis is a possible factor.
An echocardiogram should be performed if mitral valve disease or ventricular aneurysm is suspected, and a sonogram of line aorta and popliteal arteries may be necessary to rule out a pulsatile mass. The diagnosis of atheromatous emboli (fracturing of plaques) is reached by exclusion. Occasionally, this cntily presents with the appearance of livedo reticularis (a lacy network of cyanotic-looking superficial vessels on the anterior side of the leg), but a lupus syndrome must still be ruled out.
Treatment
Aneurysms must be surgically repaired. Cardiac embolism is an indication for chronic anticoagulation therapy with warfarin. Atheromatous emboli are treated with antiplatelet drugs, including aspirin.
Appropriate therapy for patients with the lupus inhibitor has not been established, although both antiplatelet drugs and anticoagulation therapy have been advocated. Recent evidence suggests that only warfarin, at the level used for treating cardiac embolism, is effeclive.
RAYNAUD’S PHENOMENON
A syndrome of peripheral vasospasm with intermittent cutaneous pallor or cyanosis.
Symptoms and Signs
Exposure to cold lypically causes blanching and then cyanosis of Ihe hands, feet, and sometimes the ears and nose. An erythematous phase follows upon entering a warm environment. These episodes can be painless or associated with varying degrees of pain, numbness, and sense of coldness. Many older persons experience only a blanching or cyanotic phase, which may develop even when the ambient temperature is not very cool. Patients lend to have cool hands and feel even in a warm environment. If the problem is severe or of long duration, sclero-dactyly may occur.
Diagnosis
Symptoms are usually unilateral if Raynaud’s phenomenon is the rc-suft of previous frostbite or a thoracic oullel syndrome; otherwise Raynaud’s phenomenon after age 40 is almost always a harbinger of internal disease. Secondary causes include hypothyroidism, drug-induced systemic lupus erythematosus, cryoglobulinemia, cryoi’ibrino-genemia, cold agglutinin disease, scleroderma, and CREST syndrome (calcinosis, Raynaud’s phenomenon, esophageal dysfunction, .vclero-dactyly, telangiectasia).
Raynaud’s phenomenon is a helpful clue to Ihe diagnosis of hypothyroidism, which must be considered even if other symptoms are lacking. Patients with scleroderma, systemic lupus erythematosus, and cryo-proteinemia may present with infarcted digits. A cryoprotein mandates evaluation for occult malignancy. Patienls with cold agglutinin disease often have a low-grade lymphoma.
Almost all patienls with scleroderma have Raynaud’s phenomenon, which can precede all other manifestations by many years. Sclero-dactyly is not diagnostic of scleroderma; diagnosis requires skin tightening in areas other than Ihe hands and feet or visceral involvement (see SCLERODERMA in Ch. 75).
Treatment
In general, treatment of Raynaud’s phenomenon per se should be conservative in the elderly. Cardiovascular reflexes are often impaired, and subclinical coronary and cerebrovascular disease may be present. Therefore, patients respond intensely to vasodilators and can develop orthostatic hypotension with serious consequences. Yet, nifedipine 10 mg orally tid is usually safe and effective. Griseofulvin 250 mg orally bid may also be helpful. Ketanscrin, a selective 5-hydroxytryptamine2 receptor antagonist, was reported to be beneficial in one large study, but the drug is not yet available in the USA. However, most patients do well enough by wearing warm clothing, avoiding extreme cold, and not smoking.
Patients with scleroderma should usually be treated more vigorously because attacks of Raynaud’s phenomenon are associated with reversible decreases in renal and cardiac blood flow and with echocardiography evidence of impaired myocardial contractility. If the patient is also hypertensive, an angiotensin converting en7yme inhibitor, which promotes renal as well as peripheral blood flow, is an excellent choice for therapy.

Occlusion of blood supply to the extremities by atherosclerotic plaques (atheroma).
Progressive atherosclerosis in the extremities is a very common, age-related disease that parallels the development of atherosclerosis in the coronary and cerebral vessels. The pathologic process, beginning many years before clinical findings are apparent, is slow and insidious. Almost 70% of a vessel’s lumen must be occluded before the disease can be clinically recognized. Atherosclerosis involves the legs much more extensively than the arms, and symptoms are usually confined to the former.
Etiology and Pathophysiology
The risk factors for peripheral atherosclerosis, similar to those for atherosclerosis elsewhere, include cigarette smoking, diabetes mel-litus, hyperlipidemia, hypertension, polycythemia, family history, homocystinuria, and in women, early hysterectomy or ovariectomy. Diabetes and smoking arc particularly important.
Since the chief determinant of blood viscosity is the hematocrit, any condition (eg, polycythemia) that increases the hematocrit increases the resistance to blood flow and shearing force against vessel walls. This causes injuries lo the intima into which platelets and lipids move and thus form atheromas. Poorly controlled diabetes mellilus also leads to intimal injury and the buildup of atheromas. Low estrogen levels, whelher from ovariectomy or menopause, hasten atheroma formation. The lipid-lowering effects of estrogen are one important reason why postmenopausal women who have no contraindications should receive estrogen replacement therapy.
How smoking damages the arteries is still unclear, but carbon monoxide and the metabolites of smoke components probably have a toxic effect on the intima. Because nicotine is a direct arterial vasoconstrictor, damage may be heightened when distal blood flow is restricted. Even after peripheral atherosclerosis becomes clinically evident, continuing to smoke accelerates arterial deterioration. In fact, the incidence of limb amputation is 10 limes higher in those who continue to smoke after developing arterial occlusion than in those who quit.
Symptoms and Signs
The cardinal and most specific symptom of peripheral atherosclerosis is intermittent claudication: pain, tightness, or weakness in an exercising muscle thai occurs on walking and is relieved promptly (in < 5 min) by rest. The pain is mosl often described as "squeezing." It results from muscle hypoxia, its coronary counterpart being angina pectoris. If (he femoropopliteal artery is occluded, pain almost always occurs in the calf; if the aortoiliac arlery is occluded, pain usually occurs in the hip and buttocks. By definition, claudication never occurs while sitting or standing still. Most important, claudication forces the person to halt; walking eilher is too painful or results in loss of muscle function and a fall.
The distance at which claudication occurs may change over time but tends to be remarkably constant from day to day if external conditions arc unchanged. Cold and windy weather, inclines, and rapid walking shorten the distance at which claudication occurs. Using canes or crutches does not improve walking distance, since muscle function is normal until hypoxia occurs. With mild claudication, a person may walk up (o six blocks without stopping, hut the usual distance is less than ihree blocks and, in severe cases, may be only a few yards.
Less specific symptoms of peripheral atherosclerosis—numbness, paresthesias, coldness, and pain on rest—relale to the foot's cutaneous circulation. Numbness and paresthesias may also be caused by concomitant diabetic neuropathy. However, foot or loe numbness that occurs on walking suggests arterial disease and can be likened to claudication. It results from maximal vasodilation of muscle arterioles, wilh stealing of blood flow from the skin.
A sense oi coldness may be secondary to vasoconstriction rather than to arterial occlusion and is very common in the elderly. A recent increase in coldness, coldness in only one limb, or coldness that persists after a night's sleep suggests arterial insufficiency. Foot pain at rest is a dire symptom, indicating lhat blood flow capacity is reduced to < 10% of normal: il must be evaluated and treated immediately. The pain is paresthetic and burning, most severe distally, and typically worse a( night, preventing sleep. Partial relief is often possible with the foot in the dependent position (ie, below heart level). Pain from ischemia must be distinguished from other causes; for example, the pain of diabetic neuropathy may be similar but is generally bilateral and extends above the feet.
Claudication is the earliest symptom in a patient accustomed to walking. However, some elderly people are relatively sedentary and rarely walk far enough to have claudication; therefore, they present later with foot pain at rest or even gangrene. Gangrene represents necrosis of tissue. It first appears as nonblanching cyanosis (ecchymosis), followed by blackening and mummification of the involved part. In diabetic or other patients with peripheral neuropathy, dependent rubor and subsequent gangrene may occur without pain.
Because older people usually have many areas of occlusion, they are unlikely to have Leriche's syndrome (localized aortoiliac occlusion), in which the distal vessels arc usually patent and the feel are healthy. Patients with Leriche's syndrome have hip claudication and impotence secondary lo hypotension in the internal iliac arteries. Elderly patients wilh aortoiliac disease generally also have femoropopliteal and tibial occlusions, so dislal flow may be seriously impaired. Leriche's syndrome should be considered in the differential diagnosis of impotence in the elderly; however, older patients wilh Leriche's syndrome may be bothered more by claudication.
Diagnosis
Examination of the peripheral pulses is key lo confirming the diagnosis of peripheral atherosclerosis. The posterior tibial pulse is always present in healthy persons, although il may be difficult to feel if the patient has edema or prominent malleoli. It is besl palpated with the patient supine and (he examiner on the same side as the pulse. Meticulous palpation under the medial malleolus is necessary: dorsiflexing and everting the fool slightly may help move the artery into a more superficial position.
The dorsalis pedis artery extends along the dorsomedial aspect of the foot and is frequently subject to vasoconstriction: its pulse is absent in about 5% of healthy persons. The lateral tarsal pulse can occasionally be felt lateral to this artery.
The popliteal artery is generally the most difficult to palpate; the patient should be supine and relaxed, wilh the knee slightly flexed. The artery may be located posteriorly, laterally, or medially in the popliteal space. Very deep palpation may be necessary in obese persons.
Measurement of pulse strength is subjective and depends on the pulse pressure, girth of the extremity, and patient age. as well as on Ihe sensitivity of the examiner. If an arlery remains patent, its pulse lends to become more prominent with aging because Ihe media loses smooth muscle and elastic tissue, predisposing lo ectasia. The upstroke of the pulse wave is more important than Ihe amplitude. Bruits heard over the femoral arteries indicate aortoiliac disease.
When the presence or strength of a peripheral pulse cannol be determined clinically, Doppler ultrasonography can be used to assess arterial patency. However, a Doppler signal does nol prove lhat pulsatile flow is adequate; a signal may be perceived when the vessel's systolic blood pressure is as low as 30 mm Hg. For a Doppler study to be satisfactory, a blood pressure cuff musl be used to measure syslolic pressure (pressure above which the signal cannot be detected). For this purpose, a normal-sized arm cuff can be placed just above the ankle. Wide cuffs can be used to measure thigh pressures, which may be falsely elevated because of difficulty in occluding the femoral artery. The Doppler instrument is placed over the artery to be tested (usually the posterior tibial or dorsal is pedis artery). The clinician must search carefully lor a Doppler signal before assuming a zero blood pressure.
The Doppler measurement is also useful in evaluating arterial insufficiency in a pulseless limb (eg. by determining the ankle-brachial index). In healthy limbs, this index should not be < I, although an index > 0.6 indicates but does not prove adequate resting blood flow to the foot. In some cases of mild arterial disease, the ankle-brachial index may be about 1 because of cuff artifact or peripheral vasoconstriction in the involved leg. Reehecking the blood pressure at the ankle after exercise is helpful. Because vasodilalion occurs after exercise, blood pressure will fall if the proximal artery is occluded; the magnitude and duration of the fall after exercise correlate with the degree of arterial insufficiency. In addition, many elderly and diabetic patients have heavily calcified arteries that are difficult to compress, thereby making ankle pressure appear falsely high. Thus, foot viability must never be based solely on a Doppler measurement; examination of the foot is essential. Other techniques for assessing the degree of ischemia (eg. plethysmography or percutaneous oxygen electrode measurements after transient arterial occlusion) require a great deal of expertise.
Temperature differences between the toes of each foot and color changes are particularly important. The fool should be elevated above heart level for 20 sec to determine whether pallor develops. A severely ischemic foot may appear pale even when horizontal. With the foot in the dependent position, pallor lasting for > 30 sec or rubor (a homogeneous, violaceous color, which may require I to2min to reach its maximum) appearing after 20 sec indicates < 10% of normal blood flow capacity. Rubor is more pronounced in the toes and extends proximally for various distances. Both prolonged pallor and rubor, well correlated with pain on resting, are grim signs. More extensive obi iterative disease may compromise tissue viability and lead to skin ulceration or frank gangrene, particularly of the toes, heels, and lateral malleoli.
In evaluating persons with atherosclerosis, serum lipid levels should be measured. A full lipid profile, including total cholesterol, HDL. LDL, and triglyceride levels, should be obtained in the fasting state. Measuring the tolal cholesterol level alone is inadequate because some persons will have normal levels of total cholesterol but abnormal levels of the other lipid parameters (see Ch. til).
Treatment
Treatment is based on disease severity as determined from history, physical examination, and the patient's general condition. Patients can be categorized into three broad groups: (I) those who are asymptomatic, (2) those who have only inlermittcnt claudication, and (3) those who have significant foot ischemia, with or without claudication.
Asymptomatic patients: Most patients with peripheral atherosclerosis, including the elderly, have no symptoms; collateral vessels adequately perfuse their feet. Many patients > 70 yr have weak or missing pedal pulses but have no difficulty with their extremities unless they experience an infection, trauma, or thermal injury, which may cause serious problems because a marginal circulation cannot meet the increased metabolic demands of the tissue. Therapy consists primarily o\’ preventive measures (see TABLE 42-1).
Patients with intermittent claudication: Medical therapy is somewhat limited in patients who have intermittent claudication. They should be given foot care instructions (see TABLE 42-1) and advised to avoid smoking, to lose weigh! if necessary, and to walk ;\s much as possible. As soon as they experience claudication, they should rest and then continue walking. In a small bul significant number of patients who follow these instructions, symptoms ameliorate within the first 3 rno.
Results of drug therapy for claudication are mixed. Vasodilators have been ineffective. Pentoxifylline, the first of a new class of drugs approved for treating claudication, decreases blood viscosity and improves red blood cell flexibility, leading to improved blood flow through arterioles and capillaries. In a double-blind, controlled study, subjects increased mean walking distance by about 50 m. However, clinical results have been disappointing. The recommended dose is 400 mg orally lid.
Questions have been raised about using β-adrenorgic blocking agents in patients who have both coronary and peripheral atherosclerosis. Except for β-blockers that have intrinsic sympathomimetic activity, these drugs are mild peripheral