4 What causes a weaker and delayed pulse in the left arm as compared to the right?

It depends on the patient’s age: in younger individuals, it is usually coarctation, in the elderly, it is instead an atherosclerotic obstruction or a dissection of the aorta. Depending on the level of obstruction, asymmetry and delay in pulses may only affect the lower extremities. Hence, the need to examine all peripheral pulses, especially in symptomatic or hypertensive patients. A pulse asymmetry can be confirmed by comparing systolic pressure of the two arms or by comparing that of lower extremities to upper extremities.

5 What is Raynaud’s phenomenon?

An exquisite sensitivity of hands and fingers to cold, but also to smoking and emotional stress. Upon exposure to the trigger, fingers exhibit a typical “triple response,” which very appropriately for Raynaud follows the colors of the French flag: initial pallor and blanching (white), followed by cyanosis (blue), and finally by rubro (red). Eventually, the fingers slowly return to their baseline color. Numbness, tingling, or pain accompanies this response. The white-blue-red response may at times be out of sequence, with patients exhibiting a blue-white-red response or even single-color responses (only blue or white).

6 What causes Raynaud’s phenomenon?

A spasm of the digital arteries, resulting in ischemia of the fingers, with pallor at first and cyanosis later (due to increased oxygen extraction from trapped and noncirculating erythrocytes). The final stage of redness coincides with the reperfusion that follows release of the arterial spasm. This also is the phase mostly characterized by numbness or pain (a bit like the numbness and pain experienced in legs that have “fallen asleep”). Severe vasospasm may even lead to infarction and dry gangrene.

7 How can Raynaud’s phenomenon be artificially triggered?

By immersing the patient’s hand in a bucket of iced water.

8 What is the clinical significance of Raynaud’s phenomenon?

It can precede several important disorders, including:

9 Who was Raynaud?

Maurice Raynaud (1834–1881) was one of the great 19th-century French physicians. The son of a university professor, he graduated in Paris at age 28 with a thesis describing his famous syndrome, which made him an instant celebrity. An excellent clinician and a beloved teacher, he also was passionately interested in literature, history, and the arts. In fact, all his life he sought the chair of Medical History at the University of Paris, but he died before this could come through. His contributions to medical knowledge included the book Medicine in Molière’s Time and an article on the Greek physician Asclepiades of Bithynia (an opponent of Hippocratic medicine and the unrivaled authority of his times, who treated celebrities like Cicero, Crassus, and Marc Antony). In 1881, Raynaud wrote an address to the International Medical Congress of London titled “Skepticism in Medicine, Past and Present,” but died before delivering it.

10 What is Allen’s test? What does it mean?

It is a bedside test for patency of the deep palmar arch and of radial/ulnar arteries (Fig. 22-5). Hence, a good way to learn about the risks of radial artery puncture and/or cannulation.

Figure 22-5 Allen’s test.

(From James EC, Corry RJ, Perry JF: Principles of Basic Surgical Practice. Philadelphia, Hanley & Belfus, 1987.)

11 Isn’t the test conducted by simultaneously compressing the ulnar and radial arteries?

Yes, it may be. This is, in fact, a variant of the Allen’s test, conducted as follows (see Fig. 22–5):

12 How do you report the results of an Allen’s test?

By indicating (1) the name and side of the artery compressed (for example, RR for right radial) and (2) refill time expressed in seconds. Thus a RR5/RU3 means that it took 5 seconds to refill the capillary bed of the right palm after releasing the right radial artery, and 3 seconds after releasing the right ulnar artery. Arteries with >15 seconds refill time should not be cannulated. Instead, the contralateral hand should be instrumented.

13 Who was Allen?

Edgar V. Allen (1900–1961) was an American physician. A native of Nebraska and a graduate of that state’s university, Dr. Allen eventually moved to the Mayo Clinic, where in 1947, he became professor of medicine. His contributions include the clinical use of coumarin anticoagulants and a landmark textbook of peripheral vascular diseases.

14 Can peripheral pulses be absent in normal individuals?

Yes. Dorsalis pedis and tibialis posterior are undetectable in 10% of healthy subjects. Congenital loss of one of the arteries usually leads to compensatory increases in the other. Still, only fewer than 2% of healthy subjects lack both pedal pulses. Hence, this is usually an important clue to the presence of peripheral vascular disease (see question 16).

15 What is peripheral vascular disease (PVD)?

An obstructive condition of the lower extremity arteries, also referred to as peripheral arterial disease. Usually caused by atherosclerosis, it affects 8–12 million Americans, with a steadily growing incidence. Although one half of all patients never experience symptoms, the condition represents a risk marker for many other diseases, such as diabetes, hypertension, coronary artery disease, cerebrovascular disease, and aneurysms. Hence, PVD patients have a fourfold to sixfold increase in cardiovascular mortality.

16 What are the symptoms of PVD?

Mostly symptoms of arterial insufficiency, such as exertional limb weakness, resting limb pain (or paresthesia), and poor healing of sores or ulcerations. The classic symptom, however, is claudication (from the Latin term for limping)—i.e., intermittent limb pain, usually triggered by activity. This affects different parts of the lower extremity, depending on which artery is compromised. Yet, whether obstruction is high or low, both pedal pulses are absent in PVD, an important diagnostic clue (see Table 22-1).

Table 22-1 Symptoms of Peripheral Vascular Disease

17 What are the physical findings of PVD?

(1) Decreased or absent pulses (as previously indicated); (2) atrophic changes in the foot (such as loss of hair, discoloration of skin, decreased warmth, impaired nail growth, pallor following elevation, and rubor following dependency); (3) vascular bruits (over the involved artery—iliac, femoral, or popliteal); and (4) increased venous filling time.

18 Can these findings predict severity of the disease?

No. Vascular bruits and other signs only indicate presence of disease; they do not correlate with severity. For severity, the standard assessment is the ankle-to-arm systolic pressure index (see Chapter 2, questions 117–119). Still, in diabetic patients with significantly abnormal ankle–brachial indexes, the following symptoms/signs predict more severe disease: (1) age greater than 65, (2) history of peripheral vascular disease or claudication in less than one block, (3) diminished foot pulses, and (4) venous filling time longer than 20 seconds.

19 What is an increased venous filling time?

It is the abnormally slow (re)filling of foot veins in peripheral vascular disease. To test for it:

20 What is a capillary refill time (CRT)?

A generally accepted bedside method for assessing peripheral perfusion. To test for it:

Still, these figures have little scientific foundation. In fact, CRT is often longer in women, the elderly, a cold environment, and poor ambient lighting. Hence, a normal CRT indicates good peripheral perfusion, but a prolonged one must be interpreted in view of other parameters, such as sex, age, blood pressure, heart rate, cardiac output, and level of consciousness.

21 What is the Buerger’s test?

Another bedside maneuver for assessing arterial perfusion to the leg. It consists of examining the color of the patient’s leg: first when elevated and then when lowered. Hence, it consists of two stages (Table 22-2). The test is considered positive for PVD when it elicits excessive pallor with elevation and intense rubor with dependency.

Table 22-2 Buerger’s Test

22 How accurate is physical examination for diagnosing PVD?

McGee and Boyko compared various findings to the gold standard of ankle-to-arm systolic pressure index (AASPI) and found the following signs to be useful and independent predictors of PVD: (1) abnormal pedal pulses, (2) femoral arterial bruit, (3) prolonged venous filling time, and (4) unilateral limb coolness. These also were independent of age, atherosclerosis risk factors, sex, and claudication. Other traditional findings, such as trophic changes of the nails and skin and prolonged capillary refill time, were instead less useful.

23 Is there any finding that argues against the presence of PVD?

Bilateral presence of pedal pulses. Still, beware that as many as one third of PVD patients may have palpable pedal pulses (see question 25).

24 How accurate is physical examination for diagnosing the distribution of PVD?

Quite accurate. More specifically, findings can predict different levels of obstruction (Table 22-3). Thus, abnormal pedal pulses, a femoral arterial bruit, prolonged venous filling time, and a unilateral cool limb predict the presence of vascular disease. Abnormal femoral pulse, iliac bruits, limb bruit, Buerger’s test, and warm knees predict instead its distribution. Moreover:

25 What are the limitations of physical exam in evaluating PVD?

26 To what lower extremity complications are diabetics uniquely predisposed?

Mostly infections and neuropathic manifestations (such as ulcers and Charcot arthropathy), both resulting in longer hospitalization and higher mortality. In fact, the “diabetic foot” is the second most common cause (after trauma) for amputation.

27 What are the predisposing factors?

Definitely atherosclerotic disease, not only of large and medium-sized arteries (aortoiliac and femoropopliteal), but also of infrapopliteal vessels, to which diabetics are uniquely prone. Still, the most important factor is peripheral neuropathy, with loss of muscular coordination and protective sensation, favoring mechanical stress during ambulation.

28 How common is peripheral neuropathy in diabetics?

Very common. Prevalence is 25% after 10 years of disease and 50% after 20 years.

29 What are the characteristics of this neuropathy?

A typical stocking-and-glove distribution, presenting initially with paresthesias (or dysesthesias), and eventually progressing to complete anesthesia. As a result of their inability to sense pressure, every year 2.2–5.9% of diabetics develop a diabetic foot ulcer. Especially afflicted are Latinos and Native Americans, among whom the disease is rampant. Hence, the need for early identification of patients at risk, since prompt and meticulous foot care reduces rates of lower extremity amputation by about 50–80%.

30 What is the best way to recognize peripheral neuropathy in diabetics?

Nerve conduction studies have long been the gold standard, but they can be time consuming, expensive, and impractical in primary care settings. Conversely, more traditional bedside screenings (loss of vibratory and position sense) are inaccurate, since many diabetics with neuropathy can still sense a cotton wisp, a pinprick, or a tuning fork. Loss of deep tendon reflexes (especially the ankle jerk), foot drop, and muscle atrophy can surely help the diagnostic process, but are often late events. Hence, the bedside standard is the Semmes-Weinstein (SW) monofilament test, which provides a simple and inexpensive tool for identifying patients at risk for diabetic ulcers.

31 What is the Semmes-Weinstein (SW) monofilament test?

A maneuver designed to test protective sensation in the foot. It measures patients’ ability to sense light touch by using a nylon probe (the SW monofilament). This comes in three sizes (4.17, 5.07, and 6.1), which buckle respectively at a constant pressure of 1, 10, and 75-g force. Birke and Sims examined all three types in 28 patients with diabetes and 72 with Hansen’s disease, and concluded that inability to sense a 10-g force pressure (exercised by a 5.07 filament) is a valid and independent predictor for the risk of foot ulceration. Hence, both the International Diabetes Federation and the World Health Organization recommend that 5.07/10-g SW monofilament tests are regularly carried out in diabetics.

32 How is the test conducted?

By having the patient lie supine with closed eyes, and then pressing the filament against a specific site of the foot, with just enough force to bend the wire for 1 second.

33 When is the test considered positive for neuropathy?

When the patient cannot feel the filament at >4/10 sites. Yet there is no real consensus on how to best use the filaments, or even how to interpret the results. In fact, studies have often relied on a different number of testing sites (from 1 to 10) and different criteria for determining protective sensation. Not surprisingly, specificity and sensitivity also have differed. Still, a recent report by Lee et al. used SW monofilament tests on 10 sites, and then evaluated the diagnostic value of each site and their combinations. They found the test to be very sensitive and specific. More importantly, they found that sensitivity and specificity at the third and fifth metatarsal heads were comparable to those of 10 sites taken together. Hence, the inability to sense touch over the plantar aspects of third and fifth metatarsals has equivalent diagnostic value to that of sensing touch in more than four of the 10 traditional test sites (with sensitivity and specificity of 93.1% and 100%, respectively). Thus, a two-site SW monofilament test is as clinically valuable as a 10-site test in screening for diabetic neuropathy. Although limited in its ability to quantify the severity of the disease, this test is simple, cost effective, and practical.

34 How do you separate an ischemic from a neuropathic (diabetic) foot ulcer?

Both occur over toes and trauma sites (especially areas with diminished sensation in diabetics). Yet, neuropathic ulcers usually have a callous rim, no pain, and little gangrene. Instead, they have evidence of neuropathy (decreased sensation and absent ankle reflex), but not necessarily other signs of peripheral vascular disease.

35 What about ulcers of chronic venous stasis?

Their hallmarks are (1) location (perimalleolar area of the inner ankle) and (2) chronic skin changes (brown hyperpigmentation, stasis dermatitis with skin thickening, and induration). Venous ulcers are also rather painless, warm, and with no gangrene.

36 What is the role of physical exam in a diabetic ulcer?

In addition to being comprehensive (diabetes is, after all, a systemic disease), the exam should:

37 Where is a diabetic foot ulcer located?

It is typically located over one of the following sites:

38 What is Charcot’s foot?

It is a neuropathic osteoarthropathy resulting from loss of both sensation (causing unrecognized microtrauma from ill-fitting shoes) and motor control (causing intrinsic muscle weakness and splaying of the foot on weight-bearing areas, thus compounding the trauma). The result is a convex foot with a rocker-bottom appearance, where small fractures remain unnoticed until bone and joint deformities become severe.

39 Which joints are most affected by Charcot’s changes?

In addition to tarsometatarsal and metatarsophalangeal joints, Charcot’s changes also can affect the ankle, causing displacement of the mortise. If neglected, calluses over pressure points will evolve into ulcerations, especially over the medial aspect of the navicular bone, the inferior aspect of the cuboid bone, and the ankle. Sinus tracts from ulcerations may then reach into the deeper planes of the foot and bone, thus leading to osteomyelitis, to which diabetics are also uniquely susceptible. Ulcers deeper than 3  mm and larger than 2   cm² are especially predisposed to this complication.

40 Are there any other causes of Charcot’s foot?

In addition to diabetes (where it affects 2% of the population), a Charcot’s foot also can occur in other peripheral neuropathies, including tertiary syphilis (which used to be the leading cause of this condition) and Charcot-Marie-Tooth disease.

41 What is edema of an extremity?

It is the swelling of a limb caused by accumulation of fluid. This could be serum (venous edema), lymph (lymphedema), or fat (lipedema, see Table 22-4).

42 What is “pitting”?

A well-defined depression in soft tissues resulting from application of pressure—something that separates it from the “brawny” edema of hypothyroidism, inflammation, and chronic venous stasis. “Pitting” is due to accumulation of interstitial fluid and thus predominantly localized (but not necessarily so) to dependent areas, like the pre-sacrum of supine patients or the shins of standing/sitting ones. The less viscous and protein-rich the fluid, the more likely the “pitting.”

43 How do you elicit pitting edema?

By pressing your thumb for 1–2 seconds over the tibia, dorsum of each foot, and retromalleolar area. Pitting severity is graded from 1 to 4, with 4 being the highest.

44 How do you grade pitting edema?

As 1+ (mild pitting, slight indentation); 2+ (moderate pitting, indentation rapidly subsiding); 3+ (deep pitting— longer indentation, leg swollen); 4+ (very deep pitting, leg very swollen).

45 How does lymphedema present? What are its causes?

Primary lymphedema is bilateral, more common in women, and with onset before 40. Secondary lymphedema is instead unilateral, equal in both sexes, and usually occurring after infections (recurrent cellulitis), radiation, surgery, or cancer. These etiologies are all at play in lymphedema of the arm, almost exclusively seen in breast cancer patients as a result of tumor, treatment (surgery/radiation), or a combination thereof.

46 What is the most common cause of neoplastic lymphedema in the lower extremities?

Metastatic prostatic cancer in men and lymphoma in women.

47 How can physical exam help in the diagnosis of edema?

The most important finding for the interpretation of edema is the patient’s venous pressure as assessed through neck veins examination (with distention arguing in favor of right ventricular or biventricular failure). Edema per se (i.e., without an assessment of central venous pressure) has little correlation with cardiac disease.

48 How do you separate edema of deep venous thrombosis (DVT) from edema of congestive heart failure?

DVT causes unilateral edema. Differential diagnosis includes Baker’s cyst, cellulitis, and venous insufficiency.

49 What is the Trendelenburg’s test?

It is a test of functionality of leg veins’ valves, first described by Sir Benjamin Brodie in 1846, almost 50 years before Trendelenburg’s report (which is why the maneuver is still referred to as the Trendelenburg-Brodie test). To carry it out:

50 How do you interpret the test?

51 Can the saphenous vein serve as a manometer of intra-abdominal pressure?

Yes. If the saphenous vein has incompetent valves, it may also function as an intra-abdominal pressure monitor. Hence, it is to the belly what the internal jugular is to the right atrium. This monitoring function can be carried out by raising the leg at various angles, and then studying the level of the column of blood in the saphenous vein both at baseline and after maneuvers that increase abdominal pressure (like coughing or straining).

52 How do you check for presence of communicating veins?

By using another maneuver devised by Trendelenburg. This consists of applying a tourniquet on the saphenous vein while the patient is still supine and the varicose veins are engorged. The leg is then raised high above the level of the heart, and varicosities are closely monitored. If they gradually disappear, this indicates that there is a communication between the saphenous and the deep veins, that the valves of these communicating veins are competent, and that the deep venous system is patent. Conversely, if the veins remain engorged, this indicates either occlusion of the deep venous system or absence of the communicating veins.

53 What is the Trendelenburg’s position?

Originally, it was a supine position on the operating table, with the bed inclined at such an angle that the pelvis was always higher than the head. The Trendelenburg’s position is still used during (and after) pelvic operations. It also is used for shock, to redirect blood from legs and abdomen into chest and brain. Since these patients are acutely ill, Trendelenburg’s position is often referred to as “the Titanic position.”

54 Who was Trendelenburg?

Friedrich Trendelenburg (1844–1924) was the son of a well-known German philosopher. After studying in Glasgow and Edinburgh, he taught vascular surgery in his native Berlin, and then Rostok, Bonn, and, ultimately, Leipzig, where he stayed as surgeon-in-chief until retiring in 1911. An innovator in his field and the founder of the German Surgical Society, Trendelenburg developed the position that still carries his name in order to operate on the pelvis. He experimented, however, in many other areas. For example, he devised a new surgery for varicose veins—hence, the aforementioned Trendelenburg’s test(s). He even attempted a pulmonary embolectomy in 1907, yet the first successful embolectomy was not performed until 1924, by one of his former students, Dr. Martin Kirshner (1924 also was the year of Trendelenburg’s death, of carcinoma of the mandible). His many interests included a passion for medical history, which prompted him to write a book on ancient Indian surgery, and even an autobiography. Trendelenburg’s name is linked not only to the test(s) and position, but also to the eponymous sign and gait (see Chapter 21, questions 176–179).

55 What is Perthes’ test?

Another bedside test of varicose veins, devised by another German surgeon (Georg C. Perthes, the same of Calvé-Legg-Perthes disease fame). It is aimed at determining patency of the deep venous system and competence of the saphenous and communicating veins’ valves. It is carried out by placing a tourniquet around the mid-thigh of a standing patient whose leg veins are fully engorged. The patient is then asked to walk for 5 minutes, and the veins are reexamined.

Perthes’ test is based on the “milking” effect that muscle compression exercises on the greater saphenous vein. As a result, walking squeezes blood from the saphenous veins into the communicating system and from there into the deep veins.

56 What is the role of palpation in assessing varicose veins of the saphenous system?

It can provide confirmation of the presence of incompetent valves. To do so, place the fingers of one hand over the engorged saphenous vein (below the knee) while at the same time tapping gently with the other hand the same vein a foot cephalad (above the knee). Valve incompetence results in transmission of the impulse downward and backwards.

57 What is the role of physical exam for diagnosing DVT?

It is part of a comprehensive approach, including review of risk factors and symptoms.

Table 22-5 Diagnosis of Deep Venous Thrombosis (DVT)

Major Criteria

Active cancer (ongoing treatment, treatment within previous 6 months. or palliative treatment)

Paralysis, bedridden >3 days, and/or major surgery within 4 weeks

Localized tenderness along the distribution of the deep venous system in the calf or thigh

Thigh and calf swelling (should be measured)

Calf swelling by >3   cm compared with asymptomatic leg (as measured 10   cm below the tibial tuberosity)

Strong family history of DVT (>2 first-degree relatives with history of DVT)

Minor Criteria

History of recent trauma (to symptomatic leg within 60 days or less)

Pitting edema in symptomatic leg only

Dilated superficial veins (nonvaricose) in symptomatic leg only

Hospitalization within previous 6 months

Erythema

Scoring Method

High probability: three or more major criteria with no alternative diagnosis, two or more major and two or more minor criteria with no alternative diagnosis

Low probability: one major criterion and two or more minor criteria with alternative diagnosis; one major criterion and one or more minor criteria with no alternative diagnosis; no major criteria and three or more minor criteria with alternative diagnosis; no major and two or more minor criteria with no alternative diagnosis

Moderate probability: All other combinations

(Adapted from Anand S, Wells P, Hunt D, et al: Does this patient have deep vein thrombosis? JAMA 279:1094–1099, 1998.)

58 What are the traditional physical findings of DVT? How valuable are they?

Based on traditional teaching, the physical exam of patients with suspected DVT should include: (1) careful inspection of the leg (looking for pitting edema, warmth, dilated superficial veins, and erythema); (2) measurement of leg circumference; (3) appreciation of a palpable cord; and (4) elicitation of Homans’ sign (development of calf pain following the forceful and abrupt dorsi-flexion of the foot). Yet, all these signs/maneuvers are quite inaccurate. Tenderness, swelling, warmth, and redness of the limb cannot adequately separate patients with or without DVT. In fact, warmth and color of the skin reflect superficial, rather than deep, circulation. A “palpable cord” is also indicative of superficial thrombophlebitis—which has no relationship to the deep vein system. Finally, skin changes, pitting edema, and dilated superficial veins may all be caused by other processes, such as venous insufficiency, leg trauma, cellulitis, obstructive lymphadenopathy, superficial venous thrombosis, postphlebitic syndrome, or a Baker (popliteal) cyst—a distended gastrocnemius-semimembranosus bursa that has ruptured into the calf, thus creating a perimalleolar crescent-shaped ecchymosis (pseudo-thrombophlebitis). And as for Homans’ sign, it has a low sensitivity and poor specificity.

59 How accurate is physical exam for DVT?

Not much. Given the previously discussed constraints, the sensitivity is only 60–88%, and the specificity 30–72%. In fact, the only important signs of DVT are tenderness and swelling. Calf asymmetry <2   cm (when measured 5   cm below the tibial tuberositas) also is abnormal and, if new, argues for DVT until proven otherwise.

60 What should then be the approach to a patient with suspected DVT?

Because of the low sensitivity and specificity of clinical exam, many authors have tried to either combine various signs and symptoms (like the Wells’ scoring system for DVT) or have recommended exclusive reliance on noninvasive tests. Still, five findings seem to be independ-ently and significantly associated with the presence of proximal DVT: (1) swelling below the knee, (2) swelling above the knee, (3) recent immobility, (4) cancer, and (5) fever. Overall, the sensitivity of a positive clinical examination (associated with the presence of one or more of these independent predictors) is 96%, although the specificity is still low (20%). The absence of any of these findings is associated with a less than 5% chance of proximal DVT. Conversely, the presence of two or more of these clinical findings is associated with a 46% chance of proximal DVT.

61 In summary, what is the role of bedside examination for the evaluation of DVT?

Still an important one. Although individual symptoms and signs are not, by themselves, very useful, a careful review of risk factors, symptoms, and signs may nonetheless help determine the pretest probability of disease. And thus, it can guide interpretation of noninvasive diagnostic tests. This rekindled value of clinical examination has in recent time led to the hypothesis that when pretest probability of disease and noninvasive tests of lower extremity veins are concordant, DVT can be effectively ruled in or ruled out, whereas when pretest probability of disease and non-invasive tests are discordant, further evaluation is necessary. This approach has led to the creation of a clinical prediction guide for the management of patients with suspected DVT

62 Who was Homans?

John Homans (1877–1954) was an American surgeon who worked with Harvey Cushing at Hopkins, and eventually became professor of Surgery at Peter Bent Brigham. His interest in peripheral vascular disease led to a monograph on the subject in 1939. He also wrote a very successful surgery textbook based on his Harvard course. Still, he did not name his sign after himself and in fact later in life tried to distance himself from it.