Despite major advances in imaging technology, the history and physical examination remains the primary measure for assessing patients with peripheral vascular disease. The goal of the medical history is to obtain a detailed vascular profile of each individual patient, focusing on the history of the present illness and associated symptoms.1
History taking is the first step in development of the patient–physician relationship. To enhance communication, eye contact with careful listening in a compassionate stance (i.e. at level with the patient, if possible) is necessary. Using vocabulary the patient understands in an easily comprehensible pace and a nonjudgmental tone is essential to establish a working relationship with the patient.
To maximize history taking, a combination of open-ended and directed questions is necessary regarding the primary concern. Open-ended questioning allows for a more thorough understanding of the patient’s concerns. In addition, valuable situational information may be unveiled that can impact patient care, such as lack of resources to take medications as prescribed. If the patient is acutely ill, however, it is reasonable to limit the patient’s time for response to allow for prompt evaluation and treatment. After the patient has been given an opportunity to discuss his or her concerns in his or her own words, directed questioning should be used to further define and clarify the patient’s symptoms.
After a short greeting, the physician inquires about the chief complaint. Then an exploration of each symptom in detail is necessary. Details about the symptoms include the location, quality, severity, timing, alleviating and aggravating factors, and associated manifestations (Table 7-1). Understanding the symptoms in the context of a pathophysiologic base will allow for recognition of disease pattern and aid in the development of a differential diagnosis.
| Location | Specifics about location of symptom. For example, is “leg pain” located in the anterior, posterior, hip, thigh, calf, foot, left or right side? Does the pain radiate or change location? |
| Quality | Specifics on the experience of the symptom. For example, is “leg pain” a sharp, dull, burning, aching, heaviness, or cramping in nature? How does the experience feel? |
| Quantity or severity | Quantifiable parameters. For example, in an analogue scale from 0 to 10, how severe is the pain? How does the symptom differ from how you were doing at baseline? |
| Timing | Clarification on onset (when symptom was first appreciated), duration (seconds, minutes, hours, or days), and frequency (daily, weekly, or monthly) |
| Setting | Clarification on when the symptom occurs. For example, does the leg pain start with walking up stairs or with prolonged periods of rest? Does the pain occur first thing after getting out of bed or during the night when sleeping? Did some event, such as a trauma, precede the symptom? |
| Alleviating and aggravating factors | Typifying the symptom. For example, what makes the leg pain better or worse? Medications? Certain positions or actions? |
| Associated symptoms | Documenting the presence or absence of potentially related symptom to others. For example, did the leg pain precede the subsequent chest pain? Or was there no associated chest pain? |
There are numerous risk factors for the development and progression of venous vascular disease. Nonreversible risk factors include age, male gender, family history of venous abnormalities, and congenital hypercoagulopathies. Modifiable risk factors include smoking and acquired hypercoagulopathic states such as those secondary to malignancy, medication use (e.g., oral contraceptives), and impaired mobility. All of these risk factors should be identifiable through the completion of a full medical history, encompassing the patient’s medical and surgical histories, current use of prescription and nonprescription medication, allergies, social habits, family history, and a review of systems as part of appropriate cancer screening.
Patients with peripheral venous disease often present with complaints of swelling or pain. What patients view as “swelling” is often their description for the accumulation of interstitial fluid, also known as edema. In the case of lower extremity swelling, patients may note their shoes fitting tighter or their socks “leaving marks” from constrictive elastic bands. When upper extremity swelling is the issue, patients complain about rings or wrist watches fitting too snugly. Other symptoms attributable to edema include periodic tiredness or achiness in the legs, especially at the end of the day or after standing up for long periods.
Although edema may occur with multiple pathologic states, its presence is commonly associated with either systemic dysfunction or abnormalities in the local circulation from peripheral vascular disease. Patients with edema from systemic disease frequently present with generalized features of volume load, including shortness of breath from pulmonary congestion (left ventricular dysfunction), ascites (cirrhosis), or anasarca (nephrotic syndrome). In contrast, edema caused by abnormalities in the lower extremity venous system is often rapid in onset and can present with isolated swelling in one or both extremities. The preceding disorders are typically associated with pitting edema. A less common form of edema occurs in lymphedema. This disorder presents classically with nonpitting limb edema.
Extremity pain can be attributable to edema but more broadly is often caused by increased venous pressure in the lower extremities secondary to venous diseases. Lower extremity pain in venous insufficiency typically occurs in any setting requiring an upright position and improves with leg elevation or wearing external support stockings. The pain, which is usually below the knee and is often described as a feeling of tightness, heaviness, or fatigue of varying intensity, is referred to as venous claudication.
In addition to position-dependent pain and swelling, patients may also present with cosmetic concerns, such as skin discoloration or varicose veins. Although varicose veins is a disease entity distinct from chronic vein insufficiency, the latter may develop as a hemodynamic consequence; therefore, the coexistence of chronic venous insufficiency (CVI) by history and its severity should be investigated.
A diagnosis of CVI is often suggested by the patient’s history and then confirmed by examination. It is also important to address whether the venous insufficiency may have been caused by a previous deep venous thrombosis (DVT) or if the patient has coexisting occlusive arterial disease. Although clues for these disease states may be established via history and examination, diagnosis often requires additional testing.
In the era of modern technology, the need for a complete physical examination may seem time consuming and unnecessary; however, a proper physical examination is essential for a variety of reasons. Close listening to the patient and careful examination not only help build a foundation of trust; they also allow for the development of a differential diagnosis for which diagnostic testing can then help confirm. In addition, proceeding with laboratory tests without first establishing a diagnostic hypothesis based on a thorough history and physical examination may produce misleading results and ultimately delay diagnosis.
To aid in diagnosis, the skilled practitioner uses the following steps during a physical examination: inspection, palpation, percussion, and auscultation. The physical examination in patients with venous and lymphatic disease requires a diligent incorporation of these steps to accurately perceive abnormalities in structure and function.
Inspection is the search for physical signs of pathology using both sight and smell. Visual inspection should begin by evaluating patient as a whole followed by close assessment of specific anatomic regions. The examiner should take note of such things as body habitus, skin color, and hair growth patterns. Using the sense of smell can also assist in diagnosing infections and poor hygiene.
After inspection, the examiner should proceed with palpation using various aspects of his or her hand. The dorsum of the hand can be used for temperature sense, and the tips of the fingers should be used for fine tactile discrimination. Accurate palpation of arterial and venous pulsations, pulsatile masses, heaves, thrills, edema, and temperature offers valuable information regarding the adequacy of perfusion, function of cardiac structures, and hemodynamics of blood flow. Palpation should also be used to evaluate for lymphadenopathy, which is often a marker for infection, malignancy, or other pathology.
Next, percussion is performed. The practitioner strikes the body surface to emit sound, which will vary in intensity based on the density of the tissues, which can be altered in disease states.
Last, the examiner should auscultate, or listen, to the heart and peripheral vasculature using both the diaphragm and bell of a stethoscope. Through auscultation, one can perceive murmurs and bruits that will aid or confirm diagnosis, as well as provide additional insights into disease processes.
The physical examination should begin with the recording of patient’s vitals signs, including blood pressure, heart rate, and respiratory rate. Height and weight should also be documented, and the body mass index (BMI) should be calculated. Then the patient should be inspected as a whole. Attention is paid to how the patient is dressed and groomed, the tone and pattern of speech, facial expressions, and presence of eye contact. The body is also examined for asymmetry and deformities. In select cases, measurement of limb circumference is useful.
Anatomy. The supraorbital and supratrochlear veins combine to form the angular vein, which then drains into the facial vein. The facial vein empties either directly into the internal jugular vein or joins the anterior branch of the retromandibular vein to form the common facial vein, which then enters the internal jugular vein.
The cavernous sinuses are located on each side of the sella turcica and the body of the sphenoid bone and contain the oculomotor, trochlear, ophthalmic, and maxillary nerves. The cavernous sinuses communicate with the pterygoid venous plexus by emissary veins and receive the superior ophthalmic vein.
Examination and Venous Disorders. Evaluation of the head should begin with inspection of the scalp and head for venous trauma or infection. Subdural hematoma may develop after only minor trauma, with patients initially having little or no symptoms. The development of headaches and localizing signs only occurs upon expansion of the initial intracranial lesion. Additional observations should be noted, such as temporal wasting, which may be a sign of poor nutritional status.
Visual inspection of the eyelids should be performed, looking for passive hyperemia, or blueness of the eyelid, which results from thrombosis of the orbital veins or from tumors and arteriovenous aneurysms of the orbit. Funduscopic examination is then used to evaluate for arteriolar and venous changes seen in systemic disease. Arterial changes that can be appreciated include those secondary to hypertension (“cotton wool” patches, flame hemorrhages, papilledema, or arteriovenous nicking), diabetes mellitus (neovascularization, microaneurysms), atherosclerosis (exudates, beading of the retinal artery), and atheromatous embolization (Hollenhorst plaques). Changes can also be seen in the venous system, such as venous nicking, tapering of the veins, or venous humping. Although retinal vein engorgement is most commonly caused by hypertensive disease, it can also result from hypercoagulable states, polycythemia vera, cyanotic congenital heart disease, leukemia, and macroglobulinemia (Figure 7-1).
Inspection of the nose should be aimed at ruling out infection. Nasal infections can spread via the angular vein to the cavernous sinus, where septic and cavernous sinus thrombosis may occur. With these pathologies, the patient often complains of pain deep in the eyes, and there may be selective ocular palsy of one of the cranial nerves within the sinus (oculomotor, trochlear, or abducens). Both eyes are involved early in the disease course, and death can be rapid, within 3 days, if treatment is not initiated.
Evaluation of the oral mucosa, tongue, and dental hygiene is also important. Furrowing of tongue is a sign of dehydration; paleness of mucosa suggests anemia; and aphthous ulcers indicate a sign of systemic disease process, such as those of autoimmune or infectious causes.
Anatomy. The cervical triangle of the neck is formed by the sternocleidomastoid muscle, the anterior border of the trapezius muscle, and the superior border of the clavicle. The veins of the cervical triangle include the retromandibular, external jugular, and internal jugular vein (Figure 7-2). The retromandibular vein is formed by the superficial temporal and maxillary veins and then divides into anterior and posterior braches. The anterior branch joins the facial vein to form the common facial vein, and the posterior branch merges with the posterior auricular vein to create the external jugular vein. The internal jugular vein begins in the jugular foramen as the continuation of the sigmoid sinus and descends into the carotid sheath, ending with the brachiocephalic vein.
Examination and Venous Disease. Inspection of the jugular venous pulsations and pressure imparts valuable information regarding the hemodynamic changes in the right side of the heart. Although these findings can be observed in the superficial veins, it is preferable for the examiner to evaluate the internal jugular veins because they are less likely to have pressure transmission interference frequently encountered from the superficial veins.
The normal jugular venous pulsation consists of three positive waves (a, c, and v) and two negative deflections (x and y) (Table 7-2, Figure 7-3).
| Wave | Increase | Loss or Decrease |
|---|---|---|
| A wave | Tricuspid valve abnormalities Increase resistance distal to tricuspid valve Pulmonary arterial hypertension Arrhythmias | Atrial fibrillation |
| V wave | Tricuspid regurgitation Atrial septal defect | Atrial fibrillation Right atrial enlargement |
FIGURE 7-3.
Jugular venous pulse waves. The a wave is reflection of atrial systole. The c wave is the bulging of the tricuspid valve early in ventricular systole. The v wave is from atrial filling while the valve is closed. The x descent comes from atrial relaxation and the y descent from opening of the tricuspid valve. ECG, electrocardiogram.
(Modified from LeBlond R, Brown DD, and DeGowin R: DeGowin’s Diagnostic Examination, 9th ed. New York: McGraw-Hill; with permission.)
The a wave is a reflection of atrial systole. This wave peaks during the first heart sound (S1) and before the onset of ventricular ejection (carotid pulse upstroke).
The c wave is the result of the bulging of the tricuspid valve into the right atrium at the beginning of ventricular systole.
The x descent follows the a and c waves and is produced by right atrial relaxation and the downward displacement of the tricuspid valve during right ventricular ejection.
The x descent is followed by the v wave, which represents atrial filling. It is created by the rise in right atrial pressure from continued inflow of blood via the venous system during late ventricular systole when the tricuspid valve is still closed. The peak of the normal v wave corresponds to the downslope of the carotid pulse and follows just after the second heart sound (S2).
The descending limb of the v wave is termed the y descent and essentially reflects ventricular filling. The right atrial pressure decreases upon the opening of the tricuspid valve and subsequent outflow of blood from the right atrium and venous system into the right ventricle. If present, the third heart sound (S3) corresponds to the nadir of the y descent. The rise in pressure after the nadir of the y descent occurs as a consequence of the continued inflow of blood from the venous system after the rapid filling phase of the right ventricle.
Abnormalities in the venous pulsations can result from various pathology. An increase in a wave amplitude occurs when the right atrium experiences resistance during atrial systole. This may be caused by abnormalities in the tricuspid valve, such as tricuspid stenosis (rheumatic or congenital), right atrial myxoma, carcinoid heart disease, tricuspid atresia, and lupus endocarditis. Other causes of increased a wave amplitude include pulmonary arterial hypertension and right ventricular outflow obstruction caused by pulmonary valve stenosis or right ventricle hypertrophy.
Arrhythmias can also lead to alterations in the a wave. In atrial flutter, multiple a waves can be appreciated because of the increase in atrial contractions (known as flutter waves). On the other hand, in atrial fibrillation, in which there is no defined atrial activity, there will be complete loss of the a wave. In reentrant tachycardias, such as atrioventricular nodal tachycardia, prominent a waves are seen because of simultaneous atrial and ventricular activation. Atrial contractions against a closed tricuspid valve, as occurs with premature atrial and ventricular beats, junctional rhythm, atrioventricular block, and slow ventricular tachycardia, produce cannon a waves.
The v wave can be altered as well. In tricuspid regurgitation, tall v waves may be appreciated. The amplitude of the v wave depends on the regurgitant volume and right atrial compliance. Associated with the regurgitant wave of tricuspid insufficiency is the carotid pulse and pansystolic murmur along the lower right and left sternal border, both of which increase in intensity during inspiration. It is important to note that the v wave may not be seen in patients in atrial fibrillation or those with dilated right atria. Prominent v waves may also be seen in patients with an atrial septal defect.
Abnormalities in the y descent, or the rapid filling of ventricle, can be suggestive of several disease states. Obstruction of right atrial outflow secondary to tricuspid stenosis or right ventricular hypertrophy leads to slowing or blunting of the y descent. Constrictive pericarditis or restrictive cardiomyopathy, conversely, produces a sharp or steep y descent. In cases of cardiac tamponade, the x and y descents are not prominent and may even be absent altogether.
After venous pulsations, examination of the jugular venous pressure (JVP) should be completed for assessment of volume status. The normal JVP is 1 to 6 mm Hg, as measured from the sternal angle to the height of the venous column. The JVP is best calculated by having the patient lie supine with the neck extended and rotated to the left, exposing the right internal jugular vein. The examiner then gradually raises the head of the table until the oscillations of the venous pulse are appreciated. In most individuals, the pulsations are maximally visualized at a 30-degree elevation of the trunk. To estimate the right atrial pressure, 5 cm is added to the height of the JVP to account for the distance of the right atrium below the sternal angle.
Alterations in JVP provide insight into disease processes. An elevated JVP indicates an increase in the right atrial pressure caused by a variety of clinical conditions, including congestive heart failure, cardiac tamponade, constrictive pericarditis, fluid overload, tricuspid valve regurgitation, and superior vena cava obstruction. Diminished venous pressure, defined as collapsed peripheral veins in a supine patient, is also possible and is seen in patients with hypovolemia, decrease venous tone, or peripheral pooling as occurs with shock.
The variation of JVP with respiration also provides useful clinical information. In normal individuals, the JVP should decrease with inspiration because of the decrease in intrathoracic pressures and subsequent increased venous return. If this does not happen or if there is a paradoxical increase, it is termed the Kussmaul’s sign and considered pathologic. A Kussmaul’s sign, which occurs with reduced ventricular compliance and right-sided volume overload, is classically associated with constrictive pericarditis but may also result from restrictive cardiomyopathy, right ventricular infarction, massive pulmonary embolism (PE), right atrial and ventricular tumors, and cardiac tamponade.
To help facilitate analysis of the JVP, the hepatojugular reflex may be used. The examiner firmly compresses the right upper quadrant of the patient or passively raises the patient’s legs for at least 10 seconds. In a normal examination, this maneuver results in a minimal and temporary increase in the JVP. In patients with increased right-sided pressures, though, a sustained elevation of more than 3 cm in the venous pressure for at least 15 seconds after termination of the maneuver is often observed.
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