Clinical Presentation And Diagnosis

Although a thrombus can form in any part of the venous circulation, the majority begin in the lower extremities. Once formed, a venous thrombus may behave in a combination of ways including: (a) remain asymptomatic, (b) spontaneously lyse, (c) obstruct the venous circulation, (d) propagate into more proximal veins, (e) embolize, and/or (f) slowly incorporate into the endothelial layer of the vessel.14 The majority of pa tients with VTE never develop symptoms. However, even those who initially experience no symptoms may suffer long-term consequences, such as PTS and recurrent

VTE. The symptoms of DVT or PE are nonspecific, and it is extremely difficult to distinguish VTE from other disorders on clinical signs alone.15 Therefore, objective tests are required to confirm or exclude the diagnosis. Patients with DVT frequently present with unilateral leg pain and swelling. Similarly, the PTS, a long-term complication of DVT caused by damage to the venous valves, produces chronic lower extremity swelling, pain, and tenderness that lead to skin discoloration and ulceration. The D-dimer test, a quantitative measure of fibrin breakdown in the serum, is a marker of acute thrombotic activity and may help to distinguish between an acute DVT and the PTS. Symptomatic PE usually produces shortness of breath, tachypnea, and tachycardia.16 Hemoptysis occurs in less than one-third of patients. The physical exam may reveal diminished breath sounds, crackles, wheezes, or a pleural friction rub during auscultation of the lungs. Cardiovascular collapse, characterized by cyanosis, shock, and oliguria, is an ominous sign.

FIGURE 10-3. Vascular injury and thrombosis. (ADR, adenosine diphosphate; GP lb, glycoprotein lb; GP llb/lla, glycoprotein llb/lla; HK, high-molecular weight kininogen; PAF, platelet activating factor-1; PAI-1, plasminogen activator inhibitor; PF-4, platelet factor-4; PGG/PGH, prostaglandins; PLA, phospholipase A; TS, thromboxane synthetase; TXA2, thromboxane A2; t-PA, tissue plasminogen activator; u-PA, urokinase plasminogen activator; vWF, von Willebrand's factor.) (From Haines

FIGURE 10-3. Vascular injury and thrombosis. (ADR, adenosine diphosphate; GP lb, glycoprotein lb; GP llb/lla, glycoprotein llb/lla; HK, high-molecular weight kininogen; PAF, platelet activating factor-1; PAI-1, plasminogen activator inhibitor; PF-4, platelet factor-4; PGG/PGH, prostaglandins; PLA, phospholipase A; TS, thromboxane synthetase; TXA2, thromboxane A2; t-PA, tissue plasminogen activator; u-PA, urokinase plasminogen activator; vWF, von Willebrand's factor.) (From Haines

ST, Witt DM, Nutescu EA. Venous thromboembolism. In: DiPiro JT, Talbert RL, Yee GC, etal., eds. Pharmacotherapy: A Pathophysiologic Approach, 7th ed. New York: McGraw-Hill; 2008:335.)

Given that VTE can be debilitating or fatal, it is important to treat it quickly and

aggressively. On the other hand, because major bleeding induced by antithrombotic drugs can be equally harmful, it is important to avoid treatment when the diagnosis is not reasonably certain. Assessment of the patient's status should focus on the search for risk factors in the patient's medical history (Table 10—1).15,16 Venous thrombosis is uncommon in the absence of risk factors, and the effects of these risks are additive. Indeed, if a patient has multiple risk factors, VTE should be strongly suspected even when the symptoms are very subtle.

Because radiographic contrast studies are the most accurate and reliable methods

18,19

for the diagnosis of VTE, they are considered the gold standards in clinical trials. ' Contrast venography allows visualization of the entire venous system in the lower extremities and abdomen. Pulmonary angiography allows the visualization of the pulmonary arteries. The diagnosis of VTE can be made if there is a persistent intraluminal filling defect observed on multiple x-ray films. Contrast studies are expensive, invasive procedures that are technically difficult to perform and evaluate. Severely ill patients often are unable to tolerate the procedure, and many develop hypotension and cardiac arrhythmias. Furthermore, the contrast medium is irritating to vessel walls and toxic to the kidneys. For these reasons, noninvasive tests, such as ultrasonography, CT scans, MRI, and ventilation/perfusion (V/Q) scans are frequently used in clinical practice for the initial evaluation of patients with suspected VTE. See the Clinical Presentation and Diagnosis of PE, and Clinical Presentation and Diagnosis of DVT textboxes.

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