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144 PA R T II / Physiologic and Pathologic Responses

Clinical Manifestations
Table 6-6 ■ DIFFERENTIAL DIAGNOSIS IN PATIENTS The classic signs and symptoms of pain, edema, warmth, ery-
PRESENTING WITH VENOUS THROMBOEMBOLISM thema, and tenderness of the leg are common with DVT, but can
also be caused by nonthrombotic events. There can also be a pal-
Inherited (Primary) Hypercoaguable States pable cord, discoloration, cyanosis, venous distention, and
Activated Protein C resistance due to factor V Leiden mutation 18
Prothrombin gene mutation prominence of the superficial veins. The size of the thrombus,
Antithrombin III deficiency the location of the affected vein, and the adequacy of collateral
Proteins C and S deficiencies channels are some of the factors that cause the variability of the
Dysfibrinogenemias (rare) clinical presentation. 24 In the past, a positive Homans’ sign,
Acquired (Secondary) Hypercoaguable States which is pain occurring in the affected calf with forceful dorsi-
Trauma flexion of the foot, was thought to be diagnostic for a DVT. How-
Pregnancy (especially postpartum period)
Immobilization (paralysis, extended bedrest, or sitting) ever, a positive Homans’ sign is not specific for thrombotic disease
Advancing age and could indicate minor muscle injury or other lower leg disor-
24
Postoperative state der. Therefore, caution must be used when interpreting Homans’
Obesity sign because any inflammation near the calf muscles may also elicit
Prolonged air travel
Malignancy similar pain. Asymmetry between two extremities may also be
Estrogens (hormone replacement therapy, oral contraceptives) present, with the affected limb being slightly larger because of the
Lupus anticoagulant or antiphospholipid antibody syndrome congestion and edema associated with the inflammatory process.
These signs and symptoms in combination with the presence of
Modified from Hoffman, R., Benz, E., Shattil, S., et al. (2005). Hematology: Basic the associated risk factors should assist in the diagnostic process.
Principles and Practice. Philadelphia: Elsevier-Churchill-Livingstone. The clinical manifestations of DVT are sometimes elusive and
should always be confirmed by objective diagnostic tests.

is that it can lead to PE. Venous thrombosis in the lower extremity Medical Management
can involve superficial leg veins, the deep veins of the calf (calf vein Objective testing and a careful history and physical examination
thrombosis), and the more proximal veins, including the popliteal should be obtained if a DVT is suspected. The patient’s history
veins, the superficial femoral, common femoral, and iliac veins. In and physical examination are important components of the diag-
superficial vein thrombosis, sometimes called thrombophlebitis, nostic process, because they may reveal an alternative cause of the
the thrombosis is the result of inflammation in the venous wall of patient’s symptoms. Diagnostic studies for DVT include B-mode
the superficial venous system and is benign and self-limiting. or duplex ultrasonography, venography, and impedence plethys-
mography. Some form of ultrasound, either compression or color
Etiology duplex, is usually the most common test used for diagnosing
The risk factors associated with VTE can be divided into two cat- DVT because it is more specific and sensitive. Venography is used
egories: primary and secondary hypercoaguable states. Virchow’s but is technically difficult to perform and requires experience to
triad (see Fig. 6-4) theory can be applied to some of these risk fac- execute the test accurately. Impedence plethysmography is also
tors (Table 6-6). used but is not sensitive to calf vein thrombosis. 19 Once the diag-
nosis of DVT is confirmed, anticoagulation will be initiated im-
Pathophysiology mediately. Prevention is also an important priority to deter further
Thrombi can form because the balance that is maintained in decompensation of the patient’s condition. Both these interven-
normal homeostasis has been disrupted. Coagulation is en- tions will be discussed and more radical interventions, such as ve-
hanced or fibrinolysis is impaired, which can lead to a hyperco- nous filters, will be discussed in the treatment of PE.
aguable state. Primary inherited disorders that cause a hyperco-
aguable state are usually deficiencies in factors that inhibit Anticoagulation
coagulation, so there is less counterbalance to the coagulation The main goal of therapy for VTE, of any origin, is anticoagula-
process. The three main deficiencies are antithrombin III, pro- tion to prevent further formation of thrombi. Depending on the
5
tein C, and protein S. Secondary hypercoaguable states may re- severity of the embolism, anticoagulation can be used conserva-
sult from endothelial activation by cytokines that will lead to tively or aggressively if thrombolytic therapy is needed to lyse a
loss of normal vessel wall anticoagulant surface functions with life-threatening clot. The Seventh American College of Chest
conversion to proinflammatory thrombogenic functions. 18 Vas- Physicians (ACCP) Consensus Conference on Antithrombotic
20
cular endothelial damage can expose circulating blood compo- Therapy recommends these drugs to be used for anticoagulation
y
y
nents to subendothelial structures that initiate thrombosis. This with VTE: the heparins, oral anticoagulants, and thrombolytic
process can also lead to vasoconstriction, which causes stasis and agents. The most common and one of the oldest drugs used for
makes it easier for platelets to detach from flowing blood. The anticoagulation is heparin. Heparin is a glycosaminoglycan that
accumulation of platelets can furnish phospholipid for the in- binds to and activates antithrombin III and reduces the formation
trinsic pathway, promoting thrombin formation by absorbing of thrombin and fibrin. The best method of administering he-
activated factor X to their surface. 18 Platelets can also undergo parin is according to a weight-based protocol, which starts with a
alterations in their surface area that can lead to spontaneous ag- bolus loading dose of 5,000 units or 75 units/kg intravenously fol-
gregation or increased adhesiveness. 18 Increased blood viscosity lowed by a heparin IV drip at 18 units/kg per hour. The dose is
may also predispose thrombosis. Patients with increased levels of then regulated by aPTT results that are sampled initially every
fibrinogen can induce erythrocyte aggregation, increasing vis- 6 hours, with the aPTT goal of 1.5 to 2 times the normal aPTT.
cosity and decreasing blood flow. The use of a heparin weight-based protocol has been found to be