Principles of surgery

Specific Considerations

Venous and Lymphatic Disease


1. Which of the following veins does not have valves?

A. Cranial sinuses

B. Portal vein

C. Iliac veins

D. All of the above

Answer: D

The inferior vena cava (IVC), common iliac veins, portal venous system, and cranial sinuses are valveless. (See Schwartz 9th ed., p 778.)

2. Heparin induces anticoagulation primarily by

A. Increasing production of antithrombin

B. Increasing the activity of antithrombin

C. Increasing conversion of factor X to Xa

D. Increasing conversion of factor XI to XIa

Answer: B

Unfractionated heparin (UFH) binds to antithrombin via a specific 18-saccharide sequence, which increases its activity over 1000-fold. This antithrombin-heparin complex primarily inhibits factor IIa (thrombin) and factor Xa and, to a lesser degree, factors IXa, XIa, and XIIa. In addition, UFH also binds to tissue factor pathway inhibitor, which inhibits the conversion of factor X to Xa, and factor IX to IXa. Finally, UFH catalyzes the inhibition of thrombin by heparin cofactor II via a mechanism that is independent of antithrombin. (See Schwartz 9th ed., p 784.)

3. The Cockett perforator veins are located in the

A. Medial thigh

B. Lateral thigh

C. Medial lower leg

D. Lateral lower leg

Answer: C

Multiple perforator veins traverse the deep fascia to connect the superficial and deep venous systems. Clinically important perforator veins are the Cockett and Boyd perforators. The Cockett perforator veins drain the medial lower leg and are relatively constant. They connect the posterior arch vein (a tributary to the great saphenous vein (GSV)) and the posterior tibial vein. They may become varicose or incompetent in venous insufficiency states. The Boyd perforator veins connect the GSV to the deep veins approximately 10 cm below the knee and 1 to 2 cm medial to the tibia. (See Schwartz 9th ed., p 778.)

4. Warfarin inhibits γ-carboxylation of which of the following?

A. Factor III

B. Factor VII

C. Factor VIII

D. Factor XI

Answer: B

Vitamin K antagonists, which include warfarin and other coumarin derivatives, are the mainstay of long-term antithrombotic therapy in patients with venous thromboembolism (VTE). Warfarin inhibits the γ-carboxylation of vitamin K–dependent procoagulants (factors II, VII, IX, X) and anticoagulants (proteins C and S), which results in the formation of less functional proteins. (See Schwartz 9th ed., p 785.)

5. Thrombolytic drugs work by

A. Converting plaminogen to plasmin

B. Increasing the activity of plasmin

C. Converting thrombin to fibrin

D. Decreasing the activity of thrombin

Answer: A

Several thrombolysis preparations are available, including streptokinase, urokinase, alteplase (recombinant tissue plasminogen activator), reteplase, and tenecteplase. All these agents share the ability to convert plasminogen to plasmin, which leads to the degradation of fibrin. They differ with regard to their half-lives, their potential for inducing fibrinogenolysis (generalized lytic state), their potential for antigenicity, and their FDA-approved indications for use. (See Schwartz 9th ed., p 786.)

6. One of the factors which prevents thrombosis in the normal venous system is

A. Smooth muscle contraction in the wall of the vein

B. Distention of the vein as volume increases in diastole

C. Endothelial production of prostaglandin

D. Endothelial production of endothelial relaxing factor

Answer: D

Veins are thin-walled, highly distensible, and collapsible structures. Their structure specifically supports their two primary functions of transporting blood toward the heart and serving as a reservoir to prevent intravascular volume overload. The venous intima is composed of a nonthrombogenic endothelium with an underlying basement membrane and an elastic lamina. The endothelium produces endothelium-derived relaxing factor and prostacyclin, which help maintain a nonthrombogenic surface through inhibition of platelet aggregation and promotion of platelet disaggregation. (See Schwartz 9th ed., p 778.)


1. Anticoagulation with heparin requires monitoring which of the following?

A. Thromboelastogram (TEG)

B. Bleeding time



Answer: D

The level of antithrombotic therapy after giving heparin should be monitored every 6 hours using the activated partial thromboplastin time (aPTT), with the goal range of 1.5 to 2.5 times control values.

This should correspond with plasma heparin anti-Xa activity levels of 0.3 to 0.7 IU/mL. (See Schwartz 9th ed., p 784.)

2. Which of the following is NOT a risk factor for venous thromboembolism?

A. Factor XI elevation

B. Protein C elevation

C. Nephrotic syndrome

D. Travel >6 hours

Answer: B

Protein C deficiency is a risk factor for thromboembolism. (See Schwartz 9th ed., p 781, and Table 24-1.)

TABLE 24-1 Risk factors for venous thromboembolism


Advanced age


Hormone replacement therapy and oral contraceptive use

Pregnancy and puerperium

Prior venous thromboembolism


Major surgery


Nephrotic syndrome

Trauma or spinal cord injury

Long-haul travel (>6 h)

Varicose veins

Antiphospholipid antibody syndrome

Myeloproliferative disease



Factor V Leiden

Prothrombin 20210A

Antithrombin deficiency

Protein C deficiency

Protein S deficiency

Factor XI elevation


Mixed etiology


Factor VII, VIII, IX, XI elevation


Activated protein C resistance without factor V Leiden

3. Full anticoagulation (steady state) when using warfarin is achieved in

A. 24 hours

B. 48 hours

C. 4-5 days

D. 7-10 days

Answer: C

Warfarin usually requires several days to achieve its full effect, because normal circulating coagulation proteins must first undergo their normal degradation. Factors X and II have the longest half-lives, in the range of 36 and 72 hours, respectively. In addition, the steady-state concentration of warfarin is usually not reached for 4 to 5 days. (See Schwartz 9th ed., p 785.)

4. The most effective therapy for lymphedema is

A. Compression garments

B. Surgical excision of the involved area

C. Surgical bypass of the obstructed lymphatics

D. Combined excision of affected areas with bypass of the obstructed lymphatics

Answer: A

An important aspect of the management of lymphedema is patient understanding that there is no cure for lymphedema. The primary goals of treatment are to minimize swelling and to prevent recurrent infections. Controlling the chronic limb swelling can improve discomfort, heaviness, and tightness, and potentially reduce the progression of disease.

Graded compression stockings are widely used in the treatment of lymphedema. The stockings reduce the amount of swelling in the involved extremity by preventing the accumulation of edema while the extremity is dependent. When worn daily, compression stockings have been associated with long-term maintenance of reduced limb circumference. They may also protect the tissues against chronically elevated intrinsic pressures, which lead to thickening of the skin and subcutaneous tissue. Compression stockings also offer a degree of protection against external trauma. (See Schwartz 9thed., p 798.)

5. Phlegmasia cerulea albans is caused by

A. Obliteration of the major deep venous channels of the leg

B. Obliteration of the major deep venous channels and the collateral veins of the leg

C. Reperfusion injury following an isolated injury to the femoral vein

D. Reperfusion injury following injury to both the femoral vein and artery

Answer: B

Massive DVT that obliterates the major deep venous channel of the extremity with relative sparing of collateral veins causes a condition called phlegmasia alba dolens. This condition is characterized by pain, pitting edema, and blanching. There is no associated cyanosis. When the thrombosis extends to the collateral veins, massive fluid sequestration and more significant edema ensues, resulting in a condition known as phlegmasia cerulea dolens. Phlegmasia cerulea dolens is preceded by phlegmasia alba dolens in 50 to 60% of patients. The affected extremity in phlegmasia cerulea dolens is extremely painful, edematous, and cyanotic, and arterial insufficiency or compartment syndrome may be present. If the condition is left untreated, venous gangrene can ensue, leading to amputation. (See Schwartz 9th ed., p 782.)

6. The incidence of deep vein thrombosis (DVT) in patients undergoing repair of a hip fracture who do NOT receive prophylaxis is greater than

A. 10%

B. 20%

C. 30%

D. 40%

Answer: D

Patients who undergo major general surgical, gynecologic, urologic, and neurosurgical procedures without thromboprophylaxis have a significant incidence of perioperative DVT (15 to 40%). The incidence is even higher with major trauma (40 to 80%), hip and knee replacement surgery (40 to 60%), and spinal cord injury (60 to 80%). (See Schwartz 9th ed., p 787, and Table 24-2.)

TABLE 24-2 Thromboembolism risk and recommended thromboprophylaxis in surgical patients


7. The most common form of lymphedema is

A. Congenital lymphedema

B. Lymphedema praecox

C. Lymphedema tarda

D. Secondary lymphedema

Answer: D

Secondary lymphedema is far more common than primary lymphedema. Secondary lymphedema develops as a result of lymphatic obstruction or disruption. Axillary node dissection leading to lymphedema of the arm is the most common cause of secondary lymphedema in the United States. Other causes of secondary lymphedema include radiation therapy, trauma, infection, and malignancy. Globally, filariasis (caused by Wuchereria bancroftiBrugia malayi, and Brugia timori) is the most common cause of secondary lymphedema.

Congenital lymphedema may involve a single lower extremity, multiple limbs, the genitalia, or the face. The edema typically develops before 2 years of age and may be associated with specific hereditary syndromes (Turner syndrome, Milroy syndrome, Klippel-Trenaunay-Weber syndrome). Lymphedema praecox is the most common form of primary lymphedema, accounting for 94% of cases. Lymphedema praecox is far more common in women, with the gender ratio favoring women 10:1. The onset is during childhood or the teenage years, and the swelling involves the foot and calf.Lymphedema tarda is uncommon, accounting for 10% of cases of primary lymphedema. The onset of edema is after 35 years of age. (See Schwartz 9th ed., p 796.)

8. The initial dose of heparin given to anticoagulate a patient with deep venous thrombosis is

A. 50 units/kg

B. 80 units/kg

C. 120 units/kg

D. 200 units/kg

Answer: B

Unfractionated heparin (UFH) therapy is most commonly administered with an initial IV bolus of 80 units/kg or 5000 units. Weight-based UFH dosages have been shown to be more effective than standard fixed boluses in rapidly achieving therapeutic levels. The initial bolus is followed by a continuous IV drip, initially at 18 units/kg per hour or 1300 units per hour. The half-life of IV UFH ranges from 45 to 90 minutes and is dose dependent. The level of antithrombotic therapy should be monitored every 6 hours using the activated partial thromboplastin time (aPTT), with the goal range of 1.5 to 2.5 times control values. This should correspond with plasma heparin anti-Xa activity levels of 0.3 to 0.7 IU/mL. (See Schwartz 9th ed., p 784.)

9. In a patient with symptomatic varicose veins where the great saphenous vein has reflux and a diameter of 1 cm, the preferred surgical treatment is

A. Sclerotherapy

B. RFA or laser ablation

C. Vein valvuloplasty

D. Surgical bypass

Answer: B

Patients with symptomatic great or small saphenous vein reflux may be treated with endovenous ablation techniques or surgical removal. Endovenous laser treatment and radiofrequency ablation (RFA) have gained in popularity in the past several years.

Injection sclerotherapy can be successful in varicose veins 3 mm in diameter and in telangiectatic vessels.

Saphenous vein ligation and stripping is still the more commonly performed procedure worldwide, and it may be the preferred therapy for patients with GSVs of very large diameter (>2 cm). (See Schwartz 9th ed., p 791.)

10. The preferred initial therapy of chronic venous insufficiency with ulceration is

A. Compression therapy with Unna’s boot or elastic stockings

B. Saphenous vein high ligation and stripping or endovenous ablation

C. Open ligation of perforator veins

D. Reconstruction of the saphenofemoral junction

Answer: A

Compression therapy is most commonly achieved with graduated elastic compression stockings. Graduated elastic compression stockings, initially developed by Conrad Jobst in the 1950s, were made to simulate the gradient of hydrostatic forces exerted by water in a swimming pool. (See Schwartz 9th ed., p 793.)

Another method of compression was developed by the German dermatologist Paul Gerson Unna in 1896. Unna’s boot has been used for many years to treat venous ulcers and is available in many versions. A typical Unna’s boot consists of a three-layer dressing and requires application by trained personnel. A rolled gauze bandage impregnated with calamine, zinc oxide, glycerin, sorbitol, gelatin, and magnesium aluminum silicate is first applied with graded compression from the forefoot to just below the knee. The next layer consists of a 4-in-wide continuous gauze dressing followed by an outer layer of elastic wrap, also applied with graded compression. The bandage becomes stiff after drying and the rigidity may aid in preventing edema formation. Unna’s boot is changed weekly, or sooner if the patient experiences significant drainage from the ulcer bed. (See Schwartz 9th ed., p 794.)

Incompetence of the perforating veins connecting the superficial and deep venous systems of the lower extremities has been implicated in the development of venous ulcers. The classic open technique described by Linton in 1938 for perforator vein ligation has a high incidence of wound complications and has largely been abandoned. (See Schwartz 9th ed., p 795.)

11. Heparin-induced thrombocytopenia (HIT) occurs most commonly

A. Within 24 hours of starting therapy

B. 3 days after starting therapy

C. 7 days after starting therapy

D. 14 days after starting therapy

Answer: C

Heparin-induced thrombocytopenia (HIT) results from heparin-associated antiplatelet antibodies (HAAbs) directed against platelet factor 4 complexed with heparin. HIT occurs in 1 to 5% of patients being treated with heparin. In patients with repeat heparin exposure (such as vascular surgery patients), the incidence of HAAb may be as high as 21%. HIT occurs most frequently in the second week of therapy and may lead to disastrous venous or arterial thrombotic complications. Therefore, platelet counts should be monitored periodically in patients receiving continuous heparin therapy. (See Schwartz 9th ed., p 785.)

12. Indications to place an inferior vena cava (IVC) filter include

A. Recurrent deep vein thrombosis (DVT) despite adequate anticoagulation

B. Contraindication for anticoagulation in a patient with proximal DVT

C. Pulmonary hypertension with recurrent pulmonary embolism

D. All of the above

Answer: A

Placement of an IVC filter is indicated for patients who develop recurrent DVT (significant propagation of the original thrombus or proximal DVT at a new site) or pulmonary embolism (PE) despite adequate anticoagulation therapy and for patients with pulmonary hypertension who experience recurrent PE. In patients who receive IVC filters for these indications, therapeutic anticoagulation should be continued. The duration of anticoagulation is determined by the underlying venous thromboembolism (VTE) and not by the presence of the IVC filter itself. Practically speaking, however, many patients who require an IVC filter for recurrent VTE are the same ones who would benefit most from indefinite anticoagulation. The other major indication for placement of an IVC filter is a contraindication to, or complication of, anticoagulation therapy in the presence of an acute proximal DVT. (See Schwartz 9th ed., p 787.)

13. Initial therapy of a professional baseball player with acute venous thoracic outlet syndrome includes

A. Observation

B. Immobilization

C. Thrombolytic therapy

D. Surgical embolectomy and correction of the underlying anomaly

Answer: C

Patients with primary axillary-subclavian vein thrombosis (ASVT) often give a history of performing prolonged, repetitive motion activities, which results in damage to the subclavian vein, usually where it passes between the head of the clavicle and the first rib. This condition is also known as venous thoracic outlet syndromeeffort thrombosis, and Paget-Schroetter syndrome. Anticoagulation therapy should be initiated once ASVT is diagnosed to prevent PE and decrease symptoms. Patients presenting with acute symptomatic primary ASVT may be candidates for catheter-directed thrombolytic therapy. (See Schwartz 9th ed., p 790.)

14. A patient develops a first episode of deep venous thrombosis following a colon resection. How long should he be treated with anticoagulation?

A. 2 weeks

B. 4-6 weeks

C. 3 months

D. 1 year

Answer: C

The recommended duration of warfarin antithrombotic therapy is increasingly being stratified based on whether the deep vein thrombosis (DVT) was provoked or unprovoked, whether it was the first or a recurrent episode, where the DVT is located, and whether malignancy is present. Current American College of Chest Physicians (ACCP) recommendations for duration of warfarin therapy are summarized in Table 24-3. In patients with proximal DVT, several randomized clinical trials have demonstrated that shorter-term antithrombotic therapy (4 to 6 weeks) is associated with a higher rate of recurrence than 3 to 6 months of anticoagulation. (See Schwartz 9th ed., p 786.)

TABLE 24-3 Summary of American College of Chest Physicians recommendations regarding duration of long-term antithrombotic therapy for deep vein thrombosis (DVT)