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CHAPTER 24
Venous and Lymphatic Disease
veins of the upper extremity are the cephalic and basilic veins
and their tributaries. The cephalic vein originates at the lateral wrist and courses over the lateral ventral surface of the
forearm. In the upper arm, the cephalic vein terminates in
the infraclavicular fossa, piercing the clavipectoral fascia to
empty into the axillary vein. The basilic vein runs medially
along the forearm and penetrates the deep fascia as it courses
past the elbow in the upper arm. It then joins with the deep
brachial veins to become the axillary vein, a landmark for
identification of the axillary vein. The median antecubital
vein joins the cephalic and the basilic veins on the ventral
surface of the elbow.
The axillary vein becomes the subclavian vein at the lateral
border of the first rib. At the medial border of the scalenus
anterior muscle, the subclavian vein joins with the internal jugular vein to become the brachiocephalic vein, with
the subclavian vein coursing anterior to the scalenus anterior muscle. The left and right brachiocephalic veins join to
become the superior vena cava, which empties into the right
atrium. (See Schwartz 11th ed., p. 981.)
2. The target organ(s) of chronic venous insufficiency
is/are:
A. Perforator veins.
B. The great saphenous veins.
C. The skin.
D. Lymphatics.
E. Venous capillaries.
Answer: C
Chronic venous insufficiency (CVI) may lead to characteristic
changes in the skin and subcutaneous tissues in the affected
limb. CVI results from incompetence of venous valves, venous
obstruction, or both. Most CVI involves venous reflux, and
severe CVI often reflects a combination of reflux and venous
obstruction. It is important to remember that although CVI
originates with abnormalities of the veins, the target organ
of CVI is the skin, and the underlying physiologic and biochemical mechanisms leading to the cutaneous abnormalities associated with CVI are poorly understood. A typical
leg affected by CVI will be edematous, with edema increasing over the course of the day. The leg may also be indurated
and pigmented with eczema and dermatitis. These changes
are associated with excessive proteinaceous capillary exudate
and deposition of a pericapillary fibrin cuff that may limit
nutritional exchange. In addition, an increase in white blood
cell trapping within the skin microcirculation in CVI patients
may lead to microvascular congestion and thrombosis. Subsequently, white blood cells may migrate into the interstitium
and release necrotizing lysosomal enzymes, potentially leading to tissue destruction and eventual ulceration.
Fibrosis can eventually develop from impaired nutrition,
chronic inflammation, and fat necrosis ( lipodermatosclerosis).
Hemosiderin deposition due to the extravasation of red cells
and subsequent lysis in the skin contributes to the characteristic pigmentation of chronic venous disease (Fig. 24-1).
Ulceration can develop with long-standing venous hypertension and is associated with alterations in microcirculatory
and cutaneous lymphatic anatomy and function. The most
common location of venous ulceration is approximately 3 cm
proximal to the medial malleolus (Fig. 24-2). (See Schwartz
11th ed., p. 983.)
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FIG. 24-1. Characteristic hyperpigmentation
of chronic venous insufficiency.
FIG. 24-2. Venous ulceration located
proximal to the medial malleolus.
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3. Venous thromboembolism (VTE) is associated with all
of the following EXCEPT:
A. Increased morbidity and mortality.
B. Pulmonary hypertension.
C. Postthrombotic syndrome.
D. No change in future risk of VTE.
CHAPTER 24
Venous and Lymphatic Disease
4. Which of the following factors is the most important in
the development of spontaneous deep vein thrombosis?
A. Stasis
B. Endothelial Damage
C. Hypercoagulability
D. All of the above
Answer: D
The incidence of VTE is approximately 100 per 100,000 people per year in the general population, with 20% of the diagnoses made within 3 months of a surgical procedure. Of the
symptomatic patients, one-third will present with pulmonary
embolism (PE) and two-thirds with deep vein thrombosis
(DVT). The estimated number of cases of VTE may well be
over 600,000 per year in the United States, making it a major
US health problem. Furthermore, death occurs in 6% of DVT
and 12% of PE cases within 1 month of diagnosis. Not only
does VTE pose a veritable threat to life, but it also places
patients at higher risk for recurrence and post-VTE sequelae
such as pulmonary hypertension and postthrombotic
syndrome, with 4% and up to 30% incidence, respectively.
(See Schwartz 11th ed., p. 984.)
Answer: C
Three conditions, first described by Rudolf Virchow in 1862,
contribute to venous thromboembolism (VTE) formation:
stasis of blood flow, endothelial damage, and hypercoagulability. Of these risk factors, relative hypercoagulability
appears most important in most cases of spontaneous VTE,
or so-called idiopathic VTE, whereas stasis and endothelial damage likely play a greater role in secondary VTE, or
so-called provoked VTE, occurring in association with
transient risk factors such as immobilization, surgical procedures, and trauma. (See Schwartz 11th ed., p. 984.)
5. All of the following are acquired risk factors for venous
thromboembolism (VTE) EXCEPT:
A. Nephrotic syndrome.
B. Factor V Leiden.
C. Malignancy.
D. Pregnancy.
E. Obesity.
F. Varicose veins.
Answer: B
The more common acquired VTE risk factors include older
age (>40 years), hospitalization and immobilization, hormone replacement and oral contraceptive therapy, pregnancy
and the recently postpartum state, prior VTE, malignancy,
major surgery, obesity, nephrotic syndrome, trauma and spinal cord injury, long-haul travel (>6 hours), varicose veins,
antiphospholipid syndrome, myeloproliferative disorders,
and polycythemia. Heritable risk factors include male sex,
factor V Leiden mutation; prothrombin 20210A gene variant;
antithrombin, protein C, and protein S deficiencies; and dysfibrinogenemias. In some patients, the cause of the thrombophilia may have both a heritable and an acquired component.
These mixed causes include homocysteinemia; factors VII,
VIII, IX, and XI elevation; hyperfibrinogenemia; and activated protein C resistance in the absence of factor V Leiden.
There may be a synergistic effect when particular multiple
inherited and acquired risk factors are present in the same
patient.
Other patient-specific factors associated with venous
thrombosis include the traditional cardiovascular risk factors of obesity, hypertension, and diabetes. VTE is more
common in whites and African Americans than Asians and
Native Americans. Certain gene variants (single nucleotide
polymorphisms) are also associated with a mildly increased
risk for VTE, and their presence may interact with other risk
factors to increase the overall risk for venous thrombosis.
(See Schwartz 11th ed., Figure 24-3, p. 984.)
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6. May-Thurner syndrome is an anatomical factor associated with increased deep vein thrombosis (DVT) formation, and is characterized by which of the following?
A. Narrowing of the left iliac vein at the site where the
right iliac artery crosses over it
B. Narrowing of the left renal vein as it traverses beneath
the superior mesenteric artery
C. Subclavian vein narrowing due to repetitive upper
extremity effort
D. A rapidly expanding hemangioma
7. All of the following are absolute contraindications to
catheter-directed thrombolysis EXCEPT:
A. Prior history of ischemic or hemorrhagic stroke
within 3 months.
B. Traumatic cardiopulmonary resuscitation within 3
weeks.
C. Known intracranial neoplasm.
D. Age > 75 years.
Answer: A
Anatomic factors may also contribute to development of DVT.
At the site where the right iliac artery crosses over the left iliac
vein, the left iliac vein may become chronically narrowed predisposing to iliofemoral venous thrombosis, so-called MayThurner syndrome. External compression of major veins by
masses of various types can also lead to venous thrombosis.
(See Schwartz 11th ed., p. 985.)
Answer: D
There are contraindications to thrombolytic therapy. Absolute
contraindications include prior history of ischemic or hemorrhagic stroke within 3 months, head trauma within 3 months,
neurologic surgery within 6 months, known intracranial
neoplasm, internal bleeding within 6 weeks, active or known
bleeding disorder, traumatic cardiopulmonary resuscitation
within 3 weeks or suspected aortic dissection. Fortunately,
serious remote bleeding is uncommon, and intracranial hemorrhage rarely occurs. The majority of bleeding complications
are limited to the venous access site. Symptomatic pulmonary embolism occurs uncommonly and is very rarely fatal.
(See Schwartz 11th ed., pp. 990–991.)
CHAPTER 24
Venous and Lymphatic Disease
8. Phlegmasia cerulea dolens is best described as:
A. Asymptomatic, but extensive deep vein thrombosis
(DVT).
B. Isolated popliteal vein thrombosis.
C. Extensive DVT of the major axial deep venous chan-
nels of the lower extremity potentially complicated by
venous gangrene and/or the need for amputation.
D. Painless lower extremity swelling.
Answer: C
Clinical symptoms may worsen as DVT propagates and
involves the major proximal deep veins. Extensive DVT of the
major axial deep venous channels of the lower extremity with
relative sparing of collateral veins causes a condition called
phlegmasia cerulea dolens (Fig. 24-3). This condition is characterized by pain and pitting edema with associated cyanosis.
When the thrombosis extends to the collateral veins, massive fluid sequestration and more significant edema ensue,
resulting in a condition known as phlegmasia alba dolens. The
affected extremity in phlegmasia alba dolens is extremely painful and edematous and pale secondary to arterial insufficiency
from dramatically elevated below lower knee compartment
pressures. Both phlegmasia cerulean dolens and phlegmasia
alba dolens can be complicated by venous gangrene and the
need for amputation. (See Schwartz 11th ed., p. 986.)
FIG. 24-3. Phlegmasia cerulea dolens of
the left leg. Note the bluish discoloration.
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9. According to the American College of Chest Physicians,
the recommended duration of long-term antithrombotic
therapy after provoked deep vein thrombosis (DVT) is:
A. 2 weeks.
B. 1 month.
TABLE 24-1 Summary of American College of Chest Physicians recommendations
C. 3 months.
D. 6 months.
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Venous and Lymphatic Disease
Clinical Subgroup Antithrombotic Treatment Duration
First episode DVT/transient risk/surgery VKA or LMWH for 3 months
First episode DVT/unprovoked VKA or LMWH for 3 months
Distal DVT/unprovoked
• Symptomatic
• Asymptomatic and no risk factors for progression
Second episode DVT/unprovoked
DVT and cancer
LMWH = low molecular weight heparin; VKA = vitamin K antagonist.
Data from Kearon C, Akl EA, Comerota A J, et al: Antithrombotic therapy for VTE disease: Antithrombotic Therapy and Prevention
of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines, Chest. 2012;
141(2 Suppl): e419S-e496S.
Answer: C
Table 24-1 (See Schwartz 11th ed., Table 24-4, p. 990.)
regarding duration of long-term antithrombotic therapy for deep vein
thrombosis (DVT)
Consider for long-term therapy if:
• Proximal DVT
• Minimal bleeding risk
• Stable coagulation monitoring
VKA for 3 months
Serial imaging in 2 weeks, if progression VKA
for 3 months
VKA for extended therapy
LMWH for extended therapy over VKA
10. Which of the following statements related to inferior
vena cava (IVC) filters is TRUE?
A. Placement of an IVC filter allows for a reduced dura-
tion of anticoagulation therapy.
B. In patients with a proximal DVT, placement of an
IVC filter reduces rate of pulmonary embolism, and
also prolongs early and late survival.
C. The rate of fatal complications related to IVC filters is
<0.12%.
D. An IVC filter is safe to leave in place after it is no
longer needed.
E. All of above.
Answer: C
When possible, anticoagulation therapy should be continued
in patients with vena cava filters. 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. In patients who
are not able to receive anticoagulants due to recent surgery or
trauma, the clinician should continually reassess if anticoagulation may be started safely at a later date.
Placement of permanent IVC filters has been evaluated as
an adjunct to routine anticoagulation in patients with proximal DVT. Routine IVC filter placement has not been shown to
prolong early or late survival in patients with proximal DVT
but did decrease the rate of PE (HR, 0.22; 95% CI, 0.05–0.90);
however, there is an increased rate of recurrent DVT in
patients with IVC filters (HR, 1.87; 95% CI, 1.10–3.20).
IVC filters are associated with acute and late complications.
Acute complications include thrombosis or bleeding at the
insertion site and misplacement of the filter. Late complications
include thrombosis of the IVC, DVT, breaking, migration, or
erosion of the filter through the IVC (Fig. 24-4). The rate of fatal
complications is <0.12%. As a result of the increasing number of
reported complications with IVC filters, the US Food and Drug
Administration (FDA) issued a warning in 2010 recommending removal of IVC filters as soon as they are no longer needed.
This was followed by an update in 2014 where the recommendation was made to remove IVC filters within 29 and 54 days
after implantation based upon a mathematical model that suggested an increased risk-to-benefit ratio at this time point. (See
Schwartz 11th ed., p. 991.)
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CHAPTER 24
A
Venous and Lymphatic Disease
FIG. 24-4. Preoperative computed tomography
imaging and intraoperative photo demonstrating
erosion of IVC filter through the IVC wall.
11. All of the following are appropriate therapies for suppurative thrombophlebitis (SVT) EXCEPT:
A. Nonsteroidal anti-inflammatory medications.
B. Antibiotics.
C. Systemic steroid therapy.
D. Removal of existing indwelling venous catheters.
B
Answer: C
Treatment of SVT is quite variable. A Cochrane Review
reported that low molecular weight heparin (LMWHs) and
nonsteroidal anti-inflammatory drugs both reduce the rate of
SVT extension or recurrence. Topical medications appear to
improve local symptoms. Surgical treatment, combined with
the use of graduated compression stockings, is associated with
a lower rate of venous thromboembolism (VTE) and SVT
progression. The treatment is individualized and depends on
the location of the thrombus and the severity of symptoms. In
patients with SVT not within 1 cm of the saphenofemoral junction, treatment consists of compression and administration
of an anti-inflammatory medication such as indomethacin.
In patients with suppurative SVT, antibiotics and removal of
any existing indwelling catheters are mandatory. Excision of
the vein may be necessary but is usually reserved for patients
with systemic symptoms or when excision of the involved vein
is straightforward. If the SVT extends proximally to within
1 cm of the saphenofemoral junction, extension into the common femoral vein is more likely to occur. In these patients,
anticoagulation therapy for 6 weeks and GSV ligation appear
equally effective in preventing thrombus extension into the
deep venous system. (See Schwartz 11th ed., p. 994.)
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12. All of the following findings on venous duplex ultrasonography (DUS) suggest acute venous thromboembolism (VTE) EXCEPT:
A. Venous distention.
B. Formation of venous collaterals.
C. Inability to compress vessel walls.
D. Loss of respiratory variation.
E. Lack of spontaneous flow.
CHAPTER 24
Venous and Lymphatic Disease
Answer: B
The examination begins at the ankle and continues proximally to the groin. Each vein is visualized, and the flow signal is assessed with distal and proximal compression. Lower
extremity deep vein thrombosis (DVT) can be diagnosed by
any of the following DUS findings: lack of spontaneous flow
(Fig. 24-5), inability to compress the vein (Fig. 24-6), absence
of color filling of the lumen by color flow DUS, loss of respiratory flow variation, and venous distention. Again, lack of
venous compression on B-mode imaging is the primary diagnostic variable. Several studies comparing B-mode ultrasound
to venography for the detection of femoropopliteal DVT in
patients clinically suspected to have DVT report sensitivities
of >91% and specificities of >97%. The ability of DUS to assess
isolated calf vein DVT varies greatly, with sensitivities ranging from 50% to 93% and specificities approaching 100%. (See
Schwartz 11th ed., pp. 986–987)
FIG. 24-5. Duplex ultrasound of a femoral vein containing
thrombus demonstrating no flow within the femoral vein.
FIG. 24-6. B-mode ultrasound of the femoral
vein in cross-section. The femoral vein does not
collapse with external compression (arrows).
R FVP R FVP
No compression Compression
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13. Heparin-induced thrombocytopenia (HIT) is characterized by which of the following?
A. Diagnosis based on prior exposure to heparin with
platelet count <120,000 and/or platelet decline of
40% following heparin exposure
B. Results from heparin-associated antiplatelet antibod-
ies directed against platelet factor 4 complexed with
heparin
C. Low incidence in patients with repeat exposure to
heparin
D. Minimal association with thrombotic complications
14. Direct thrombin inhibiting medications include which
of the following?
A. Warfarin
B. Enoxaparin
C. Argatroban
D. Fondaparinux
Answer: B
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 HAAbs 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.
HIT is diagnosed based on previous exposure to heparin,
platelet count < 100,000, and/or platelet count decline of
50% following exposure. All heparin must be stopped and
alternative anticoagulation initiated immediately to avoid
thrombotic complications, which may approach 50% over
the subsequent 30 days in affected individuals. (See Schwartz
11th ed., p. 988.)
Answer: C
Direct thrombin inhibitors (DTIs) include recombinant hirudin, argatroban, and bivalirudin. These antithrombotic agents
bind to thrombin, inhibiting the conversion of fibrinogen to
fibrin as well as thrombin-induced platelet activation. These
actions are independent of antithrombin. The DTIs should
be reserved for (a) patients in whom there is a high clinical
suspicion or confirmation of HIT, and (b) patients who have a
history of HIT or test positive for heparin-associated antibodies. In patients with established HIT, DTIs should be administered for at least 7 days, or until the platelet count normalizes.
Warfarin may then be introduced slowly, overlapping therapy
with a DTI for at least 5 days. (See Schwartz 11th ed., p. 988.)
CHAPTER 24
Venous and Lymphatic Disease
15. All of the following are components of the treatment of
lymphedema EXCEPT:
A. Extremity compression and elevation.
B. Prophylactic antibiotics.
C. Intermittent pneumatic compression therapy.
D. Lymphatic massage.
Answer: B
Bed rest and leg elevation. Elevation is an important aspect
of controlling lower extremity swelling and is often the first
recommended intervention. However, continuous elevation
throughout the day can interfere with quality of life more
than lymphedema itself. Elevation is an adjunct to lymphedema therapy but is not the mainstay of treatment.
Intermittent pneumatic compression therapy. The use of
IPC with a single-chamber or multichamber pump temporarily reduces edema and provides another adjunct to the use of
compression stockings. These devices have been shown to be
effective in reducing limb volume; however, use of compression stockings is necessary to maintain the volume reduction
when the patient is no longer supine because fluid transport
is not associated with the transport of macromolecules (proteins) from the tissue. Typically, IPC is used for 4 to 6 hours
per day at home when the patient is supine, with pressure
ranges between 30 and 60 mm Hg demonstrated to be most
effective.
Lymphatic massage. Manual lymphatic drainage is a form
of massage developed by Vodder that is directed at reducing
edema. In combination with the use of compression stockings, manual lymphatic drainage is associated with a longterm reduction in edema and fewer infections per patient per
year.
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Antibiotic therapy. Patients with lymphedema are at
increased risk of developing cellulitis in the affected extremity due to microscopic breakdown in the skin barrier either
secondary to swelling or unrecognized and untreated tinea
pedis. Recurrent infection can damage the lymphatics, aggravating the edema and increasing the risk for subsequent
infection. Staphylococcus and β-hemolytic Streptococcus are
the most common organisms causing soft tissue infection.
Aggressive antibiotic therapy and elevation with compression are recommended at the earliest signs or symptoms of
cellulitis. The drug of choice is penicillin or a cephalosporin
active against Streptococcus for 5 days. In patients with recur-
rent cellulitis despite methods to reduced edema, treatment
with monthly intramuscular injections of benzathine penicillin 1.2 MU, twice-daily erythromycin 250 mg, or penicillin V
1 g daily has proven effective at suppression. (See Schwartz
11th ed., pp. 1001–1003.)
16. Mesenteric vein thrombosis (MVT) is associated with all
of the following EXCEPT:
A. MVT is less common in patients with hypercoagu-
lable states, malignancy, or cirrhosis.
B. 5% to 15% of cases of acute mesenteric ischemia
occur as a result of MVT.
C. Patients with MVT are treated with fluid resuscita-
tion, heparin anticoagulation, and bowel rest.
D. Computed tomography (CT) scan and magnetic res-
onance imaging (MRI) are 100% sensitive and 98%
specific for MVT.
Answer: A
Five percent to 15% of cases of acute mesenteric ischemia
occur as a result of MVT. Mortality rates in patients with
MVT may approach 50%. The usual presenting symptom
is nonspecific abdominal pain and distention, often accompanied by nausea, vomiting, and diarrhea. Peritoneal signs,
suggesting intestinal infarction, are present in fewer than half
of MVT patients. MVT is more common in patients with
a hypercoagulable state, malignancy, and cirrhosis. MVT
occurs as a rare complication of laparoscopic surgery.
Most cases of MVT are diagnosed with contrast-enhanced
CT scanning or MRI in the course of an evaluation for
abdominal pain. The sensitivity and specificity for CT and
MRI approach 100% and 98%, respectively. Ultrasound can
also be used and has reported sensitivity and specificity of
93% and 99%, respectively.
Patients with MVT are treated with fluid resuscitation,
heparin anticoagulation, and bowel rest. (See Schwartz
11th ed., p. 996.)
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The Esophagus and Diaphragmatic Hernia
1. Locations of anatomic narrowing of the esophagus seen
on an esophagram include all of the following EXCEPT:
A. Lower esophageal sphincter.
B. Crossing of the left mainstem bronchus and aortic
arch.
C. Thoracic outlet.
D. Cricopharyngeal muscle.
2. The cervical esophagus receives its blood supply primarily from the:
A. Internal carotid artery.
B. Inferior thyroid artery.
C. Superior thyroid artery.
D. Inferior cervical artery.
E. Facial artery.
Answer: C
Three normal areas of esophageal narrowing are evident on
the barium esophagogram or during esophagoscopy. The
uppermost narrowing is located at the entrance into the
esophagus and is caused by the cricopharyngeal muscle. Its
luminal diameter is 1.5 cm, and it is the narrowest point of the
esophagus. The middle narrowing is due to an indentation
of the anterior and left lateral esophageal wall caused by the
crossing of the left main stem bronchus and aortic arch. The
luminal diameter at this point is 1.6 cm. The lowermost narrowing is at the hiatus of the diaphragm and is caused by the
gastroesophageal sphincter mechanism. The luminal diameter at this point varies somewhat, depending on the distention of the esophagus by the passage of food, but has been
measured at 1.6 to 1.9 cm. These normal constrictions tend to
hold up swallowed foreign objects, and the overlying mucosa
is subject to injury by swallowed corrosive liquids due to their
slow passage through these areas. (See Schwartz 11th ed.,
p. 1010.)
Answer: B
The cervical portion of the esophagus receives its main blood
supply from the inferior thyroid artery. The thoracic portion receives its blood supply from the bronchial arteries,
with 75% of individuals having one right-sided and two leftsided branches. Two esophageal branches arise directly from
the aorta. The abdominal portion of the esophagus receives
its blood supply from the ascending branch of the left gastric artery and from inferior phrenic arteries (Fig. 25-1).
On entering the wall of the esophagus, the arteries assume a
T-shaped division to form a longitudinal plexus, giving rise to
an intramural vascular network in the muscular and submucosal layers. As a consequence, the esophagus can be mobilized from the stomach to the level of the aortic arch without
fear of devascularization and ischemic necrosis. Caution
should be exercised as to the extent of esophageal mobilization in patients who have had a previous thyroidectomy with
ligation of the inferior thyroid arteries proximal to the origin
of the esophageal branches. (See Schwartz 11th ed., p. 1013.)
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