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T. Gabriel et al.
Physical Exam
Patients with DVT may exhibit swelling, tenderness, erythema, rmness along the leg, as well as
a positive Homan’s sign. Patients with Homan’s
sign experience increased calf pain with dorsiexion of the foot; however, this is a poor predictor of DVT.
Pathology/Description
DVTs can develop due to stasis of blood ow
within the deep vein system, endothelial injury,
or because of a hypercoagulable state, known as
Virchow’s Triad [9]. DVTs occur in 300,000–
600,000 people in the United States per year [7].
For common risk factors, see Table27.4.
Symptoms will develop in the affected limb.
Most patients will experience pain, swelling,
warmth, erythema, hyperpigmentation, aching,
throbbing, and limb heaviness. If patients experience chest pain, shortness of breath, tachypnea,
tachycardia, or unexplained cough with DVT,
they should be screened for pulmonary embolus
[10] (Chap. 22).
Imaging andDiagnosis
D-dimer can be tested, but it is not recommended
given low specicity. Diagnosis of DVT is
obtained via visualization of thrombus in the
vein. Venous duplex for evaluation of DVT is the
gold standard (Fig. 27.6); however, computed
tomography venography (CTV) can also be
obtained (Fig. 27.7). Interventional venogram
can be diagnostic as well therapeutic. Patients
Table 27.4 Risk factors for DVT
Family history/genetics History of prior
thrombotic event
Malignancy Spinal cord injury/
paralysis
African American race Tobacco use
Oral contraceptives Pregnancy (6weeks
postpartum)
Surgery within 3months Venous catheters
Prolonged immobility-travel,
cast
Age >40years and risk
doubles with every 10years
Congestive heart failure Sickle cell disease
Autoimmune disorders Hypercoagulable states
Hospitalization
Hypertension
Fig. 27.6 Femoral vein that does not collapse with pressure. The lack of compression is suggestive of thrombus
and DVT at the yellow arrow

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recommend if thrombus has propagated (even if
remaining in the distal veins).
lated DVTs who are experiencing severe symptoms. Apixaban, dabigatran, edoxaban, or
rivaroxaban over VKA is recommended in the
rst 3 months (treatment phase), and AC alone
over interventional therapies (thrombolytic,
mechanical, or pharmacochemical) for acute
DVTs. Oral Xa inhibitor (apixaban, edoxaban,
rivaroxaban) over LMWH is recommended for
Fig. 27.7 CTV to evaluate IVC stented segment. Dark
thrombus formation is seen on the right side of the stented
IVC segment
initiation and treatment phases for patients with
cancer. VKA (with INR target 2.5) is recommended for patients diagnosed with triple
antiphospholipid syndrome.
who have unprovoked DVT should undergo
hypercoagulable workup. EKG, echocardiogram
(to evaluate for right heart strain), CT angiography of the chest, or ventilation-perfusion (VQ)
scan may be used to evaluate for pulmonary
embolism.
mendations on duration of treatment. Patients
with acute DVT without contraindication for AC
should begin a treatment phase of 3 months of
AC. At the completion of 3 months, patients
should be assessed for extended therapy. Therapy
should be extended for patients if the VTE was
unprovoked or provoked by a persistent risk factor (prefer DOAC over VKA).
Management
DVT include thrombolysis, catheter-directed
The aim of DVT management is to reduce risk of
thrombus propagation and embolization, relieve
acute symptoms, and reduce risk of lasting complications [11]. DVTs are managed with anticoagulation (AC). Intravenous options for this
include systemic regular dose unfractionated
heparin in the acute setting. Therapeutic lowmolecular- weight heparin (enoxaparin) or oral
anticoagulation can be used in the acute, subacute, or chronic phase. Oral anticoagulants
include direct-acting oral anticoagulants
(DOACs) (apixaban, dabigatran, edoxaban, rivaroxaban) or warfarin (vitamin k
antagonists-VKA).
The CHEST Guidelines can help aid clinician
decision-making based on DVT classication.
CHEST recommends serial imaging (weekly
venous ultrasound) for 2 weeks instead of
anticoagulation in patients with isolated distal
DVT of the leg without severe symptoms or risk
factors for extension. Upon repeat imaging, AC is
not recommended if no extension is seen and is
therapy, and thrombectomy. Thrombolysis,
catheter- directed thrombolysis, and surgical
thrombectomy are reserved for extensive proximal lower extremity DVT (iliofemoral) for those
with severe symptoms, threatened limb (phlegmasia), and with thrombus burden for <14days
[11] (see Table27.5). For these patients, the benet of more aggressive intervention may outweigh the associated risks [13]. The 2016 AC
Forum and 2020 NICE recommend individual
risk-to- benet analysis for catheter-directed therapy (CDT) and that patients with iliofemoral
DVT who have symptoms for <14 days, good
functional status, life expectancy of 1+ years, and
low risk for bleeding be considered for CDT [13].
sound to evaluate DVT if symptoms worsen—
this will evaluate for thrombus propagation.
Swelling and leg heaviness may persist for
those with extensive DVTs, despite surgical
intervention and post intervention therapies.
This can be alleviated by consistent use of com-
287
CHEST recommends AC for patients with iso-
The CHEST guidelines also provide recom-
Surgical interventions for management of
Patients should undergo repeat venous ultra-

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T. Gabriel et al.
Table 27.5 Contraindication to thrombolysis and DVT
[12]
Absolute Relative
Recent intracranial
hemorrhage (ICH)
Severely uncontrolled
HTN
Cerebral vascular
lesion-neoplasm
Ischemic stroke within
3months
Possible aortic
dissection
Head trauma or facial
trauma within
3months
Recent intracranial or
spinal surgery
Active bleeding
(except menses)
Streptokinase within
6months
History of uncontrolled HTN
Severe hypertension at
presentation (SBP >180, DBP
>110)
CPR >10min within last
3weeks
Remote ischemic stroke
Dementia
Pregnancy
Major surgery within 3weeks
Internal bleeding within
2–4weeks
Active peptic ulcer disease
Noncompressible vascular
puncture
pression garments, leg elevation, and regular
exercise. Patients can begin wearing compression garments once a DVT is deemed stable,
and not propagating. Compression garments
help support venous structure and reduce
venous stasis. There is no evidence that the use
of graduated compression garment reduces the
risk of DVT.Bed rest is not recommended after
DVT diagnosis while starting anticoagulation
therapy [11].
Clinical Pearls
• Aside from patient with asymptomatic distal
DVT, patients without contraindication to AC
should be treated for a minimum of 3–6months
with the option of extending duration of
therapy.
• When selecting AC, DOACs are preferred
over VKA EXCEPT in patients with
moderate- severe liver disease or antiphospho-
lipid syndrome [7].
• Oral Xa inhibitor (apixaban, edoxaban, rivar-
oxaban) over LMWH is recommended for ini-
tiation and treatment phases for patients with
cancer.
• Clinicians should weigh risk of bleeding when
considering anticoagulation. Risk factors for
major bleeding while taking AC include age
>65, alcohol use, liver failure, renal failure,
anemia, antiplatelet therapy, cancer, reduced
functional capacity, frequent falls, prior bleeding issues, prior stroke, and recent surgery
[11].
• An inferior vena cava (IVC) lter may be
placed in patients with acute proximal DVT of
the leg who have contraindication to AC.
• It is important to educate patients on modiable risk factors to prevent new or recurrent
thrombotic events. These risk factors include
medication compliance, smoking cessation,
heart healthy diet, regular exercise, weight
management, and surgical prophylaxis.
• Phlegmasia dolens is a rare and life- threatening
complication of extensive, acute DVT
[14].Surgical intervention due to arterial perfusion compromise and risk of limb loss may
be needed.
References
1. Britannica, The Editors of Encyclopaedia. “artery”.
Encyclopedia Britannica, 6 Jun. 2023, https://www.
britannica.com/science/artery. Accessed 29 July 2023.
2. Berger J, Davies M. Overview of lower extremity peripheral arterial disease. UpToDate. 2021.
www.uptodate.com/contents/overview- of- lowerextremity- peripheral- artery- disease?source=history_
widget#H16453723. Accessed 14 Mar 2022.
3. Hussain MA, Al-Omran M, Creager MA, Anand
SS, Verma S, Bhatt DL. Antithrombotic therapy for
peripheral artery disease: recent advances. J Am Coll
Cardiol. 2018;71:2450–67.
4. Douketis J. Overview of the venous system. 2021.
https://www.merckmanuals.com/home/heartand- blood- vessel- disorders/venous- disorders/
overview- of- the- venous- system.
5. Moore KJ, Tabas I.Macrophages in the pathogenesis
of atherosclerosis. Cell. 2011;145(3):341–55, www.
cell.com/abstract/S0092- 8674(11)00422- 3. https://
doi.org/10.1016/j.cell.2011.04.005.
6. Lip, etal. Overview of the treatment of lower extremity deep vein thrombosis. 2022. https://www.uptodate.

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289
com/contents/overview- of- the- treatment- of- lowerextremity- deep- vein- thrombosis- dvt.
7. Ortel, et al. American Society of Hematology 2020
guidelines for management of thromboembolism:
treatment of deep vein thrombosis and pulmonary
embolism. 2020. https://ashpublications.org/bloodad-
vances/article/4/19/4693/463998/American- Societyof- Hematology- 2020- guidelines- for.
8. Kushner A, West P, Pillarisetty L.Virchow triad. 2021.
https://www.ncbi.nlm.nih.gov/books/NBK539697/.
9. Themes, UFO.Peripheral vascular disease. Thoracic
Key. Southern California Vascular Institute. 2017.
https://thoracickey.com/peripheral- vasculardisease- 2/, https://calvascular.net/peripheral- vasculardisease/. Accessed 14 Mar 2022.
10. Venous thromboembolism. n.d.. https://www.nhlbi.
nih.gov/health- topics/venous- thromboembolism.
11. Wilburn & Shian. Deep venous thrombosis and pulmonary embolism: current therapy. 2017. https://
www.aafp.org/afp/2017/0301/p295.html.
12. Baig & Bodle. Thrombolytic therapy. 2021. https://
www.ncbi.nlm.nih.gov/books/NBK557411/.
13. Stevens, et al. Antithrombotic therapy for VTE
disease: second update of the chest guidelines
and expert panel report. 2021. https://journal.
chestnet.org/article/S0012- 3692(21)01507- 5/
fulltext?_ga=2.38742947.1844619104.1647184408-
751823456.1647184408.
14. Chaochankit & Akaraborworn. Phlegmasia cerulea
dolens with compartment syndrome. 2018. https://
www.ncbi.nlm.nih.gov/pmc/articles/PMC6200621/.

Diseases oftheAorta
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TracyTotten andFrankR.Arko III
28
Aneurysm
Anatomy andPhysiology
The term aneurysm describes dilatation of any
blood vessel greater than 1.5× increase in diameter compared with expected normal diameter.
Excluding intracranial vessels, arterial aneurysms are most prevalent in the infrarenal aorta
[1]. Aortic aneurysms are commonly associated
with concomitant aneurysm of the ascending
aorta, thoracic aorta, iliac, femoral, or popliteal
arteries.
Arterial walls are made up of three layers:
tunica intima, media, and adventitia. A true aneurysm involves dilation of all intact layers of the
arterial wall due to remodeling of the extracellular matrix (ECM) (Fig.28.1).
T. Totten (*)
Atrium Health/Sanger Hearth and Vascular Institute,
Charlotte, NC, USA
e-mail: tracy.totten@atriumhealth.org
F. R. Arko III
Vascular and Endovascular Surgery, Atrium Health/
Sanger Heart and Vascular Institute,
Charlotte, NC, USA
e-mail: Frank.Arko@atriumhealth.org
Pathology/Description
Aneurysmal degeneration of the aorta is a multifactorial, systemic process generally felt to be
due to alterations in vascular wall biology leading to a loss of vascular structural proteins (viz.,
collagen) and wall strength. Biomechanical
forces, including stress across the arterial wall,
are also felt to play a role [3]. As the aorta
enlarges, turbulent ow develops within the
aneurysm due to the ow dynamics and can lead
to thrombus formation along the aortic wall [4].
This can lead to distal embolization.
Classication
The shape of aneurysms is dened as fusiform or
saccular. A fusiform aneurysm is a ballooning on
all sides of the aorta, whereas a saccular aneurysm is a focal enlargement which is one sided. A
false aneurysm (pseudoaneurysm) develops from
arterial injury with subsequent hematoma formation and does not involve all three layers of the
arterial wall (Fig.28.2).
Aneurysms can occur throughout the entirety
of the aorta. Location of aneurysms includes the
aortic root, ascending aorta, aortic arch, thoracoabdominal aorta (Type I, II, III, IV), suprarenal
aorta, juxtarenal, and infrarenal aorta. Abdominal
aortic aneurysms (AAAs) are a leading cause of
death in the United States [1]. AAAs are classi-
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
R. Musialowski, K. Allshouse (eds.), Cardiovascular Manual for the Advanced Practice Provider,
https://doi.org/10.1007/978-3-031-35819-7_28
291

292
Internal Elastic Lamina
aneurysm
aneurysm
aneurysm
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T. Totten and F. R. Arko III
External Elastic Lamina
Physiological
ECM
remodeling
smooth muscle cell
fibroblast
collagen
Glycosaminoglycans (GAGs)
Tu nica Intima
Proteoglycan
MMPs
TIMPs
Macrophages
Neutrophils
Tu nica Media
Tu nica Adventitia
Adverse ECM
remodeling
leading to
aortic aneurysm
Fig. 28.1 Extracellular matrix, regional heterogeneity of the aorta, and aortic aneurysm [2]
diameter and length, with diameter being the
important risk factor for rupture (Table28.1).
Risk Factors
Aortic aneurysms often occur in the setting of
other concomitant diseases. Most AAAs are
related to atherosclerotic disease (Table28.2).
Incidence of AAA increases in males age
Fusiform
Saccular
aneurysm
Saccular and
fusiform
Pseudo
Fig. 28.2 Types of aneurysm
ed based on anatomical location, shape, and
size (Fig.28.3).
Depending on the location and size of the
aneurysmal segment, the management and classication can vary. Aneurysm size is described by
greater than 60 years and females greater than
70years of age. Males are more likely to develop
AAA than females. However, females are more
likely to rupture at a smaller size than males [5].
Genetic conditions that are known to be associated with developing aortic aneurysms include
Ehlers-Danlos syndrome (EDS) and Marfan’s
syndrome. These conditions are more concerning
in patients who present with aneurysms at a
younger age. There is high association between
smoking and development of aneurysm.

THORA
ANEUR
YSM
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CIC AORTIC
YSMS
293
AORTIC ANEURYSMS
THORACIC AORTIC ANEURYSMS
ABDOMINAL
AORTIC ANEURYSM
Fig. 28.3 Aortic aneurysm morphology and location
Table 28.1 Size and rupture risk [5]
Size of aneurysm Annual risk of rupture
Small (3–3.9cm) No increased risk
Medium (4–4.9cm) 1%
Large (5–5.9cm) 5–10%
Very large (6–6.9cm) 10–20%
Giant (7–7.9cm) 20–40%
>8cm 30–50%
Table 28.2 Risk factors for aneurysm development
Atherosclerotic disease Any tobacco use
Family history Male sex
Genetic predisposition PAD/PVD
Autoimmune/inammatory
process
Remote aortic
surgery
Infection Hypertension
Age >60years Caucasian race
Obesity Trauma
NORMAL AORTA
NORMAL AORTA
DESCENDING THORACIC
AORTIC ANEURYSM
ABDOMINAL AORTIC ANEURYSM
SUPRARENAL
ABDOMINAL
AORTIC ANEURYSM
AORTIC ROOT
ANEURYSM
PARARENAL
ABDOMINAL
AORTIC ANEURYSM
AORTIC ARCH
ANEURYSM
JUXTARENAL
ABDOMINAL
AORTIC ANEURYSM
Asymptomatic screening is recommended in
patients with tobacco use.
Signs andSymptoms
AAAs are commonly asymptomatic and found
incidentally during workup for other disease processes or on an age-related screening exam.
Symptomatic patients can present with a wide
array of symptoms. This may include abdominal,
back, or ank pain. If there is evidence of a large
AAA, the patient can present with obstructive
symptoms such as gastric outlet obstruction
(GOO), nausea/vomiting, urinary symptoms due
to obstruction of ureters, and inferior vena cava
compression and deep vein thrombosis (DVT). If
ASCENDING THORACIC
AORTIC ANEURYSM
INFRARENAL
ABDOMINAL
AORTIC ANEUR

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T. Totten and F. R. Arko III
an AAA has evidence of thrombus along the aortic wall, a patient may present with embolic
changes (i.e., claudication, discoloration of toes,
and feet).
Physical Exam
When examining the vascular patient for a concern of aortic aneurysm, it is important to complete a full vascular exam. This includes a full
abdominal examination, lower extremity, and
peripheral pulse examination including palpation
of the popliteal fossa for pulsatile masses, auscultation of carotid bruits, and cardiac auscultation.
The provider must keep in mind the following list
of physical exam ndings as the patient may
present with any of the following (Table 28.3).
Do not rely on a physical exam to diagnose a
AAA since it is a difcult clinical diagnosis.
Always check distal pulses due to risk of embolic
disease and concomitant PAD.
and surveillance of AAA and lower extremity
aneurysms [5]. This is also the cheapest and least
invasive. It is not uncommon that an abdominal
CT scan will be ordered for a patient during
workup of abdominal pain revealing an incidental nding of AAA. Non-contrasted abdominal
CT scans can help to identify AAAs but are not
an ideal study for surgical planning. A CT angiography of the abdomen and pelvis is the most
accurate modality for preoperative workup or
concern for ruptured AAA.A CTA chest/abdomen/pelvis should be considered for any thoracic
or thoracoabdominal aortic aneurysm. MRI of
the lumbar spine can also help to identify AAA
but are not ideal studies for AAA and are not
appropriate for surgical planning (Fig.28.4).
Management
Aortic aneurysms are managed medically with
regular imaging surveillance until they reach size
criteria for surgical intervention. A goal of aneu-
Imaging
When working up an AAA, there are many different imaging modalities. Duplex ultrasound
(DUS) is the modality of choice for screening
Fig. 28.4 Infrarenal AAA pre-EVAR with heavy thrombus (DARK) and atherosclerotic burden (calcication in wall
of aorta) on CT imaging
Table 28.3 Physical ndings consistent with AAA
Abdominal pulsatile mass Enlarged popliteal pulse
Aortic bruit Painful aortic palpation
Abdominal, inguinal, or
ank pain
Embolic changes in lower
extremity

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295
rysmal disease is early detection, surveillance,
and elective repair to prevent complications of
rupture, thrombosis, or embolism. The diagnosis
and treatment will depend on stability of the
aneurysm [5]. Vascular surgery referral can be
placed for any aortic aneurysm. Any incidence of
ruptured aortic aneurysms requires emergent
operative repair.
Medical management is indicated for stable
aortic aneurysms of less than 5.5cm in males and
less than 5.0cm in women. Modiable risk factors in the medical management of aortic aneurysms include smoking cessation, management
of hypertension, cholesterol, obesity, and atherosclerotic disease. Medical therapy includes antiplatelet therapy, statin drugs, and blood pressure
management with a goal of normotension. Betablocker therapy is preferred as rst-line agent.
Full anticoagulation is needed if thromboembolic
disease distal to an aneurysm is identied with
mural thrombus within the aneurysm. Avoid the
use of uoroquinolones as they have been shown
to increase size of AAA and complications associated with rupture or dissection.
Once an aneurysm is diagnosed, DUS surveillance is obtained and is based on size and location (Table28.4).
The timing of surgical intervention is often
guided by size of the aneurysm (Table28.5).
Table 28.4 Aneurysm surveillance AAA
Aneurysm size
<4.0cm Annually
4.0–5.0cm Every 6months
>5.0 C TA
Table 28.5 Aneurysm size and indication for surgical
intervention
Rapid growth 0.5cm over 6months
Ascending and abdominal >5.5cm males, >5.0cm
females
Ascending and abdominal Marfan’s >5.0cm male,
4.5cm female
>4.5cm ascending root if aortic valve disease
involvement
Isolated aortic arch >5.5cm
Popliteal >2.5cm asymptomatic
Common iliac >3.5cm asymptomatic
Duplex imaging frequency
Surgical intervention is then further dened
based on endovascular repair versus open repair.
EVAR is the most common repair, but there are
still cases in which open repair is preferred.
Endovascular repair is dened as EVAR (endovascular aortic repair), TEVAR (thoracic endovascular repair), and FEVAR (fenestrated
endovascular aortic repair).
Open aortic repair is completed with aortic
bypass grafting with either aortoiliac, aortobifemoral bypass graft, or straight aortic tube graft
for patients without iliac artery involvement.
Open repair may be indicated in younger patients
who are otherwise healthy; patients with anatomy
not conducive to EVAR, including short or angulated infrarenal aortic neck; and multiple branch
vessels increasing risk for endoleak. Patients
with connective tissue disorders may be favored
for open repair.
Endovascular aortic repair is completed via
percutaneous or open arterial access.
Straightforward EVAR can be completed with
procedural sedation versus general sedation.
Open access may be indicated in patients with
concomitant peripheral arterial disease, small
access vessels, or prior surgical interventions.
Depending on the complexity of the repair,
alternative access sites may also be indicated
including brachial artery or open axillary artery
conduit. Repair is completed by placing a bifurcated endograft within the aorta thereby excluding the aneurysm sac (Fig. 28.5). Prior to
completion, a nal angiogram is imaged to ensure
no evidence of endoleak at the remainder of the
case. Occasionally, assistive devices are used to
aid with the seal zone including xation devices,
coiling, or onyx glue in patients with a short
neck.
Open aortic repair is completed via midline
or retroperitoneal incision (Fig. 28.6). The
extent of repair is based on anatomical involvement of iliac and femoral arteries or concomitant PAD. The incision is carried down to the
abdominal cavity exposing the aorta. A retroperitoneal approach is performed with the
patient in right lateral decubitus position through
a left ank incision. The proximal and distal
arteries are then clamped, repair is completed

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Fig. 28.5 EVAR treatment of AAA with exclusion of residual thrombus
Table 28.6 Types of endoleaks (EL)
1 abProximal (a) distal (b) graft attachment site leaks
2 Retrograde ow into the sac via aortic side
branches (i.e., lumbar, mesenteric)
3 Defect in the graft either d/t fabric tear or
disconnection of modular overlap
4 Graft wall porosity
5 Increase in maximum aneurysm diameter with no
identiable endoleak; endotension
a
Intervention is indicated for Types 1, 3, and 2 when EL
sac with increasing aortic size [6]
T. Totten and F. R. Arko III
Fig. 28.6 Open aorto-bi-iliac bypass with Dacron graft
by replacing the aneurysmal segment with synthetic graft, the aneurysm is then oversewn, and
the abdomen is closed.
Postoperative surveillance of EVAR of the
infrarenal segment can be completed with aortic
duplex in the vascular surgery clinic. An endoleak
is dened as ow outside of the endograft and
within the remaining AAA sac, risking continued
aneurysm growth (Table28.6).
Clinical Pearls
• Consider screening patients with risk factors
for AAA given they are commonly
asymptomatic.
• Fluoroquinolones are contraindicated in
patients with history of aortic aneurysm or
dissection as there is an increased risk of
aneurysm and dissection with this drug
class.
• Consider TTE screening for ascending aortic
aneurysm with new diagnosis of AAA and
vice versa.
• Endocarditis prophylaxis should be recommended with any patient s/p aortic graft.
• There is risk for genetic inheritance of aneurysms, thus recommend family screening.
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