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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 dorsi­exion 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 Table27.4.
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 andDiagnosis
D-dimer can be tested, but it is not recommended given low specicity. 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 (6weeks
postpartum) Surgery within 3months Venous catheters Prolonged immobility-travel, cast Age >40years and risk doubles with every 10years 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 classication. 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 <14days [11] (see Table27.5). For these patients, the ben­et of more aggressive intervention may out­weigh the associated risks [13]. The 2016 AC Forum and 2020 NICE recommend individual risk-to- benet 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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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 3months Possible aortic dissection Head trauma or facial trauma within 3months Recent intracranial or spinal surgery Active bleeding (except menses) Streptokinase within 6months
History of uncontrolled HTN
Severe hypertension at presentation (SBP >180, DBP >110) CPR >10min within last 3weeks Remote ischemic stroke
Dementia
Pregnancy
Major surgery within 3weeks
Internal bleeding within 2–4weeks 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 3–6months
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 modi­able 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, etal. Overview of the treatment of lower extrem­ity deep vein thrombosis. 2022. https://www.uptodate.
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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 oftheAorta
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TracyTotten andFrankR.Arko III
28
Aneurysm
Anatomy andPhysiology
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.
Classication
The shape of aneurysms is dened 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
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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 (Table28.1).
Risk Factors
Aortic aneurysms often occur in the setting of other concomitant diseases. Most AAAs are related to atherosclerotic disease (Table28.2).
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 clas­sication can vary. Aneurysm size is described by
greater than 60 years and females greater than 70years 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
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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 (3–3.9cm) No increased risk Medium (4–4.9cm) 1% Large (5–5.9cm) 5–10% Very large (6–6.9cm) 10–20% Giant (7–7.9cm) 20–40% >8cm 30–50%
Table 28.2 Risk factors for aneurysm development
Atherosclerotic disease Any tobacco use Family history Male sex Genetic predisposition PAD/PVD Autoimmune/inammatory process
Remote aortic
surgery Infection Hypertension Age >60years 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 andSymptoms
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 difcult 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 (calcication 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 5.5cm in males and less than 5.0cm in women. Modiable 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 identied 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 (Table28.4).
The timing of surgical intervention is often guided by size of the aneurysm (Table28.5).
Table 28.4 Aneurysm surveillance AAA
Aneurysm size <4.0cm Annually
4.0–5.0cm Every 6months >5.0 C TA
Table 28.5 Aneurysm size and indication for surgical intervention
Rapid growth 0.5cm over 6months Ascending and abdominal >5.5cm males, >5.0cm females Ascending and abdominal Marfan’s >5.0cm male,
4.5cm female >4.5cm ascending root if aortic valve disease involvement Isolated aortic arch >5.5cm Popliteal >2.5cm asymptomatic Common iliac >3.5cm asymptomatic
Duplex imaging frequency
Surgical intervention is then further dened 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 dened 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
identiable 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 dened as ow outside of the endograft and
within the remaining AAA sac, risking continued aneurysm growth (Table28.6).
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.