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2 components of Aorta
thoracic (ascending, arch, descending); Abdominal
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3 layers of aorta:
Intima; Media; Adventitia
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Intima:
thin, inner layer (delicate, easily traumatized)
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Media:
thick middle layer (*strength of the aorta comes from media)
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Adventitia:
somewhat thin outer layer (contains mainly collagen)
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Strength of the aorta lies in:
media (= laminated, intertwining elastic tissue/ multiple layers, in a spiral manner, max tensile strength w/ distensible & elastic
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Pseudoaneursym
well defined collection of blood & conn tissue outside vessel wall
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Atherosclerotic vs inflammatory
inflame = extreme of atherosclerotic aneurysm
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pathogenesis of AAAs:
multifactorial: genetic, environ, hemodynamic & immunological; Chlamydia pneumoniae?
-
Aorta most affected by atherosclerotic process:
infrarenal abdominal aorta
-
most common site of AAA formation:
infrarenal abdominal aorta
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Atherosclerotic dz of aorta may produce:
stenotic obstrusion or aneurysmal dilatation
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Aneurysm types
Saccular; fusiform
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Most common aneurysm type
Fusiform
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Has a fairly symmetrical dilation (involves full circumference of aortic wall)
Fusiform
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More localized dilation (outpouching of a portion of aortic wall)
Saccular aneurysms
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Flow disturbance thru the aneurysmal aortic segment:
blood may stagnate along walls, cause mural thrombus (may embolize)
-
Aneurysm defn:
1.5x or > the normal diameter of the vessel.
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Aneurysm type cf prevalence
Abdominal more common than thoracic aneurysm
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Half of newly detected AAAs are:
<5cm (& 2/3 eventually require repair)
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AAA & COPD:
COPD pts: rupture of smaller AAAs more likely
-
AAAs usually involve:
aortic bifurcation (& often involve common iliac arteries)
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AAA & Rupture
80% rupture into left retroperitoneum (may contain it); remainder rupture into peritoneal cavity (=> uncontrolled hemorrhage & rapid circulatory collapse)
-
Healthy, young normal aorta: size
about 2 cm
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Considered Aneurysm at size:
> 3 cm
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AAA Incidence in Men vs Women
10:01
-
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AAAs arise in areas of:
dense athero-sclerosis, eroding & weakening the wall which leads to dilatation then rupture
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90% of AAAs originate where:
below renal arteries (infrarenal); 10% suprarenal
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Infrarenal aneurysm may exhibit:
stenosis (narrowing) of aorta
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AAA: Surgery recommended when:
>5 cm*
-
Decline of aortic elasticity & distensibility is accelerated in pts with:
HTN, hyperlipidemia, & atherosclerosis of coronaries & other arteries.
-
Loss of aortic elasticity
loss of elastin & increase in collagen (=> lack of distensibility)
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AAA: Risk Factors
Tobacco; Age; HTN; lipid; Atherosclerosis; Male; FH
-
FH in AAA:
1/4 of AAA pts have first degree relative with hx of AAA
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Initial dx test to screen for & follow known AAA =
Abdominal US:
-
Abdominal US: advantages
100% sensitivity, no contrast, low cost
-
AAA: CT scan
pre-op or if US indeterminate; better defines shape & location/ extent of AAA
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AAA: Catheter aortography may:
underestimate diameter
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AAA Risk Factors for Rupture
Size (5cm female, 6 cm male); rapid progression (>1cm/yr); female; FH; unctrld HTN; SMK; COPD
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AAA Surveillance
Trend: bigger AAA, more frequent surveil
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AAA: for average risk pts, a threshold of ?? cm in diameter is appropriate for elective repair
5.5 cm
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AAA: what may prompt earlier endovasc repair?
Rapid expansion (>1 cm/yr) & pt preference (in 4.5-5.5 cm range)
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AAA Endovascular repair: No justification for:
endovascular repair at smaller diameters
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AAA: for women, elective endovasc repair is appropriate at:
4.5 or 5.0 cm
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AAA Prognosis
80% mortality with rupture
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AAA mgmt:
Risk factor mod (stop SMK, aggressive HTN & Lipid Rx), med mgmt to slow progression
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AAA operative mortality:
Elective = 2-5%, Expanding = 5-15%, Ruptured: >50%
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Criteria for Endovascular Repair: Proximal neck:
length: min 15 mm; diameter: max 28 mm; angulation: <60 degrees
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Criteria for Endovascular Repair: Iliac arteries
Common iliac a.: variable diameters; ext iliac a. <7 mm
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USPSTF Screening Guidelines: repair what in who?
large AAA (> 5.5 cm) in men btw 65-75 w/ Hx of SMK; No gdln for men 65-75 no hx SMK; gdln against screen in women
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USPSTF AAA Screen Consensus stmt
All M 60-85; All F 60-85 w/ 1 or more CVD risk factor; M&F > 50 w/ FH AAA
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Thoracic aneurysm: prevalence
Far less common than AAAs
-
Thoracic aneurysm: classified by:
pt of aorta involved ( ascending, arch or descending TA)
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Thoracoabdominal AA =
desc TA extends distally to involve AA
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TAAA: prevalence
Less common than AAA w/ diff pathogenesis; 60% = aortic root & ascend A; 40% desc A; 10% arch
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Sm mx cell drop out & elastic fiber degen w/ media of cystic spaces filled w/ mucoid matl =
Cystic medial necrosis
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Cystic medial necrosis occurs most frequently in:
ascending aorta
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Cystic medial necrosis leads to:
aortic wall weakening => fusiform aneurysm
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Aneurysm from cystic medial necrosis often involve:
aortic root & may consequently result in AI
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CMN is accelerated by:
HTN (occurs somewhat w/ aging)
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CMN assoc with:
conn tissue dz (Marfan, Ehlers-Danlos syndrome, RA); aortic valve replacement
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Asc TA: Etiologies
CMN, Bicuspid valve; AI; Arteritis/ Vasculitis; Collagen vasc dz (RA, Marfan, Ehlers-Danlos, Reiter); HTN; Syphilis; Atherosclerosis
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Ascending aneurysms usually caused by:
CMN
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If Asc aneurysm due to atherosclerosis, assoc with:
diffuse aortic atherosclerosis
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Aortic Arch aneurysms often contiguous with:
aneurysms of asc OR desc A & can be caused by any of the etiologies above.
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Desc TA: predominant cause =
atherosclerosis
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Desc TA: tend to originate:
just distal to origin of L subclavian; may be fusiform or accular
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A Arch A: Etiologies
Ext of Asc or Desc aneurysms; Hx trauma or deceleration injury
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Desc TA: called thoracoabdominal if they:
extend below level of diaphram into abd aorta
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TAA: Spontaneous rupture prevalence
less common than AAA (bc inc of Sx due to compression of surrounding structures)
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TAA: Tx: >5 cm
surgery (if Sx or rapid expansion: then sooner)
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Sx pts or w/ AI:
Inc incidence of rupture
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TAA: Clinical Findings
> 50% pts ASx at dx; Sx due to vascular consequence or mass effect
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TAA: Vascular Sx
AI with CHF, or thromboembolism causing stroke, lower extremity or mesenteric ischemia, renal infarct
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TAA: Mass Effect
SVC syndrome, tracheal deviation, cough, hemoptysis, dysphagia, hoarseness
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Ascending or arch An can cause compression of:
SVC or innominate v. => obstruction of venous return
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Desc/ arch An: may cause compression of:
trachea or main stem bronchus => tracheal deviation, wheezing, cough & positional dyspnea, hemoptysis or recurrent pneumonitis
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Desc/ arch An: Compression of esophagus can cause:
dysphagia & compression of recurrent laryngeal n. can cause hoarseness
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TAA: Clinical Findings
Pain ( 25% pts) from direct compression of intrathoracic structures or chest wall; substernal or in back/ neck; steady, deep & severe?
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TAA Rupture:
excruciating pain; may be assoc w/ aortic dissection
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Rupture occurs most commonly into:
L intrapleural space or mediastinum; results in severe hypotension
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Desc An rupture into:
adjacent esophagus => life threatening hematemesis
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TAA Evaluation
CXR; Echo (TTE vs TEE); CT/ MRI
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TAA: CXR for dx:
CXR NOT dx alone (need CT or MRI to r/out if CXR neg)
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TAA: Pos CXR:
Must differentiate from anterior mediastinal mass (ie thymoma, lung CA)
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TAA: if surgery required, need:
coronary angiography
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Echo: TTE vx TEE
TTE only good to visualize aortic root (good for Marfan); TEE to visualize entire aorta, but is semi invasive (CT/ MRI better)
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TAA Mgmt: major factors in rupture risk
Size & rate of growth
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TAA Mgmt: Annual growth rate for <5cm aneurysm
2%
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TAA Mgmt: Annual growth rate for 5-5.9 cm
3%
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TAA Mgmt: Annual growth rate for >6 cm
7%
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TAA: Inc rupture risk at smaller diameters with:
Marfan; bicuspid valve
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Asc Aorta: surgery indicated at:
≥ 5.5 cm (=/> 5.5)
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Marfan/ Bicuspid Valve: surgery indicated at:
≥ 5.0 cm (=/> 5.0)
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Aortic valve replacement: surgery indicated at:
≥ 4.0 cm (=/> 4.0)
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Desc Aorta: surgery indicated at:
≥ 6.0 cm (=/> 6.0)
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Aortic Root Replacement: Bentall:
Dacron graft w/ prosthetic valve sewn directly into aortic annulus; coronary arteries reimplanted into the graft (op mortality risk 5%)
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Aortic Root Replacement: David =
valve sparing Bentall (re-implant native valve within dacron graft)
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TAA: Prognosis
M&M higher than with AAA; 5 yr if unrepaired (>6 cm) is 20-25% (most deaths due to rupture or CAD)
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TAA: 1 month op mortality =
8-20%
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TAA: op complications
pulmo comps & damage to laryngeal or phrenic n., carotid or subclavian a. poss
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Aortic dissection: incidence
3/100,00/yr (at least 7,000 cases/yr in the US)
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Aortic dissection: usual direction of extension
antegrade (driven by the forward force of aortic blood flow); sometimes retro from site of intimal tear
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Tear in aortic intima usu preceded by medial wall degen/ CMN =
aortic dissection
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Aortic dissection: intimal tear in aorta creates a false lumen between:
media & adventitia
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Aortic dissection: time course
May be acute or chronic
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Aortic dissection: >95% occur in the:
Ascend aorta just distal to aortic valve or just distal to L subclavian at lig arteriosum
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Intimal tears resulting in dissection: prevalence:
65% Ascend A; 20% Desc A; 10% A Arch; 5% Abd A.
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Aortic Dissection: M vs F
Men > women 2:1 (peak incidence 60-70 y.o.); 2,000-3,000 cases/yr
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Aortic Dissection: Increased risk in:
pregnancy (1/4 of all female cases <40 yrs & most in last trimester); conn tissue dz (Marfan, Ehlers Danlos); Bicuspid Aortic Valve or Coarctation
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Aortic Dissection: 80% of pts are:
Hypertensive
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Aortic Dissection: Debakey I =
Ascending A extending to distal
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Aortic Dissection: Debakey II =
Ascending aorta only
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Aortic Dissection: Debakey III =
Descending aorta only
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Aortic Dissection: Stanford A =
Any involvement of ascending aorta
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Aortic Dissection: Stanford B =
Not involving ascending aorta
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Aortic Dissection: Proximal =
DeBakey Types I & II or Stanford Type A
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Aortic Dissection: Distal =
DeBakey Type III & Stanford type B
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Aortic Dissection: Clinical Findings
Acute: sudden, severe excruciating ripping chest pain (ascending) or scapular (descending); most hypertensive or nml
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Aortic Dissection: PE
Pt appears to be in shock; pulse discrepancy or syncope (tamponade)
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Aortic Dissection: poss Sx devt
Acute aortic regurgitation (CHF indicates valve involvement); focal neuro (CVA may develop)
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Aortic Dissection Eval: CXR =
wide mediastinum, poss L sided pleural effusion
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Aortic Dissection Eval: Echo =
98% sensitive, 99% specific, +/- pericardial effusion, done bedside
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Aortic Dissection Eval: CT helpful in:
acute presentation
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Aortic Dissection Eval: MRA/MRI useful for:
serial follow up
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Aortic Dissection Eval: EKG =
LVH, nonspecific or inferior abnormalities (dissections preferentially extend into Right coronary ostium)
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Aortic dissection: CXR =
Wide aortic silhouette & mediastinum; Left pleural effusion; 10%-20% normal
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Aortic Dissection: mgmt: Type A =
Surgical repair, may require AVR
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Aortic Dissection: mgmt: Type B =
Medical therapy
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Aortic Dissection: mgmt: Type B: Exceptions to med tx:
Rupture, Limb/ visceral ischemia, Saccular morphology, ongoing pain, uncontrolled HTN, Marfan, AI
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Aortic Dissection: mgmt: Chronic & asymptomatic =
medical Rx
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Aortic Dissection: mgmt: All pts =
aggressive BP control; yearly imaging or if increased Sx
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Aortic Dissection: Prognosis
Op mortality of type B 2x that of type A (bc comorbid illness)
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Aortic Dissection: 5 yr survival: repaired Type A =
70-80% repaired type A
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Aortic Dissection: 5 yr survival: repaired Type B =
50-70% repaired type B
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Aortic Dissection: Prognosis: chronic type B
30% => progressively enlarging aneurysm that eventually requires repair
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Most common cause of chronic lower limb occlusive disease
Atherosclerosis
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PAD hx
Hx of intermittent claudication or rest pain
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PAD location: Buttock/Hip:
Aortoiliac disease
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PAD location: Thigh:
Common femoral artery
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PAD location: Upper calf:
superficial femoral artery
-
PAD ad location:
Lower calf: popliteal artery
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PAD location: Foot:
tibial/peroneal artery
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PAD S/S
Diminished peripheral pulses, femoral bruits, cool skin temp, abnormal skin color, poor hair growth
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PAD Clinical Findings
Intermittent Claudication; ischemic rest pain; ulceration; tTissue necrosis
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Intermittent Claudication:
mx pain in LE induced by exercise and relieved with rest; highly reproducible
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Intermittent Claudication: contrasts with:
pseudoclaudication of spinal stenosis (normal pulses/color)
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PAD: Diff dx
Baker Cyst; Chronic compartment syn; Arthritis; Nerve root compression; Spinal stenosis; Venous claudication
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PAD Screen: ABI: Normal
1.0+ (blood pressure augments distally)
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PAD Screen: ABI: < 0.9
dx of peripheral vascular dz
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PAD Screen: ABI: < 0.7
intermittent claudication
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PAD Screen: ABI: < 0.4
rest pain
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PAD Screen: ABI: < 0.1
impending tissue necrosis
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PAD Mgmt:
Risk factor mod; SMK cessation; Walking program; antiplt tx (aspirin & clopidogrel); Pletal Trental; revascularization (Surgery vs Stenting)
-
ABIs performed to assess:
Asx PAD or mild to mod claudication
-
ABIs helpful to predict:
CLI (Critical Limb Ischemia) & amputation; wound healing; or to screen/ monitor
-
Acute arterial occlusion: Clinical features
Pain; Pulseless; Pallor; Paresthesia; Paralysis; Poikilothermia
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Acute art occlusion: Etiologies:
Embolism; Thrombus in situ
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Acute art occlusion: some d/t embolism: from:
heart, aorta, large arteries
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Acute art occlusion: Thrombus in situ: d/t:
atherosclerotic plaque, trauma, hypercoagulable dz
-
Acute art occlusion: Clinical Findings
Valvular dz or valvular prosthesis Ischemic dz (post MI/ plaque rupture); Paradoxical emboli from DVT of leg rarely produce emboli
-
Acute art occlusion: 80-90% of arterial emboli arise from:
the heart
-
Acute art occlusion: A-fib prevalence
present in 60-70% (thrombus forms in left atrial appendage)
-
Acute Arterial Occlusion Tx
Revascularization; IV heparin; Intra-arterial thrombolytic therapy; Surgical thromboembolectomy; Surgical bypass
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Venous Dz
Varicose V; Chronic Venous Insuff; Superficial Thrombophlebitis; DVT
-
Dilated, tortuous alterations of the saphenous v. & tributaries (lie immed under skin in the Les)
Varicose Veins
-
Varicose V. pathology related to:
venous valve incompetence & subsequent venous reflux from increased pressure
-
Varicose V. Clinical Findings
Asymptomatic to dull, aching pain or discomfort of legs usu worse after prolonged standing
-
Emboli from heart: destinations
50%-60% to LEs, 20% to cerebrovasc; 10-20% to UEs/ renal/ mesenteric circ
-
Varicose v: Increased frequency after:
pregnancy
-
Varicose Veins: DDx
Secondary VV d/t: chronic venous insufficiency of deep vein; Retroperitoneal venous obstruction; Arteriovenous fistula; congenital venous malformation
-
Varicose: complications
Thrombophlebitis
-
Sluggish blood flow in varicose v. => local thrombosis =
Thrombophlebitis
-
Thrombophlebitis: predisposing conditions =
pregnancy, local trauma, long periods sitting
-
Thrombophlebitis rarely:
ascends in trunk of Gr saphenous v. & leads to thrombosis of femoral vein
-
Varicose V. Tx:
Graduated compression stockings (TED); Elevate legs; endovenous ablation (radiofrequency vs laser); sclerotherapy; greater saphenous vein stripping (older)
-
Chronic V. Insuff: Pathophys:
Functionally inadequate v. valves in LEs d/t bad leaflets (do not coapt)
-
Chronic V. Insuff: valve damage poss d/t:
post-thrombotic syndrome (scarred/thick) or dilatation of vein & unable to coapt
-
Chronic V. Insuff: Clinical Findings
Hx DVT/ leg trauma; EDEMA (below knees); brawney skin pigmentation & venostasis ulcer (above ankles); pruritic, dull discomfort(esp w/ long standing)
-
Chronic V. Insuff: DDx
LE edema d/t: CHF; chronic renal dz; decomp liver dz; Lymphedema (usually unilateral); Autoimmune; PAD
-
Chronic V. Insuff: Tx
Grad compression stockings; avoid long stand/ sit; elevate legs; last: pneumatic leg compressions
-
Inflammation, induration, erythema & tenderness along a superficial vein =
Superficial Thrombophlebitis
-
Superficial Thrombophlebitis usu involves what vein:
long saphenous v.
-
Superficial Thrombophlebitis: spont occur in pt with:
PG, blunt trauma, IV infusion, thromboangitis obliterans, abd ca;
-
Superficial Thrombophlebitis : assoc with DVT how often:
20% of cases
-
Superficial Thrombophlebitis: Clinical Findings
linear erythema, induration, & dull tenderness along affected vein
-
Superficial Thrombophlebitis: Fever & chills suggest:
septic phlebitis (IV line)
-
Superficial Thrombophlebitis: Circular lesion more consistent with:
cellulitis
-
Superficial Thrombophlebitis: prevention:
Avoid prolonged standing
-
Superficial Thrombophlebitis: Tx
local heat & elevation, bed rest, NSAIDs; Sx usually resolve in 7- 10 days
-
Superficial Thrombophlebitis: Tx: if progressive recurrence =
Ligation surgery
-
Superficial Thrombophlebitis: Tx if extension into deep venous system =
Anticoagulation
-
Superficial Thrombophlebitis: Prognosis
usually benign & brief (Varicose v. etiology: recurrent)
-
Septic thrombophebitis mortality =
20% (usu Staph (Antibx & vein excision)
-
Phlebitis of saphenous vein rarely:
extends to deep veins (potential for PE)
-
Thromboembolus of deep veins of LEs (deep saphenous) or pelvis =
DVT
-
DVT: 80% develops in:
deep veins of the calf
-
DVT: 20% develops in:
femoral or iliac vein
-
Virchow’s Triad:
Stasis, Vascular Injury, Hypercoaguable State
-
DVT: Precipitators:
Long bedrest/ immobility (surg), long air travel, malignancy, nephrotic syndrome
-
DVT Clinical Findings
50% Asx; dull aching pain in calf/leg, worse with ambulation; edema in affected limb, palpable cord, low grade temp, tachycardia; Homan sign 50% of time
-
Wells Criteria: Clinical evidence for DVT =
3 points
-
Wells Criteria: PE the No. 1 dx =
3 points
-
Wells Criteria: HR > 100 bpm =
1.5 points
-
Wells Criteria: Immobilization/Surgery in past 4 wk =
1.5 points
-
Wells Criteria: Previous DVT/PE =
1.5 points
-
Wells Criteria: Cancer =
1 point
-
Wells Criteria: Hemoptysis =
1 point
-
Wells Criteria: Score of <2:
makes dx highly unlikely
-
Wells Criteria: Score of > 6:
highly likely
-
DVT Evaluation
D-dimer; LE Doppler/ US; if PE suspected, VQ scan versus spiral CT; hypercoaguable w/u if no identifiable predisposing event
-
D-dimer results:
negative result is helpful; pos results non-specific
-
DVT Tx
Hep (vs LMWH) & concomitant warfarin loading; warfarin; Thrombolytic tx; embolectomy; IVC filter
-
warfarin tx for DVT
(INR 2.0 – 2.5); idiopathic 6 mos 1st event; non-idiopathic or recurrent event: consider indefinite tx
-
DVT complications
PE; ischemic limb; varicose v.; chronic venous insufficiency
-
DVT Prevention in Surg pts: Low risk:
Minor surg in pt < 40 yrs w/ no additional risk factors
-
DVT Prevention in Surg pts: mod risk:
Minor surg in pt < 40yrs w/ an additional risk factor or surg in pt 40-60 years of age
-
DVT Prevention in Surg pts: High risk:
Surgery in pt > 60 years or in pt 40-60 with risk factors
-
DVT Prevention in Surg pts: Highest Risk:
Surg in pt > 40 yrs w/ multiple risk factors or hip/knee arthroplasty or major trauma spinal cord injury
-
DVT: Risk factors:
age, cancer, prior VTE, obesity, heart failure, paralysis, hypercoaguable state
-
DVT Prophylaxis in Surg pts: Low risk:
Early ambulation, pneumatic stockings
-
DVT Prophylaxis in Surg pts: Mod risk:
SubQ unfract hep or LMWH +/- pneumatic compression
-
DVT Prophylaxis in Surg pts: High risk:
SubQ LMWH
-
DVT Prevention in medical pts
No formal risk assessment; pneumatic compression stockings for low risk pts; unfract hep or LMWH for other pts w/ systemic illness limiting mobility esp w/ other risk factors
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