Professional Documents
Culture Documents
Arteries diseases
Thoracic aortic aneurysm
Abdominal aortic aneurysm (AAA)
Aortic dissection
Peripheral arterial disease (PAD)
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DEFINING THORACIC AORTIC
ANEURYSM
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Abdominal Aortic Aneurysm (AAA)
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Acute Aortic Dissection
Classification
DeBakey :
Most common aortic emergency Type I:
I: involve the ascending aorta, aortic arch and the
Incidence double that of ruptured decending aorta
Type II:confined
II:confined to the ascending aorta
abdominal aortic aneurysms Type III:
III: confined to the descending aorta
Type IIIA:
IIIA: above the diaphragm
Without treatment, 36-
36-72% of patients Type IIIB:
IIIB: below the diaphragm
will die within 48 hours (one week Stanford:
Stanford:
Type A:involve
A:involve the ascending aorta
mortality of up to 91% ) Type B:
B: do not involve the ascending aorta
Acute: less than 2 weeks
Chronic: more than 2 weeks
Intramural Hematoma
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Aortic Dissection
Classic presentation includes acute-
acute-onset,
severe chest/back pain described as tearing
or ripping
Atypical presentations are common
15% of patients report NO pain
Supportive findings include pulse deficit, new
aortic regurgitation, tamponade, and focal
neurological deficits
Majority of patients have no specific physical
findings
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Clinical Findings(II) Ancillary Evaluation
Physical Examination Routine Lab. Tests: non-
non-specific
pulse deficits and discrepancies in BP EKG: shows LVH reflecting long-
long-standing
between limbs are key diagnostic clues hypertension
pulse deficits (50%) the EKG is useful in excluding myocardial
aortic regurgitation(50%) infarction
neurologic findings(20%): altered
sensorium,
sensorium, hemiplegia,
hemiplegia, hemianesthesia,
hemianesthesia,
gaze preference to the affected side
Radiography (I)
Chest X ray
mediastinal widening(75%)
calcium sign
sign -uncommon but highly specific, >5mm
double-
double-density appearance of the aorta
a localized bulge along a normally smooth aortic
contour
a disparity in the caliber between the descending and
ascending aorta
obliteration of the aortic knob
displacement of the trachea or nasogastric tube to the
Abnormal CXR finding a 1- 1-cm separation between the
right by the dissection
intimal calcification and the adventitial outline of the descending
descending
pleural effusions(left)
aorta (the calcium sign), consistent with aortic dissection.
Transesophageal Echocardiography
Radiography(II) of Aortic Dissection
Echocardiography
transthoracic approach: M-M-mode & 2-
2-D=low
sensitivity and specificity
transesophageal = more accuracy and very
sensitive, can be done in ER (safer).
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Radiography (III) Radiography(IV)
Computed Tomography limitations of CT scan:
scan:
dilatation of the aorta it dose not provide information about the presence of aortic
identification of an intimal flap regurgitation
differential rates of flow in true and false lumina no information about the relationship of the dissection to the
the clear demonstration of both the true and false major arterial branches of the aorta
lumina time-
time-consuming and requires the patient to be outside ER
advantages over aortography:
aortography:
greater contrast resolution and detects small or delayed
differences in the opacification of true and false channels
may be able to detect a thrombosed false lumen despite
nonopacification
does not require arterial catheterization
Radiology(V) Radiography(VI)
Aortography
disadvantages of aortography:
aortography:
filling of a false channel or channels with or without an
most invasive, most expensive
intervening intimal flap
risks of intravenous contrast material
distortion of the true lumen by either a patent or
inadequate detection of pleural leak
thrombosed false lumen
advantages of aortography:
aortography:
thickening of the aortic wall by more than 5-
5-6 mm
accurate for determining the site of the intimal tear
caused by a thrombosed false lumen
and extent of the dissection
displaced intimal calcification
easily demonstrated aortic regurgitation
the only procedure that demonstrates the extent
and location of dissection into aortic side branches
Differential Diagnosis
Radiography(VII)
Chest pain is the most common symptom in AD
Magnetic Resonance Imaging Acute myocardial infarction
shows the site of intimal tear, type and pain is more typically pressurelike but may radiate to the
extent of dissection, presence of aortic arms or neck
pain does not typically migrate over time
insufficiency, and differential flow velocities
CK-
CK-MB levels are elevated
in the true and false channels and in the Pulmonary embolus
aortic side branches pain is generally respirophasic
advantages:
advantages: hypoxemia secondary to ventilation/perfusion mismatch
no contrast material, no ionizing radiation, Pericarditis
noninvasive pain typically changes with position
auscultation may reveal a pericardial friction rub
EKG is common diagnostic(ST-
diagnostic(ST-segment elevation
prominent in V5-
V5-6 and lead I)
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Treatment(I) Treatment(II)
Emergency Department Definite Therapy
Objective: maintaining systolic blood pressure between 100 and Type A:
A: acute aortic dissections require surgical treatment
120 mmHg the only contradiction to immediate surgical repair of a type
Antihypertensive agents: A dissection is the simultaneous occurrence of a
Sodium nitroprusside:
nitroprusside: 50-
50-100mg +D5W 500ml infused at a rate of
0.5~3 ug/min
ug/min
progressing stroke
Beta-
Beta-adrenergic blocker:reduce the heart rate to 60-60-80/m Type B : medical management mortality is 15- 15-20%(same as
Propranolol:
Propranolol: 1mg IV q 5 min, MAX initial dose < 0.15mg/kg surgery done)
Metoprolol Surgery indications: persistent pain, uncontrolled
Esmolol hypertension, occlusion of a major arterial trunk, frank aortic
Trimethaphan camsylate:
camsylate: a ganglionic blocking agent leaking or rupture, or development of a localized anerysm.
anerysm.
500mg +D5W 500ml infused at a rate of 1- 1-2 mg/min
Labetalol:both
Chronic aortic dissection: control of blood pressure using
Labetalol:both alpha and beta-
beta-blockade properties
initial bolus 10-
10-20 mg, then infuse of 1-
1-2 mg/min beta-
beta-blocking agents(most common)
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RISK FACTORS
Older age (> 40 years)
Male gender
Smoking
Diabetes mellitus
Hyperlipidemia
Hypertension
Hyperhomocysteinemia
1%-2%
Critical
Limb Ischemia
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WHAT CAUSES INTERMITTENT INTERMITTENT CLAUDICATION IS
INDICATIVE OF SYSTEMIC
CLAUDICATION? ATHEROSCLEROSIS
PRIMARY SITES
OF INVOLVEMENT
Femoral & Popliteal
arteries: 80-
80-90%
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HOW DOES AN INTERMITTENT
CLAUDICATION PATIENT PRESENT
CLINICALLY? DIFFERENTIAL DIAGNOSIS
CALF HIP/THIGH/BUTTOCK
Leg pain caused and reproduced by a certain Venous occlusion Arthritis
degree of exertion Tight bursting pain / dull Persistent pain, brought on
Relieved by rest ache that worsens on by variable amounts of
exercise
Not affected by body position standing and resolves Associated symptoms in
Atherosclerotic lesions usually found in arterial with leg elevation other joints
segment one level above affected muscle group Positional pain relief Spinal cord compression
Calf claudication more commonly due to disease Chronic compartment History of back pain
syndrome Symptoms while standing
in femoral arteries and less commonly due to Positional pain relief
disease in popliteal or proximal tibial or peroneal Tight bursting pain
Positional pain relief FOOT
arteries; Hip/Thigh/Buttock claudication due to Arthritis
Nerve root compression
aortoiliac disease Positional pain relief
Buerger disease
(thromboangitis obliterans)
Am J Cardiol 2001; 87 (suppl): 3D-13D Bakers cyst Am J Cardiol 2001; 87 (suppl): 3D-13D
Positional pain relief
Action for relief Stand Sit, change position Am J Cardiol 2001; 87 (suppl): 3D-13D
NEJM 2001; 344: 1608-1621
Time to relief <5 minutes 30 minutes
Also see Table 4 of Hirsch AT, et al. J Am Coll Cardiol. 2006;47:e1-e192.
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Ankle-
Ankle-Brachial Index Values and Ankle-
Ankle-
Clinical Classification Brachial
Index
Clinical Presentation Ankle-
Ankle-Brachial Index
Normal > 0.90
Claudication 0.50-
0.50-0.90
Rest pain 0.21-
0.21-0.49
Tissue loss < 0.20
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The history and physical examination (pulse
evaluation and careful examination of the leg)
are usually sufficient to establish the
diagnosis
Atheroembolic disease
Vascular tumor
Thrombotic disorders
Trauma Iliac syndrome of the No leg pain Atypical
leg pain
Classic
claudication
Chronic critical
limb ischemia
Acute limb
ischemia
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GOALS OF TREATMENT
To relieve exertional symptoms and improve
walking capacity
To improve quality of life
To reduce total mortality as well as cardiac
and cerebrovascular morbidity and mortality
REVASCULARISATION PROCEDURES
EXERCISE PROGRAM
Improves walking ability Incapacitating claudication
Requires motivation and personalised Limb-
Limb-threatening ischemia (pain at rest, non-
non-
supervision healing ulcers and/or infections or gangrene)
Benefits lost if not maintained on regular If symptoms persist despite medical therapy
basis
Overall effectiveness limited
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MEDICAL THERAPY USED IN PAST FOR MANAGING
INTERMITTENT CLAUDICATION SYMPTOMS
ANTIPLATELET THERAPY
Vasodilators (e.g. verapamil,
verapamil, isoxsuprine,
isoxsuprine, Aspirin
cinnarizine,
cinnarizine, xanthinol nicotinate, Clopidogrel (CAPRIE Study)
cyclandelate)
Several controlled trials have No studies have shown that
found no evidence of clinical aspirin or clopidogrel improves
efficacy of drugs of this class claudication symptoms
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UNIQUE MECHANISM OF ACTION Contraindications to Cilostazol Use
Platelet Vasodilation TG
aggregation and z peripheral blood flow HDL
activation Antiproliferative effect
CHF=congestive heart failure.
Pletal (cilostazol) Package Insert. Rockville, Md: Otsuka America Pharmaceutical, Inc; 1999.
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Endovascular Treatment for Claudication: Endovascular Treatment for Claudication
Iliac Arteries
Provisional stent placement is indicated for use in iliac arteries
as salvage therapy for suboptimal or failed result from balloon Endovascular intervention is not indicated if there is no
dilation (e.g. persistent gradient, residual diameter stenosis significant pressure gradient across a stenosis despite flow
>50%, or flow-limiting dissection). augmentation with vasodilators.
Surgery for Critical Limb Ischemia Surgery for Critical Limb Ischemia
Femoral-
Femoral-tibial artery bypasses should be constructed with
Bypasses to the above-
above-knee popliteal artery should be autogenous vein, including ipsilateral greater saphenous vein,
constructed with autogenous saphenous vein when possible.
or if unavailable, other sources of vein from the leg or arm.
Bypasses to the below-
below-knee popliteal artery should be
constructed with autogenous vein when possible. Composite sequential femoropopliteal-
femoropopliteal-tibial bypass, or bypass
to an isolated popliteal arterial segment that has collateral
Prosthetic material can be used effectively for bypasses to the outflow to the foot, are acceptable methods of
below knee popliteal artery when no autogenous vein from
ipsilateral or contralateral leg or arm is available. revascularization and should be considered when no other
form of bypass with adequate autogenous conduit is possible.
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Buergers disease (Thromboangitis
(Thromboangitis Histology:
obliterans)
obliterans) Localised inflammatory changes occur in walls of
arteries and veins leading to thrombosis.
Definition:
It is occlusive disease of small & medium size
Clinical picture:
arteries, thrombophlebitis of superficial or deep
The usual symptoms and signs of arterial
veins & Raynauds syndrome.
occlusive disease are present.
Gangrene of the toes and fingers is common and
It occurrs in male patients with heavy smoking &
progressive.
usually under the age of 30 years.
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When cooled, these vessels constrict & the part
Raynauds Disease becomes blanched & incapable of finer movements.
The capillaries then dilate & fill with slow flowing
deoxygenated blood, the digits therefore becoming
Small artery, arteriole vasospasm swollen & dusky.
White, blue, red As the attack pass off, the arterioles relax, oxygenated
blood returns into the dilated capillaries & the digits
become red.
Often accompanied by pain.
Mortality is 25% and risk of amputation is 20%. After prolonged arterial obstruction, reperfusion may not be
fully attainable due to distal edema and thrombi forming in
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11-27%of elderly have peripheral arterial disease the microcirculation.
Smoking, diabetes, hyperlipidemia, hypertension and Peripheral nerves and skeletal muscle are very sensitive to
homocysteinemia are significant risk factors ischemia and irreversible damage can occur within 6 h of
anoxia
At least half of the patients with coronary or cerebrovascular
disease have PVD Non-
Non-embolic ischemia is due to atherosclerosis of the
vessels
Pathophysiology Etiology
Progression of ischemic injury can occur Thrombotic occlusion is significantly more common cause of
through several mechanisms: acute limb ischemia than is embolism.
a) propagation of clot to include collateral vessels
Emboli originate from the heart in 80-
80-90 % with atrial
b) ischemia-
ischemia-related distal edema leading to high fibrillation being the cause in two thirds of all peripheral
compartment pressures emboli.
c) fragmentation of clot in the microcirculation Mural thrombus in the ventricle after recent myocardial
infarction is the second most common cause.
d) edema of the microvasculature cells
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Etiology Etiology
Other causes of emboli include atrial myxomas, vegetations Thrombosis unrelated to atherosclerotic disease can occur
from valve leaflets, and parts of prosthetic devices such as at an area of vessel injury during invasive studies.
mechanical valves.
Peripheral arterial supply can be obstructed by vasospastic
Noncardiac causes include thrombi from aneurysms and or inflammatory conditions like Raynaud disease and
atheromatous plaques. Thromboangitiis obliterans (young smokers)
Iatrogenic embolization can happen during angiograhic Limb ischemia can also seen with central causes like
procedures of the aorta and larger vessels thoracic aortic dissection and Takayasu arteritis.
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Treatment
Goals of therapy include restoration of
blood flow, preservation of limb and life,
and prevention of recurrent thrombosis
Current practice includes UFH to prevent
clot extension, venous thrombosis, the
appearance of thrombi distal to the
obstruction, and reocclusion.
Fluid resuscitation and treatment of heart
failure and dysrhythmias are sometimes
necessary to improve limb perfusion.
Definite treatment includes surgery or
thrombolysis
2- Immediate surgical revascularization is indicated in class IIb, or class I, IIa when Compartment syndrome
thrombolysis is not possible or contraindicated
& muscle necrosis
A combination of different procedures can be done:
Arterial exploration at different sites
ttt
Arterial thrombectomy
Bypass surgery based on pre-operative angiography if
available or intra-operative angiography Fasciotomy
Longitudinal incision of the skin & deep fascia to release pressure over swollen muscles
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Amputation:
Upper Extremity Ischemia
Done for irreversible ischemia with permanent tissue
damage (turgid muscles, fixed cyanosis) Upper extremity arterial occlusion is less
common.
There is a well-
well-developed collateral
The level of amputation is decided according to the level of
palpable pulse. circulation around the shoulder and elbow,
thus arterial occlusion is better tolerated.
Palpable popliteal pulse -------------- Below knee amputation
Usual causes are vasospasm, arteritis,
Absent popliteal pulse ---------------- Above knee amputation trauma, hypercoagulable state, plaque
rupture, thoracic outlet syndrome,
aneurysms.
Treatment includes heparinization and
surgical thrombectomy.
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