Vascular

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Vascular

• Arterial system

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Aneurysmal Vascular Disease

• Defined as a permanent localized enlargement of
  an artery to more than 1.5 times its expected
  diameter.
• Aneurysms can develop at any location in the
  arterial tree but are most commonly found in the
  aorta, iliac, popliteal, and femoral arteries, in
  decreasing order of frequency.
• The primary clinical significance of centrally
  located aneurysms (intrathoracic and
  intra-abdominal) is related to the risk of
  aneurysm rupture, whereas the primary clinical
  significance of peripheral aneurysms is related
  to the risk of thrombosis or embolism.
• Aneurysms are classified according to anatomic
  site, morphology, and etiology. The most common
  aneurysm morphology is a fusiform, symmetrical
  circumferential enlargement involving all layers
  of the artery wall. Aneurysms may also be
  saccular with aneurysmal degeneration affecting
  only part of the arterial circumference.
• The most common etiology of aneurysms is
  atherosclerotic degeneration of the arterial
  wall. The pathogenesis is a multifactorial
  process involving genetic predisposition, aging,
  atherosclerosis, inflammation, and localized
  proteolytic enzyme activation. Most aneurysms
  occur in elderly people, and the prevalence of
  aneurysms increases with increasing age.
  Aneurysms can also occur in younger, genetically
  susceptible individuals with Ehlers- Danlos and
  Marfan syndromes. Other etiologies include
  localized infection that results in mycotic
  aneurysms and the rare tertiary stage of
  syphilis. Aortic aneurysms may also occur with
  aortic dissection. Aneurysmal enlargement can
  also result from hemodynamic causes such as
  poststenotic arterial dilation or arteriovenous
  fistulas.
• Pseudoaneurysms (false aneurysms) are localized
  arterial disruptions caused by blunt or
  penetrating trauma, vascular intervention, or
  anastomotic disruption.

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Incidence

• The average age of patients with abdominal aortic
  aneurysms is 75 years, about 10 years older than
  the average age of patients with clinically
  significant arterial occlusive disease. Abdominal
  aortic aneurysms are more common in men than in
  women.
• White men have a higher prevalence than black men
  or women.
• Smoking is the most important risk factor
  .Prevalence of aneurysms is approximately 10 in
  men with hypertension or with clinical evidence
  of peripheral, carotid, or coronary arterial
  disease. There is a definite, familial incidence .

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Abdominal Aortic Aneurysms(AAA)

• The natural history of abdominal aortic aneurysms
  is to enlarge and rupture.
• Treatment strategies are designed to prevent this
  complication.
• Higher enlargement rates have been associated
  with arterial hypertension, chronic obstructive
  lung disease, family history.
• In less than 5 of abdominal aneurysms, the first
  clinical manifestation is embolization to the
  lower extremity. This complication is not related
  to the size of the aneurysm and constitutes an
  independent indication for repair.
• Risk of Rupture
• The single most important factor associated with
  rupture is maximal cross-sectional aneurysm
  diameter.
• AAA more than 5 .5cm should be treated even a
  symptomatic .
• The most powerful factors that increase the risk
  of rupture are chronic obstructive pulmonary
  disease and pain.

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Clinical Presentation of AAA

• Most abdominal aortic aneurysms are asymptomatic
  before rupture,most aneurysms are discovered on
  routine physical examination with the palpation
  of a pulsatile abdominal mass or on imaging while
  investigating an unrelated problem. Approximately
  80 of aneurysms are identified incidentally on
  abdominal ultrasound, computed tomography (CT),
  magnetic resonance imaging (MRI), or plain
  abdominal radiograph.
• Symptomatic Aneurysms can be associated with
  vague abdominal and back discomfort.
  Occasionally, spinal erosion is the cause of back
  pain, and large aneurysms may be associated with
  early satiety and occasionally vomiting.
• Acutely expanding aneurysms produce severe, deep
  back pain or abdominal pain radiating to the
  back. This may be accompanied by tenderness to
  palpation of the aneurysm. This presentation
  often precedes rupture and urgent treatment is
  required.
• Less than 5 of patients with abdominal aortic
  aneurysm have evidence of embolization, usually
  small, to the distal arteries of the lower
  extremities. As many as 12 of aneurysms present
  for the first time with acute aneurysm rupture.
• About 5 of aneurysms present with nonspecific,
  idiopathic retroperitoneal fibrosis. These
  aneurysms are referred to as inflammatory
  aneurysms. They are often associated with pain,
  fever, and fibrosis, which may involve the
  ureters and cause ureteral obstruction.

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Diagnosis

• Physical examination is useful for the diagnosis
  of abdominal aortic aneurysms, especially in thin
  patients and patients with large aneurysms. An
  important feature on physical examination is
  detection of expansile pulsation, where the gap
  between both hands placed on either side of the
  aneurysmv widens with each systole. This finding
  separates the aneurysm from normal aortic
  pulsations, which can be normally palpated in
  thin subjects, particularly those with lordotic
  spines, and young women, and whenever a mass
  overlies the aorta and transmits them.
• Abdominal aortic aneurysms are occasionally
  discovered on plain abdominal or on a lumbar
  spine radiograph by the characteristic eggshell
  pattern of calcification.
• Abdominal ultrasound is the most widely used
  noninvasive test for diagnosing and following up
  abdominal aortic aneurysms. Ultrasound is
  accurate in demonstrating the presence of an
  aortic aneurysm and in measuring transverse
  diameter .Useful for screening and for
  surveillance of small aneurysms and may prove
  useful for follow-up after endovascular repair.
• CT is the most precise test for imaging aortic
  aneurysms. CT scanning clearly demonstrates the
  size and extent of aortic aneurysms and their
  relation to renal and iliac arteries. Renal
  artery stenoses, accessory renal arteries, and
  renal and renal vein anomalies are clearly
  evident. CT has largely replaced arteriography
  for evaluation of aortic aneurysmal disease.
• MRI and MR angiography accurately demonstrates
  aortoiliac aneurysmal disease and is useful for
  planning and for follow-up of endovascular
  repair. It is less sensitive than CT scanning in
  identifying accessory renal arteries and grading
  renal artery stenoses.
• Arteriography ?

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A, Ultrasonography demonstrates an abdominal
aortic aneurysm. Note the posterior mural
thrombus within the aneurysm sac. B,
Three-dimensional CT image illustrates the
presence of an infrarenal abdominal aortic
aneurysm.
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Treatment and Preoperative Evaluation

• All patients with symptomatic AAA , and a
  symptomatic AAA with diameter more than 5.5 cm
  should be treated on elective base .
• Patients with aneurysms are most often elderly
  and frequently have coexisting cardiac,
  pulmonary, or renal disease, which increases the
  risk of aneurysm repair. Complete preoperative
  evaluation and careful patient selection can
  reduce perioperative risk. Because history,
  physical examination, and electrocardiography
  (ECG) has been largely superseded by stress or
  thallium cardiac scintillation scan and the
  dobutamine echocardiogram. Other tests include
  measurement of the ejection fraction by
  echocardiogram or multigated acquisition scan and
  continuous portable ECG monitoring. Patients who
  are found to have significant coronary artery
  disease may be referred for catheter-based or
  surgical coronary revascularization before
  surgical repair of the aneurysm.
• Pulmonary function studies can serve as a rough
  prognostic guide and should be optimized before
  surgical intervention.
• Preoperative renal function is an important
  determinant of perioperative morbidity and
  influences the use of contrast agents in
  diagnostic tests or at the time of endovascular
  repair.

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Operative Technique of Open Surgical Repair
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Endovascular abdominal aortic aneurysm repair
involves aneurysm exclusion with an endoluminal
aortic stent-graft introduced remotely, usually
through the femoralartery.
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RUPTURED ABDOMINAL AORTIC ANEURYSM

• The most dreaded complication of abdominal aortic
  aneurysms is aneurysm rupture. Aneurysms can
  rupture freely into the peritoneal cavity or into
  the retroperitoneum (leaking ). Free
  intraperitoneal rupture is usually an anterior
  rupture and is usually accompanied by immediate
  hemodynamic collapse and a very high mortality
  rate. Retroperitoneal ruptures are usually
  posterior and may be contained by the psoas
  muscle and adjacent periaortic and perivertebral
  tissue.
• Both types of rupture present with acute
  excruciating back and abdominal pain, accompanied
  by pallor, diaphoresis, syncope, and other
  symptoms and signs related to blood loss and
  hypovolemic shock. Occasionally, patients may
  have chest pain induced by retroperitoneal blood
  loss or hypovolemia, misleading the physician to
  suspect primary myocardial ischemia.
• Patients with ruptured aortic aneurysms require
  immediate surgical repair. Blood should be
  rabidly prepared.
• Resuscitation ?
• Stable patients with a questionable diagnosis may
  undergo CT scanning. In patients not stable
  enough to undergo CT scanning, the presence of an
  aneurysm can be confirmed by bedside ultrasound.
• Acutely expanding aneurysms may present with
  abdominal pain and tenderness on palpation. These
  are prone to rupture and should be repaired on an
  emergent basis.

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Peripheral Arterial Occlusive Disease

• Adverse events are due to the effects of impaired
  circulation on critical end organs (e.g., brain,
  heart, abdominal viscera) or extremities.
• Atherosclerosis is the most common and is a
  complex, chronic inflammatory process that
  affects the elastic and muscular arteries.
• Other causes of arterial occlusive disease,
  although far less common than atherosclerosis ,
  must also be considered, especially in patients
  who do not fit the risk factor profile outlined.
  These include thromboangiitis obliterans
  (Buergers disease), Takayasus arteritis, giant
  cell/temporal arteritis, and other less common
  vasculitides.
• Each of these disorders has unique clinical,
  radiographic, and anatomic features

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AtherosclerosisRisk Factors and Pathology

• Firmly Established
  Relative
  Factors
• Hypercholesterolemia
  Advanced age
• Cigarette smoking
  Male gender
• Hypertension
  
  Hypertriglyceridemia
• Diabetes mellitus
• 
  
• 
  
  Sedentary lifestyle
• 
  
  Family history
• The disease is both systemic and segmental,with
  clear predilections for certain locations within
  the arterial tree and relative sparing of others.
  The earliest lesions (i.e., fatty streaks) may be
  detected in childhood in susceptible individuals.
• The pathologic hallmark of atherosclerosis is the
  atherosclerotic plaque. There are several major
  components of plaque smooth muscle cells,
  connective tissue (matrix), lipid, and
  inflammatory cells (predominantly macrophages).
  Platelets may adhere to dysfunctional
  endothelium, exposed matrix, and
  monocytes/macrophages

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Presentation of CHRONIC OCCLUSIVE DISEASE OF THE
LOWER EXTREMITIES

• Reproducible ischemic muscle pain resulting from
  inadequate oxygen delivery during exercise.
  Claudication distance is an indicator for the
  severity and the site is related tom the site of
  arterial occlusion. Eg Symptoms or signs of
  occlusive disease of the bifurcation of the
  abdominal aorta (Leriche syndrome) include
  Claudication of the buttocks and thighs
  associated with impotence , absent pulse in both
  femoral arteries
• As opposed to the patient with claudication, who
  has cramping pain with exercise, the patient with
  more advanced critical ischemia complains of pain
  at rest.
• Rest pain occurs when blood flow is inadequate to
  meet resting metabolic requirements. In the lower
  extremity, ischemic rest pain is localized to the
  forefoot .The patient with rest pain is often
  awakened by severe discomfort in the forefoot and
  hangs the affected extremity off the bed for
  temporary relief of symptoms.
• Patients often have trophic changes, such as
  muscle wasting, thinning of skin, thickening of
  nails, and hair loss in the distal affected limb.
  
• Rest pain is an ominous symptom and usually
  requires revascularization because this form of
  advanced ischemia generally progresses to tissue
  loss.
• The patient with critical ischemia is at risk for
  tissue infection or gangrene resulting from
  arterial insufficiency.

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Diagnostic Modalities in Peripheral Arterial
Occlusive Disease

• A key principle in the treatment of peripheral
  atherosclerosis is the hemodynamic assessment of
  circulatory impairment, which assumes paramount
  importance in comparison to the anatomic presence
  or distribution of lesions.
• Segmental pressure measurements in the limb can
  be used to localize and grade hemodynamically
  significant lesions, as well as the overall
  degree of circulatory impairment. The single most
  useful index is the ankle pressure, which can be
  obtained simply at the bedside with a handheld
  Doppler probe and pressure cuff.
• Because the ankle pressure varies with central
  aortic pressure, it is commonly indexed to the
  brachial artery pressure as a ratio
  (ankle-brachial index ABI). In normal resting
  subjects, the ABI is slightly greater than unity
  (1.0 to 1.2).
• There is a correlation between the severity of
  signs and symptoms of arterial insufficiency and
  the ABI, such that claudicants usually fall in
  the 0.5 to 0.7 range, whereas critical ischemia
  (rest pain or tissue necrosis) most commonly is
  associated with an ABI less than 0.4. In addition
  to preoperative assessment, the ABI can be used
  to follow up patients after arterial
  reconstruction as a measure of technical success
  or subsequent graft failure.
• Exercise (treadmill) testing may be used in
  patients with claudication. It is particularly
  useful in the evaluation of patients with
  atypical symptoms, normal resting pulse .A normal
  exercise test rules out arterial insufficiency
  explicitly. In addition, exercise testing has
  been used to quantify the degree of impairment in
  arterial claudication self reporting of walking
  distance is notoriously unreliable.
• Doppler and Duplex Ultrasonography
• Arteriography( preoperative )
• Computed tomography (CT) with intravenous
  contrast medium administration can also delineate
  vascular anatomy.
• Magnetic resonance angiography (MRA)

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Color Duplex ultrasound images with Doppler
velocity profiles
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Angiogram
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Complications of Contrast Arteriography

• Puncture Site or Catheter Related
• Hemorrhage/hematoma
• Pseudoaneurysm
• Arteriovenous fistula
• Atheroembolization
• Local thrombosis
• Contrast Agent Related
• Major (anaphylactoid) sensitivity reaction
• Minor sensitivity reactions
• Vasodilation/hypotension
• Nephrotoxicity
• Hypervolemia (osmotic load)

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Therapeutic Interventions in Arterial Occlusive
Disease

• Medical Management Targeted to reduce
  progression, induce regression, and prevent
  morbid endpoints of lesion formation.
• For all patients and the only treatment for
  milled claudication
• Risk factor management is the primary approach.
• Lipid-lowering therapy uses both dietary
  treatment and an increasing pharmacopeia with
  specific effects on different lipid subclasses.
  These drugs include niacin, bile acid-binding
  resins, clofibrate, and gemfibrozil.
• Smoking cessation is clearly of paramount
  importance.
• Others Hypertension , Diabetes mellitus,
  anemia, respiratory disease
• Antiplatelet therapy Aspirin remains the
  cornerstone of platelet therapy. Newer
  antiplatelet agents have been developed with
  everincreasing potency and more specific
  antiaggregative effects. For the present,
  low-dose aspirin is the most widely accepted
  antiplatelet prophylaxis for patients with
  cardiovascular disease.

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Surgery

• Indication
• 1- critically eschimic limp( what )

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Surgery

• Surgical Bypass Grafting
• Natural vs. synthetic

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In situ method of infrainguinal reconstruction.
Saphenofemoral
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Surgical Endarterectomy
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Endovascular Surgery.Percutaneous Angioplasty,
Stenting.
A hemostatic arterial sheath showing the inner
dilator and hemostatic valve
A variety of selective catheters
that are used for
peripheral interventions.
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Intravascular stents
An inflated angioplasty balloon catheter
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ACUTE THROMBOEMBOLIC DISEASE

• Unlike the brain, which suffers infarction after
  only 4 to 8 minutes of ischemia, or the
  myocardium, which infarcts after 17 to 20
  minutes, the lower extremity may be salvaged
  after up to 5 to 6 hours of profound ischemia.
• Etiology
• I)Embolism
• Cardiogenic 80(Rheumatic valvular heart disease,
  Prosthetic heart valves, Atrial fibrillation ,
  Myocardial infarction , Bacterial or fungal
  endocarditis).
• Noncardiac 10(Aneurysmal disease, Proximal
  artery , Paradoxical emboli)
• Idiopathic 10

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aortic bifurcation known as a saddle embolus.
right popliteal artery.
occlusive left femoral embolu
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II) Thrombosis

• Acute thrombosis generally occurs in vessels
  affected by preexistent atherosclerosis. As such,
  there is generally some degree of collateral
  vessel development and the resultant ischemia is
  often less severe than with acute embolic
  disease. A particularly severe form of ischemia
  results from distal vascular thrombosis of the
  extremities, which may occur in the setting of
  sepsis or with hypercoagulable states. The most
  common hypercoagulable states associated with
  acute arterial thrombosis are antithrombin III
  deficiency, lupus anticoagulant (antiphospholipid
  antibody), and protein C deficiency. Although
  usually associated with venous thrombosis,
  activated protein C resistance caused by the
  spontaneous mutations of factor V Leiden may also
  cause arterial thrombosis.
• Acute thrombosis of a previous arterial bypass
  graft may also lead to recurrent ischemia. The
  degree of ischemia depends on the location of the
  graft and the original indication for surgery.
  Early graft occlusions (within 2 months of
  surgery) are usually caused by technical or
  judgmental errors.

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Presentation and Evaluation

• The classic presentation of patients with acute
  ischemia of the extremities may be recalled by
  the five Ps pain, pallor, pulselessness,
  paresthesias, and paralysis.
• Pain is the most common complaint in alert
  patients. The sudden onset of severe ischemic
  pain in a previously asymptomatic patient is most
  suggestive of an embolic occlusion. Patients with
  spontaneous thrombosis often have had chronic
  symptoms of claudication or various degrees of
  pain before the acute event.
• Pallor is a common cool, waxy-appearing white
  extremity with no signs of cutaneous blood flow.
  Conversely, a partial occlusion may result in
  only delayed capillary refill with pallor on
  elevation of the extremity and rubor on
  dependency.
• The absence of arterial pulses on examination
  will alert the surgeon to both the location of
  the arterial occlusion and the degree of
  ischemia. Patients with acute arterial embolism
  generally have normal palpable pulses above the
  occlusion with a complete absence below. The
  pulse immediately above the occlusion may be
  particularly prominent with a water-hammer
  quality that results from limited arterial
  outflow.
• A handheld continuous-wave Doppler examination
  plays an important role in the initial evaluation
  of patients with acute vessel occlusion. The
  presence of even monophasic Doppler signals over
  the pedal vessels affirms distal vascular patency
  and at least short-term viability of the distal
  tissues. Conversely , a complete absence of
  arterial flow is most suggestive of profound
  ischemia and calls for immediate
  revascularization.

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• The peripheral nerve is the tissue that is most
  sensitive to ischemia. As such, the degree of
  neurologic dysfunction is a sensitive barometer
  of the degree of ischemia. With mild ischemia,
  the findings may be subjective and subtle. Early
  paresthesias may be characterized as a numbness
  of the toes or a slight decrease of sensation of
  the foot compared with the contralateral
  extremity to light touch or pinprick.
• With severe ischemia, however, profound sensory
  loss may lead to complete anesthesia of the foot,
  indicative of impending tissue loss without early
  revascularization.
• Weakness of the extremity is another important
  sign of neurologic ischemia of the extremity.
  Patients with an aortic saddle embolus may have
  bilateral paralysis and anesthesia from the waist
  down.
• In patients with severe ischemia characterized by
  anesthesia and paralysis, it is important to
  distinguish reversible from irreversible ischemic
  changes. Patients with prolonged ischemia have
  palpable firmness to the extremity muscle and
  stiffness to the extremity indicative of muscle
  rigor. Reperfusion of such an extremity does not
  restore function and can result in severe
  systemic injury. Primary amputation is the safest
  form of management in such cases.

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Management

• Because evaluation of patients with acute
  arterial occlusion generally differs for patients
  who have suffered embolic versus thrombotic
  occlusion, it is important to make the
  appropriate clinical distinction. Patients with
  emboli tend to have risk factors (e.g., atrial
  fibrillation, recent myocardial infarction,
  prosthetic heart valve), a more sudden onset of
  symptoms (no prior claudication), and unilateral
  findings (normal contralateral extremity).
• Patients with acute arterial occlusion should be
  anticoagulated with an intravenous heparin bolus
  (5000 to 10,000 units) and begun on a continuous
  infusion at 1000 units/hr.
• When the history and physical examination
  implicates an embolus as the source of occlusion,
  the subsequent evaluation should be simple and
  direct. Routine preoperative blood work and a
  chest radiograph are obtained, and a 12-lead
  electrocardiogram is performed. Because arterial
  emboli are removed by direct arterial cut down
  and removal of the embolus( Embolictomy ), there
  is generally no need for preoperative
  arteriography. When the diagnosis of embolus is
  questionable or the site for simple arterial
  cutdown and arteriotomy unclear, a preoperative
  arteriogram may be useful to define the anatomy
  and guide the revascularization procedure.

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Management

• Arteriograms of intraarterial emboli often
  demonstrate an abrupt cutoff of the artery with a
  rounded meniscus at the site of the embolus
  .Conversely, the embolus may appear as an
  intraluminal defect with partial flow around it.
• Postoperatively, when the embolus has been
  removed and the limb revascularized, and the
  patient is stable, the evaluation should be
  completed by documentation of the source of the
  embolus. In most cases, this involves
  transesophageal echocardiography.
• Thrombotic arterial occlusion undergo an initial
  arteriogram to delineate the arterial anatomy and
  define the best mode of revascularization. In
  most cases, the site of thrombotic occlusion is
  well delineated. In patients with a satisfactory
  inflow and outflow vessel with a long segment of
  occluded vessel, the best option is generally to
  proceed to surgery and perform a surgical bypass
  procedure.

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Thrombolytic Therapy

• Fibrinolytic drugs enhance conversion of
  plasminogen to plasmin, which is then capable of
  degrading fibrin clot. These agents have been
  used in both systemic and local fashion to
  achieve lysis of both arterial and venous
  thrombi. It is used as an important adjunct to
  PTA or surgical interventions that directly
  address the underlying atherosclerotic lesions,
  restoring perfusion to the downstream bed. The
  two major drugs in current use are urokinase and
  tissue plasminogen activator (tPA).
• Contraindications to Thrombolytic Therapy
• Absolute 1-Recent major bleeding
  2-Recent stroke
• 3-Recent major surgery or
  trauma 4-Irreversible ischemia of end organ
  5-Intracranial pathology
  6- Recent ophthalmologic procedure
• Relative 1-History of gastrointestinal bleeding
  or active peptic ulcer disease
• 2-Underlying coagulation abnormalities 3-
  Uncontrolled hypertension
• 4-Pregnancy 5-Hemorrhagic retinopathy
• An important consideration in evaluating patients
  for thrombolytic therapy is the severity of
  ischemia and the time interval for restoring
  perfusion before irreversible tissue injury has
  occurred. Patients with signs of irreversibility
  such as major neurologic impairment should not
  undergo attempted thrombolysis.

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Vascular Trauma

• Penetrating trauma typically results in varying
  degrees of laceration or transection of the
  vessel. The severed ends of a completely
  transected artery often retract and undergo spasm
  with subsequent thrombosis. Therefore, a
  lacerated or incompletely transected vessel
  typicall bleeds more profusely than a completely
  transected one.
• Blunt trauma results in disruption of the
  arterial wall, ranging in severity from small
  intimal flaps to extensive transmural damage with
  either extravasation or thrombosis. Deceleration
  injury causes deformation of the arterial wall.
  Tight plaster ,fracture .
• Bleeding from a lacerated vessel can be free or
  contained, the latter leading to pseudoaneurysm
  formation.
• An arteriovenous fistula is the result of a
  traumatic communication between an injured artery
  and vein.
• Limb loss is more likely to result from blunt
  trauma and high-velocity gunshot injuries, mainly
  because of the significantly greater damage to
  bone and soft tissue of the injured extremity.
  Low-velocity gunshot injuries and stab wounds
  rarely lead to limb loss.
• Iatrogenic injury may occur either at the target
  site of the intervention (e.g., a coronary
  artery) or at the access site (e.g., the common
  femoral artery). The latter is more common and
  sometimes requires surgical repair .Every cardiac
  catheterization or arterial line insertion is, in
  fact, a form of vascular injury, where the
  physician relies on the patients hemostatic
  mechanism to plug the hole and repair the damage..

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Temporary intravascular shunt
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Buergers disease

• Buergers disease is exclusively associated with
  cigarette smoking. The disease is more prevalent
  in the Middle East and Asia. Occlusive lesions
  are predominantly seen in the muscular arteries,
  with a predilection for the tibial vessels. Rest
  pain, gangrene, and ulceration are the typical
  presentations.
• Recurrent superficial thrombophlebitis
  (phlebitis migrans) is a characteristic
  feature.
• The diagnosis is suspected in younger patients
  who are heavy smokers and do not have other
  atherosclerotic risk factors.
• Angiography often reveals diffuse occlusion of
  the distal extremity vessels. The arterial
  involvement appears to progress in a distal to
  proximal fashion.
• Revascularization options are therefore usually
  limited. The disease virtually always shows
  clinical remission if smoking cessation can be
  achieved. Sympathectomy has a limited role in
  patients with ulcerations.

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Raynauds phenomenon

• Raynauds phenomenon is characterized by
  recurrent, episodic vasospasm of the digits
  brought on by cold exposure or emotional stress.
  Exposure to cold initially produces pallor of the
  digits, followed by cyanosis, and is accompanied
  by pain and paresthesias. Rewarming leads to
  marked rubor caused by a hyperemic response. The
  clinical spectrum of severity is broad and may
  include ulceration or loss of digits in patients
  with protracted periods of ischemia. Progression
  to tissue loss implies persistent vascular
  occlusions beyond the vasospastic component.
• Primary (Raynauds disease) and secondary causes
  are recognized. Secondary Raynauds phenomenon
  has been associated with a variety of
  rheumatologic, hematologic, and traumatic
  disorders, as well as a number of drugs and
  toxins. Treatment is centered around minimizing
  exposure to the triggering stimulus and
  pharmacologic (calcium channel blockers,
  sympatholytics) therapy. Sympathectomy may play a
  role in patients with severe digital ischemia and
  ulceration.

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Others

• Takayasus arteritis (pulseless disease)
  commonly afflicts younger female patients and has
  a higher prevalence in those of Eastern European
  or Asian descent. The arterial pathology is
  focused on the aorta and its major branches.
  Surgical treatment is often indicated for
  ischemic manifestations and should only be
  undertaken when active inflammation is under
  control (i.e.,normalized erythrocyte
  sedimentation rate).
• Temporal arteritis (sometimes referred to as
  giant cell arteritis) predominantly afflicts
  patients older than 50 years of age, with a
  slight (21) female preponderance. The
  superficial temporal, vertebral, and major aortic
  arch branches may be involved. As in Takayasus
  disease, there are often signs of systemic
  inflammation. Ischemic symptoms are common,
  including claudication of facial or extremity
  muscles and retinal ischemia. Headache is a
  common symptom. Blindness, usually irreversible,
  is a dreaded complication. Once the clinical
  diagnosis is suspected, treatment must be prompt
  and consists of high-dose corticosteroid therapy.
  Surgery is rarely indicated except in cases of
  major aortic branch involvement with ischemic
  symptoms.

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Aortic dissection

• Acute aortic dissection is the most common
  catastrophic event involving the aorta. A tear in
  the intima allows blood to escape from the true
  lumen of the aorta, dissects the aortic layers,
  and reroutes some of the blood through a newly
  formed false channel. The weakened aortic wall is
  highly susceptible to acute rupture and
  chronically prone to progressive dilation.
  Arterial hypertension and connective tissue
  disorders (particularly Marfan syndrome) may
  predispose patients to dissection. The cause of
  the initial tear remains unknown, but the
  histology of the aortic wall typically exhibits
  medial degeneration.

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Classification Left, Stanford type A, DeBakey
types I and II. Right, Stanford type B, DeBakey
type III.
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• Conventionally, aortic dissection is termed acute
  when a clinical diagnosis is made within 14 days
  following the onset of symptoms and chronic after
  14 days.
• When a dissection involves the ascending aorta,
  it is commonly referred to as a Stanford type A.
• Dissection without involvement of the ascending
  aortamost often with the intimal tear in the
  descending thoracic aortais referred to as a
  Stanford type B or DeBakey type III.
• DeBakey classification further distinguishes
  ascending aortic dissection with involvement of
  the descending thoracic aorta (DeBakey type I)
  from ascending aortic dissection without
  involvement of the descending thoracic aorta
  (DeBakey type II).
• Approximately 20 of aortic aneurysms and
  dissections are related to hereditary connective
  tissue disorders.Marfan syndrome is the most
  common of these disorders. Skeletal, ocular, and
  cardiovascular complications characterize Marfan
  syndrome, with aortic aneurysm and dissection as
  the major cause of morbidity and mortality.

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AORTIC DISSECTIONClinical Presentation

• Abrupt excruciating pain epitomizes the onset of
  acute aortic dissection. Chest pain is present in
  about two thirds of patients and back pain
  invariably accompanies dissections that begin
  distal to the aortic arch. Pain may migrate as
  the dissection progresses distally. Patients with
  ascending aortic dissections may have associated
  aortic valve insufficiency with dyspnea and a
  diagnostic loud pansystolic murmur.
• Other acute symptoms and signs related to aortic
  branch occlusion can cause cerebral infarction,
  myocardial infarction, abdominal malperfusion,
  limb ischemia, and paraplegia.
• Serious life-threatening complications typically
  occur during the acute phase, and surgery on the
  acutely dissected aorta is high risk, associated
  with considerable bleeding due to the friability
  of the aortic wall.

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Treatment

• Acute type A dissection most often requires
  emergency surgical repair because of the
  associated high risk of death due to rupture,
  tamponade, and/or aortic valve insufficiency .The
  patient who is unstable with suspected type A
  acute aortic dissection is immediately
  transferred to the operating room and evaluated
  by TEE. If dissection is confirmed then repair is
  undertaken at once . Surgery in the case of the
  hemodynamically stable patient is less urgent,
  and the patient is first transferred to an acute
  care setting until confirmation of the diagnosis
  is made.
• For acute type B aortic dissection the treatment
  of choice is generally medical therapy aimed at
  pain control and the correction of hypertension .
  Patients are admitted to an intensive care unit
  and observed closely. Surgical repair is most
  often reserved for dissection complicated by
  aortic rupture, abdominal malperfusion, limb
  ischemia, intractable pain, or uncontrollable
  hypertension. Approximately 20 of patients .
  with acute type B aortic dissection require
  surgical therapy

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Arteriovenous Fistula

• Abnormal connection between artery and vein,
  congenital or acquired, located anywhere in body
• Congenital systemic effect is minimal usually
  noted in infancy or childhood
• Acquired enlarges rapidly, can cause heart
  failure continuous bruit be heard palpable
  thrill and increased skin temperature proximal
  vein dilatation, diminished distal pulse, distal
  coolness
• Magnetic resonance imaging (MRI) is study of
  choice for peripheral arteriovenous malformation
  angiography precisely delineates arteriovenous
  fistula
• Treatment
• Monitor small peripheral fistulas
• If treatment is needed, most are managed with
  radiographic embolization head and neck, pelvis
  best
• Operative management ligate all feeding vessels

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Carotid Body Tumor

• Carotid body normally 36 mm nest of
  chemoreceptor cells of neuroectodermal origin
  responds to decrease in PO2, increase in PCO2,
  decrease in pH, or increase in blood temperature
• Tumors of carotid body cervical chemodectomas,
  10 metastatic
• Symptoms and signs include slow enlargement of
  asymptomatic cervical mass rarely, hypertension
  secondary to release of catecholamines rarely,
  cranial nerve dysfunction from tumor extension
  mass mobile in horizontal plane but not vertical
  plane
• Duplex ultrasound is often diagnostic
• Differential Diagnosis
• Metastatic nodes from squamous cell cancer
• Thyroid cancer
• Carotid aneurysm
• Treatment
• Preferred treatment is complete excision and
  arterial reconstruction if possible
• Complications gt50 incidence of cranial nerve
  dysfunction after resection

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Thoracic Outlet Syndrome

• Variety of disorders caused by arterial,
  venous, or nerve compression at base of neck
• Symptoms and signs are predominantly
  neurologic pain, paresthesias, numbness in
  brachial plexus trunks (ulnar most common) hand
  numbness often wakes patients from sleep motor
  deficits indicate long duration
• Adson test weakened radial pulse with arm
  abduction and head rotated to opposite side
• Tinel sign light percussion in supraclavicular
  fossa produces peripheral sensations
• Subclavian artery compression bruit, distal
  emboli, or arterial occlusion
• Subclavian vein compression thrombosis of vein
  leading to extremity pain and swelling (effort
  thrombosis called Paget-von Schrötter syndrome)
• Differential Diagnosis
• Carpal tunnel syndrome
• Cervical disk disease
• Treatment
• Postural correction and physical therapy
• If surgical repair warranted, thoracic outlet
  decompression
• Surgery is indicated for arterial disease,
  venous compression, neurologic symptoms not
  attributable to other disease, failure of
  conservative therapy after 36 months