Vascular Surgery - Rush Review of Surgery

Question 1

Which of the following is not an independent risk factor for the development of coronary and peripheral atherosclerosis?

• Smoking
• Hypercholesterolemia
• Diabetes Mellitus
• Hypertension
• Hypercoagulable conditions

Answer 1

Hypercoagulable Conditions

• Associated with an increased risk for thrombosis but they have not been to be an independent risk factor for atherosclerosis.

**Why are other answers wrong? **

• Smoking is a risk factor because of the release of oxidative free radicals, which damage the vascular endothelium
• Hypercholesterolemia with total serum levels greater than 200 mg/d and elevated low density lipoprotein fractions is also associated with an increased risk
• Diabetes and hypertension are independent risk factors in proportion to their severity

Question 2

Which of the following describes chronic leg ulcers?:

• Cause of ulcers cannot be determined by their locations on the leg
• Venous ulcers are seldom located on the foot
• Arterial ulcers are seldom located on the leg
• Leg ulcers affect diabetic patients less often than other patient groups
• Ulcer healing is improved more significantly with balloon angioplasty than with arterial bypass

Answer 2

Venous ulcers are seldom located on the foot

• Chronic venous insufficiency causes characteristic dermal changes, including hyperpigmentation, thickened skin and ulceration in the gaiter region.
• Venous ulcers usually occur at the medial malleoli but seldom extend below ankles.

**Why are other answers wrong? **

• Arterial ulcers form at the distal aspect of the region that has compromised arterial circulation.
  
  • Usually result in ulcers of the toes or foot but islands of ischemia can occur more proximally on the leg - anterior aspect.
• Diabetic patients can form neutrophilic ulcers - neuropathy that afflicts patients with long standing diabetes causes wasting of the muscles of the foot and collapse of the standard architecture of the foot which leads to pressure points between toes and at the metatarsal heads.
• Strict avoidance of weight bearing is essential for these pressure ulcers to heal when arterial circulation is adequate.
  
  • If arterial circulation is inadequate then usually an arterial leg bypass operation is needed - although balloon angioplasty could be used.

Question 3

Which of the following is characteristic of ischemic extremity rest pain?

• Initially occurs mostly in the morning
• Can be relieved by placing the involved extremity in the supine position
• Usually located at the toes
• Can be relieved by intravenous heparin
• Can be relieved with cilostazol (Pletal)

Answer 3

Can be relieved by intravenous heparin

• IV heparin cuases vasodilation by promoting release of nitric oxide - thereby promoting extremity arterial circulation.
• Can reduce rest pain until arterial circulation can be improved with a bypass operation or angioplasty.

**Why are other answers wrong? **

• Extremity angina occurs most commonly at night because when patients with severe lower extremity arterial insufficiency lie supine - they lose the added benefit of gravity for perfusion in the lower extremity.
• Patients with noctural ischemic rest pain quickly disocver that walking, standing or sleeping in a chair relieves this pain which is centered over the metatarsal heads not the toes.
• Pain in the toes suggest gout or an infection
• Cilostazol improves claudication impaired distance walking but has not been shown to be effective in treating ischemic rest pain.

Question 4

Which of the following characteristics of leg from venous insufficiency or lymphedema is true?

• Edema forms when hydrostatic pressure in the interstitum is higher than that in the lymphatics or venules
• Venous insufficiency causes pigmentation and hypertrophic changes in the skin over the ankle and results in late lymphedema with fibrosis
• Lymphedema can be diagnosed by ultrasound imaging
• Operative intervention can treat venous insufficiency and is commonly used for lymphedema
• Lymphedema may be pitting in form

Answer 4

Venous insufficiency causes pigmentation and hypertrophic changes in the skin over the ankle and results in late lymphedema with fibrosis

• edema formation
  
  • goverened between hydrostatic and oncotic pressure in the interstitium versus lymphatics and venules
  • hyperpigmentation with cicatrix formation in the gaiter regionis pathognomonic of venous insufficiency
    
    • caused by breakdown of extravascular red blood cells and subcutaneous scar tissue (liposclerosis)
  • with severe cases of untreated chronic venous insufficiency - scar tissue formation can cause local destruction of the leg lymphatics and secondary formation of lymphedema.
    
    • Any severe hypoproteinemia can cause lymphedema
• Lymphedema may appear early as a pitting form but after subsequent protein deposition in the extremity and damage to the lymphatics the adipose tissue fibroses and skin thickens.
• Venoush insufficiency can be recognized clinically by filling of varices as well as on color Doppler imaging
  
  • because of the size of lymphatics they are not visible on ultrasound imaging and only nonspecific lymphedema are not generally performed.
• Operations for venous insufficiency include peforator vein ligation, varicose vein ligation and stripping, deep vein valvoplasty, laser and radiofrequency ablation of the greater and lesser saphenous veins

Question 5

Fasciotomy should be performed in patients with which of the following signs or symptoms?

• Tense fullness of the compartment in an otherwise asymptomatic patient
• Extremity ischemia for longer than 4 hours
• Progressively worsening neurologic signs after revascularization
• Traumatic injuries to the popliteal artery
• Compartmental pressure higher than 15 mm Hg and unreliable findings on physical examination

Answer 5

Progressively worsening neurologic signs after revascularization

• Compartment syndromes occur whenever tissue pressure within a confined anatomic space becomes sufficiently elevated to impair venous return.
  
  • It can be caused by bleeding within a compartment or by reperfusion edema.
  • Successful treatment is based on early, accurate diagnosis. There is no absolute pressure above which the syndrome invariably occurs, but nutrient blood flow in the muscle ceases between 30 and 40 mm Hg.
  • However, isolated measurement of compartment pressure is neither
    sensitive nor specific for determining the degree of muscle ischemia.
  • Fasciotomy is indicated when measured compartment pressure is within 20 to 30 mm Hg of diastolic blood pressure.
• Prolonged ischemia is associated with compartment syndrom because of the reperfusion injury and release of free radicals.
• Diminished or absent pulses is a late finding, after which irreversible neurologic damage may have occurred.
• Compartment syndromes are best diagnosed by having a high index of suspicion.
  
  • A tense compartment alone in the absence of elevated pressures or
    physical findings is not an absolute indication for fasciotomy
• Traumatic injury to the popliteal artery is not an absolute indication forfasciotomy unless the repair/revascularization occurred more than4 hours after the time of injury.

Question 6

In a low-resistance arterial vascular system, at which percent
reduction in diameter does a stenosis become flow limiting?

• 10%
• 20%
• 40%
• 50%
• 80%

Answer 6

50%

• In low-resistance arterial systems, such as the internal carotid artery, total blood flow across a stenosis does not decrease until the diameter is reduced by approximately 50%.
• This corresponds to a 75% reduction in cross-sectional area. Total blood
• flow is maintained by increasing the velocity. Shear stress (drag along the wall) and viscosity limit further increases in velocity once the reduction in diameter exceeds 50%.
• This hemodynamic fact is the reason for not repairing short stenoses of less than 50% because total blood flow is not altered.
• A longer stenosis increases shear stress and causes a lesser degree of stenosis over a long enough length to be flow limiting.

Question 7

What is the most common cause of a congenital hypercoagulable
disorder?

• Protein S deficiency
• Protein C deficiency
• Antithrombin III deficiency
• Activated protein C resistance (APC-R; factor V Leiden mutation)
• Homocysteinemia

Answer 7

Hemostasis is a finely tuned balance between
coagulation and fibrinolysis. The existence of a congenital defect
in procoagulant or anticoagulant proteins can shift this balance
and cause increased bleeding or increased thrombotic tendencies,
respectively. Hypercoagulable states are the most common
cause of early bypass graft failure in young adults who require
vascular interventions for limb salvage. More than 50% of patients
younger than 50 years who require a lower extremity bypass
and experience early graft thrombosis have a hypercoagulable
state.

Protein C, protein S, and antithrombin III deficiencies have
been known to exist for years, but until recently a specific inherited
hypercoagulable state could not be identified in as many as 80%
of patients.
It is now known that APC-R is the most common inherited
hypercoagulable state; it is found in more than 50% of patients
with inherited thrombotic tendencies. The cause of APC-R is an
amino acid substitution in factor V of glutamine for arginine 506.
Patients with APC-R have a poor anticoagulant response to APC,
a vitamin K–dependent anticoagulant protein. When protein C is
activated, it normally degrades activated clotting factors Va and
VIIa. The altered factor V, or Leiden mutation (named for the
Dutch city where it was first found), is resistant to the degrading
action of APC. The altered, activated factor V retains its procoagulant
activity, and the hemostatic balance is shifted toward
thrombosis.
Antithrombin III is the major plasma inhibitor of thrombin.
Heparin performs its anticoagulant function by forming a trivalent
molecule of heparin–antithrombin III–thrombin to inactivate
thrombin. This deficiency is rare, with an incidence of only 1 in
5000. Thrombotic events are usually triggered by trauma, surgery,
or pregnancy.
Proteins C and S are both vitamin K–dependent anticoagulant
proteins synthesized by the liver. The incidence of congenital
protein C deficiency is 1 in 200. Proteins C and S deficiencies are
found in 20% of patients younger than 50 years with arterial thrombosis,
but the combined incidence is much less than the incidence
of APC-R.
Treatment of antithrombin III, protein C, and protein S deficiencies
is lifelong warfarin anticoagulation. Heparin must be
given before initiating warfarin anticoagulation in these patients to
protect against warfarin-induced skin necrosis. All patients with
thrombosis who are to receive warfarin therapy should be administered
heparin during the first 3 to 4 days of warfarin therapy
because the half-life of the anticoagulant protein C is much less
because it is degraded much faster than the procoagulant vitamin
K–dependent factors II, IX, and X.
Mild homocysteinemia exists in 5% to 7% of the population.
Elevated levels of homocysteine occur because of a defect in the
pathway that metabolizes methionine. Treatment of homocysteinemia
is with the B vitamin folate, 1 to 5 mg/day.

Question 8

What is the most common cause of an acquired hypercoagulable
state?

• Smoking
• Heparin-induced thrombocytopenia (HIT)
• Antiphospholipid antibody (e.g., lupus anticoagulant)
• Warfarin
• Oral contraceptives

Answer 8

Smoking

• most common cause of acquired hypercoagulability.
• It is the most important factor that determines the short- and long-term results of any vascular intervention.
• The mechanisms of action of smoking are multiple and include both vasoconstriction and a measurable elevation in plasma fibrinogen levels, which itself is a risk factor for thrombosis.

**Why are other answers wrong? **

• The next most common cause of acquired hypercoagulability is HIT.
  
  • This condition affects 2% to 3% of all patients who receive heparin. Antibodies form to heparin because it is obtained from bovine or porcine sources.
  • The clinical manifestations are a falling platelet count, increasing resistance to anticoagulation with heparin, and new paradoxical thrombotic events while undergoing heparin treatment.
  • Treatment of HIT is cessation of all heparin. Warfarin-induced skin necrosis is unusual as long as heparin is administered for the first 3 days that warfarin is given.
• Antiphospholipid syndrome is common and affects 1-5% of the population.
  
  • Specific types are lupus anticoagulant and anticardiolipin antibodies.
  • Because the incidence of APS increases with age, 50% of patients older than 80 years have APS.
  • This syndrome is recognized by prolongation of the baseline partial thromboplastin time (PTT)
  • Brain thromboplastin is the reagent used for triggering the intrinsic clotting system where the PTT is measured.
  • Patients with APS have serum antibodies that consume this reagent - thereby resulting in a prolonged PTT.
  • This is an unforgiving hypercoagulable state - with an incidence of thrombotic complications approaching 50%.
• Warfarin and oral contraceptives are less common causes.

Question 9

A 70-year-old man who had undergone repair of an endovascular abdominal aneurysm 1 year earlier collapses and complains of back and abdominal pain. His blood pressure is 90/40 mm Hg. The patient denies a history of peptic ulcer or alcohol abuse. What is the most likely diagnosis?

• Aortoenteric fistula
• Bleeding duodenal ulcer
• Ruptured abdominal aortic aneurysm (AAA)
• Pancreatitis
• Diverticulitis

Answer 9

**Ruptured abdominal aortic aneurysm (AAA) **

• The diagnosis of a ruptured abdominal aortic aneurysm must be considered in a patient with abdominal pain, back pain, and hypotension.
• After endovascular repair, an endoleak (persistent flow within an aneurysm sac despite an excluded aneurysm) develops in up to 50% of patients.
  
  • Type 1 endoleak occurs when a persistent channel of blood flow develops as a result of an inadequate or ineffective seal at the graft ends.
  • Type 2 endoleak occurs when there is persistent collateral blood
    flow retrograde into the aneurysm sac from patent lumbar arteries
    or the inferior mesenteric artery.
  • Type 3 is a graft defect endoleak, such as when the sections pull apart.
  • Type 4 is a graft fabric porosity endoleak.
• However, only about 1% of patients with stent graft repair of AAAs have a late rupture.