Vascular Diseases

Dr. Derek Meeks D.O. Director of Clinical Systems Touro University, Nevada

Vascular Diseases
Objectives:
Be able to recognize, diagnose and treat the following: following:  Peripheral Arterial Disease  Aortic Aneurysm  Aortic Dissection  Deep Vein Thrombosis  Pulmonary Embolus

Vascular Diseases


Systemic Vasculature -Aortic disease* -Peripheral vascular disease* Pulmonary Vasculature -Pulmonary Hypertension -Thromboembolic disease* Renovascular

Systemic Vasculature Peripheral Vascular Disease



Peripheral Vascular Disease (PVD) -Most common etiology=Atherosclerosis*etiology=Atherosclerosis* plague buildup within the vessel walls.

Peripheral Vascular Disease

  

PVD worsens with age Half of all CAD pts have PVD. It mostly affects the lower extremities.*

Peripheral Vascular Disease Symptoms

SYMPTOMS: CLAUDICATION! CLAUDICATION!

Claudication =Aching, cramping, fatigue, weakness in the calves, thighs or buttocks brought on by walking and completely relieved after a few minutes of rest.  Relieved with rest.* Worse with exertion. Predictable.*
 

As PVD progresses, symptoms may occur at rest progresses, -often involve the toes and are worse at night. Ischemic foot ulcers may develop.

Peripheral Artery Disease Physical Exam

Physical Examination:** Examination:  Smooth, shiny, hairless skin (lower extremities)* Muscle atrophy.  Diminished or delayed distal pulses*
  

Audible bruits over the involved arteries Severe ischemia causes pallor, cyanosis, decreased skin temperature, ulceration and may cause gangrene* gangrene*

Peripheral Artery Disease

Diagnosis
Diagnosis:
  

 

 

Usually made by signs and symptoms* symptoms* Ultrasound* may quantify the extent of dz. May also help dx those patients with noncompressible vessels. AnkleAnkle-Brachial Index**: In normal patients, the systolic blood Index**: pressure in the leg is slightly higher than in the arm (ankle-brachial (ankleindex > 1.0). In PVD, the index decreases. <.9=PVD* AnkleAnkle-Brachial index decreases with disease progression and with exertion. Angiography considered gold standardrarely needed for standard diagnosis but may help define the vascular anatomy prior to surgery. Magnetic Resonance Angiography (MRA) CT Angiography

Interpretation of Ankle-Brachial AnkleIndex

Peripheral Artery Disease

Treatment
3 Phases: 1)Conservative 2)Medical 3)Surgical 1) Conservative:  Lifestyle changes: -Regular walking* may increase the distance walking* prior to claudication by 100%-400%! 100%-Smoking cessation -switch to another form of Rx if resting ischemia or nonhealing ischemic ulcers develop

Peripheral Artery Disease

Medical Treatment
Pentoxifylline*? Effectiveness. leads to Pentoxifylline*? vasodilation, vasodilation, decreased platelet aggregation, and increases walking distance by 28%-100%. 28% Cilostazol**Studies look very favorable. Cilostazol**Studies  Lipid lowering agents*  Hypertensive agents*  Aspirin*  Clopidogrel (Plavix)* Plavix)*


Peripheral Artery Disease

Surgical Treatment

Revascularization (percutaneous or surgical) is indicated for:  -severe claudication that is resistant to medical therapy*,  -limb-threatening ischemia*, or limb -vasculogenic impotence.

Acute Limb Ischemia

Vascular Emergency!!
Sudden occlusion of a peripheral artery is caused by either arterial embolism or thrombosis in situ.  Arterial emboli usually originate in the cardiac chambers in the setting of prepreexisting cardiac disease such as MI, CHF or atrial arrhythmias (A-Fib). (A

Acute Limb Ischemia

Symptoms:
 

Arterial embolism: Sudden onset of symptoms embolism: without history of claudication. Pain!* Thrombosis in situ: History of claudication which situ: suddenly assumes a crescendo pattern over a few days. Cold, cyanotic (bluish) extremity* Absent pulses distal to the occlusion* Diminished motor and/or sensory function.

Physical exam:
  

Acute Limb Ischemia

Diagnosis:
 

HandHand-held Doppler* can assess flows at different arterial segments. Transesophageal echocardiography (TEE) to determine the potential cardiac source.*

Treatment:
   

Anticoagulation! IV Heparin* Embolectomy* CatheterCatheter-directed infusion of plasminogen activator (tPA), a fibrinolytic* Emergent amputation if tissue necrosis.

Acute Limb Ischemia

Abdominal Aortic Aneurysm

A bulging area of the aorta. Degenerative process in the aorta which leads to a bulging (ballooning) in the area of weakness.  A normal aorta is about 2 cm in diameter.  >5cm is concerning*  Major concern of AAA s is rupture which is an immediate lifelife-threatening condition.
 

Aortic Aneurysm


Abdominal Aortic Aneurysm is a common

vascular disease in older adults*. adults*. -Affects 4-8% men and .5-1.5% women over the age 4.5of 65 years. Risk Factors: Factors: Age, Smoking, Hypertension and Family History

Causes: Causes:
Atherosclerosis*, Atherosclerosis*, Cystic Medial Necrosis (Marfans, EhlersEhlers-Danlos), vasculitis with connective tissue giantdisease (Takayasu s arteritis, giant-cell arteritis), chronic infection (syphilitic aortitis), and trauma.

Abdominal Aortic Aneurysm (AAA)

Abdominal Aortic Aneurysm

Gradually grows in size.  Risk of rupture is low until the diameter reaches >5 cm* cm*  Death usually quickly follows rupture of the AAA.


Symptoms/Signs:** Symptoms/Signs:**  Nontender pulsatile mass below umbilicus if <5 cm.*  Hypotension, acute abdominal/back pain should Hypotension, prompt consideration of aneurysm rupture.*****

Abdominal Aortic Aneurysm

Diagnosis:
 

Duplex ultrasonography* CT, MRA allow visualization of the thoracic and abdominal aorta and iliac arteries and its branches.*

Abdominal Aortic Aneurysm Treatment:

Smoking cessation  Close blood pressure control*  Cholesterol reduction.  Small aneurysms (<5 cm) should be treated medically with close observation.  Aneurysm surgical repair-for patients with large repairaneurysms or rapid expansion.** -Open surgical repair or percutaneous endovascular graft placement.* placement.*


Aortic Dissection


Intimal layer is torn from the aortic wall leading to the formation of a false lumen in parallel with the true lumen. Typically occurs in the thoracic aorta*

Aortic Dissection
Risk Factors:  Hypertension*  Cocaine use*  Trauma*  Hereditary connective tissue disease*  Vasculitis

Aortic Dissection
Classifications: Stanford system=Type A system=Type or B  Type A involves the ascending aorta*  Type B involves the distal aorta.*

Aortic Dissection
Debakey System= System=  Type I=dissecton involves the entire aorta  Type II=involves only the ascending aorta  Type III=involves only the descending aorta

Aortic Dissection
Type A Symptoms:  Acute onset severe chest pain or back pain.** pain.**  Abdominal pain -common*  Syncope -common*  Stroke-common* Stroke Retrograde propagation of the dissection can cause pericardial tamponade or coronary artery dissection with acute myocardial infarction.  Aortic valve involvement causes severe aortic insufficiency with acute pulmonary edema.  May propagate anteriorly to compromise flow in the Carotid and Subclavian arteries leading to stroke or upper limb ischemia.

Aortic Dissection
Type B symptoms:
      

Acute chest or back pain** Lower extremity ischemia and ischemic neuropathy.* Pulse deficits* Neurologic deficits* Tachypnea, Tachycardia Narrow pulse pressure Hypotension, jugular venous distention (JVD) and pulsus paradoxus may indicate a pericardial tamponade.

Aortic Dissection
Diagnosis:


 

Transesophageal echocardiography (TEE)* MR angiography CT angiography*angiography*good in an emergency

Aortic Dissection
Treatment: Treatment:  Type A-fatal without emergent repair.* Arepair.*  Type B- Medical therapy.* Btherapy.* -However, surgery is indicated if compromised blood flow to the legs, kidneys or other viscera.  Tight blood pressure control to avoid aneurysms and further growth of dissections.*

Raynaud s Phenomenon
A vasospastic disease of the small arteries. Mainly affecting the toes and fingers.*  Episodic bilateral digital pallor, cyanosis and rubor.*  Precipitated by cold or emotional stress.  Relieved by warmth.  If idiopathic, it is called Raynauds disease.  If associated with a possible precipitating systemic or regional disorder (autoimmune diseasse, arterial diseasse, occlusive disease, etc), it is called Raynauds phenomenon.


Raynauds Phenomenon

Raynaud s Phenomenon
Symptoms:


Recurrent episodes of digital ischemia, with characteristic whitewhiteblueblue-red color sequence.**

Raynaud s Phenomenon
Symptoms: Symptoms:  Pallor*  Cyanosis*  Erythema (reactive hyperemia)*  Physical exam can be completely normal between attacks.*  May have digital ulcers or thickening of fat pad (sclerodactyly).

Raynaud s Phenomenon
Treatment:
  

Avoid cold temperatures** temperatures** Protect hands Aspirin Calcium channel blockers reduce frequency and severity of vasospastic episodes.*

Buerger s Disease (Thromboangiitis Obliterans) Obliterans)



A non-atherosclerotic disease of the smallnonsmallmediummedium-sized arteries, veins and nerves of the arms and legs affecting mostly young men before the age of 45 years. Inflammatory process* of the vessels=vasculitis vessels=vasculitis These patients have a hypercoagulable condition. In acute exacerbations, a highly inflammatory thrombus may affect both the arteries and veins.

  

Buerger s Disease
Cause: Cause: Unknown. All patients have a history of heavy tobacco addiction.* Progression of the disease is strongly linked to continued tobacco use Symptoms:  Claudication of the feet, legs, hands or arms.**  Skin changes (ischemia, ulcerations) found mainly in the extremities*

Buerger s Disease

Buerger s Disease
Diagnosis:
 

Clinical presentation and biopsy.* Histologic feature=inflammatory intramural thrombi within the arteries and veins with sparing of internal elastic lamina and other arterial wall structures.* Complete tobacco abstinance is the most effective

Treatment:
 

treatment!** Iloprost=Prostacyclin analog reduces limb ischemia and improves healing. Surgical amputation required in >40% of those patients who do not quit smoking.*

GiantGiant-Cell Arteritis
Pathophysiology:
Inflammation of the lining of the medium-large mediumarteries.*  Large vessel vasculitis*  Immune-mediated* Immune Elderly* (>50 yrs)  Females>males

Giant Cell Arteritis

Symptoms:  Headache from Temporal arteritis.*  Jaw claudication from ischemia of masseters*  Visual loss due to Ophthalmic artery dz.*  Chest pain may suggest Aortic aneurysm or Dissecting Aneurysm.

GiantGiant-Cell Arteritis
Physical Exam:  Scalp tenderness in the temporal artery area!*  Low grade fever  Pale, edematous fundus*  Diastolic murmur of aortic regurgitation. Studies:  Elevated C-reactive protein and Sed. Rate* C Anemia  Diagnosis confirmed by biopsy of arterial tissue*

GiantGiant-cell Arteritis
Treatment:  High dose corticosteroids**  Start treatment when highly suspicious (before biopsy results)*  Methylprednisolone (Solumedrol)* 250mg IV q 6 hrs for 3 days followed by oral steroids (prednisone 80mg q day)

Case Study


74 year old female comes into your office complaining of a right sided headache that has been getting worse over the last 3 days. Pain is moderate to severe, constant, throbbing and located in the right temporal area. What is your most likely diagnosis?

Takayasu s Arteritis
Granulomatous vasculitis of the aorta, its main branches and the pulmonary artery.*  Rare polyarteritis of unknown cause with a special predilection for branches of aortic arch.  Results in segmental stenoses, occlusion, and stenoses, aneurysms.  Common in young women of Asian descent.  Inflammatory process in the vascular wall can lead to stenosis and/or aneurysm formation*.  Hypertension is the most common sign**


Takayasu s Arteritis
Physical findings: findings:  Bruits over Subclavian art. and aorta*  Diminished brachial pulses*  Low brachial artery blood pressure.* Diagnosis:  Made primarily on clinical presentation

Takayasu s Arteritis
Treatment:
Corticosteroids are 1st line**  Immunosuppressive agents: Methotrexate* and cyclophosphamide help prevent relapse and disease progression.  Revascularization (percutaneous or surgical)


Arteriovenous (AV) Fistulas

Abnormal vascular communications which shunt blood flow from the arterial system directly into the venous system, bypassing the capillary beds that normally ensure optimal tissue perfusion and nutrient exhange.  May be congenital or acquired.


AV Fistula

Arteriovenous (AV) Fistulas

Symptoms:
      

Pulsatile mass* mass* Symptoms related to compression of an adjacent organ. Bleeding from spontaneous rupture.* rupture.* Systolic and Diastolic bruits and thrills over the AVM or fistula. Bone malformation (if in skeletal muscle) or pathologic fracture. Neurologic deficits or seizures (if AVM is in brain)* High output heart failure

Arteriovenous (AV) fistulas

Diagnosis:
MR angiography  CT angiography  Conventional angiography


Arteriovenous (AV) Fistulas

Treatment:
Surgical resection  Transcatheter embolization  Pulse laser irradiation  Surgical closure if AV fistula is from trauma.


Venous Thromboembolic Disease*



The presence of coagulated blood, or thrombus in a vein. Encompasses both DVT (Deep Venous Thromboembolism) and PE (Pulmonary Embolus). High incidence. 1 per 1000 patients

Venous Thromboembolic Disease

Predisposing Factors  Virchows Triad (3 predisposing factors)** 1. Endothelial damage 2. Venous stasis 3. Hypercoagulation

Venous Thromboembolic Disease



Trousseau s Syndrome : Migratory thrombophlebitis with noninfectious vegetations on the heart valves typically in the setting of mucinmucin-secreting adenocarcinoma. Hypercoagulable states: Include hereditary states: diseases such as deficiencies in antithrombin III, protein C, or protein S.* A search for identifiable risk factors in patients with VTE will be negative in 25-50% of patients. 25-

Deep Vein Thrombosis

Etiology: Etiology: -Surgery (esp. of hip or leg or abdomen)* -Immobility (bedrest, long travel)* -Birth control pills * -Atrial Fibrillation* -Cancer* -Heart failure* -Pregnancy* -Venous catheters*

Deep Vein Thrombosis

Most DVT s begin in the calf.  Without treatment, 15-30% of these clots 15propagate to the proximal calf veins.  The risk for PE then becomes much higher 4040-50% compared to 5-10%. 5 Involvement in upper extremities is much less common.


Deep Vein Thrombosis

Symptoms:
Pain and/or swelling!!**  Many are asymptomatic  Upper extremity DVT can develop the superior vena cava syndrome of facial swelling, blurred vision and dyspnea.  Thoracic outlet obstruction can compress the brachial plexus leading to unilateral arm pain associated with hand weakness.


Deep Vein Thrombosis

Physical exam: exam:  Tenderness, erythema, warmth, and swelling below the site of thrombosis.**  Pain with dorsiflexion of the foot (Homans sign*) may be present.  Palpable tender cord.  Dilated superficial veins  Low grade fever

Deep Vein Thrombosis

Physical findings (cont.):  Thoracic Outlet Syndrome (TOS)(TOS)compression of the neurovascular structures at the superior aperture of the thorax.  Adson s Test:  Wright s Test

Deep Vein Thrombosis

Diagnosis:
D-Dimer-Highly sensitive indicator of DVT Dimer Duplex ultrasonography  MR angiography can help detect Subclavian vein DVT s that are obscured by the clavicle. (Hard to get MRI s in the ER)  Contrast venography-no longer the gold venographystandard.


Contrast Venography

Deep Vein Thrombosis

Treatment: Treatment:  1st-Heparin (IV), Lovenox (SQ)(SQ)-Prevent thrombus propagation and to maintain the patency of venous collaterals.  2nd-Warfarin (Coumadin)-start after above (Coumadin)medications.  Benefit of anticoagulation is debatable in DVT s limited to the calf, since PE risk is low.

Deep Vein Thrombosis

Upper extremity DVT in young patients: may consider thrombus removal by: -fibrinolytic infusion thru a catheter inserted directly into the affected vein. -mechanical fragmentation of the thrombus


Purpose is to prevent/minimize the postpostthrombotic syndrome (chronic arm pain, swelling, hyperpigmentation, and ulceration.

Deep Vein Thrombosis

Inferior Vena Cava filter*-consider in filter*patients with proximal DVT who: 1. either have an absolute contraindication to anticoagulation or 2. develop recurrent PE despite adequate anticoagulation. -These filters reduce the incidence of PE but they increase the risk of recurrent DVT.


Inferior Vena Cava Filter

Pulmonary Embolism
 PE occurs when a

thrombus dislodges from the deep veins of the upper or lower extremities and embolizes to the arterial blood supply of the lungs where it then blocks a pulmonary artery.

Pulmonary Embolism
A very common problem/complication. -Severely underdiagnosed.  Predisposing factors are the same as for DVT  In acute PE, areas of lung tissue are ventilated but underunder-perfused.


Pulmonary Embolism
Symptoms:*** Symptoms:  Sudden onset of dyspnea*  Pleuritic chest pain*  Anginal chest pain  Hemoptysis  Syncope

Pulmonary Embolism
Physical findings: findings:  Tachypnea**  Tachycardia**  Crackles  Wheezing  Pleural rub

Pulmonary Embolism
Diagnosis:
Arterial blood gas (ABG)-may reveal (ABG)hypoxia.*  Spiral CT of chest**  Chest x-ray-not very helpful x-ray D-dimer*


Pulmonary Embolism
Diagnosis (cont.):  VQ study=WAS gold standard. Too nonspecific.  Spiral Chest CT angiography=Quick, effective. Modality of choice**.  Lower extremity ultrasound (can be helpful)  Pulmonary angiography-only use if above angiographystudies are inconclusive.

Pulmonary Embolism Diagnostic Algorithm

Pulmonary Embolism
Treatment:  Anticoagulation-Immediate! IV UFH** Anticoagulation Warfarin (Coumadin)*-After starting UFH. (Coumadin)* Thrombolytics*-reserve for patients with Thrombolytics*hypotension and/or severe hypoxemia.

Pulmonary Embolism Treatment (cont.)

How long do we continue anticoagulation? - 3 to 6 months after a PE due to trauma or surgery. -Indefinitely for VTE due to cancer -Indefinitely for idiopathic VTE  Stop anticoagulation if unmanageable bleeding.


Venous Thromboembolism Prophylaxis

 

Prophylaxis for high risk patients. Prophylaxis involves: Heparin, LMWH, and pneumatic involves: stockings, TED hose, early ambulation Surgical patients.* Hospitalized patients with acute illness, especially with history of CHF, respiratory illness, acute inflammatory disease and those expected to be immobilized for 3 days or longer. Imprecise science.