Vascular disease

Chronic venous insufficiency Venous Insufficiency: Epidemiology

Introduction: Prevalence of CVI increases with age

Definition  escapement of blood from its normal path of flow, refluxing down the vein Women>men
- (back flow)
Women: 40-49
Chronic venous insufficiency  wide spectrum of morphological functional abnormalities Men: 70-79
- Venous dilation
- Valvular pathology
- Reflux
Venous Insufficiency: Risk Factors Venous Insufficiency: Anatomy

Family history of venous disease Venous network in the lower extremities divided into 3 networks
Smoking - Superficial vein  great/small saphenous
Sedentary lifestyle - Deep veins  anterior/posterior tibial, superficial/deep femoral, iliac popliteal &
High estrogen state peroneal
Pregnancy - Communicating veins

DVT renders venous valve incompetent and thereby causes backflow and increase venous
pressure. A sedentary lifestyle minimizes pump action of calf When functioning correctly – movement of legs causes blood to be pumped inward and upward
past the valves.
Venous Insufficiency: Pathophysiology Venous Insufficiency: Pathophysiology

Inadequate muscle pump Scarred and thickened valve leaflets

Inadequate function - Secondary damage from DVT
- Valvular incompetence - Trauma
- Venous dilation - Excess pressure
Increase hydrostatic pressure causes edema from leaking capillaries Venous dilation
- Lose the reflex constriction of the pre-capillary arterioles that occurs when standing - Leg trauma
Venous stasis ulceration - Congenital AV fistulas
- Neoplastic obstruction
- Complicated by obesity
Venous Insufficiency: History Venous Insufficiency: Physical Exam

Early stage  bothersome Edema

Middle phase  less severe - Lower extremities pitting edema
Advance phase  worsening again Hyperpigmentation
- Medial lower leg
Common sx: - Skin is taught and shiny
Burning, cramping, aching, swelling, throbbing, heaviness, restless leg, leg fatigue Visible dilated venous
Pain improves when Venous Insufficiency: Physical Exam. - Telangiectasias
Warmth tend aggravate while cold relieves them - Reticular veins
- Varicose veins
Physical Exam: Dermatitis Physical Exam: Varicosities
Venous stasis dermatitis  inflammatory skin disease is the earliest cutaneous sequala of CVI
Dilated tortuous veins in the lower extremities
- Potentially aching
- Increase frequency after pregnancy
 -
Physical Exam: Lipodermatosclerosis

Stasis panniculitis and lipomenbranous changes

Skin induration, increase hyperpigmentation, swelling and redness
Bowling pin appearance

Physical Exam: Atrophie Blanch

- Scarring of the lower extremities secondary to CVI

Physical Exam: Ulcerations

Venous stasis ulcer
- Shallow, superficial, irregular borders
- May have related edema, phlebitis and infection

Physical examination: Venous disability scoring

Venous stasis dermatitis Score 0 – asymptomatic
Varicosities Score 1- symptomatic, able to carry out usual activities without compression therapy
Lipodermatosclerosis Score 2- symptomatic, able to carry out usual activities with compression therapy
Atrophie blanch Score 3- symptomatic, unable to carry out usual activities even with compression therapy or
Venous stasis ulceration limb elevation
Venous Insufficiency: Diagnostics Venous Insufficiency: Treatment
Venous duplex ultrasound – study of choice for venous insufficiency
- Assess: superficial reflux, degree of deep reflux & degree of obstruction Regular maintenance
- Diagnosis of venous insufficiency made when there is a retrograde/reverse flow Conservative treatment
greater than o.5 seconds under ultrasound - Leg elevation
- Exercise
Magnetic resonance venography – second best choice - Compression therapy (stocking from mid-foot to knee, at least 30mmHg)

Of note  consider performing ankle-branchia index to rule out concomitant arterial disease Venous ablation is reserved for those with discomfort and ulcer refractory to medical
management and conservative treatment
- Primary goal is to correct insufficiency by removing major reflux pathways
Venous Insufficiency: Treatment

Venous stasis ulcer

Once swelling has been decreased
Apply unna boot
- Semi rigid boot gauze boot with calamine and zinc oxide layer
- Change every 2-3 days
Thrombophlebitis/ phlebitis

Introduction – inflammation of the vein

Can become migratory- trousseau sign of malignancy
Etiology Thrombophlebitis: Presentation

Irritation of IV catheter insertion Induration

Irritation soultions through IV Edema
Trauma Tenderness
IV drug use 90-95% at the site of thrombosis

(hard, warm, very tender)

Thrombophlebitis: Diagnostics Thrombophlebitis: Treatment

Venous ultrasound for detection of thrombosis Uncomplicated (WARN)

W: warm compress
A: analgesic
R: rest/elevation
N: NSAIDS

Involvement of saphenofemoral or iliofemoral

- Treat as DVT  anti-coagulant for 4 weeks

Admit:
- Extensive involvement
- Septic signs
- Progression despite treatment

Thromboangiitis Obliterans

Introduction: Thromboangiitis Obliterans: Pathophysiology

Buerger’s disease
Unknown
Nonatherosclerotic, segmental, inflammatory disease that affects small-medium size arteries and Definite relationship to cigarette smoking
veins of the extremities

Men < 40 years old

Asian and eastern European descent
Smoking
Thromboangiitis Obliterans: Clinical Presentation Thromboangiitis Obliterans: Diagnostics

TRIAD of claudication of the affected extremities (distally), Raynaud’s phenomenon, migratory MRA or angiography
superficial vein thrombophlebitis

Progresses  severe digital ischemia, trophic nail changes, painful ulcerations, gangrene

Physical examination:
- Normal brachial and popliteal pulse
- Reduced radial, ulnar and tibial pulses
- Toe lesions usually involved
Thromboangiitis Obliterans: Treatment and Prognosis

No specific treatment for this disease

Abstention from smoking
Referral to vascular surgeon

Prognosis is worse is continue to smoke  amputation

Venous thrombosis
Venous Thrombosis: Epidemiology Venous Thrombosis: Pathophysiology

Men > women Virchow’s triad:

Caucasians/African Americans > Asians & Hispanics
Death of DVT  associated with pulmonary embolism
Venous stasis
- Occurs as a result of anything that slows/obstructs venous flow
- Result in increased viscosity and formation of micro-thromboli
vascular damage
- Intrinsic or secondary to external trauma
Hypercoagulability
- May be the result of biochemical imbalance of circulating clotting factors

Venous Thrombosis: Risk Factors Venous Thrombosis: Clinical Presentation

Risk factors (PALM ICP) Produces pain and limb edema that are often mild or absent
- Pregnancy and the postpartum period - Edema is the most specific symptom of DVT
- Age - Leg pain occurs in 50% of patients
- Long plane or car trips > 4 hours in the last previous 4 weeks Pain occurs with dorsiflexion of the foot (holman sign)
- Major surgery in previous 4 weeks Discoloration of lower extremities  erythematous or violaceous color
- Immobilization for > 3 days Tenderness occurs
- Cancer
- Previous DVT DVT cannot be diagnosed or excluded based on physical exam! YOU NEED A DIAGNOSTIC
TESTING, MUST BE PERFORMED
Venous Thrombosis: Diagnostics Venous Thrombosis: Diagnostics

Routine blood test  D-Dimer Ultrasound is 1st line imaging – ease of use, absence of irradiation, high sensitivity
Gold standard is still  venography w/ pedal vein cannulation, IV contrast injection, serial limb
Know the WELLS criteria for DVT – ppt 49 radiography

MRI is the next best test

Venous Thrombosis: Treatment Venous Thrombosis: Treatment
Primary goal is to prevent pulmonary embolism, reduce morbidity, and reduced developing
post-thrombotic syndrome Most patients with confirmed proximal vein DVT may be safely treated on an outpatient basis

Anticoagulant is the mainstay for this treatment Exclusions for outpatient management
- LMWH*, UFH - Unavailable or unable to arrange close follow up care
- Oral factors Xa inhibitors (Xarelto, Eliquis) - Unable to follow instructions
- Fondaparinux Absolute contraindications to anti-coagulant treatment
- BRIDGE to warfarin - Intracranial bleeding
- INR: 2.0-3.0 - Severe active bleeding
- Bridge (5-10days) to dabigatran (Pradaxa) or edoxaban (savaysa) - Recent brain, eye, or spinal surgery
- Continue for 3-6 months for 1st DVT then for at least 1 year for subsequent - Malignant hypertension
Venous Thrombosis: Treatment

Thromolytics can result in intracranial bleeding

Only use when:
- Contraindicated to anti-coagulants
- Phegmasia cerula dolen
- Symptoms for more than 14 days

if pregnant, warfarin is contraindicated

- Extend LMWH
Patients with unexplained DVT  consider occult malignancy

Raynaud’s Phenomenon
Introduction: exaggerated vascular response to cold temperature or emotional stress Raynaud’s – Pathogenesis

Episodic digital ischemia Exposed to cold environment or touches a cold object

Idiopathic: - Digit turns white – ischemic phases – vasospasm
- Women 20-40 years old Capillaries and venules dilate reactivity
- Mostly fingers – can include nose, penis and earlobes - Cyanosis: deoxygenated blood
- Secondary disease - Sensation of cold or numbness or paresthesia
Rewarming =- blood flow into the dilated arterioles and capillaries
- Bright red color – reactive hyperemia
- Throbbing, painful sensation
Raynaud’s – Clinical Presentation

Manifested by sharply demarcated color changes of digital skin

• Abnormal vasoconstriction of digital arteries and cutaneous arterioles due to
a local defect in normal vascular responses is thought to underlie the
primary form of this disorder
Diagnosis- none needed

Raynaud’s – Treatment and Prognosis

- Smoking cessation
- Dress warmly to avoid cold exposure
Can use CCB
KNOW THIS - Dihydropyridines, nifedipine, amlodipine
- Refer for digital sympathectomy
Peripheral arterial disease

Peripheral artery disease Atherosclerotic PAD – Pathogenesis

Stenosis or occlusion of the aorta or arteries of the limb
Formation of atherosclerotic plaques  subsequent stenosis and arterial occlusion
Atherosclerotic PAD: leading cause of PAD in those >40 years old
Risk factors: Femoral and popliteal – 80-90%
- Cig. Smoking Tibial and peroneal arteries – 40-50%
- DM Abdominal aorta and iliac femoral – 30%
- Dyslipidemia
- You know the rest. Prefers arterial branch points
- Increase turbulence
- Altered sheer stress
- Intimal injury
Atherosclerotic PAD – Clinical Presentation, Early Atherosclerotic PAD – Clinical Presentation, Severe

Asymptomatic >50% Resting blood flow cannot accommodate basal metabolic needs of the tissues
Claudication - ulceration or gangrene
- pain, cramp, aches, fatigue, numbness in muscle during exercise - rest pain
- relived by rest - feeling of cold or numbness
erectile dysfunction - worse at night (patient supine)
- bilateral common iliac disease - improve when legs are in a dependent position
- poor nail growth and decreased hair growth on toes and legs
PAD – Clinical Presentation Atherosclerotic PAD – Clinical Presentation

Arterial ulcers: Decreased or absent pulses

- full thickness Bruits over narrowed arteries*
- punched out appearance Hair loss
- smooth edges Smooth and shiny skin
- bright red granulation tissues in wound bed Decreased in skin temperature*
Pallor
Muscle atrophy
Cyanosis

Atherosclerotic PAD – Diagnostics Classifications

Normal  > 0.90
Ankle brachia index* Claudication  0.40-0.90
Arterial ultrasound and treadmill stress testing* Rest pain  0.21 – 0.49
 Tissue loss  <0.20
ABI has 99% specificity and 94-97% sensitivity
Segmental limb pressure – once arterial occlusive disease has been verified using the ABI, the Atherosclerotic PAD – Diagnostics
level and extent of disease can be determined using segmental limb pressure

Magnetic resonance angiography of a patient with intermittent claudication, showing stenoses

of the distal abdominal aorta and right iliac common iliac artery (A) and stenoses of the right
and left superficial femoral arteries (B).
Atherosclerotic PAD – Treatment Atherosclerotic PAD – Treatment

Risk factor modification: Treatment of hypercholesterolemia with statins

Smoking cessation
Diet/exercise **Platelet inhibitors, including Aspirin and clopidogrel, reduce the risk of adverse CV events

Controlling blood pressure Cilotazol 100mg

- ACE inhibitors may reduce the risk of CV events in patients with symptomatic PAD
- BB do not worsen claudication Follow-up every 4-6 months
- ECHO
- Carotid ultrasound
- ABI annually
Atherosclerotic PAD – Refer
Conservative treatment is not working
Invasive treatment consideration:
- Percutaneous transluminal angiography (PTA), stent placement, bypass

stent placement
Revascularization Indications Revascularization Indications
Claudication causing lifestyle deterioration refractory to pharmacologic intervention and
Gangrene, non-healing ulcers & ischemic rest pain (limb threatening ischemia) behavioral modification
 Atherosclerotic PAD – Prognosis Atherosclerotic PAD – Patient Education
Meticulous care of feet  clean & moisturizers
1/3 to ½ patient with symptomatic PAD have evidence of CAD Well-fitting and protective shoes to reduce trauma
Elastic support hose should be avoided

Patient with claudication should be encouraged to exercise regularly and at progressively more
strenuous levels

Acute arterial occlusion

(sudden cessation of blood flow to an extremity)

Embolism  commonly cardiac, aorta, and large arteries Acute Arterial Occlusion – Clinical Presentation
Thrombus in situ
- Most commonly femoral Within 1 hour:
- Iliac artery, aorta, popliteal & tibioperoneal arteries - Severe pain, pallor, paresthesia, coldness, numbness, paralysis if severe
- Originate from proximal sites of atherosclerosis and aneurysms
- Originate from areas of trauma  catheters & arterial punctures
- Hypercoagulable states
Arterial dissection
Trauma
muscle stiffening, mottling, may have absent tendon reflexes
Blue toe syndrome- palpable pulse

Acute Arterial Occlusion – Diagnostics

Acute extremity pain/ lost pulse  imaging done in OR

- MRA
- CTA
- Catheter-based arteriography

These are used to confirm the diagnosis and demonstrate the location and extent of occlusion.
However, they should be performed in the OR because waiting on results with jeopardize the
viability of the limb
If light touch sensation is still intact, you may wait to order tests in ER
5 P’s
Acute Arterial Occlusion – Treatment

IV heparin bridge to warfarin  immediate IV heparin bolus

Intraarterial thrombolytic therapy with recombinant tissue plasminogen activator

Arterial Aneurysm
(abdominal, thoracic and peripheral)

Abdominal aortic aneurysm AAA – Pathogenesis

Dilation of the aorta > 3 cm
Males > females Atherosclerotic lesions decrease integrity of the vessel walls

Risk factors 90% originate BELOW the renal arteries

- Family history of aneurysms Usually involves the aortic bifurcation and common iliac arteries
- Atherosclerosis, PAD
- >60 years old
- Smoking
- HTN
- Aneurysm of the femoral or popliteal
- Obesity
Regular exercise and a diet rich in fruits, veggies, and nuts reduce the risk

The natural history is one of progressive expansion

- Variable and depends on diameter and other factors
- Most important of which is ongoing smoking
AAA – Clinical Presentation AAA – Diagnostics

Most asymptomatic until rupture** Found incidentally during workup or routine screening

Mid-abdominal discomfort radiating to lower back Study options:

- Constant or intermittent Unruptured  abdominal US
Rupture: Suspected ruptured.  CT
- Severe abdominal and back pain (ripping/tearing) planning repair  CT with contrast
- Hypotension
- Syncope screening frequency for US
- Periumbilical ecchymosis or flank ecchymosis 65-74 year old with smoking history
- Q2 years if <4cm
- Q6 months > 4cm
AAA – Treatment

Refer if > 4cm or if tender

Elective repair
- > 5.5 cm or rapid expansion of > 0.5 cm in 6 mos
Ruptured aneurysm
- Lethal

Thrombus in the aneurysm is NOT NOT NOT NOT an indication for anticoagulant
AAA – Prognosis

Risk of rupture in 1 year

- 12% if >6 cm
- 25% if > 7 cm
Thoracic aorta aneurysm

Less than 10 % Thoracic Aortic Aneurysm – Clinical Presentation

Mostly due to atherosclerosis Asymptomatic

Depends on size and position of aneurysm
False aneurysm in traumatic deceleration injuries  partial tear of the aorta Substernal back or neck pain

Pressure on trachea, esophagus and superior vena cava

- Dyspnea
- Stridor
- Brassy cough
- Dysphagia
- Edema in the neck and arms
- Distended neck vein
Thoracic Aortic Aneurysm – Clinical Presentation Thoracic Aortic Aneurysm – Diagnostics
Suspected  CXR
Stretching the left recurrent laryngeal nerve causes hoarseness - Widened mediastinum
Rupture  acute onset of chest pain radiating to the back
- Bleeding rarely contained leading to death : ( CT modality of choice to exclude mimicking lesions
Thoracic Aortic Aneurysm – Treatment

Refer for repair > 5 cm

Especially descending aorta

Peripheral arterial aneurysms

Caused by atherosclerotic disease Peripheral Arterial Aneurysms – Clinical Presentation

Manifestation d/t embolism and thrombosis

70% involve the popliteal artery

First sign may be d/t acute arterial occlusion

Peripheral Arterial Aneurysms – Diagnostics Peripheral Arterial Aneurysms –Treatment and Prognosis

Arterial ultrasound Refer for repair

Abdominal US if popliteal aneurysm present (r/o AAA) - > 2 cm in diameter
- Lined with thrombus at any size
For reconstruction: CTA & MRA
Aortic dissection
Spontaneous intimal tear develops, and blood dissects into media of the aorta Aortic Dissection – Pathogenesis

Risk: Repetitive torque

Bicuspid aortic valve Hypertension
Coarctation of the aorta Smooth muscle, elastic tissue or collagen disorders
Connective tissue disorder

MEDICAL EMERGENCY

Aortic Dissection – Clinical Presentation Aortic Dissection – Diagnostics

Sudden onset of severe, persistent chest pain CT scan is immediate study choice
- Ripping/tearing pain - Include chest and abdomen
- Radiating down the back or anterior chest
- Rarely radiates to the neck ECG
Abdominal pain Radiograph
Hypertension/hypotension - Widened mediastinum
Syncope - Abnormal aortic contour
Hemiplegia or paralysis of lower extremities may occur
Intestinal ischemia

Aortic Dissection – Treatment

Medical emergency- consult CV surgeon

Lower BP to 100-120 systolic (ideal) or 120-130

- Beta blockers (best option)
- Labetalol 10-20 mg IV over 2 minutes, then 20-40 mg q10 min
- Esmolol 0.1-0.5
- May add nitroprusside (vasodilator)