vascular diseases

1. VASCULAR DISEASES II
Edwin E. Nyambi, DMSc, MPAS, PA-C
edwinnyambi@atsu.edu
Cardiovascular Medicine & Surgery
CCPA5012

2. OCCLUSIVE DISEASE

3. ESSENTIALS OF DIAGNOSIS
• Claudication: cramping pain/tiredness in the calf, thigh, or hip while walking.
• Diminished femoral pulses
• Tissue loss (ulceration, gangrene) or rest pain

4. GENERAL CONSIDERATIONS
• Lesions in the distal aorta/proximal common iliac arteries
• Occur in white males—main risk fact is cigarette smoking
• Disease progression can lead to complete occlusion of one or both common iliac
arteries—occlusion of entire abdominal aorta to the level of the renal arteries.

5. CLINICAL FINDINGS
Signs/Symptoms
• Pain; thigh, buttocks
• Males (erectile dysfunction)
• Limb fatigue/weakness of limbs during ambulation
• Symptoms are relieved with rest, reproducible when patient walks
• Pulses; femoral and distal are absent/weak
• Bruits; can be heard over the iliac, aorta and femoral arteries

7. CLINICAL FINDINGS
Bruits
• https://www.youtube.com/watch?v=PrlTdsJ7lWg

8. CLINICAL FINDINGS
Doppler and Vascular Findings
• Ankle-brachial index (systolic blood pressure of ankle vs radial artery by Doppler) is
reduced to below 0.9 (normal; 0.9-1.2)
• Ankle: dorsalis pedis and posterior tibialis

9. CLINICAL FINDINGS
Imaging
• CT angiography and magnetic resonance angiography can identify the anatomic
location of the disease

10. DISEASE
CLASSIFICATION

11. DISEASE
CLASSIFICATION

12. TREATMENT
Medical & Exercise Therapy
• Cardiovascular risk reduction
• Cigarette smoking cessation
• Antiplatelet therapy (Aspirin 81 mg or Clopidogrel 75 mg daily + low-dose rivaroxaban 2.5
mg BID + Cilostazol 100 mg BID-vasodilator and improve walking distance)
• Lipid and blood pressure management (Atorvastatin 80 mg daily)
• Weight loss
• Nicotine replacement therapy (Bupropion or Varenicline)
• Exercise

13. TREATMENT
Endovascular Therapy
• Angioplasty and stent: https://www.youtube.com/watch?v=OFBa-hquW6s
Surgical Intervention
• Aorto-femoral bypass graft which bypasses the diseased aorta or iliac artery
• Graft from axillary artery to femoral arteries or from contralateral femoral artery can be
used

14. TREATMENT
When to refer
• Patients with progressive reduction in walking distance
• Interference with activities of daily living
• Vascular surgeon consult

15. TREATMENT
When to admit
• Evidence of chronic limb-threatening ischemia; lower extremity rest pain, tissue loss
• Limb ischemia

16. CHRONIC VENOUS DISEASE
Formerly known as Venous Insufficiency

17. EPIDEMIOLOGY
• Chronic vein abnormalities are present in up to 50 percent of individuals

18. PATHOPHYSIOLOGY
• Inadequate muscle pump function
• Incompetent venous valves

19. RISK FACTORS
• Advancing age
• Family history
• Ligamentous laxity (hernia, flat feet)
• Prolonged standing
• Increased body mass index
• Smoking
• Sedentary lifestyle
• Lower-extremity trauma
• High estrogen states
• Pregnancy

20. PRESENTATION
• Pain
• Leg heaviness or aching
• Swelling
• Dry skin
• Tightness
• Skin irritation
• Heaviness
• Muscle cramps
• itching
• Dilated veins
• Lipodermatosclerosis
• Ulceration

23. DIAGNOSIS
• Duplex ultrasound
• Presence of venous reflux

24. MANAGEMENT
• Leg elevation
• Exercise
• Compression therapy
• Topical dermatologic agents
• Wound management
• Ablation therapy
• Surgical excision
• Sclerotherapy (Chemical ablation)
• Thermal ablation

25. VARICOSE VEINS

26. ESSENTIALS OF DIAGNOSIS
• Dilated, tortuous superficial veins in the legs.
• Asymptomatic/aching/discomfort or pain.
• Hereditary.
• Increased frequency post partum

27. GENERAL CONSIDERATIONS
Risk factors
• #1: Post-partum
• High venous pressure; from prolonged standing/heavy lifting
Hallmark of disease
• Progressive venous reflux and venous hypertension

28. GENERAL CONSIDERATIONS
Pathophysiology
• The superficial veins are involved; great saphenous vein and its tributaries + short saphenous
vein (posterior lower leg).
• Distention of the vein prevents the valve leaflets from fitting together, creating incompetence and
reflux of blood toward the foot.
• Focal venous dilation and reflux leads to increased pressure and distention of the vein segment
below that valve---failure of the next lower valve.
• Perforating veins that connect the deep and superficial systems become incompetent---blood reflux
into the superficial veins from the deep system---increased venous pressure/distention.

29. GENERAL CONSIDERATIONS
Pathophysiology
• Secondary varicosities can develop as a result of obstructive changes/valve damage in the
deep venous system following thrombophlebitis, or because of proximal venous occlusion due
to neoplasm or fibrosis.
• Congenital or acquired arteriovenous fistulas or venous malformations are also associated with
varicosities and should be considered in young patients with varicosities.

30. GENERAL CONSIDERATIONS
Symptoms and Signs
• Dull, aching heaviness or a feeling of fatigue of the legs brought on by periods of standing is
the most common complaint.
• Itching from venous eczema may occur either above the ankle or directly overlying large
varicosities.
• Dilated, tortuous veins of the thigh and calf are visible and palpable when the patient is
standing.
• Varicose veins may progress to chronic venous insufficiency with associated ankle edema,
brownish skin hyperpigmentation, and chronic skin induration or fibrosis.
• ***A bruit or thrill is never found with primary varicose veins and, when found, alerts the clinician to
the presence of an arteriovenous fistula or malformation.

31. GENERAL CONSIDERATIONS
Imaging
• The identification of the source of venous reflux that feeds the symptomatic veins is necessary
for effective surgical treatment.
• Duplex ultrasonography.
• Reflux arises from the greater saphenous vein in most cases

32. TREATMENT
A. Nonsurgical Measures
• Elastic graduated compression stockings (20–30 mm Hg pressure) reduce the venous pressure
in the leg and may prevent the progression of disease.
• Good control of symptoms can be achieved when stockings are worn daily during waking hours
and legs are elevated, especially at night.
• Compression stockings are indicated and effective for elderly patients or patients who do not
want surgery.

33. TREATMENT
B. Varicose Vein Sclerotherapy
• Direct injection of a sclerosing agent induces permanent fibrosis and obliteration of the target
veins.
• Chemical irritants (eg, glycerin) or hypertonic saline are often used for small, less-than-4-mm
reticular veins or telangiectasias.
• Foam sclerotherapy is indicated for treatment of the great saphenous vein, varicose veins larger
than 4 mm, and perforating veins.

34. TREATMENT
C. Surgical Reflux Treatment
• Reflux; surgical vein stripping (removal) or endovenous treatments using thermal devices (laser
or radiofrequency catheter), cyanoacrylate glue injection, or foam sclerosant injection.
• Endovenous interventions can often be performed with local anesthesia and the early success is
equal to vein stripping.
• Long-term success; highest with vein stripping and thermal treatments

35. THROMBOPHLEBITIS, SUPERFICIAL
VENOUS

36. KEY FEATURES
Essentials of diagnosis
• Red, painful induration along a superficial vein, at the site of a recent intravenous line
• Marked swelling of the extremity
General Considerations
• Common in pregnant or postpartum women
• Also seen in individuals with varicose veins
• May be also be caused by;
• Trauma
• Deep venous thrombosis (DVT) (in about 20% of cases)
• Short-term venous catheterization of superficial arm veins
• Longer term peripherally inserted central catheter lines

37. KEY FEATURES
General Considerations
• Can be a manifestation of systemic hypercoagulability secondary to abdominal cancer
• Pulmonary emboli are rare (associated with DVT)
• Observe intravenous catheter sites daily for signs of local inflammation

38. CLINICAL FINDINGS
Signs and Symptoms
• Dull pain of the vein around the site of injection
• Thickness, erythema, and tenderness of the vein
• Process may be localized and can involve the great saphenous vein and its tributaries
• Inflammatory reaction generally subsides in 1–2 weeks; a firm cord may remain for much longer
• Proximal extension of hardness and pain with chills/high fever suggest septic phlebitis
Differential Diagnosis
• Cellulitis
• Erythema nodosum
• Erythema induratum

40. DIAGNOSIS
Laboratory Tests
• Blood culture: the most common causative organism is usually Staphylococcus aureus. Fungi
can also be a causative agent
Imaging Studies
• Duplex ultrasonography is gold standard

41. DIAGNOSIS
Medications
• NSAIDs
• Septic thrombophlebitis
• Antibiotics (Vancomycin + ceftriaxone); if cultures are positive, continue for 7–10 days or for 4–6 weeks if
complicating endocarditis cannot be excluded
• Systemic anticoagulation; heparin or fondaparinux
• Prophylactic dose low-molecular-weight heparin/fondaparinux is recommended for superficial
thrombophlebitis of the lower limb veins (5 cm and/or longer)
• Full anticoagulation; rapidly progressing disease

42. DIAGNOSIS
Surgery
• indicated when process infection progresses toward the saphenofemoral or cephalo-axillary junction
Therapeutic Procedures
• Local heat
• Bed rest with leg elevation

43. VENOUS THROMBOEMBOLISM
(VTE)
Deep Vein Thrombosis (DVT) and Pulmonary Embolism (PE)

44. EPIDEMIOLOGY
• Approximately 1 percent of hospital admissions in the US are for VTE.
• It has been estimated that there are 900,000 cases of pulmonary emboli (PE)
and deep vein thrombosis (DVT) per year resulting in 60,000 to 300,000
deaths.
• The vast majority of these deaths occur in untreated patients, where the
diagnosis is made postmortem or not diagnosed, and attributed to another
etiology (eg, myocardial infarction, cardiac arrhythmia).
• About two-thirds of VTE cases are associated with a hospitalization within the
prior 90 days, emphasizing the importance of medical illness, major surgery,
or immobilization as risk factors.

45. VTE PHYSIOLOGY
•Virchow’s Triad
•Venous Stasis
•Vessel Wall Injury
•Hypercoaguable state

46. VTE RISK FACTORS
• History of immobilization or prolonged hospitalization/bed rest
• Recent surgery
• Obesity
• Prior episode(s) of venous thromboembolism
• Lower extremity trauma
• Malignancy
• Use of oral contraceptives, hormone replacement therapy, IV drugs (abusers, street
drugs).
• Pregnancy or postpartum status
• Stroke
• Inherited Thrombophilia
• Factor V Leiden, Protein C/S Deficiency, Lupus

47. DVT EPIDEMIOLOGY
• Male to female ratio is 1.2:1
• Typically occurs in individuals older than 40
• Can be distal (calf)
• More common
• Can be proximal (popliteal, femoral, or iliac)
• More commonly associated with the development of PE

48. DVT PRESENTATION
• Swelling, pain, and erythema of the involved extremity
• Palpable cord (reflecting a thrombosed vein)
• Difference in calf diameters
• Warmth
• Superficial venous dilation
• + Homan’s Sign (Not very reliable)
• Calf pain with resisted dorsiflexion
of the foot

49. EVALUATION
•Malignancy is a risk factor for the development of venous
thromboembolism. However, prospective studies do not
demonstrate improved survival with aggressive diagnostic
testing for cancer in those with a first idiopathic DVT

50. Wells Score

51. DIAGNOSIS
• D-dimer
• Doppler Ultrasonography/Compression ultrasonography
• Venography
• If ultrasonography is not available

52. TREATMENT
• Patients with DVT should be treated acutely with LMW
heparin, fondaparinux, unfractionated intravenous heparin, or
adjusted-dose subcutaneous heparin.
• For most patients, warfarin should be initiated simultaneously with the
heparin, at an initial oral dose of approximately 5 mg/day.
• Inferior vena cava filter placement is recommended when there is a
contraindication to, or a failure of, anticoagulant therapy in an
individual with, or at high risk for, proximal vein thrombosis or PE.

54. DURATION OF THERAPY
• Patients with a first thromboembolic event in the context of a reversible or
time-limited risk factor (eg, trauma, surgery) should be treated for three
months.
• Patients with a first idiopathic thromboembolic event should be treated for a
minimum of three months. Following this, all patients should be evaluated for
the risk/benefit ratio of long-term therapy.
• Indefinite therapy is preferred in patients with a first unprovoked episode
of proximal DVT who have a greater concern about recurrent VTE and a
relatively lower concern about the burdens of long-term anticoagulant
therapy.
• Most patients with advanced malignancy should be treated indefinitely or
until the cancer resolves.

55. PULMONARY EMBOLISM
• Obstruction of the pulmonary artery or one of its branches by material
(eg, thrombus, tumor, air, or fat) that originated elsewhere in the body
• More common in males than females
• In the United States, PE accounts for approximately 100,000 annual
deaths

56. PE PRESENTATION
• Dyspnea
• Pleuritic pain
• Cough
• Symptoms of DVT
• Hemoptysis
• Shock – RARELY
• Asymptomatic - COMMON

57. DIAGNOSIS
•Hemodynamically stable patient
•Clinical + Pretest Probability
•D-dimer
•Computed Tomographic Pulmonary Angiography
•Ventilation Perfusion Scanning (if CTPA is not available or
contraindicated)
•Hemodynamically unstable patient
•Bedside echocardiography

59. ANTICOAGULATION
• Achieve therapeutic level of anticoagulation within the first 24 hours of
treatment
• Low Molecular Weight Heparin (LMWH)
• SQ Fondaparinux
• IV Unfractionated Heparin (UFH)
• When Creatinine Clearance (CC) is ≤30 mL/min
• Persistent hypotension due to PE
• SQ UFH
• When CC is ≤30 mL/min
• Bridge to Warfarin oral tablets (5 days and until INR is between 2.0 and 3.0)

60. DURATION OF THERAPY
•1st
PE with reversible risk factor = 3 months
•1st
PE without cause = 3 months then reassessed
•Recurrent PE = 3 months then reassessed

61. VIDEO
•https://www.youtube.com/watch?v=inz0BTSbTMw

62. PULMONARY ARTERIOVENOUS
MALFORMATIONS

63. INTRODUCTION
• In normal pulmonary circulation; blood lives the right ventricle of the heart through
the pulmonary artery.
• The entire blood is routed to the pulmonary capillary bed adjacent to the alveoli;
allows for gas exchange.
• After drainage from pulmonary capillaries, the blood returns to the heart through the
pulmonary veins.
• Pulmonary arteriovenous malformations (PAVMs) are abnormal vascular
connections between pulmonary arteries and pulmonary veins—prevents exposure
of blood to normal pulmonary capillaries
• Leads to hypoxemia—shunting of deoxygenated blood into the pulmonary venous system
and into the systemic circulation.

64. INTRODUCTION
• The size of the abnormal connections are larger than the size of pulmonary
capillaries—allows for transmission of particles in the blood stream (like venous
thromboemboli) from the venous circulation into the arterial circulation.
• Leads to complications (i.e stroke or septic emboli).
• Pulmonary arteriovenous malformations was first described by Churton in 1897;
‘autopsy case report of a 12-year-old boy with hemoptysis, epistaxis and edema’.
• In the 20th
century, pulmonary arteriovenous malformations were found to be
associated with hereditary hemorrhagic telangiectasia (HHT; also known as
Osler-Weber-Rendu syndrome)-mucocutaneous telangiectasia and pulmonary
arteriovenous malformations of various organ systems + lung.
• At least 60% of pulmonary arteriovenous malformations were found to be associated with
hereditary hemorrhagic telangiectasia.

65. PATHOLOGY
• Pulmonary arteriovenous malformations are made of 3 components; a vascular
aneurysmal sac, a feeding artery (or arteries) and a draining vein.
• Commonly found in the lower lobes of the lung

67. CLINICAL MANIFESTATIONS
• Dyspnea on exercise; 14-59% of patients
• Exercise intolerance
• Hemoptysis
• Epistaxis
• Hypoxemia; effect of right-left intrapulmonary shunting
• Platypnea (shortness of breath in the upright position)
• Orthodeoxia; oxygen desaturation (by <2%) of arterial blood in the upright
position—improved in the recumbent position
• Pulmonary bruit; heard in lower lung during inspiration
• Cutaneous finding; telangiectasis (small, dilated blood vessels found near the surface
of skin) and clubbing

70. CLINICAL MANIFESTATIONS
• Polycythemia (secondary erythrocytosis); 75% of patients—increased stroke risk
• Occurs as a compensatory mechanism for chronic hypoxemia through increased
erythropoiesis

71. COMPLICATIONS
• Pulmonary; hypoxemia
• Hemorrhage; rupture of pulmonary arteriovenous malformations—bleeding into
airways, hemoptysis, bleeding into pleural space
• Hemorrhage is Increased in pregnancy; increase in cardiac output, blood volume, vascular
distensibility, hormonal effects—increased risk of bleeding
• Pulmonary hypertension can lead to right heart failure
• Neurologic; migraine headaches (most common neurologic finding), ischemic strokes
transient ischemic attacks (TIAs) and brain abscesses
• Occur because pulmonary arteriovenous malformations allow small emboli to bypass the
pulmonary capillary bed into systemic circulation
• Brain abscess; occurs due to loss of pulmonary capillary filtration—passage of septic emboli
into systemic arterial circulation
• Patients should receive prophylactic antibiotics prior to dental procedures and other
nonsterile procedures that can cause bacteremia
• B

72. DIAGNOSIS
• Patients with a known or suspected diagnosis of hereditary hemorrhagic telangiectasia
(HHT; also known as Osler-Weber-Rendu syndrome) whose initial diagnosis is negative for
pulmonary arteriovenous malformations should be screened after puberty, after pregnancy,
within 5 years of planned pregnancy and every 5-10 years.
• Screening assesses for right to left shunting—contrast echocardiography, confirm diagnosis with
chest CT scan

73. TREATMENT
• Conservative management; asymptomatic patients with small feeding arteries (<2 mm
diameter) should have CT imaging performed every 3-5 years
• Embolization (also known as embolotherapy) is standard first-line intervention
• A CT scan should be obtained within 6-12 months following embolotherapy and repeat
every 3-5 years in asymptomatic patients
• Surgery: restricted to cases that are not amenable to embolization or those involving
hemorrhage.

74. QUESTIONS?