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Diseases of blood vessels
Dr. Mohammed Hajhamad, MB.ChB. (Egypt) M.S (Malaysia)
Department of SurgeryInternational Medical School
Management and Science University
Contents Introduction Diagnosis and
investigations Aneurysmal diseases and
dissectionThoracic aortic aneurysmAortic dissectionAAAOthers
Acute arterial occlusion Buerger disease Inflammatory arteritis and Arterial diseases of upper
limb
Diseases of venous systemIntroductionVTESVTVaricose VeinsChronic Venous insufficiency
Lymphedema
Arterial diseases … introduction
Peripheral arterial disease occurs in 12 percent of adult population.
It affects around 8-10 million people in US.
Most common presentation is intermittent claudication.
These patients have significantly higher risk of death compared with healthy controls of similar age.
Arterial diseases … diagnosis
Vascular history: Intermittent claudication (describe) TIA or stroke symptoms Mesenteric ischemia Previous vascular intervention Up to 30 percent of vascular
patients are diabetics. Most of them are smokers.
Arterial diseases … diagnosis
Vascular examination: Pulses (2+, 1+, 0 or 3+) Foot: for pallor on elevation, rubor on
dependency, ulceration or gangrenous toes.
Upper limbs for signs of ischemia or ulcerations.
Ankle-brachial index ABI (n>1) Aortic (aneurysm), carotid (bruits) and
vascular graft (stenosis) examination.
Arterial diseases … investigations
Duplex Scan (B-mode and Doppler US)- Carotid arteries stenosis- Bypass grafts of lower limbs- Abdominal aorta- DVT
Segmental pressures (ABI) Angiography,
- invasive (arterial access)- contrast … renal, drug interaction and allergy.- hydration status of the patients
CT-Angiography MR-Angiography
Arterial diseases … medical management …
Smoking cessation (reduce 10-mortality 54% 18%)
Control blood pressure (stroke and coronary events)
Reducing blood lipid levels Correction of elevated homocysteine level
(elevated in 60% of vascular patients) Tight control of blood sugar Exercise programs (24% reduction in
cardiovascular mortality) (30 minutes, 3 times/week)
Others: cilostazol (intermittent claudication), Aspirin and Clopidogrel.
Aneurysmal disease … introduction
Aneurysm: focal dilatation of an artery greater than 1.5 times its normal diameter.
Classification:Shape: fusiform, spindle-shaped, saccularWall constituents: true (by wall of the artery) false or pseudo (partly by wall and partly by adjacent structures.Etiology: dissecting, mycotic or traumatic.
Aortic aneurysm … Thoracic Incidence is estimated to be 5.9 per 100,000 per
year. Etiology:
- nonspecific medial degeneration (fragmentation of elastic fibers and loss of smooth muscles) most common.- Aortic dissection, two channels, weak outer layer.- Genetic disorders> Marfan syndrome, 75-85% have ameurysm.> Ehlers-Danlos syndrome, esp. type IV> Familial aortic aneurysm> Bicuspid aortic valves- Post-stenotic dilatation- Infection- Aortitis (Takayasu, Giant cell arteritis, Rheumatoid aortitis)- Traumatic
Clinical manifestations Asymptomatic, incidentally discovered Signs and symptoms are related to the segment
involved.1. Local compression and erosion
pain, radiate to neck and jaw (mimicking angina) airways compression hoarseness of voice dysphagia, hematemesis
2. Symptoms related to aortic valve insufficiency widened pulse pressure diastolic murmur heart failure
3. Distal embolization, to intercostals, visceral, renal or lower limbs.
4. Rupture
Investigations Plain x-ray, CXR, AXR and spine. Echocardiography (transthoracic or
trans-esophageal) CT Angiography MR Angiography Aortography (rarely used) and
cardiac catheterization
Treatment Aim is to prevent fatal rupture. Indication for surgery:
5-6 cm sizerate of dilatation > 1 cm/yearpatients with connective tissue disorders.
Pre-operative workupCardiacPulmonaryRenal
Surgical options:Resection of aneurysmal sac, replacement by a graft, reconstruction of branches.
Aortic dissection … Thoracic It’s a progressive separation of the aortic
wall layers, usually occurs after a tear in the intema and inner media, resulting in formation of two or more channels.
5-10 patients/million/year. If not treated, 50% die within 24 hours and
60% die within a month. Risk factors:
- smoking- hypertension- atherosclerosis- hypercholesterolemia- connective tissue disorders.
Clinical manifestations Sever chest pain radiate to the back
(tearing) Acute heart failure and dysponea due to
involvement of aortic valve. Cardiac tymponade Rupture shock and death Depending on vessels involved
- coronaries ischemic pain- carotid stroke- celiac liver failure- renal renal failure - ischemic limbs
Investigations Diagnosis usually delayed, 39% diagnosed
only after 24 hours. Clinical suspicion index is the critical point. Discrepancy between extremity
pulse/pressure is classic. CTA MRA Echocardiography Coronary angiogram in selected patients
Treatment Blood pressure control (permissive
hypotension 60-70 mmHg) Analgesia. According to location:Proximal aorta urgent graft replacement of
ascending aorta.Distal aorta pharmacotherapy
stabilization surgery.Endovascular treatment can be considered.
Abdominal aortic aneurysm (AAA)
AAA usually grows at a rate of 0.4 cm/year Risk of rupture is related to diameter of the
aneurysm.5 cm 3-5%/year7 cm 19%/year Intervention is indicated for all aneurysm 5
cm or above.
Abdominal aortic aneurysm (AAA)
Male and female are equal Progressive loss of elastin with increased
metalloprotease activity. Proteolysis and inflammation are the
driving forces in AAA. Normal 12 % elastin, in aneurysm only 1 % Family history is significant, For parents with AAA, up to 29% of
siblings found to have AAA.
Abdominal aortic aneurysm (AAA)
Mostly asymptomatic, indecently discovered.
Abdominal and low back pain GI bleed Pulsatile mass in the epigastric regionDiagnosis:1. USG2. CTA Treatment:Surgery, aneurysm opened longitudinally,
thrombus evacuated, graft is inserted, end-to-end anastomosis.
EVAR
Abdominal aortic aneurysm (AAA)
Post-operative complications: Pneumonia Ileus Renal failure Lower limb ischemia Colonic ischemia Spinal cord ischemia Graft infection
Ruptured Abdominal aortic aneurysm (RAAA)
Mortality is 50% Most patients die at home before reaching
the hospital Most patients are unaware of having AAA Sudden onset of sever abdominal or back
pain. Fainting Shock Once diagnosis made operation theater
Other aneurysms Iliac artery aneurysm Popliteal aretery aneurysm Femoral artery aneurysm Hepatic artery aneurysm Splenic artery aneurysm Renal artery aneurysm
Acute arterial occlusionLower limbs
One of the most common vascular emergency of lower limbs
Causes:1. Arterial embolism2. Thrombosis3. Graft occlusion4. Dissection5. Trauma (penetrating or blunt)
Manifestations5 P(s)1. Pain2. Pallor3. Paresthesia4. Paralysis5. Pulselessness+ Poikilothermia (perishing cold)Most common at femoral bifurcationTypically at foot and calf
treatment Immediate anticoagulation,
IV Heparin 800 u/kg as loading dose 180 u/kg/h infusion
Analgesia Oxygen Hydration
Surgery:femoral emobolectomy +/- faciotomyBypass
Endovascularcatheter directed thrombolysisthrombectomy (aspiration or mechanical)
Acute arterial occlusionMesenteric artery
GI blood supply is via CA, SMA and IMA Chronic or acute occlusion
Mortality 50-75% Early recognition is vital
Acute arterial occlusionMesenteric artery
Clinically:Acutesever abdominal pain, out of proportion to the findings.Sudden onset of bowel crampsbloody diarrheaChronic:abdominal anginaweight loss as patients afraid to eat
Diagnosis CTAMesenteric arteriography
Acute arterial occlusionMesenteric artery
Treatmentfluid resuscitationsystemic anticoagulationcorrect metabolic acidosisbowel resection if gangrene
Chronic revascularization, either by endartrectomy of bypass.
Acute arterial occlusionRenal artery
70% due to atherosclerosis Fibromuscular dysplasia of renal artery Renal artery aneurysm AVM
Presentation:Usually with hypertensionDiagnosis: Renal duplex scanCTAMRA
Acute arterial occlusionRenal artery
TreatmentMedical therapy:
antihypertensiveTransluminal balloon angioplasty and stentingSurgical revascularization
Inflammatory arteritis and vasculitides
Buerger Disease Takayasu arteritis
Giant cell arteritisBehcet diseasePolyarteritis nodosaRaynaud syndromeFibromuscular dysplasia
Buerger Disease(Thromboangiitis obliterans)
Progressive nonatherosclerotic segmental inflammatory disease that affects small and medium size arteries and veins of upper and lower limbs
Typically smokers men between 25-50 years There is thrombosis of vessels Start at age of 40, at foot, leg, arms or hands
with claudicating and ulceration Treatment is by stopping smoking
no role for bypass or graftingamputation of necrotic tissue and wound care
Takayasu Arteritis More case reports from
Japan ,India, South-east Asia, Mexico
No geographic restriction No race – immune Incidence-2.6/million/year-
N.America/Europe The incidence in Asia is 1
case/1000-5000 women.
Takayasu Arteritis Age 10-40 Primarily aorta Present with constitutional symptoms Fever, anorexia, weight loss, arthralgia and
malnutrition. With progression of disease patient presents with
vascular insufficiency- renal artery stenosis, retinopathy, aortic regurgitation, cerebrovascular symptoms, angina, congestive heart failure
ESR, CRP and WCC are elevated Treatment with steroids and cytotoxic agents Surgery (bypass) for advanced cases
Raynaud Syndrome Group of symptoms associated with peripheral
spasm mainly in upper limbs. Typically intermittent spasm in responds to
stimuli, like cold, smoking, or emotional stress. Color changes, pallor cyanosis redness 70-90% in women Diagnosis is clinically, angiogram for sever cases No curative treatment Life style modification, gloves, hand warmers,
stop smoking, avoid vibrating instruments CCB Surgery for debridement and ulceration
CHRONIC VENOUS INSUFFICIENCY
(CVI)
CVI Occurs when the vein valves become dysfunctional
and impairs venous blood return.
Affects up to 20% of adults.
By age 50 ~40% of women and 20% of men have significant vein problems.
More people lose work time from vein disorders then from artery disease. 1.
RISK FACTORS Advancing age Family history of venous disease Ligamentous laxity (eg, hernia, flat fleet) Prolonged standing Increased body mass index Smoking Sedentary lifestyle Lower extremity trauma Prior venous thrombosis (superficial or deep) Arteriovenous shunt Hereditary conditions High estrogen states Pregnancy 2.
PROGRESSION OF VEIN DISEASE
ASYMPTOMATIC SUPERFICIAL VENOUS DILATATION
Telangiectasias (intradermal)
Reticular veins (subdermal)
PROGRESSION OF VEIN DISEASE
ASYMPTOMATIC VS SYMPTOMATIC VARICOSE VEINS (subcutaneous)
PROGRESSION OF VEIN DISEASE
Leg edema
PROGRESSION OF VEIN DISEASE
Skin changes Hyperpigmentation
PROGRESSION OF VEIN DISEASE
Skin changes Stasis dermatitis
PROGRESSION OF VEIN DISEASE
Skin changes Corona phlebectatica
a. venous cups (veins)
b. telangiectasias
c. reticular veins
d. stasis spots (capillaries)
PROGRESSION OF VEIN DISEASE
Lipodermatosclerosis a form of panniculitis just above the
ankles. 9.
PROGRESSION OF VEIN DISEASE
Venous stasis ulceration(s)
EVALUATION VENOUS DOPPLER ULTRASOUND Evaluate for deep and superficial
venous thrombosis. Evaluate for incompetent veins with significant reflux disease. Evaluate for incompetent perforating veins and tributaries.
MANAGEMENT OF CVI LEG ELEVATION – heart level for 30 minutes 3-4
times daily improves micro-circulation reduces edema, and promotes healing of venous ulcers.4.
EXERCISE – daily walking and simple ankle flexion exercises.
MANAGEMENT OF CVI Compression therapy - avoid contraindications such as
cellulitis or significant arterial occlusive
disease.
MANAGEMENT OF CVI – COMPRESSION THERAPY
Compression bandages – elastic or non-elastic with single or multi-layers.
MANAGEMENT OF CVI – COMPRESSION STOCKINGS
MANAGEMENT OF CVI PNEUMATIC COMPRESSION THERAPY
MANAGEMENT OF CVI – SKIN CARE
Skin cleansing – wash with a mild non-soap cleanser (e.g. Dove, Olay, Caress).
Emollients – provides a film of oil to lubricate the skin (e.g. Vaseline, Lubriderm, Aveeno).
Barrier preparations – physically block chemical irritants and moisture.(e.g. Zinc oxide, Vaseline).
Topical corticosteroids – often used to treat stasis dermatitis. 4.
MANAGEMENT OF CVI – VENOUS STASIS ULCERS
Surgical debridement – used to remove devitalized tissue.
Enzymatic agents – used to break down necrotic tissue (e.g. Santyl).
Growth factors – synthesized by many cell types such as platelets, neutrophils, and epithelial cells (e.g. Regranex).
Bioengineered tissue – used for a variety of non-healing ulcers (e.g. Apligraf, Dermagraft).
Skin grafting – an option for non-healing ulcers. 4.
MANAGEMENT OF CVI – ABLATION THERAPY
Indications – patients with persistent signs/symptoms of venous disease after a minimum of 3 months of medical therapy (e.g. compression) and documented reflux (e.g. >0.5 seconds of reflux GSV).
Absolute contraindications – acute DVT or phlebitis and pregnancy. 5,6.
Radiofrequency versus laser endovenous ablation therapy.
MANAGEMENT OF CVI - SCLEROTHERAPY
DETERGENT AGENTS - Sodium tetradecyl sulfate - Polidocanol OSMOTIC AGENTS - Hypertonic saline - Glycerin
DVT Epidemiology and Etiology
Annual incidence of venous thromboembolism (VTE) is 1/1000
DVT accounts for one half of VTE Majority of lower extremity DVT arise
from calf veins but ~20% begin in proximal veins
About 20% of calf-limited DVTs will propagate proximally
DVT – VTE Risk Factors Malignancy Surgery Trauma Pregnancy Oral
contraceptives or hormonal therapy
Immobilization Inherited
thrombophillia
Presence of venous catheter
Congestive failure Antiphospholipid
antibody syndrome
Hyperviscosity Nephrotic
syndrome Inflammatory
bowel disease
DVT – Clinical Presentation Classically = calf pain, tenderness,
swelling, redness and Homan’s sign› Overall sens/spec = 3-91%› Unreliable for diagnostic decisions
Wells developed and tested a clinical prediction model for DVT
Wells PS, Anderson DR, Bormanis J, et al. Value of assessment of pretest probability of deep-vein thrombosis in clinical management. Lancet 1997;350 (9094):1795-8.
DVT – Imaging Available imaging and ancillary
tests:› Compression US – first line
test, high sens/spec› Venography – gold standard› MRI – Lower quality evidence
only at present› Impedance
plesmythography – not in US› Complete lower extremity
US – experimental
PE Epidemiology and Etiology
100-200,000 deaths per year due to PE Most PE arise from lower extremity DVT In patients with DVT, 40-60% will have
a PE on V/Q scanning
“Pulmonary embolus is not a disease. It is a complication of DVT.” Ken Moser MD
PE Clinical Presentation
Dyspnea, pleuritic pain and cough most common symptoms
Tachypnea, rales and tachycardia most common signs
ABG limited value for diagnosis EKG and CXR often abnormal, but
usually lacking specificity to aid diagnosis
PIOPED Study. JAMA. 1990;263(20):2753-59. Stein PD, Goldhaber SZ, Henry JW. Chest 1995;107:139-43
CXR FINDINGS Hampton’s Hump: -wedge-shaped configuration at
lung periphery due to infarcted lung
Westermark sign: -pulmonary oligemia
PE – Imaging Studies PIOPED study quantified the value of
V/Q scans in diagnosing PE› Normal/near-normal scans exclude PE in
low-moderate risk patients› High probability scans confirm PE in
moderate-high risk patients› Drawbacks: more difficult test and 73%
patients had indeterminate scans LE compression US showing DVT helps
diagnostically, but a negative study insufficient to exclude VTEPIOPED Study. JAMA. 1990;263(20):2753-59
PE – Helical CT (CTA) Eng performed a systematic review (SR) of all
studies & SRs on CTA prior to 2003› Only 1/6 SRs and 3/8 primary studies found CTA >90%
sensitive for PE In a similar SR in 2005 Roy concluded
› Negative CTA could safely exclude PE in low risk patients
› Negative LE US plus negative CTA could exclude PE in moderate risk patients
At the time of those SRs no studies of faster multidetector CTA (MDCT) were available
Eng J, Krishnan JA, Segal JB, et al. AJR 2004;183(6):1819-27. Roy PM, Colombet I, Durieux P, et al. BMJ 2005;331(7511):259.
VTE – Other Therapy Issues Anticoagulation same for DVT & PE Thrombolysis - risk/benefit uncertain;
clinical outcomes generally not improved Vena cava filters
› Contraindication to anticoagulation› Rarely survivors of massive PE› Rare patients with recurrent VTE on
adequate anticoagulation› Prophylaxis in certain high risk patients
Lymphedema
Lymphedema An abnormal accumulation of protein-
rich fluid in the interstitium, causing chronic inflammation and reactive fibrosis of the affected tissues
Usually in an extremity, but can also occur in the head, neck, genitals, and abdomen
Lymphedema Affects 1% of the American population
(2.5 million people) Still poorly understood in the medical
community Largest cause of lymphedema in the
world is Filariasis (considered secondary lymphedema)
Filariasis is a parasitic infiltration into the lymphatics that is very common in third world countries (affects 90 million people)
Types of Lymphedema Primary lymphedema is a result of
lymphatic dysplasia.› May be present at birth› Can develop later in life without known
cause Secondary lymphedema is much
more common.› Result of surgery, radiation, injury, trauma,
scarring, or infection of the lymphatic system
Secondary Lymphedema
Primary Lymphedema
Lymphedema
Primary lymphedema Lymphangiodysplasia – general malformation Hypoplasia – fewer than normal # of lymph
collectors Aplasia – absences of collectors in a distinct
area Milroy's Disease is congenital lymphedema
evident at birth Meige’s Syndrome is primary lymphedema
onset at puberty (lymphedema praecox) Lymphedema Tardum is primary lymphedema
onset after age 35
Secondary lymphedema There is a known cause for the presence of
edema Surgery: breast cancer, melanoma,
prostate/bladder cancer, lymphoma, ovarian cancer, hip replacements
Radiation therapy Trauma – scarring, crush injury Infection CVI Obesity Self-induced
Angiosarcoma Can develop after long-standing lymphedema “Stewart - Treves Syndrome” Angiosarcoma after mastectomy was first
described in 1948 by Stewart and Treves Signs: reddish-blue and blackish-blue lumps that
rapidly increase in size, bleed easily and ulcerate at an early stage
Very rare & poor prognosis
Lymphedema is a disease. All other edemas are symptoms.There is no cure for lymphedema.There is only management.
Diagnosis of
Lymphedema
Physical exam and history are most important.
Characteristics of Benign Lymphedema
Slow onset, progressive Pitting in early stages Cellulitis is common Rarely painful but discomfort is common Skin changes – hyperkeratosis, papillomas,
lichenification Ulcerations are unusual Starts distally
› Toes square, positive Stemmer’s sign› Dorsum of foot “buffalo hump”› Loss of ankle contour› Asymmetric if bilateral
History What is the reason for the swelling? How long has the extremity been swollen? How fast did the edema progress/develop? What are the underlying diseases? Is there pain? Other conditions? Other treatments? Medications?
Inspection Location of swelling (distal or proximal) Any skin changes Lymphatic cysts, fistulas Ulcers Scars or radiation burns Papillomas Hyperkeratosis
Palpation Temperature – indicative of infection Stemmer sign is (+) when a thickened cutaneous
fold of skin at the dorsum of the toe or finger cannot be lifted or is difficult to lift. Positive Stemmer’s sign is indicative of lymphedema.
Skin folds Pitting Fibrosis Muscular status
Diagnostic Tests
Direct lymphography: invasive, oily contrast injected into a surgically exposed lymphatic vessel. Damaging. Has been replaced by CT, MRI, US.
Lymphoscintigraphy: noninvasive, assesses dynamic process in superficial and deep lymphatics
CT MRI These tests are often not performed due to lack
of clinical importance
Differential Diagnosis
Lipedema Chronic venous insufficiency Acute deep vein thrombosis Cardiac edema Congestive heart failure Malignancy/active cancer Filariasis Myxedema Complex regional pain syndrome
Lipedema Mainly in women Bilateral, symmetrical edema
from iliac crest to ankles Dorsum of feet never involved (-) Stemmer’s sign Little or no pitting No cellulitis Painful to palpation Bruise easily
CVI Gaiter distribution Non-pitting Brawny Hemosiderin staining Fibrosis of subcutaneous
tissue Atrophic skin
Acute DVT Sudden onset Unilateral Painful Cyanosis (+) Homan’s sign Potentially lethal (PE) Diagnosis with venous doppler Not treatable with PT
Cardiac edema Right heart insufficiency Greatest edema distally Always bilateral Pitting Complete resolution with elevation No pain May treat with PT if cleared by
Cardiologist
Congestive Heart Failure Bilateral heart failure Pitting edema Orthopnea, paroxysmal noctural
dyspnea, DOE Jugular venous distension Diagnosis with physical exam, chest x-
ray, cardiac echo
Malignant lymphedema
Pain, paresthesia, paralysis Central location, proximal onset Rapid development, continuous progression Swelling and nodules in supraclavicular fossa Hematoma-like discoloration (angiosarcoma) Ulcers and non-healing open wounds Recurrent malignancy
Filariasis
Prevalent in 3rd world countries; Can still be treated successfully with CDT. Most therapists in the US will never encounter Filariasis.
Lymphedema Treatment Options
Pneumatic compression pump Surgery Complete decongestive therapy (CDT) Elastic support garments Medications
Pneumatic Compression Pumps
Advantages:1. Can be used at home by patients2. Fast application3. Financially lucrative for DME vendors ($4000 per pump)
Surgery
Microsurgical techniques Liposuction Debulking/Reduction procedures
Skin and Nail Care Eliminate bacteria and fungal growth
by using medicated powders, hydrocortisone cream where indicated.
Reduce the risk of infection by avoiding injury, cleaning all injuries immediately, calling MD at first sign of infection.
QUESTIONS
REFERENCES1. 2012 Vascular Disease Foundation. 8206 Leesburg Pike, suite 301, Vienna
Virginia 22187.2. Alguire PC, Scovell S. Overview and medical management of lower extremity
chronic venous disease. 2012 UpToDate.3. Venous stasis and arterial ulcer comparison. February 1, 2009. http://
www.lhsc.on.ca/Health_Professionals/Wound_Care/venous.htm.4. Alguire PC, Mathes BM. Medical management of lower extremity chronic
venous disease. 2012 UpToDate.5. Scovell S. Radiofrequency ablation for the treatment of lower extremity
chronic venous disease. 2012 UpToDate.6. Ihnat DM. Endovenous laser ablation for the treatment of lower extremity
chronic venous disease. 2012 UpToDate.7. Collins KA. Classification of lower extremity chronic venous disorders. 2012
UpToDate.8. Greenberg DL, Scovell S. Liquid and foam sclerotherapy techniques for the
treatment of lower extremity veins. 2012 UpToDate.9. Alguire PC, Mathes BM. Pathophysiology of chronic venous disease. 2012
UpToDate.