Vascular surgery Frankovičová M. Dept. of vascular surgery, VUSCH
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Vascular surgery
Frankovičová M.
Dept. of vascular surgery, VUSCH
Physiology of arteries
Blood supply to organs
Blood pressure control
Only 20% of blood in arteries
Examination methods
History
Pain
Other diseases
Clinic
Aspection (changes in
skin texture, necrosis)
Palpation • Pulse
• Temperature
• Pathologic mass
Auscultation
Imagine methods
Ultrasound
Doppler
Duplex image ultrasound
CT-A
MRI-A
AG
Angiography – Gold standard !!! DSA Positive
• Excellent to distinguish
• Possibility of intervention
Disadvantage • Invasive – possibility of damage- PSA
• Allergy - iodine contrast medium
CI Allergy
Renal failure
Endovascular treatment
Conservative treatment
Endovascular treatment
Surgery
Options of endovascular treatment
Dilatation
Trombolysis
Embolization
Endovascular treatment
Indication
Better for short isolated stenosis
Better for proximal vessels
PTA alone, PTA and stent
covered – stentgrafts, treatment of
aneurysms
Endovascular thrombolysis
Arterial
Peripheral arteries
Venous
Phlebothrombosis
Surgical treatment
Embolectomy
Endarterectomy
Implantation of venous interpositum- traumas
Resection
Bypass
Bypass
Types
Anatomic
Extra anatomic
Grafts
Saphenous vein
Prothesis
Donor saphenous graft
Injuries
Sharp Bleeding
Distal ischemia
Blunt, deceleration Dissection
Rupture
Trombi
Dg Clinical presentation, Doppler, AG
Reconstruction
Direct suture ???
Suture with patch
Interposition of venous
graft
Treatment of the damage of other
structures
Acute limb ischemia
Etiology
Emboli of cardiac origin
Dissection, acute thrombosis, peripheral
aneurysm, trauma
Localization
Clinic 5P
5 P
Pain
Pulslessness
Paleness
Paresthesia
Paralysis
Cold
Acute limb ischemia
History: Cardiac reason !!!
Dg. Clinical examination, Doppler, AG
Treatment:
Embolectomy
Fogarthy balloon catheter
Trombolysis-peripheral
Acute limb ischemia
Complication
Revascularization sy,
Compartment sy
Differential dg: PAOD
To find an origin of embolization!!!!
ACI stenosis
Blood supply by int. carotid a. is 3-4x higher than vertebral artery
AS Stenosis
Dg Doppler, AG
Indication Over 70% asymptomatic
Over 50% symptomatic, or bilateral
CI Occlusion of ACI, stroke in progression
AAA
Aneurysm of abdominal aorta
Etiology- AS
Clinical presentation
Asymptomatic
Pressure
Peripheral embolization
Dg: ultrasound, CTA, MRI
TEE, exclude thoracic aneurysm
Therapy of AAA
Indication more than 5 cm in diameter,
important to consider general status
Th
Tube graft
Bifurcation graft
Rupture of AAA
Clinical presentation
Intensive pain
Pulsatile mass in abdomen
Shock
Dg: ultrasound, CT
Th: urgent surgery, stentgraft
Bad prognosis
Peripheral arterial occlusive disease
PAOD
Etiology
AS
Buerger´s disease, mucinous cystic degeneration,
popliteal entrapment sy
Most common presentation: chronic limb
ischemia
Fountain classification
I. without symptoms
IIa. Intermittent claudication above 100m
IIb. Intermittent claudication below 100m
III. Rest pain
IV. Trophic changes of skin, necrosis
Dg History, clinical presentation, Doppler
AG
Critical limb ischemia
Rest pain requiring anodynes for more
than 14 days
Resting ankle systolic pressure below 50
torr
Treatment
Conservative
Antiagregation drugs, ACEi, statins,
proslaglandins,
Stop smoking
Endovascular
Surgery
Surgery
Aorto-illiac region
Ao BiF bypass
One illiac artery - cross over F-F bypass
Femoro-popliteal region
F-P bypass
Crural region
Femoro event popliteo crural bypass
Pedal bypasses
Diabetic foot
Pathophysiology
Microangiopathy leads to neuropathy –
decreases awareness of injury
Impaired tissue metabolism favor bacterial
growth and poor healing
Diabetes increases risk of AS
macroangiopathy
5x more gangrenes than AS
Clinical presentation
Painless deep ulcers
Painless necrosis
Chronic ulceration
Infection !!! – wet gangrene
Palpapable pulse at ADP a ATP
Therapy
Treatment of infection ATB
Necrectomy, amputation – 15 x more often than AS
Conservative with compensation of diabates
Endovascular treatment
Arterial reconstruction with saphenous graft
Physiology
Rest
Hydrostatic
pressure 120 torr
Negative
pressure
Rest
pressure
Muscles
contraction
200 torr
Lower limb venous systems
Deep 90%
Superficial 10%
Perforating veins
Valves!!!
Incidence
Venous disorders are 10x more often than
arterial
Men 15-30%
Women 40%
Superficial vein thrombosis
Etiology
Aseptic form ( paravenous infusion )
Septic form
Superficial inflammation, tenderness, increased warmth
Heparin ung, local compression, ATB, mobilization,
LWMH by more severe forms
Deep vein thrombosis
Occlusion of deep venous system by
thrombus
Etiology: Wirchov´s trias
Hypercoagulative status
Venous stasis
Endothelium damage
Deep venous thrombosis of
lower limb Localization
Calf veins
Femoral veins
Pelvis veins
Upper limb
Clinical presentation
Silent
Tenderness
Swelling of calf
Praetibial veins
Hommans´ sign
Diagnostics
Doppler ultrasound of venous system
D-dimers
Phlebography
Therapy
LWMH 2x 0,1ml on every10kg – also without admission
Continual heparin infusion 30000j a day. Monitoring of aPTT + immobilization
Intravascular thrombolysis- Tissue activator of plasminogen
Complication of DVT
Pulmonary embolism
Arterial flow disturbance
Post thrombotic changes
Check
Hematologic disorders
Malignancy Abdominal ultrasound, Chest X-ray
Tumor markers
Urology
Long term Compression
ANP, LWMH, Warfarin
Prevention
Compression stockings, bandage
Early postoperative mobilization
LWMH
Caval filters
Caval filters
Chronic venous insufficiency
Varicous veins
Saphenofemoral reflux
Insufficient perforators
Post thrombotic syndromes
Damage of valves due to
recanalization of deep venous
thrombosis
Predisposition
Obesity
Pregnancy
High hydrostatic pressure
Weak muscle pump
Etiology
Reflux 90%
Superficial
Deep
Obstruction 10%
Post-thrombotic
Non-thrombotic
CEAP classification of CVI
Class 0 No visible or palpable signs of venous disease
Class 1 Telangiectases, reticular veins, malleolar flare
Class 2 Varicose veins
Class 3 Edema without skin changes
Class 4 Skin changes attributed to venous disease
Class 5 Skin changes with healed ulceration
Class 6 Skin changes with active ulceration
Etiologic classification
EC - Congenital
EP – Primary: Chronic venous disease of undetermined cause
ES – Secondary: Chronic venous disease with an associated known cause (post- thrombotic, post-traumatic, other)
A Anatomic distribution
AS1-5 Superficial veins
AD6-16 Deep veins
AP17-18 Perforating veins
P Pathophysiologic dysfunction
PR Reflux
PO Obstruction
PR,O Reflux and obstruction
Diagnostics
Clinical presentation
Trendelenburg I,II
Perthes
Doppler ultrasound
Phlebography
Treatment
Conservative
Venotonic drugs
Compression
Avoid long standing
Sclerotization
Surgery
Operative treatment
Superficial
90% efficacy
Varicous veins
S-F back flow
Insufficient perforators
Deep
Superficial
Classic
Crossectomy
Stripping of VSM
Ligation of perforators
Avulsion of collateral varices
Complications
Hematomas
Lesion of femoral artery
Lesion of femoral vein
OK
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