Vascular SurgeryBack to Basics

Dr. George E. Hajjar

Vascular and Endovascular Surgery

The Ottawa Hospital

OUTLINE

• Peripheral vascular disease• Acute limb ischemia• Mesenteric ischemia• Aortic dissection • Aortic Aneurysm• Varicose veins• Chronic venous insuffciency

Peripheral Vascular Disease: PVD• Atherosclerotic disease involving the lower extremities

• Predisposing factors: smoking, male gender, hypercholesterolemia, HBP, Family history, and diabetes.

• Marker of generalized arterial involvement. Cardiac, renal, mesenteric cerebrovascular.

• Most commonly involves:Aorotiliac segment in younger patients 45-55Fem-pop segment in 55-75Tibioperoneal segments 75 + and diabetics

• Symptoms: usually claudication, can progress to rest pain and gangrene if risk factors are not controlled.

Clinical Features - Claudication

• Pain (cramping, weakness in legs) with exertion.*Buttocks and thighs if AI segment is involved*Calves if SFA is involved*In step of foot if tibial segment is involved

• Relieved by short rest • Reproducible • Physical exam:

Chronic arterial skin changesRubor on dependency/Pallor on elevation ( Buerger sign)Absent pulses

Clinical Features - Claudication

What is Le Riche Syndrome in PVD:

• A. Pain in both hips when walking• B. Pain and gangrene in both feet .• C. Impotence due to pudendal artery blockage• D. Bilateral thigh claudication with impotence

Leriche syndrome

• Bilateral buttock or lower leg claudication

• Impotence

• Caused by poor arterial flow through aortoiliac segment

• Hypoperfusion of the internal iliacs

PVD: Clinical signs• Rubor on dependency

pooling of blood in foot due to lack of pressure, and increased capillary dilatation

• Foot is cold. Often mistaken for cellulitis.

• Trophic skin changes

PVD: Investigation

• Clinical exam and documentation of pulses

• Nonivasive:(diagnose and screen)Ankle/brachial pressure index: ABIDuplex scan

• More Invasive: (Plan for treatment)CTAAngiogram

ABI:

• Normal ABI is 1• Helps in diagnosing PVD, quantifies the degree, monitors disease

progression, and assesses success of intervention.• Inacurate in diabetics and severely calcified distal vessels that cannot

be occluded by a pressure cuff.• Can be misleading in patients with subclavian artery stenosis

Question

Which of the following statements about ABI is incorrect:

• A. Easily reproducible• B. Monitors therapy• C. Quantifies degree of disease• D. Might give a false positive result• E. Determines the location of arterial occlusion

• Answer E

PVD : Approach to treatment.

• Determine degree of impairment and unmask other systems cardiac, cerebral etc…that might be involved

• A. Claudication: social, economical, Activity of daily living (ususally treated conservatively)B. Rest pain: Pain at night in foot when leg is elevated. Frequent awakening , relieved by garvity and hanging foot over the edge of the bed.C. Tissue loss or gangrene.

• Rest pain and tissue loss usually treated surgically

Treatment

• CONSERVATIVE• risk factor modification. Cessation of smoking. Good hyperglycemic control,manage

hypercholesterolemia• exercise program , walking.• anti platelet (ECASA, clopidrogel) for MI / stroke risk• Follow up.

• surgical• Minimally invasive ( Angioplasty/stent..) less morbid less durable• Bypass surgery :more invasive, better durability.

Question:

Which statement about patients with claudication is TRUE:

A. They will progress to severe ischemia and limb loss if not surgically treated early.

B. Despite adequate risk factor control, progression is inevitableC. Eventual limb loss is seen in 40-50% of the cases if followed long enoughD. About 50% will experience a cardiac event in five years follow up

Acute Limb Ischemia

Acute Limb Ischemia

Mrs. Witelegg

• ID:• 75 yo lady who lives by herself in an apartment. She is active,

walks her dog ~2 kms daily without any difficulty. She takes pride in the fact that she has not needed to see a doctor in the last 10 years.

• PMHx/PMSx:• remote TAH-BSO• social smoker quit in the 1960’s• no h/o DM, CAD, HTN, dyslipidemia, stroke, CRF

Acute Limb Ischemia

Mrs. Witelegg

• HPI:• While watching TV, she had sudden onset of numbness

in her right leg. Her leg felt “like it went dead”, and she couldn’t ambulate. After a few minutes she experienced constant, severe pain starting in the toes, eventually involving the entire right leg. She called her neighbor and then brought her in to the Civic emergency department.

Acute Limb Ischemia

• What is acute limb ischemia?• Sudden interruption of blood flow to the extremities threatening

its viability

• Causes:

a. Arterial embolus

b. Trauma: penetrating, blunt, iatrogenic

c. Arterial graft occlusion

Acute Limb Ischemia

Differs from PVD:

• A. No collateral circulation

• B. Profound ischemia

• C. Severe pain

• D. Permanent limb damage/ loss is inevitable if not treated

• E. Acute vascular emergency.

Acute Limb Ischemia

Acute leg ischemia clinical signs:

• The six Ps:

1. Paraesthesia

2. Pallor

3. Pain

4. Poikilothermia(Polar

5. Paralysis

6. Pulselessness

Acute Limb Ischemia

Mrs. Witelegg

• O/E– She is in distress from pain in R leg– BP:140/90 mmHg, HR:150 bpm– pulse: irregularly irregular– Normal heart sounds, good a/e bilat– No pulsatile masses in her abdomen– No carotid, abdominal or femoral bruits– Pulses:

• L: + femoral, + politeal, + DP, + PT• R: - femoral, - popliteal, - DP, - PT

– R foot is colder and paler than L– Decreased sensation in R foot– Able to move toes but difficulty with

plantar and dorsi flexion– Absence of trophic changes in her lower

extremities (no hair loss, thickened nails, or thin, flaky or shiny skin)

Acute Limb Ischemia

Acute leg ischemia clinical signs:

• Degrees of Acute Limb Ischemia.

• 6-8 hrs critical time of reversible ischemia.Class Sensory deficit Motor deficit Prognosis

1 None None Not immediately threatened

2a Mild-moderate None Salvageable if treated promptly

2b Significant Mild-moderate Salvageable if immediately treated

3 Profound Profound Irreversible limb damage- likely amputation

Acute Limb Ischemia

Mrs. Witelegg

• Your working diagnosis is acute limb ischemia.

• You order CBC, electrolytes, BUN, Cr, PTT/INR (all of which comes back normal), type and cross-match blood, and a saline infusion is started.

• CXR is unremarkable

• ECG is as follows:

Acute Limb Ischemia

Mrs. Witelegg

• What is the most likely etiology of ALI in Mrs. Witelegg?• Cardiogenic embolism

• What in her history and physical supports this diagnosis?• Lack of atherosclerotic risk factors• no previous claudication (she walked her dog 2 km/day)• Irregularly irregular pulse• Completely normal left extremity pulses

• Based on her physical examination, what is the highest point of obstruction of arterial flow?

• R ileo-femoral region

• How long can a limb be without blood flow before irreversible tissue damage ensues?

• 4-6 hrs

Acute Limb Ischemia

Mrs. Witelegg

• What is the surgical management of this condition?

• R femoral embolectomy

• Can we proceed to the OR without any imaging studies? If not what studies can be perfomed?

• Because of the classic history and physical findings, and because of the presence of class 2b ischemia, immediate surgery is indicated without delay for imaging.

• Angiography can be performed in certain conditions of ALI– when the suspected etiology is arterial thrombosis (i.e. in

preparation for bypass surgery)– when the patient has class 1 or 2a ischemia

Mrs. Witelegg

• What medical therpay is available for ALI and when is it indicated?

• Lytic therapy (i.e. with t-PA) is used to dissolve the clot. It is a good option in the setting of acute arterial or graft thrombosis. It is not indicated in the setting of trauma or when the patient can not wait more than 24-48 hrs, as the therapy requires that period of time for clot dissolution. ( i.e. class 1 or early 2a ischemia)

• IV Heparin will not dissolve the clot but will prevent further propagation, and is only indicated if there is a delay to surgery

Acute Limb Ischemia

Mrs. Witelegg

• The patient is booked for emergency embolectomy

• Under local anaesthesia, a small incision is made over the R groin. The femoral artery is exposed and controlled with vessel loops. A small arteriotomy is made and the clot is removed proximally and distally using a fogarty balloon embolectomy catheter.

• The arteriotomy is repaired and the foots “pinks up” after blood flow is returned. There is a palpable DP and PT pulse.

• The patient is returned to the recovery room.

Acute Limb Ischemia

Mrs. Witelegg

• At 3 am you get paged by the recovery room nurse. Mrs. W is complaining of significant pain in her leg, it is more swollen and the DP and PT are no longer palpable.

• In addition, her urine output has diminished and she is peeing out dark urine which tested positive for “blood” on the urine dipstick.

Acute Limb Ischemia

Mrs. Witelegg

• What is happening to Mrs. W?

– Reperfusion syndrome: occurs as a result of blood flow going back into previously damaged tissue, causing rhabdomyolysis and compartment syndrome..

• Rhabdomyolysis: Liberated myoglobin from dead muscle cells enters the blood stream resulting in renal tubular obstruction and direct nephrotoxicity causing renal failure. Myoglobinuria is a false positive on the urine dipstick test for blood.

• Compartment syndrome: Free oxygen radicals are created with reperfusion. These result in increased tissue edema, with in the limited facial compartments of the lower leg, this further decreases capillary blood flow and worsens the ischemia and tissue damage, causing further edema. Pain out of proportion, pain on passive stretch and high pressures in the compartments suggests compartment syndrome.

Acute Limb Ischemia

Mrs. Witelegg

• How should reperfusion syndrome be managed?

– Compartment syndrome is a surgical emergency and is managed by 4-compartment fasciotomies.

– Rhabdomyolysis should be managed with aggressive IV fluids, diuresis and alkalinization of urine.

Question:• Ischemia reperfusion syndrome is characterised by all of the

following EXCEPT:

• A. Leg swelling• B. Pain on passive dorsiflexion of the foot• C. Oliguria• D. Hypokalemia• E. High CK levels

Mesenteric ischemia

• Classification :

• Acute: embolic, thrombotic, dissecting• Chronic: atherosclerotic• Low flow: cardiogenic shock, vasopressors• Venous: Hypercoagulable , Pancreatitis, intraabdominal Ca,

cirrhosis.

Mesenteric ischemia: presentation• Acute :

sudden onset of severe abdominal pain, out of proportion to physical findings.Soft abdomen early on, later might develop signs of rigidity and peritonitisSilent abdomenMedical emergency. Early recognition and treatment prevents intra-abdominal

catastrophy and reduce amount of bowel loss.• Chronic:

Chronic abdo pain,usually post prandial.Classic triad: post prandial abdo pain, weight loss, and food phobia.Treatment usually surgical interventional vs bypass

• Low flow:Usually sicker patients. ICU /CCU settingon massive ionotrops hemodynamic or septic shockTreatment is usually supportive, improving hemodynamics and treating underlying cause

Mesenteric ischemia: Investigations

• Plain abdominal films:Usually not very helpful early on.Calcifications may be seen in chronic mesenteric disease

• Later stages may show:Thickening of bowel loops and thumb printing, air fluid levelsFree intraperitoneal air, air in bowel wall (pneumatosis intestinalis) air in portal vein signal advanced ischemic bowel and intestinal gangrene.

Mesenteric ischemia: Investigations• CTA :

Most useful.Shows bowel perfusionmesenteric vessels.Helps in finding etiology: Thrombotic/embolic/dissectionetc…better sensitivity to other all other findings: pneumatosis, thickening , intra-abdominal fluids etc..

• Angiography:provides diagnostic and therapeutic optionvasodialator infusion to relieve spasmplanning intervention in chronic ischemia. Operative vs stenting.

Mesenteric ischemia: Question• In the early stages of acute superior mesenteric artery

occlusion the most common findings are:

A. severe abdominal painB. guarding and reboundC. absent bowel sounds D. bowel edema on plain xrayE. A and D onlyF. A and C onlyG. all of the above

• Answer: F

Mesenteric ischemia: Question• The classic triad in chronic mesenteric ischemia includes which of the

following:

A. Post prandial abdo pain B. Post prandial diarrheaC. ConstipationD. Weight lossE. NauseaF. Post prandial vomitingG. Fear of eating

• Answer A, D, and G

AORTIC DISSECTION

Vascular Surgery – Back to Basics

Definition

• spontaneous tear in aortic intima allowing blood to be driven between the aortic intima and media

– acute < 2 weeks– chronic > 2 weeks

Etiology

• HYPERTENSION, usually uncontrolled

• TRAUMA, usually deceleration injury (falls, MVAs, Iatrogenic catheter manipulation)

• other: cystic medial necrosis, atherosclerotic ulcer, connective tissue disease (Marfan’s syndrome, Ehlers-Danlos syndromes), congenital conditions (coarctation of aorta, bicuspid aortic valves, PDA)

Epidemiology

• incidence 5.2 in 1,000,000• male:female = 3:1• small increased incidence in African-Canadians (related to

higher incidence of hypertension)• lowest incidence in Asians

Classification

• DeBakey

• Type I - involves ascending and descending aorta

• Type II - ascending aorta only• Type IIIA - descending thoracic

aorta• Type IIIB - Type IIIA plus

abdominal aorta

• Standford

• Type A - ascending aorta and aortic arch; emergency

• Type B - aorta distal to subclavian artery; emergency surgery if complications of dissection

Clinical Features• SUDDEN ONSET SEVERE “TEARING” CHEST PAIN

RADIATION TO THE BACK (INTERSCAPULAR)

• severe hypertension• asymmetric BP’s and pulses between arms• ischemic syndromes due to occlusion of aortic branches:

coronary (MI), carotid (stroke, Horner’s syndrome), splanchnic (ischemic gut), renal (kidney failure) ischemic legs with iliac involvement.

• “unseating” of aortic valve cusps (new diastolic murmur)• rupture into pleura (dyspnea, hemothorax) or peritoneum

(hypotension, shock) or pericardium (tamponade)

Investigations

• CT scan is the gold standard

• CXR• pleural cap• widened mediastinum• left pleural effusion with extravasation of

blood

• TEE• ECG: LVH (90%), +/- MI, pericarditis, heart block• aortography, MRI Usually not needed.

Treatment

• Type A• may require putting patient on pump, hypothermic circulatory arrest, valve

replacement, coronary re-implantation of aortic root

• resection of intimal tear, reconstitution of flow through true lumen, replacement of the affected aorta with graft

• EMERGENCY CARDIAC SURGERY

• Type B• MEDICAL MANAGEMENT

monitoring in intensive care settingstrict BP controllong term follow up needed, to monitor for aortic wall aneurysmal degeneration

• very rarely urgent operation for complications (expansion, rupture, gut/leg/renal ischemia, ongoing pain)

• New treatment with stenting being assessed as a preferred modality of Rx.

Aortic dissection: question

• Which of the following is least likely to be associated with Thoracic aortic dissection:

• A. severe chest painB. severe abdo painC. oliguriaD. Ischemic legE. anisocoria F. left sided hemiplegia and absent right radial pulseG. E and FE. all of the above can be a feature of aortic dissection

• Answer is E

Definition• localized dilation of an artery that

is 2 x its normal diameter

• true aneurysm: involving all vessel wall layers

• false aneurysm: disruption of aortic wall with containment of blood by some layers of the aorta or a fibrous capsule made of surrounding tissue (penetrating trauma, infections, contained perforated aortic ulcer)

AORTIC ANEURYSM

Etiology

• ATHEROSCLEROTIC association most common• DEGENERATIVE (matrix metalloproteinases)

• infection• cystic medial necrosis• trauma• vascultitis• connective tissue disease (Marfan syndrome, Ehlers-Danlos)

Epidemiology

• incidence 5 to 32 per 100,000 for AAA

• high risk groups:• 65 years and older• male:female = 4:1• smokers• peripheral vascular disease, CAD, CVD• family history of AAA

Clinical Features

• Vast majority ASYMPTOMATIC.Incidental finding

• RUPTURE• back pain• hypotension/syncope• pulsatile abdominal mass• ~100% mortality if untreated, 50% mortality with surgery

2-4% mortality if treated electively

• Triad: back pain, hypotension, syncope = ruptured AAA until proven otherwise.

AAA diagnosis.• Clinical exam unreliable in mid to large frame patients.

• Usually identified on US for other problems(Prostate, Cholecystitis, other abdominal patjologies), very sensitive

• Lumbar spine x-ray can show calcifications in the aneurysm wall in up to 50% of cases

• CTA, MR very sensitive but not readily available

• Angiography: invasive, can have a significant false negative and does not adequately estimate outer aortic wall diameter.

AAA: ScreeningThe best screening modality for AAA is :

A. CTA since it is highly sensitive, and specific

B. Angiography since it has the highest specificity

C. If not clinically palpated with a good physical exam no other testing is needed

D. Ultrasonography is the best screening tool

E. A lumbar plain xray is the cheapest and most effective screening modality

AAA: Screening

• Answer: D• US remains the least invasive, very sensitive, readily available, easily reproducible, and

most cost effective tool for screening AAA, with high specificity and sensitivity

AAA: Screening. Who?• All males over 65Years of age.• Recent studies in UK showed yield not as high as expected.

• CSVS recommendations:*all males over 65YO*Females over 65 with:first a degree relative with AAASmokers.

• “Selective” screening:any person over 65 YO with :*with first degree relative with an AAA*who ever smoked

Natural history• Greatest risk is rupture• Distal embolization

• Occlusion

• Risk of rupture depends on size• <5 cm <5% / yr• 5-6 cm 10% / yr• 6-7 cm 15-20% / yr• >7 cm >20% / yr

• Risk of dying from aneurysm surgery = 3~5%Largely due to CAD

Treatment

• Operate when

• AAA reaches 5.5 cm in an otherwise healthy individual

• >5 mm expansion in 6 months• symptomatic AAA• Rupture

• contraindications: life expectancy < 1 year, terminal disease (cancer), significant co-morbidities (recent MI, unstable angina), severe dementia, advanced age

Treatment

Treatment: Surgical

• open surgery with graft replacement*proven durability*higher rate of peri-op complications*longer hospital stay, gen anaesthesia*no need for long term follow up

• Endovascular aneurysm repair

*less morbidity, less mortality 2%vs 4% (endoleak, graft limb occlusion)*Shorter hospital stay, regional or local anaesthesia, percutaneous *higher rate of intervention*continued need for follow up and repeat CT scan or US

• Cost?

Venous disease

Venous anatomy of the leg

• Superficial system: Long and short saphenous

• Deep system: usually parallels the arterial supply

• Perforator system: communicates superficial to deep system.

•

Venous flow

• Normal flow: Distal to proximal , superficial to deep• Controlled by:• The muscle pump• Competent valves• Gravity• Central obesity and increased intra-abdominal pressure• Pregnancy• Increased intrathoracic pressure, CHF, COPD• Venous obstruction, Clot, tumor.

Varicose veins: Definition

• distended torturous superficial veins due to incompetent valves in the deep, superficial or perforator systems

• distribution: greater or lesser saphenous vein and tributaries

Etiology

• primary• main factor: inherited structural

weakness of valves• contributing factors: age, female,

occupations requiring long hours of standing, pregnancy, obesity

• Secondary• deep vein thrombosis, tumors, trauma• congenital anomalies :arteriovenous fistula

Epidemiology

• 10 - 20% of the population

• >50% over the age of 50• F>M

Clinical Features

• History • Ankle ache• Fatigued legs• swelling around the ankles• aggravated by prolonged standing (end

of day)

• P/E• dilated and tortuous superfical veins • Trendelendberg test • raise leg and compress saphenous vein

at thigh; have patient stand; if vein fills quickly from top down then incompetent valves; use mulitple tourniquets to localize incompetent veins

Symptomatology:

• Usually benign natural history

• Most are cosmetic concerns

• Ache, heaviness, fatigue and Leg swelling

• recurrent superficial thrombophlebitis, painful but benign.

• hemorrhage: external or subcutaneous

• rarely leads to venous stasis changes causing ulcerations

Investigations

• Physical exam, Trendelenburg test

• Duplex ultrasound to assess...• reflux of blood at sapheno-femoral junction• Deep venous incompetence• Perforator incompetence

• Descending venography

Treatment

• Compression stocking therapy

• Saphenous vein stripping surgery • disabling symptoms

• Laser vein or radio frequency ablation less invasive• Principle of treatment:

stop the refluxremove or ablate the conduitexcise or sclerose the varicosities.

Superficial thrombophlebitis:Clinical Features

• Usually involves GSV and its branches

• pain and swelling along course of involved vein

• Erythema and warmth• An inflammatory process• Very rare risk of PE, no need for

anticoagulation• Rx : Anti-inflammatory meds• Recurrent migrating thrombophlebitis:

rule out hypercogulable states, malignancy, or sepsis

Chronic Venous Insufficiency: Definition

• chronic elevation of deep venous pressure and blood pooling in lower extremities leading to venous hypertension

Etiology

• valvular incompetence usually due to a remote DVT.

• chronic venous obstruction

• Venous hypertension

• Secondary varicose veins

• calf muscle pump dysfunction

Clinical Features

• ankle ache and edema - relieved by foot elevation

• Chronic congestion: leads to • hyperpigmentation (hemosiderin

deposits)• Proteinaceous subcutaneous tissue

accumulation, inflammation,dermatosclerosis, fibrous tissue , capillary constriction in the dermis and skin ischemia

• ulceration– shallow and irregular– Medial aspect of lower leg (Gaitor

area)– Can be very painful, difficult to heal

Investigations

• duplex ultrasound to assess

• Reflux at sapheno-femoral junction

• Deep system incompetence

• chronic occlusion from an old DVT/trauma

• Descending venogram

Treatment

• CONSERVATIVE

• compression stockings/layered compression bandages• leg elevation, avoid prolonged standing

• surgical• surgical ligation of perforators in region of ulcer, greater

saphenous vein stripping if incompetent

•GOOD LUCK