PERIPHERAL VASCULAR

DISEASE:
ARTERIAL & VENOUS DISEASE
SUPERVISOR : ASST. PROF DR AHMAD FAIDZAL OTHMAN
Peripheral arterial disease

● Acute limb ischemia

● Chronic limb ischemia
● Aneurysm
 Acute limb ischemia

DEFINITION

A sudden decrease in limb perfusion that threatens limb viability which occurs within 14 days after symptom onset

CLINICAL FEATURES

6 P : Pain (sudden onset), Pulselessness, Perishing cold, Pallor, Paraesthesia (nerve ischaemia), Paralysis (muscle ischaemia)

Symptoms Signs

Pain - sudden onset and continuous, usually in one Limb appearance : pallor or bluish discoloration,
periphery mottled skin (fixed vs blanching), skin blistering
Temperature : cold
Perishing cold - sudden onset and continuous,
Pulses (via palpation and confirm with Doppler) :
usually in one periphery absent
Paraesthesia or numbness - sudden onset, usually in Sensation loss
one periphery Progressive paralysis and foot drop
 ETIOLOGY

Embolus (most common)

- Mostly due to large cardiogenic emboli : Atrial fibrillation, myocardial

infarction, prosthetic heart valves
- Common site of emboli : common femoral bifurcation (most common),
popliteal trifurcation, aortic bifurcation ‘saddle embolus’

Thrombosis

- Causes : Acute plaque rupture, hypovolemia, thrombosis of popliteal

aneurysm, increased blood coagulability
- Usually thrombosis happened in chronically stenosed vessel (i.e.
atherosclerotic vessel), thus less severe in presentation due to collaterals
had already developed

Trauma
INVESTIGATION

Blood : FBC, renal profile, coagulation profile, ABG

(Lactate), creatinine kinase, LDH

Bedside : Doppler ultrasound, ECG, Ankle Brachial Systolic

Index (ABSI)

Imaging : CT angiography, MR angiography

PRINCIPLE OF MANAGEMENT

IMMEDIATE

1. Early anticoagulation with IV Heparin 5000 U bolus followed by IV Heparin infusion at 1000U/hour -to prevent
propagation of thrombus proximal and distal to occlusion
2. Improve existing perfusion : keep foot dependent, avoid heel pressure, 100% oxygen supplementation, correct hypotension
3. Revascularization - surgical or endovascular

Surgical revascularization Endovascular revascularization

Embolectomy Thrombolysis
Thrombectomy Angioplasty
Bypass grafting Stenting
Fasciotomy (in profoundly ischaemic limb to prevent
compartment syndrome) *risk of severe complications such as stroke and bleeding within
Amputation 30 days of treatment

4. Post-operative anticoagulation with heparin

5. Treat underlying causes / risk factors

*Currently, hybrid intervention is being practiced whereby endovascular surgery under intraoperative angiography is being simultaneously
performed following surgical thromboembolectomy.
Chronic limb ischemia

- Most commonly caused by atherosclerosis Risk factors

Intermittent claudication - Hypertension
- Dyslipidemia
- Cramping pain in leg muscles on walking
- Diabetes Mellitus
- Relieved by rest
- Cigarette smoking
- Fixed claudication distance but can be reduced if
walking uphill
Chronic Limb Threatening Ischemia

- The end result of arterial occlusive disease

- High risk of leg amputation and cardiovascular complications

Defined as:

(1) recurrent foot pain at rest that requires regular use of analgesics with
ankle systolic pressure <50mmHg or toe systolic pressure <30mmHg
(2) a nonhealing wound or gangrene of the foot or toes,
Physical findings

- Shiny smooth skin

- Muscle wasting
- Presence of ulcers or gangrene
- Absent or diminished pedal pulses
- CRT>2 secs
- Positive Buerger’s test
Investigations

Laboratory 1. Full blood count

investigations 2. Renal profile
3. Creatine kinase

Ankle Brachial Pressure - Normal: 0.9-1.2

Index (ABPI) - ABPI ≤0.4

Duplex Ultrasonography - GSUS: estimation of plaque narrowing

- Color Doppler: estimation of flow velocities

CT Angiography, MR
Angiography
 Management of CLTI

Conservative Medical Surgery

Lifestyle measures 1. Blood pressure 1. Revascularization

- Smoking cessation control - Angioplasty
- Diet modification 2. Antiplatelet therapy- - Stenting
- Systematic exercise Aspirin - Bypass
3. Pain management 2. Amputation
Follow-up

- Lifelong follow-up
- Rehabilitation
- Nutritional status
- Patency of bypass graft after revascularization
- Close follow-up of coronary artery and cerebrovascular disease
Reperfusion Injury
- Reperfusion exacerbating the cellular damage already
caused by ischemia
- Can present as
- Acute heart failure
- Cerebral dysfunction
- SIRS
- Multi-organ failure
- Can be attenuated by reducing the extent and duration of
tissue hypoperfusion
Aneurysm

● Defined as localised area of pathologically excessive arterial

dilatation with at least 50% increase in the diameter of vessels.
● Relatively uncommon; found mainly in males over 70 years age.
● Etiology : Atheromatous, mycotic ( bacteria rather than fungal ),
collagen disease, traumatic
● Morphology : True aneurysm or pseudoaneurysm
● Aneurysm may occur in the aorta, iliac, femoral, popliteal,
subclavian, axillary, carotid, cerebral, mesentric, splenic and renal
arteries and its branches.
True aneurysm False aneurysm

Dilatation of all three layers of vessel Dilatation artery not involving all 3 layers
(intima, media, adventitia ) Eg: collection of blood or hematoma that
has leaked out of the artery but is then
confined by the surrounding tissue.
 Abdominal aortic aneurysm
● The most common type of large vessel aneurysm and is found
in 2% of the population at autopsy
● Small (3cm to 4.4cm across)

Medium (4.5cm to 5.4cm across)

Large (5.5cm or more)

Risk factor

- Hypertension
- Hyperlipidemia
- COPD
- Family history of AAA
- Cardiovascular disease or history of stroke
- smoking
 Principle of management
INDICATIONS OF AAA SURGERY INVESTIGATIONS
- Periodic monitoring ultrasonography
• Size of aneurysms of 5-5.5 cm diameter or more - CT scan ( elective operation is planned)
• Aneurysm expand more than 0.5 cm per year

• Presence of saccular aneurysm

TYPES OF SURGERY
• Symptomatic (Abd pain, back pain, ureteric - Open abdominal aortic aneurysm
obstruction or embolism ) surgery
- Endovascular aneurysm repair
• Leaking/ruptured aneurysm (medical emergency)
Clinical manifestation of ruptured AAA

1. Typically presented with palpable pulsatile abdominal mass with pain and
has transient collapse (hypotension)

2.If happened to rupture in the vena cava, there will be large arteriovenous
fistulae. Symptoms include tachycardia, congestive heart failure (CHF), leg
swelling, abdominal thrill, machinery-type abdominal bruit, renal failure, and
peripheral ischemia.

3. if rupture into the fourth portion of the duodenum- patient will present with
symptoms of UGIB & massive haemorrhage
Management

1. Resuscitation and stabilization

2. Allow permissive hypotension to facilitate investigation
3. Blood investigation and vitals monitoring
4. CT scan to plan/ decide for surgery
5. Definitive repair : open surgery or endovascular aneurysm repair
Principle of aortic aneurysm surgery
● Aorto-iliac & femoral aneurysm- tube
graft/bifurcation graft of synthetic material
● Popliteal aneurysm- autogenous saphenous
vein

Open abdominal aortic Endovascular aneurysm repair

aneurysm surgery

- Standard approach of • Minimally invasive technique using stent

midline/transverse graft
abdominal incision • Perform mostly under general anesthesia
-Perioperatively can be local
anticoagulated • Possible complications
-endovascular leak
-Possibility secondary intervention
-life long follow up
 Extracranial cerebral arterial insufficiency
( Carotid artery insufficiency )
Pathophysiology • Often results in stenosis with cerebral blood flow
becoming impaired when luminal narrowing
exceeds about 70%
• Caused by carotid atherosclerotic plaque, usually
patients have high cardiovascular risk,
• Might present with Transient Ischemic Attack

Investigations •Duplex Doppler scanning

•Carotid angiography- invasive with risk of stroke
• Magnetic resonance angiography- estimate degree of
stenosis

Management -Medical antiplatelet therapy (aspirin 75-150mg or clopidogrel 75mg daily)

-Surgical endarterectomy (removing thrombus)
-Minimally invasive stenting
Venous Thromboembolism

● 3rd most common CVD after MI and CVA. VTE

● Overall VTE rates 100 per 100,000 in the populations
per year, 70% are hospital acquired
● VTE comprises of Deep Vein Thrombosis (DVT) and
Pulmonary Embolism (PE)
● The risk of symptomatic VTE:
○ Highest within 2 weeks of surgery
○ Remains high for another 2 - 3 months DVT PE
● Risk of fatal PE:
○ Highest 3 - 7 days following surgery
VTE - Pathogenesis

● Venous thrombi originate in venous valve pockets

from sites of venous stasis or following vessel wall
injury.

● The symptoms of VTE are caused by obstruction of

venous outflow by thrombi, causing inflammation of
the vein wall, inflammation of the tissues surrounding
it or embolisation into the pulmonary circulation
VTE - Sign & Symptoms Risk Factors
1. Unilateral leg pain (Calf)) ● Active cancer
2. Diffuse & massive swelling whole leg - ● Obesity (BMI >30kg/m2)
occluded ileofemoral vein ● OCP
3. Painful white leg & edema - ● HRT
4. Phlegmasia alba dolens ● immobilisation
5. Painful blue leg & discolored - Phlegmasia ● Previous VTE
caerulea dolens ● Family hx of VTE
6. Pitting edema - ankle ● Medical comorbidities
7. Dilated superficial veins ○ IHD
8. Tenderness - deep veins course ○ Metabolic, endocrine pathologies
○ Acute infectious disease
Classical PE: ○ Inflammatory conditions
○ Sickle cell disease
● Sudden dyspnea ○ Thalassemia
● Cardiovascular collapse ○ Varicose veins
● Pleuritic chest pain
● Pleural rub
● hemoptysis
DVT WELL’s Score
PE WELL’s Score
VTE - Investigations VTE - Prophylaxis

DVT

● Color duplex ultrasound

PE

● CTPA
● D-dimers test (-ve predictive value)
VTE - Prophylaxis

MECHANICAL PHARMACOLOGICAL

1. Graded Elastic Compression 1. LMWH

Stockings (GECS) 2. Fondaparinux
2. Intermittent Pneumatic Compression 3. Unfractioned heparin
(IPC) 4. Warfarin
3. Venous Foot Pump (VFP) 5. Oral Direct Thrombiin Inhibitors
6. Oral Direct Factor Xa Inhibitors
VTE - Pharmacological Management

1. Start LMWH (enoxaparin or tinzaparin) or fondaparinux as soon as possible and continue for at least 5
days or until the INR is 2 or above for 2 consecutive days
● Enoxaparin dose is 1 mg/kg twice daily
● Tinzaparin dose is 175 IU/kg once daily
● Fondaparinux dose is 7.5 mg daily
2. Start warfarin at 5 mg daily within 24 hours of diagnosis and continue for 3 months
3. For severe renal impairment: Intravenous unfractionated heparin with dose adjustment based on APTT
4. For patients with PE and haemodynamic instability: offer IV UFH and consider thrombolytic therapy
5. Rivaroxaban: 15 mg twice daily for the first 21 days followed by 20 mg once daily for continued treatment
and prevention of recurrence
VTE - Thrombolytic Mx Mechanical Intervention
1. DVT 1. Compression Stocking
● Venous thrombectomy
● Thrombolytic therapy: Catheter
directed thrombolysis
2. PE 2. Vena cava filters
● Thrombolytic therapy a. To prevent PE secondary to DVT
● Pulmonary embolectomy b. Small device to stop blood clots
○ Emergency procedure from going to the lungs
following failed conservative
c. INdication:
measures
○ Recently, percutaneous i. When pt is contraindicated
catheter directed for anticoagulants
embolectomy devices had ii. When pt have large free
been developed floating iliocaval thrombus

AGENTS: tissue plasminogen activator (tPA),

100mg IV over 2 hours Thrombolytic therapy
Low Molecular Weight Heparin

Introduction: Overdose Signs

● Anticoagulants ● Nose bleed

● Example: Dalteparin, Enoxaparin ● Unusual bleeding
● Easy bruising
MOA ● GI bleed

Reversal Agent: Protamine Sulphate

Varicose
Vein
NURUL AIN NADIA MD AMIN
1811924
INTRODUCTION
DEFINITION: dilated, tortuous and prominent
superficial veins in the lower limb
● Common worldwide
● 20%- 20 years
● 80%- 60 years
● Women > men (6:1), esp at 2nd & 3rd trimester
● Only 12% reported to develop symptoms and
complications of varicose veins:
○ Eczema
○ Phlebitis
○ Lipodermatosclerosis
○ Ulceration
○ Bleeding
PATHOPHYSIOLOGY
CLINICAL PRESENTATION
SYMPTOMS & SIGNS EXAMINATION

● Cosmetic concerns ● Examine

● Pain ○ Extent & severity Skin
● Aching changes- swelling, ulcer,
● Heaviness varicose eczema
● Fear of future leg ulcers ○ Distribution of varicose vein
● Bleeding or worry about varicosities ● Visible standing- Cough impulse,
bleeding thrill, or saphenovarix at SFJ.
● Varicose eczema or ulcers ● Tourniquet test
● Ankle oedema
● Recurrent superficial thrombophlebitis
TOURNIQUET TEST
Elevate limb and ensure veins are emptied by massaging distal to
proximal. Apply tourniquet tightly around upper thigh

A then stand patient up. Does tourniquet prevent veins filling

and removing it cause rapid filling from above? If so, main
communication is at the sapheno- femoral junction. If veins fill
rapidly with tourniquet in place, repeat the test with tourniquet
above the knee

B. If this controls filling, then main communication is mid-thigh

perforator. If this tourniquet fails to control filling, repeat below
knee

C. If this controls filling, communication is likely to be short

saphenous-popliteal or medial knee perforator incompetence. If
no tourniquet controls filling, communication is probably by one
or more distal perforating veins, often post-thrombotic in origin

D. Note that 80% of varicose veins involve the long saphenous

system, sometimes with short saphenous incompetence as well.
CEAP
classification
system
INVESTIGATION

1. Colour duplex
Gold Standard

2. Handheld Doppler (HHD)

Delineate patterns of reflux

3. Contrast Venography

4. Intravenous Ultrasound (IVUS)

5. MR Venography
Suspect congenital vascular
malformation- assess extent of lesion
and arterial component.
 MANAGEMENT

CONSERVATIVE SURGICAL ENDOVENOUS TREATMENT

- for symptomatic relief INDICATION: aching legs , ● Radiofrequency ablation

haemorrhage, superficial (RFA)
● Elastic stockings when thrombophlebitis, venous skin ● Endovenous LASER
prolonged standing changes ablation (EVLA)
● weight reduction ● Ultrasound guided foam
● elevate legs when sitting ● High Saphenous Ligation sclerotherapy (UGFS)
● avoid constricting ● Long saphenous vein
garments stripping
● Analgesia ● Avulsion of varicosities
Chronic Venous Insufficiency
- inadequate venous drainage for at least 2 weeks and often much longer
- Usually presents with a chronically swollen limb and/or typical skin changes of venous
insufficiency around the ankle ( may have ankle ulceration)

Etiology

Primary : symptomatic presentation without a precipitating event , might be due to congenital

defects or changes in venous wall biochemistry. Alteration integrity of the vein promoting dilation
and valvular incompetence

Secondary : due to DVT which triggers an inflammatory response subsequently injuring the vein
wall.

Non-modifiable risk Modifiable risk

Female, Non-thrombotic iliac vein Smoking, obesity, pregnancy,use of oral

obstruction ( May-Thurner syndrome) contraceptives, prolonged standing, DVT
and venous injury
Pathophysiology
- due to reflux or obstruction of venous blood flow
- Valvular incompetence of superficial veins, deep veins or perforating veins,
- Causing venous hypertension of lower extremities
- Superficial incompetence due to weakened or abnormal shaped valves, or widened
venous diameter
- Prevents normal valve congruence
- DVT causing inflammation, valve scarring, adhesion and luminal narrowing.
- Persistent elevated venous hydrostatic pressure may result in lower extremity pain,
edema and venous microangiopathy.
Clinical Presentation
History taking Examination

- initial presentation such as pitting - general examination

edema, lower limb discomfort, fatigue - Detailed assessment of the lower limb
and itching such as examination of ulcers, distal
- Disease progression- changed skin pulses and neuropathy
pigmentation, ulcer formation - Trendelenburg test- differentiate
- Inquire about history of the causative whether superficial vein
hypercoagulable condition, previous valve or deep system
usage of OCP, previous DVT
- Inquire about the patient’s
occupation and level of physical
activity
Investigation and Management

Investigation

- Duplex ultrasonography- identify the region of affected anatomy

- Invasive venography - done in patient suspected vein stenosis
- ABSI - can be done to exclude arterial pathology

Management

- Based on severity and nature of disease

- Treatment goals: reduce discomfort and edema, stabilize skin appearance
- Conservative treatment : leg elevation, weight management, compression therapy
- Superficial vein : endovenous therapy, foam sclerotherapy, thermal ablation
- Valvuloplasty
- Compression stockings
Ulcers
Venous Arterial Neuropathic

History Prior deep venous Cigarette smoking, Diabetes, other

thrombosis, stroke, diabetes, dyslipidemia, causes of peripheral
miscarriage, obesity, intermittent claudication neuropathy
multiple pregnancies, pain
upon standing

Location area between the lower Pressure points, toes Plantar aspect of
calf and the medial and feet, lateral foot, tip of the toe,
malleolus malleolus, and tibial lateral to fifth
areas metatarsal

Pain Mild to moderate Severe Painless

Other Varicosities, peripheral Weak/absent peripheral Peripheral

physical edema, stasis dermatitis pulses, prolonged CRT, neuropathy with
findings pallor on leg elevation decrease sensation
Ulcers
Venous Arterial Neuropathic

Ulcer
characteristic

shallow and flag margin, Punched out and deep, Deep, surrounded by
moderate-to-heavy exudate, irregular shape, callus, insensate
slough at base with unhealthy wound bed,
granulation tissue presence of necrotic
tissue, minimal exudate,
unless infected

Treatment Compression therapy, leg Revascularization, Off-loading pressure,

elevation, surgical anti-platelet medication, typical growth factors
management management of risk
factors
THANK YOU!