Current trends in the management of PVD- CME

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CURRENT TRENDS IN THE MANAGEMENT OF PVD DR. R.MURALIDHAR CONSULTANT VASCULAR & ENDOVASCULAR SURGEON JUPITER HOSPITAL & INSTITUTE OF VASCULAR SURGERY BANGALORE

PVD- Peripheral Vascular Diseases: 

PVD- Peripheral Vascular Diseases I - Arterial Diseases II - Venous Diseases

I – Arterial Diseases: 

I – Arterial Diseases Etiology Atherosclerosis Diabetes Mellitus TAO – Buergers Disease

Risk factors: 

Risk factors Diabetes Mellitus Smoking Hypertension Hypercholesterolemia Hypertriglyceridemia

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The atherothrombotic process Normal Fatty streak Atherosclerotic plaque Fibrous plaque Plaque rupture/ fissure & thrombosis Clinically silent MI, unstable angina, stroke, critical leg ischaemia, cardiovascular death Increasing risk factors normal Fatty streak Atherosclerotic plaque Fibrous plaque Plaque rupture - thrombosis Clinically silent PVD, claudication Acute limb ischemia Increasing age & risk factors

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DIABETES An introduction

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Top 10 countries in the prevalence of Diabetes India China USA Indonesia Japan Pakistan Russia Brazil Italy Bangladesh WHO & IDF 2004

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Top 3 countries & the numbers People with Diabetes Rank Country 2000 2030 1 India 32 80 mill 2 China 21 42 mill 3 USA 18 30 mill WHO & IDF 2004

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The Origin Diabetes -Siphon (Greek) means melting down of the flesh and limbs into urine Mellitus - Sweet sweet urine being symptom of disease.

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Definition A metabolic disorder of carbohydrates , fats & proteins characterized by persistent elevated glucose levels in blood DIABETES

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Polyuria Polydipsia Glycosuria Polyphagia Asthenia Blurring of vision Loss of weight Symptoms

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Risk Factors for Diabetes Family history Obesity/central obesity Hypertension Abnormal lipids hyperglycemia during pregnancy Age above 30 yrs Stress Sedentary lifestyle Impaired glucose tolerance

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Pancreas A lobulated gland functioning as an exocrine and endocrine (Secrete hormone directly into blood stream) organ. The exocrine portion consists of Acini which secretes pancreatic juice which passes through common bile duct into the duodenum. The endocrine portion consists of Islets of Langerhans cosisting of alpha, beta and delta cells which secretes glucagon, insulin and somatostatin respectively.

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Pancreas

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Islets of Langerhans in Pancreas

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Islets of Langerhans in Pancreas Alpha cells: Form 15-20% of Islets and produce Glucagon – Stimulates the release of glucose into blood stream. Beta cells: Form 70-80% of Islet cells and produce Insulin – Is essential for body’s cells use of glucose as energy source. Facilitates the movement of glucose away from blood stream. Delta cells: Form about 5% of the Islet cells and produce Somatostatin – Inhibits the release of insulin and gastrin.

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Classification of Diabetes Type 1 (IDDM) Type 2 (NIDDM) < 5% of cases 90 % of cases ß cells are dead Malfunctioning of ß cells / or peripheral cells Insulin not present Insulin is low / normal/ / negligible even high ID IR

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Insulin Deficiency(ID) Malfunctioning of ß cells Quantity of insulin secreted is less Insulin is not secreted in biphasic manner

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Diagnosis of diabetes symptoms and plasma glucose  140 mg/dl fasting plasma glucose  110 mg/dl

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Type 1 diabetes mellitus usually autoimmune destruction of insulin-producing pancreatic islet  cells over months absolute insulin deficiency rapid presentation with thirst, polyuria, weight loss, blurred vision thrush, lethargy, dizziness usually thin and ketotic at presentation

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Type 1 diabetes typical onset < 30 years can start at any age sudden onset severe symptoms recent weight loss usually thin spontaneous ketosis absent C-peptide markers of autoimmunity Type 2 diabetes typical onset > 20 years can start at any age gradual onset may be no symptoms often no weight loss usually obese not ketotic detectable C-peptide no autoimmune markers

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Type 2 diabetes mellitus usually insulin resistant with inadequate insulin production to maintain normal glucose levels onset (usually gradual) at any age, usually >20 years usually overweight or obese but not ketotic and often no symptoms at presentation higher rates in UK Asian and Afrocaribbean people Worldwide very high prevalence in rural to urban migrant communities

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Treatment of diabetes type 1 type 2 GDM diet, exercise & insulin diet, exercise metformin or sulphonylurea alone metformin and sulphonylurea metformin, sulphonylurea & thiazolidinedione insulin diet insulin

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Diet Exercise OHA ( Oral Hypoglycemic Agents ) Monotherapy Increase the dose of OHAs Combination of OHAs Insulin injections Management of Type-2 Diabetes

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Diet

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Complications of diabetes retinopathy nephropathy neuropathy Vasculopathy coronary artery disease cerebrovascular disease peripheral vascular disease

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Diabetic nephropathy Affects 25% of type 1 and type 2 diabetes patients Risk factors similar to those for retinopathy Is a progressive condition leading to renal failure Characterised by proteinuria and high blood pressure

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Diabetic neuropathy Affects type 1 and type 2 diabetes patients similarly Risk factors similar to those for retinopathy may lead to loss of sensation in feet foot ulceration erectile dysfunction gastroparesis and vomiting postural hypotension

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Diabetic foot ulcers with amputation in other foot Diabetic Foot Ulcers

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Magnitude of Problem Among the persons with diabetes 15% may experience foot ulcer in their life time. The risk of lower extremity amputation is 15-46 times higher in diabetics than in persons who do not have diabetes. Clinical studies have shown that foot ulcer precedes 85% of non-traumatic amputations among diabetic patients.

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Management of Diabetic Foot Ulcers Primary goal “To obtain wound closure’’ Objectives of diabetic foot ulcer treatment are Reducing the risk of infection & amputation Improving function & quality of life Reducing health care cost

Diabetic vascular complications: 

Diabetic vascular complications coronary artery disease cerebrovascular disease peripheral vascular disease

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PERIPHERAL VASCULAR COMPLICATIONS *MACROANGIOPATHY *MICROANGIOPATHY Block in the medium sized arteries-Ischaemia. Peripheral Neuropathy-Susceptible to trauma Microangiopathy - spread of Infection. Hyperglycaemia - Infection

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Clinical presentations

Clinical presentation - Ischemia: 

Clinical presentation - Ischemia Acute Chronic Acute on Chronic Pallor Claudication All the features Pain Ulceration of acute ischemia Paresthesia Gangrene One/more toes/ Paralysis fingers-gangrene Pulselessness Proximal lesion

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Claudication Ischemic Neurological Venous insufficiency Typically in muscles Along the lateral Whole leg & posterior aspect of limb Appears on walking Aggravated by climbing / Appears on standing for long time lifting weights Cramp like pain Radiating / burning pain Bursting pain / feeling of tiredness Relief by rest Lying down Elevation or exercises Weak / absent pulses Normal pulse Normal pulse

Investigations: 

Investigations Routine investigations – lipid profile, blood sugar, ECG,PFT. Non Invasive – Pocket Doppler, Duplex scan Invasive – Angiogram Tran lumbar Aortogram & follow Tran femoral retrograde Angiogram( DSA ) Magnetic resonance Angiogram ( MRA )

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Non Invasive Vascular Lab Pocket Doppler being used to record ankle pressure. Calculate ankle: brachial index. Useful for bedside assessment of ischemia

COLOUR DOPPLER STUDY: 

COLOUR DOPPLER STUDY

TAO – MRA of a young male with extensive blocks in both lower limbs: 

TAO – MRA of a young male with extensive blocks in both lower limbs

MRA of another male showing bilateral blocks – Symptomatic on left side: 

MRA of another male showing bilateral blocks – Symptomatic on left side Presented with gangrene of left great toe. Had severe lung compromise due to smoking Hence not fit for Aorto – Profunda bypass as it needed Laparotomy . Underwent Right CFA to left profunda bypass using Goretex Graft. Did extremely well and his left foot was saved .

Left popliteal block: 

Left popliteal block

First Aortic surgery at SDUMC,Kolar: 

First Aortic surgery at SDUMC,Kolar

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68 year old diabetic & smoker. Gangrene with severe rest pain. Angio showing SFA block. Femoro popliteal bypass using GSV. Tran tarsal amputation done. Well granulating after 2 month s

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Left common iliac artery to popliteal bypass using 7 mm 70 cm synthetic graft [Goretex]

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Heal ulcer showing good granulation one month after the surgery

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2nd toe disarticulated and healing well. After debridement huge granulating ulcer healing well and has covered all the tendons

Diabetic foot: 

Diabetic foot After Fem-Pop bypass, exposed calcaneum was shaved to put a SSG. Well taken SSG after 2 weeks.

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Large abscess in diabetic foot

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SYMPATHECTOMY IMPROVES CUTANEOUS PERFUSION DIVERTS BLOOD FROM MUSCLES RELEIVES REST PAIN CLAUDICATION MAY WORSEN SUPERFICIAL SKIN ULCERS HEAL UTILITY OF LAPAROSCOPE

Endovascular Therapy: 

Endovascular Therapy Angioplasty with / without stenting Indications – short segment lesions stenoses aorta / iliacs Types – Intraluminal angioplasty( PTA) Sub intimal angioplasty

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Left upper limb ischemia Tips of index, thumb and middle fingers are gangrenous Thumb and middle fingers recovered fully following thrombolysis Distal half of index finger had to be amputated

Left Subclavian artery angioplasty and stenting: 

Left Subclavian artery angioplasty and stenting Ac ischemia of left upper limb Ulcerated palque with thrombus in the LSA at the origin of vertebral artery Good result after plasty and stenting Intra-arterial thrombolysis

Conclusion: 

Conclusion PVD is very common but needs to be identified Diabetes is a major contributor Smoking is the main cause of limb loss If identified early many limbs and lives can be saved Endovascular therapy – innovative & useful

Conclusion: 

Conclusion Awareness has improved in the last few years about vascular diseases Availability of synthetic grafts – is a major breakthrough Bypass is more affordable With plenty of latest techniques overall limb salvage is better and mortality is reduced

VENOUS ANATOMY: 

VENOUS ANATOMY SUPERFICIAL VENOUS SYSTEM DEEP VENOUS SYSTEM PERFORATOR SYSTEM

FLOW IN LEG VEINS: 

FLOW IN LEG VEINS Normally from superficial to deep system due to “calf-muscle pump”. Hence pressure in sup system is less than that of deep system. In deep veins it is from below upwards assisted by valves

What happens in CVI ?: 

What happens in CVI ? Flow is from Deep to Sup system. This occurs at : Saph- femoral Jn Saph- pop jn Perforators Flow in deep veins is reversed

Effect of this in CVI: 

Effect of this in CVI Superficial veins ( GSV &/or SSV ) become dilated, tortuous & incompetent. Hence called Varicose veins. Causes venous hypertension in sup veins.

Macrovascular changes – reversal of flow: 

Macrovascular changes – reversal of flow Microvascular changes – Stasis – dilatation of venous side of capillaries. Migration of blood pigments (hemosiderin) into subcut tissue –hyperpigmentation – eczema – itching- ulceration and non healing.

Types of CVI: 

Types of CVI Primary – no etiologic factor can be identified ( Idiopathic) Secondary – Following DVT

Incidence of CVI: 

Incidence of CVI Common in certain occupations like – teachers, police, conductors, surgeons especially vascular surgeons who stand and operate for long hours. 3 per 1000 in general population

Etiology: 

Etiology Hereditary Contributed by occupations Pregnancy with large fetus- causes compression of iliac veins. Post-menopausal – hormonal- progesterone. Obesity – esp. central Pelvic mass

Clinical features: 

Clinical features Cramp like pain in calf Heaviness & swelling in leg Eczema, pigmentation and itching Blanket like skin – thick & rough Scratching – ulceration – bleeding Sup / deep venous thrombosis

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Venous Ulcer Lipodermatosclerosis

Investigations : 

Investigations Colour doppler studies – non invasive & very useful In diagnosis & assisting for surgery

Investigations: 

Investigations Venography or phebography Rarely employed now Invasive and cumbersome Flow quantification not possible

INDICATION FOR INTERVENTION: 

INDICATION FOR INTERVENTION Patent Deep Veins Established reflux at SF or SP or perforators. Symptomatic limb Complications

Management: 

Management Compression – stocking / bandage Elevation & exercises Medications – bioflavonoids Calcium dobesilate Sclerotherapy

SCLEROTHERAPY: 

SCLEROTHERAPY Injection of sclerosant into the dilated veins – intense inflammation, collapse Sclerosants – STD, cyanoacrylate, etc Disadvantages – discoloration of the skin, hypopigmentation, scarring

Management: 

Management Surgery – definitive form of treatment Two schools of thought Aggressive ( saphenectomy ) Conservative ( SF flush ligation without stripping) Types – SF flush ligation (Trendelenberg operation) SP flush ligation Ligation of incompetent perf GSV stripping

Saphena femoral flush ligation: 

Saphena femoral flush ligation Small oblique incision in groin Ligate and divide all tributaries Flush ligation at SF junction and divide

Large dilated GSV mass after superficial thrombophebitis: 

Large dilated GSV mass after superficial thrombophebitis

Concomitant venous surgery and Skin grafting: 

Concomitant venous surgery and Skin grafting Had an ulcer for 12 years and given up hopes of healing After the initial preparation of the ulcer Taken up for both venous surgery and split skin grafting Had SF, SP & multiple perforator incompetence

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VENOUS ULCER GRAFTED

Complications of CVI: 

Complications of CVI Bleeding Ch. non healing ulcer Sup. Thrombophlebitis / DVT Cellulitis – infective gangrene Venous gangrene Osteomyelitis of tibia

Complications of surgery: 

Complications of surgery DVT – Pulmonary embolism Minor wound complications like groin collections, infection, etc Recurrence

Adjuvant treatments: 

Adjuvant treatments Low molecular weight heparins- dalteparin Antiplatelet &/or antecoagulation esp. post thrombotic CVI Elevation & Exercises Elastic crepe bandage / compression stockings Change in occupation

Prevention: 

Prevention Keeping body weight under control Regular walking & exercises Spring walking to improve calf pump Hormonal treatment Avoiding long hours of standing / journeys

Conclusion: 

Conclusion CVI is very much prevalent- but underdiagnosed Surgery is safe & effective Other options are still to be proven Controlling risk factors like obesity is important in preventing recurrence

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Thank You