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1

Raynaud’s Phenomenon

  • Primary: occurs without signs or symptoms of other disorders.
  • Secondary: causative underlying disease (most commonly a connective tissue disease-CTD)
  • –Systemic sclerosis –Inflammotroy muscle disease –Systemic lupus –Sjorgens syndrome –vasculitis

–White (vasoconstricted phase - ischemia)

–Blue (cyanosis)

–Red (when blood returns - hyperperfusion)

2

Raynaud’s Phenomenon

Treatment

–Avoidance of cold or sudden temp changes

–Avoidance of beta blockers

–Smoking cessation

–Vasodilating Ca2+ channel blockers

–Topical Nitric Oxide patches

  • Systemic side effects, so not always used

–Phosphodiesterase inhibitors

  • Enhance effect of NO, acts on smooth muscle to cause vasodilation
3

Livedo reticularis

  • Linked with enlargement of the blood vessels
  • Net-like dark area of skin surrounding pale centre

Cause

  • Unknown cause
  • Can be a sign of Polyarteritis Nodosa, autoimmune disease-arteries in the organs are damaged
  • Cancer
  • Emboli to skin
  • Treatment

Protection from exposure to cold

4

Acrocyanosis

  • Sympathetic nerves cause constriction or spasms in the peripheral blood vessels that supply blood to the extremities
  • Diagnosis

–Observation of the main clinical symptoms

–Blue and sweaty hands and/or feet

–Lack of pain

Treatment

  • Ca2+ channel blockers and Alpha-1 antagonists reduce symptoms
5

Acute and Chronic Pernio

  • Acute pernio manifests several hours following exposure
  • Chronic pernio may persist even after environmental temperatures are no longer cold
  • Cutaneous lesions present 12-24 hours after cold exposure
  • Red macules, papules, nodules, or plaques, which may form vesicles or ulcerate
    • Last 1-3 weeks
    • Complications include
    –Infection –Loss of skin pigmentation –Scarring

Treatment

  • Pharmacological management

–Based on anecdotal evidence only

–Topical and systemic steroids

–Vasodilators

–IV calcium followed by IM vitamin K

–Ultraviolet B radiation

6

Primary Lymphoedema

Lymphoedema congenita

  • Onset before one year of age

Lymphoedema praecox

  • Develops from one to 35 years of age

–Familial (Meige’s Disease, Autosomal dominant)

–Non familial

Lymphoedema tarda

  • Develops after 35 years of age
    • May be associated with nodal dysplasia & lymphatic obstruction
    –Suggests and acquired cause (mutation in lymph system)
7

Secondary Lymphoedema

–Surgery

–Radiation therapy

–Tumor compression/obstruction

–Traumatic injury

–Infection

–Lymphoproliferative disease

–Tumor/cancer involvement

–Filariasis (parasitic infection)

8

Lymphoedema Pathogenesis

  • Lymphatic damage and fluid stasis also leads to scar tissue/fibrosis development

–Collagen and fibrin deposition to vessel walls, therefore further blocking lymph flow

  • Fluid stasis increases susceptibility to infection with cycle initiated for further lymphatic damage
9

Lymphoedema : Clinical Signs

  • Oedema of involved anatomy
  • Usually no skin ulcerations seen
  • if present, more consistent with chronic venous insufficiency
  • Stage 1

–oedema is pitting, affected

area often returns to normal by morning

  • Stage 2

–oedema is non-pitting, chronic soft-tissue inflammation causes early fibrosis

  • Stage 3

–oedema is brawny & irreversible, largely due to soft-tissue fibrosis

10
  • Inability to pinch skin at the base of the second toe due to it’s thickness

Kaposi-Stemmer sign

11

Lymphoedema

Treatment Goals

  • Improve cosmesis
  • Preserve skin integrity
  • Soften subcutaneous tissues
  • Avoid infection or lymphangitis
  • Decrease limb size
  • Avoid contracture of the involved limb
  • Most importantly: patient & family education
12

Lymphoedema complication

Lymphangitis

13

Lymphoedema

Treatment Options: Pharmacological

  • Antibiotics

–Should always have on hand to begin treatment with first signs of infection

–Should cover Gram positive organisms (most common pathogen Group A Strep)

  • Diuretics

–Can decrease water and sodium in the interstitial fluid, but have no impact on protein status

14

Normal Venous Flow

Dynamic Flow

Flow in arterial system dependent on pumping action of the heart + elasticity &muscular activity of the arteries

Phasic Flow

Effect of respiration on normal venous flow

Arms and neck - flow towards heart increases during inspiration due to negative intra-thoracic pressure produced

Legs - with inspiration the diaphragm descends, increasing intra-abdominal pressure slowing flow

Muscle Pump

Most highly developed in calf muscles

Venous sinusoids act as a ‘bellows’, with muscle contraction emptying the bellows

Negative Pressure

Superficial veins lie outside fascia, however they are emptied by a vacuum effect as the blood in the deep veins is squeezed towards the heart

15

Venous Disorders

lVaricose Veins

lOedema

lVenous thrombosis

lSuperficial thrombophlebitis

lDeep vein thrombosis

lVenous insufficiency

lVenous ulceration

16

Varicose Veins

A dilated, elongated and tortuous vessel

Aetiology

Venous hypertension resulting from valve incompetence or vein obstruction

Primary or secondary

Skin changes (e.g., induration, pigmentation, eczema) typically affect medial malleolar (‘gaiter’) region

Ulcers may develop after minimal trauma to an affected area

Due to poor tissue viability from reduced capillary exchange

17

Venous Oedema

Swelling of soft tissue / fluid accumulation > Interstitial fluid that is protein-poor and has low viscosity

↑ capillary filtration that lymphatics cannot filter efficiently

Peri-malleolar region > proximally

18

Dermatological changes

Haemosiderin

are yellow to brown iron rich pigments that are caused through breakdown of red blood cells and may occur in various tissues throughout the body due to both localised and systemic causes

19

Venous stasis dermatitis

Skin changes associated with CVI have been linked with chronic inflammation

Eczematous process which occurs in the lower legs as a result of insufficient venous return

20

Lipodermatosclerosis

skin changes due to inflammation of subcutaneous adipose tissue of the lower legs that often occurs in patients who have long term CVI

dermis and subcutaneous tissue becoming indurated and fibrosed with the lack of pitting oedema; the skin also becomes atrophic, loses sweat glands and hair follicles, and becomes variably pigmented

21

Atrophie Blanche

smooth, ivory-white atrophic plaques of sclerosis

fibrotic with low blood flow and may contain telangiectasias

22

Telangiectasia

Broken or dilated small superficial blood vessels (spider veins).

23

Varicose Veins - treatment

Conservative

Compression stockings – improve haemodynamics whilst standing. Can be removed in bed at night

Non compliance an issue

Need to be fitted correctly

Can be graduated or non graduated

Circular or flat knit

Ablation

Injection of sclerosant

a chemical agent injected into veins to cause localized thrombosis and eventual fibrosis and obliteration of the vessels

Laser Ablation

Heat generated by laser destroys intimal lining, leading to thrombotic occlusion and acute inflammation

24

Venous Thrombosis

Virchow’s Triad

Vessel wall (tunica intima) injury or change

lStasis of blood

lAbnormal tendency for blood to coagulate

25

Superficial Thrombophlebitis

lAetiolgy and predilection for Great Saphenous Vein unknown.

lLocal trauma and/or unusual activity may precipitate

lMay be recurrent, developing in another section of saphenous vein in the same leg

lResolves rapidly with reduced activity, compression, elevation, anti-inflammatory drugs and anti-coagulants

26

Deep Vein Thrombosis

Stasis due to

Muscle pump inactivity,

Hypercoagulable state which is a biological reaction to injury

Local trauma to veins

General clinical signs

Swelling (unilateral)

Erythema over tissues

High fever

Dilation of superficial vessels in a supine position

diagnostic tests

Doppler

Too subjective, relies on sound only

Venous duplex

Detects blood flow in vein and material in lumen

Treatment

Anticoagulation preventing extension of the thrombus

Heparin (7-10 days)

Warfarin 5-7 days post heparin withdrawal

Continue for 1-2 months

Clot lysing drugs (thrombokinins) injected transvenously in selected cases

Thrombectomy (surgical removal of clot) used rarely

Elastic Compression Stockings

27

Vasculitis Examples:
Giant Cell Arteritis

  • Clinical symptoms

–Headaches

–Tongue claudication and necrosis

–Joint pain

–Facial pain

–Fever

–Vision impairment (sometimes permanent visual loss in one or both eyes)-ophthalmic artery

  • Treatment

–Corticosteroids

–Typically 40 to 60 mg of prednisone

–Symptomatic improvement 24-72 hours

28

Vasculitis Examples:
Wegener’s Granulomatosis

  • Affects mainly upper & lower respiratory tracts, glomerulonephritis, may involve any other organ.
  • Typically occurs in middle age
  • Arthritis - about half of all with this disease
  • Untreated, kidney failure + death > 90% of patients

–Glomerulonephritis

  • Treatment

–Corticosteroids

29

Vasculitis Examples:

Thromboangitis Obliterans

–Single known predisposing factor is cigarette smoking

–Begins with distal ischaemia

–Histopathology-high cellular and inflammatory thrombus minimal involvement of the blood vessel wall

–Occlusive lesions of vessels in leg may à symptoms similar to IC

  • Allen's Test Video

–Elevate hand, make a fist for 30 seconds

Treatment

  • Pain Relief
  • Smoking cessation

–Prior to irreversible tissue damage

  • Oral or IV iloprost (prostacyclin) – vasodilator (smooth muscle relaxant)
  • Surgical Sympathectomy
  • Surgical intervention
30

Entrapment Syndromes

  • Popliteal artery particularly susceptible
  • Compression during exercise àischaemia
  • Caused by anatomical abnormalities e.g. medial head of the gastroc being abnormally lateral, displacing the popliteal artery
31

Cystic Adventitial Disease

  • Cysts within peripheral arterial wall
  • Localised stenosis or vessel occlusion
  • Clinical presentation

–Sudden onset unilateral claudication

–Possible paraesthesia

  • Diagnosis

–Duplex scan followed by MRI

32

Arterial Fibrodysplasia

  • Diagnosis through angiography
  • Treatment

–Intraluminal dilation by angioplasty

33

Spontaneous Arterial Dissection

  • 90% association with hypertension
  • Clinical features

–Severe localised pain with sudden onset

–Ischaemia distal to affected vessel with progressive claudication

–Treatment through vascular bypass

34

Venous Claudication

  • Sequelae of a DVT or compression of vein
    • Aetiology
    –High venous pressure –Inadequate venous collateral circulation
  • Venous obstruction must be determined by ultrasound/venography
  • Treatment

–Poor outcomes

–Venous bypass/stenting

–Thrombectomy generally followed by re-occlusion

35

Arterial Embolus

Treatment

  • Antithrombotics
  • Surgery

–Embolectomy

–Bypass

–angioplasty

36

Neurogenic claudication

  • Lumbosacral radiculopathy due to narrowing of vertebral canal
  • Compression of intraspinal neurovascular structures
  • Ischaemia of spinal cord, cauda equina or nerve roots during exercise
37

Intermittent Claudication
Treatment: Pharmacological

  • Pentoxifylline

–Improves erythrocyte deformability

–Reduces fibrinogen and platelet aggregation

–Decreases blood viscosity

–Contraindicated in renal disease

  • Cilostazol

–Vasodilator (through smooth muscle contraction)

–Inhibition of platelet activity

–Inhibition of smooth muscle proliferation

38

Acute Limb Ischemia

  • Acute obstruction due to embolism or thrombus of a stenotic artery
  • 6 P’s:

–Pain

–Perishingly cold

–Pallor

–Paraesthesia

–Pulseless

–Paralysis

  • Diagnostic testing

–Doppler

–Vascular imaging

  • Treatment

–Anticoag. therapy (heparin ↓mortality &morbidity)

–Should begin prior to revascularistion

–Warfarin (highly effective in prevention)

39

Chronic Critical Limb Ischaemia

  • Associated with numerous risk factors described previously for PAD

Clinical Presentation

  • Ischaemic rest pain

Treatment

  • Revascularisation
  • Platelet inhibition with aspirin therapy (should be preoperative)
  • Lumbar sympathectomy