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Venous Insufficient Ulcers Flashcards

1
Q

Recurrences rates in venous ulcers

A

26-69% high

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2
Q

Venous system

A
  • Low-pressure system
  • Carries blood from tissue capillaries back to the heart
  • High in CO2 and metabolic wastes
  • 15 mmHg (capillaries on venous side)
  • 0 mmHg up one reaching right atrium via vena cava (5 mmHg)
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3
Q

Anatomy of venous system

A
  • Three layers, innermost produces enzymes which help reduce clot formation
  • Layers are thin and there is less smooth muscle
  • Veins more extensible than arteries and able to accommodate greater volumes of blood
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4
Q

Total blood volume stored in veins

A

70%

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5
Q

Intact valves

A

Reflux of blood is prevented during calf muscle relaxation

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6
Q

Damaged valves

A

Reflux of blood can occur during calf muscle relaxation and may cause venous hypertension (get retro-grade flow)

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7
Q

Perforating veins

A

Pierce the fascia connecting the deep and superficial vein systems throughout the lower leg
- Contain bicuspid valves that only allow unidirectional flow towards the heart preventing retrograde venous flow

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8
Q

Deep veins

A

Located within muscles and roughly run parallel to the arteries, contain one-way valves
- Greater pressure than superficial

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9
Q

Superficial veins

A

Contain same type of valves as deep but not surrounded by muscle (no muscle pump)
- Assist with temperature regulation

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10
Q

Calf muscle pump

A

Helps to return venous blood back to body, applies pressure on deep veins and valves pushing blood towards heart

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11
Q

Respiratory pump

A

Helps to get venous blood back to body via negative pressure pulling blood from LE

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12
Q

Venous hypertension

A

All pathophysiology of venous insufficiency starts here

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13
Q

Causes of venous hypertension

A
  • Vein dysfunction (failure of one-way valves)
  • Calf muscle pump failure
  • Combination
  • All leads to pooling of venous blood in LE
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14
Q

Fibrin cuff theory

A

Fibrinogen leaked out from capillaries creating barrier to diffusion of oxygen and nutrients
- Fibrinogen -> insoluble layer of fibrin -> fibrosis of capillaries themselves -> no gas exchange or waste elimination

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15
Q

Inflammatory trap theory

A

WBC adhere to vessel walls, activate inflammatory process -> releasing proteolytic cells -> endothelial damage

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16
Q

Cytokine dysregulation

A

Trapping of growth factors making them unavailable for repair of damaged tissue -> tissue in chronic inflammatory phase

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17
Q

Varicosity

A
  • Primary venous distention may be caused by inherent weakness within the vein itself
  • Dilated veins with increased length and tortuosity
  • May be present for years prior to ulceration
  • Peripheral edema from CHF, pregnancy, obesity, limited mobility cause secondary venous distention by decreasing VR (venous return?)
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18
Q

Calf muscle pump failure

A
  • Calf weakness, paralysis, OA, or decreased mobility decreases muscle pump
  • Occupations requiring prolonged standing without movement are at an increased risk of developing VI and ulcers
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19
Q

Trauma and VI

A

Minor injury may initiate wound formation (brush against thorn bush, itching dry skin) to already at risk tissue

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20
Q

Previous venous ulcer

A
  • High recurrence rate
  • Repeat ulcer happen for same reason first one began
  • Less tensile strength and elasticity of scar tissue
  • Precipitation factors not addressed
21
Q

Advancing age and VI

A
  • Decreases inflammatory and immune responses
  • Decreased collagen synthesis & tensile strength
  • Increase skin atrophy
  • Increased number of co-morbidities
22
Q

Diabetes

A
  • Microvascular disease and impaired immunoreactivity
  • Impaired all three phases of wound healing
  • Poor glucose control -> hyperglycemia
  • Greater the hyperglycemia the greater the adverse affect on wound healing and greater risk of infection
23
Q

Homan’s sign

A
  • Identification of deep veins thrombosis
  • Ankle passively dorsiflexed with knee extended
    + result: pain with test movement, tenderness with deep palpation of gastroc
  • Not very sensitive or specific
  • Positive test can be found with superficial phlebitis or MSK injuries ie. Achilles tendinitis
  • If + request further medical assessment especially if they have a history of reduced activity or long periods of sitting
24
Q

Co-existing arterial and venous insufficiency occurs in … of all LE ulcers

A

15%, called mixed wounds
- Until proven otherwise, arterial insufficiency should be suspected in all chronic LE ulcerations

25
ABI <0.7
Contraindication to compression as management of venous wounds
26
Trendelenburg test
- Identifies vein incompetence - Pt supine with leg elevated 45 deg x 1min -> severe tourniquet lightly around distal thigh to occlude SUPERFICIAL veins -> pt stands up -> release tourniquet and watch for vein distention up to 1 minute - If veins fully distend < 5 sec before tourniquet released = incompetence in perforator veins - Time to venous distention < 10 seconds = superficial vein incompetence
27
Rubor of dependency test
- Assess foot in sitting -> pt placed in supine with limb elevated to 60 deg x 1 minute or until veins drained by gravity (leg becomes pale = arterial insufficiency) -> place limb in dependent position and record superficial vein refill time - Refill < 5 seconds =venous insufficiency - Refill > 20 seconds =arterial insufficiency - Leg becomes hyperemic (bright red) = arterial insufficiency
28
1+ edema
Barely perceptible depression
29
2+ edema
Easily identified depression <15 sec to resolve
30
3+ edema
Depression takes between 15-30 sec to resolve
31
4+ edema
Depression lasts > 30 sec
32
Cardinal signs of venous stasis
- Firm (indurated) - Brawny edema - Hemosiderin staining - Ankle flare - Atrophie Blanche - Eczema - dermatitis - Lipodermatosclerosis 0 fat in dermis that is sclerotic - Palpable pulses - Irregular borders - Shallow - Weepy, lots of fluid - Medial malleolus - Heavily contaminated - Usually painless - not getting hypoxic pain
33
Hemosiderin staining
- Seen with chronic venous insufficiency - From a by-product of the breakdown of RBC’s forced into the interstitium by venous HTN - RBC contains hemoglobin which breaks down into Hemosiderin - Skin becomes stained a dark pigment (dark purple/brown) due to hemosiderin/iron deposition
34
Ankle flare
- Inverted champagne bottle appearance - Piano leg - From extensive lipodermatosclerosis - fat pushed into dermis that becomes fibrotic -> firmness pushes fluid into calf
35
Varicose eczema/dermatitis
- Itchy, erythematous, weeping and scale areas of skin
36
Contact dermatitis
- Local allergic reaction to preservatives, emulsifiers and/or dressing components are common - Over 50% venous ulcer pts have allergy to lanolin and some topical antimicrobials - Erythema and pruritis, increasing discomfort and perpetuating inflammatory process, ends where contact ends - Higher cotton content in clothes less offending than synthetic fibers
37
Gold standard of treatment for patients with venous insufficiency ulcers
COMPRESSION - Enhances calf muscle pump - Improved venous return - Decreases peripheral edema - Reduces venous distention - Increases tissue oxygenation - Softens lipodermatosclerosis and fibrosis - Protects limb from further trauma - Limits need for bed rest or prolonged elevation
38
Nonelastic compression
- Resist deformation and thus maintain a fixed volume compartment around leg - When calf contracts, it meets resistance of bandage and deep veins are compressed forcing blood proximally - Graduated compression** most compression applied distally and less proximally
39
Elastic compression
- Elastic bandages not appropriate for management of venous ulcers - Expands every time calf muscle moving and loses effect of calf muscle pump - Difficult to get consistent pressure
40
Contraindication to compression therapy for patients with venous insufficiency
- Arterial insufficiency with ABI <0.7 - Acute infection - Pulmonary edema - Uncontrolled or severe congestive heart failure - Active DVT - Claustrophobia
41
Compression stockings
- Graduated compression must exceed venous intralumenal pressure *Class II (30-40 mmHg) mimics compression that would be gotten from multi-layer compression* - Regular use reduces edema and ulcer recurrence - Measure for garments after edema has been reduced as much as possible - Measure after pt gets OOB or after elevating legs above heart for about 1-2 min
42
Vasopneumatic compression devices
- Decrease venous HTN - 60 min 5x/wk - 90 sec on/30 sec off - 40 - 45 mmHg - Rapid inflation better than slow - Contraindications: DVT, active CHF
43
Therapeutic exercise
- Ankle pumps when sedentary and throughout the day to increase venous return - Light aerobic exercise will improve: - Respiratory pump -> increasing venous return - Calf muscle pump - Weight loss - Control blood sugar
44
Toe brachial pressure index
Used when calcification occurs at the ankle - Medical testing method
45
Vascular duplex ultrasound scanning
- Painless exam using US to image blood movement - Allows for identification of location of impaired blood flow - Refer to vascular surgeon when ABI <0.5 - Medical testing method
46
Sclerotherapy
Foam/liquid solution injected into spider or varicose vein -> collapses veins that are incompetent - Nonsurgical medical tx for VI
47
Endovenous thermal ablation
Laser or high-frequency radio waves to heat large veins -> collapses incompetent veins - Nonsurgical medical treatment for VI
48
Surgical treatment for VI
- Ligation and stripping (through two small incisions) - Phlebectomy (microincision) for surface varicose veins - Subfascial endoscopic perforator surgery - clips placed to block incompetent perforation veins - Vein bypass - one vein to another one

Integumentary (14 decks)

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