Sections 3 & 4

Explain normal venous return

LE blood flow: Flow from the arteries, down through capillaries and back up through the veins. The superficial veins drain through perforators into the deep venous system. The venous blood must return against gravity

What are the three types of veins?

Superficial, perforated, and deep

What does effective return of blood flow from the venous system need?

Effective return depends on patent veins, competent valves, and muscle pumps

What is a major muscle pump of the LE?

The calf especially during walking

What is venous insufficiency?

Valve incompetence and/or venous obstruction allows reflux and pooling in the LE

How can venous insufficiency happen?

If the valves fail, obesity, pregnancy, valsalva maneuver all affect the pressures within the venous system and create a return problem

What does persistent venous HTN promote?

Edema, inflammatory changes, skin discoloration, tissue fibrosis and eventual ulceration

What are some factors of the LE that can increase venous pressure?

Failure of the calf pump, limited ankle motion, immobility or obstruction can increase venous pressure

Which veins are located between the epidermis and the fascia?

Perforating Veins

What is the stasis theory of venous ulcer development?

(Homans 1917): In his theory he coined the term post-phlebitis syndrome which is from the overstretching of veins and damage to valves led to a pooling of blood. Stagnant pond concept implies poor oxygenation

What is the hyperoxygenation theory of venous ulcer developement?

Blalock (1920): demonstrated that oxygen content in persons with chronic venous insufficiency (CVI) was actually higher than normal (stagnant pond concept started to lose favor). This lead to thoughts that arteriovenous shunting was occurring

What is the AV Fistula/Shunting theory of venous ulcer development?

(Puilacks and Barraquer 1953): shunting of arterial blood, implies poor oxygenation but this is not what we were finding

What is the fibrin cuff theory of venous ulcer development

(Browse and Burnand 1982): increase in venous pressure led to fibrinogen leaking from vessels. A layer of fibrin was laid down which was though to prevent the passage of oxygen and waste products, but later seen that the fibrin layer was macro molecular layer and that oxygen and waste products could pass

• Elevated venous pressure causes leakage of fibrinogen and other macromolecules into the interstitium.

• Fibrin deposits around capillaries were proposed to form a 'cuff' that interferes with oxygen/nutrient diffusion.

What is the leukocyte trapping theory of venous ulcer developement?

(Coleridge Smith 1988): WBC adhesion and activation led to destruction of venous capillaries and tissue hypoxia, which is tied somewhat with the fibrin cuff theory

• Venous hypertension slows microcirculatory flow and promotes leukocyte trapping/adhesion.

• Activated leukocytes release inflammatory mediators and proteolytic substances that can injure endothelium and surrounding tissue.

What is the ischemia/reperfusion theory of venous ulcer development?

(Greenwood 1995): Edema leads to ischemia in tissue, and as edema resolves tissue reperfusion occurs with free radicals that cause tissue damage

What is the accepted central mechanism of venous ulcer development?

Ambulatory venous hypertension

What is ambulatory venous hypertension?

• In a normal limb, walking and calf-muscle contraction lower distal venous pressure by propelling blood proximally.

• With incompetent valves, obstruction, or an ineffective calf pump, venous pressure fails to fall appropriately during ambulation.

What is the management for ambulatory venous hypertension?

• External compression/ compression and ambulation/calf-pump activity are central because they counteract venous hypertension and promote return.

Who was responsible for the theory of the fibrin cuff as the cause of venous ulceration?

a.) Homan

b.) Browse and Bernard

c.) Puilacks and Barraquer

d.) Blalock

b.) Browse and Bernard

What is the normal presentation of a venous ulcer?

The ulcer is fairly superficial, large but not deep in appearance, a deep granular base to them, heavy to moderate exudate coming out can be quite heavy, can have pain or discomfort (low level pain might complain of discomfort or achy feeling), these tend to be recurrent, fibrinous in nature (form a layer across the wound that we may need to debride), typical location is just distal to proximal medial malleolus. Can also see periwound changes such as lipdodermatosclerosis, hemosiderosis

What is a champagne bottle leg?

small ankle and very swollen calf

What does chronic edema and inflammation contribute to?

• Chronic edema and inflammation contribute to hemosiderin deposition, skin changes, fibrosis/ lipodermatosclerosis, and ulceration.

What are the risk factors for developing chronic venous insufficiency?

1. Family history (maternal)

2. Hx of CHF, DVT, recent edema, DM

3. Obesity/Pregnancy

4. Severe trauma to LE

5. Excessive vigorous exercise (intra-abd/leg pressure)

6. Multiple pregnancies

How does severe trauma to the LE cause chronic venous insufficiency?

Anytime you damage the system enough to cause bleeding then you have damaged the lymphatic and venous systems. The venous system relies heavily on the lymphatic system to remove the tissue fluid from the area

What is Lenton's Perforator?

Lenton's Perforator: damage to perforator down at the ankle level that we see many ulcers developing around that area

What is the most accepted theory of venous ulcer pathogenesis?

a.) Ischemia-Reperfusion Injury

b.) Leukocyte trapping

c.) Fibrin Cuff

d.) Ambulatory Hypertension

d.) Ambulatory Hypertension

What are the clinical classifications of venous disease?

• C0: no visible or palpable signs of venous disease.

• C1: telangiectasias or reticular veins.

• C2: varicose veins.

• C3: edema.

• C4: skin/subcutaneous changes associated with chronic venous disease; includes pigmentation/eczema and more advanced fibrotic changes.

• C5: healed venous ulcer.

• C6: active venous ulcer.

What are the different types of etiology classifications?

Classification: Congenital (Ec)

Primary (Ep)

Secondary (post thrombic) - (Es)

No venous cause identified (En)

What are the different types of anatomy classifications?

As- superficial veins

Ap- perforator veins

Ad- deep veins

An- no venous location identified

What are the different types of pathophysiology classifications?

Pr: Reflux

Po: Obstruction

Pr,o: reflux and obstruction

Pn: no venous pathophysiology identified

What is pathophysiology reflux?

when you empty the vein, the flow should move through superficial to deep and back up the heart, after the pump has pushed the blood up does it come back

How do you test for pathophysiology obstruction?

doppler test (rapid swooshing noise should happen when squeezing the leg)

What is Lipodermatosclerosis?

Lipodermatosclerosis: the skin becomes very hard and leathery in appearance, particular around the periwound

What does it mean if a patient has a CEAP clinical classification of C6s?

An active, symptomatic ulcer is present

The discoloration seen in the periwound tissue in venous disease is due to what?

hemosiderosis

What is hemosiderin?

Hemosiderin is the agent that is deposited in the tissue that stains the tissue and it is a byproduct of the heme on hemoglobin. AS you know RBC are turned over our body, but if they get into the tissues and lice out in this area they will break off the hemoglobin and release the pigment hemosiderin and that goes in and stains the tissue. This is permanent staining

What is the trendelenburg test?

• Position patient supine and elevate the limb to assist emptying of superficial venous blood (stroke the lower extremity).

• Apply a proximal-thigh tourniquet tight enough to obstruct superficial venous return without occluding deep venous flow.

• Have the patient stand and immediately inspect the saphenous/superficial venous system for filling/distention by release the tourniquet quickly and observe whether additional venous filling occurs.

How do you interpret the trendelenburg test?

• Filling while the tourniquet is still applied suggests incompetence of the deep/perforator system because superficial flow is blocked.

• No initial filling followed by filling after tourniquet release suggests superficial venous incompetence.

• Initial filling with the tourniquet on plus additional filling after release suggests combined superficial, deep, and perforator involvement.

How will the patient complain of pain if they are suffering from a venous ulcer?

The patient will most likely complain of pain while in a dependent position and will report feeling better if their leg is propped up on something

How should you describe the characteristics of an ulcer?

Location, shape, depth, color, fibrin, exudate, periwound, pain

What is Air Plethysmography?

Take a blood pressure cuff that's very lightly inflated (just enough to secure it to the leg and you have the person supine, and have them stand up and see if there is any reflux because this cuff measures any expansion that occurs as the fluid comes back down the leg

If the wound is not steadily healing by this tme frame what should you do?

By 4 weeks and the wound looks the same or has gotten worse then something else is wrong. This is an indication for the patient to be referred and get a biopsy done, venous ulcers can change to carcinoma without you knowing anything differently

Which of the following sets of characteristics would be most associated with a venous ulcer?

a.) Mild exudation, deep wound, moderate pain

b.) Moderate to heavy exudation, shallow wound, mild pain

c.) No exudation, shallow wound, moderate pain

d.) Heavy exudation, deep wound, severe pain

b.) Moderate to heavy exudation, shallow wound, mild pain

What is the prevalence of peripheral artery disease?

Prevalence at 2.6% → 10 million diagnosed

Note: Many are asymptomatic until the disease is advanced

What are some causes of arterial ulceration?

Embolic Clots

Arteriosclerosis

Sickle Cell Disease

Necrotizing vasculitis

Hypertensive Ulcer

How is sickle cell disease a cause of an arterial ulcer?

red cell takes on discoid appearance, and usually trap on venous side of capillary these develop ulcers that have venous characteristics but are extremely painful

How is necrotizing vasculitis a cause of an arterial ulcer?

vessel wall necrosis due to neutrophil infiltration. Thought to be a result of chemotactic factors in the complement cascade

What is a hypertensive ulcer also known as?

Martorell ulcer

What is a hypertensive ulcer?

A cause for an arterial ulcer and is very painful and develops in association with poorly controlled HTN, women more than men and usually 50-60 year olds

What is Thromboangitis Obliterans/ Buerger's Disease?

2nd most common arterial occlusive disease, young male smokers, distal necrosis in upper and lower extremities, major inflammatory component (WBC occlusion of smaller vessels)

What type of ulcer generally presents in the lower extremity, exhibits pain out of proportion to ulcer size and is associated with uncontrolled HTN?

Martorell's

What is a typical arterial ulcer presentation?

Punched out appearance, clearly defined margins, often deep, pale, dry, generally painful. Usually located over the toes, dorsal foot, lateral malleolus. Usually these patients are wanting to be in a dependent position

What are some limb characteristics of arterial ulcers?

Slow hair growth, faint or absent pulses, pale skin, thin limb without edema, rubor of dependency, cool skin with temp gradient distally (gets cooler as you move distally)

What is the pulse grading system?

0 is absent

1+ Weak or diminished

2+ is normal pulse

3+ is increased force

4+ is bounding

Thready: Weak force with rapid rate (difficult to count)

What is triphasic pulse?

The compression force of systole going into diastole and then the recoil of the vessel - generally associated with a healthier peripheral arterial sign than monophasic flow

What are the pulse sites?

• Femoral pulse: groin region.

• Popliteal pulse Posterior tibial pulse

• Dorsalis pedis pulse

How should you check for a femoral pulse?

Groin region

How should you check for a popliteal pulse?

posterior knee; often more difficult to palpate because of the HS but need to place these on slack by bending the knee.

How should you check for a posterior tibial pulse?

posterior/inferior to the medial malleolus, push up against the malleolus and should get a good pulse.

How should you check for a dorsalis pedis pulse?

Find the extensor tendon for your great toe, come over laterally on dorsum of the foot (between the 2nd and the 3rd digits

How do you perform a capillary refill test?

Always examine the limb before doing the test (the limb should be a pinkish color because it is a mixture of arterial and venous blood. Apply enough pressure to blanch the nail bed or distal tissue, then release and observe return of color.

What is a normal vs abnormal finding in the capillary refill test?

Normal Finding: Capillary reperfusion should happen in <3 sec,

If >15 seconds then indicates problem with arterial supply to that extremity

What is the Rubor of Dependency test?

• Elevate the limb and assist with venous return. The limb is going to be elevated for 30-60 seconds and observe for pallor as arterial inflow becomes inadequate against gravity.

• Return the leg to dependency and observe the time and character of color return.

What would a true pathological case look like when performing the rubor od dependency test?

In a person with a true pathological case the filling will take longer than 15 seconds and the bottom of the foot and the dorsum will turn a bright red, but will be delayed

What is the venous filling test?

Elevate the limb and assist venous return in the elevated position, you then are going to stand the patient up and quickly see if the veins refill.

What are the normal values?

If they fill spontaneously then that's testing venous problem not the arterial system. Normal filling time will be between 5-10 seconds. If delayed fill that takes greater than 15 seconds that is an abnormal test that shows compromised arterial flow

What is ABI?

Ankle brachial index compares systolic pressure at the ankle with systolic pressure at the arm to estimate lower-extremity arterial perfusion.

How do you perform an ABI?

• Patient should rest supine before testing.

• Obtain brachial systolic pressures with Doppler.

• Obtain ankle systolic pressures at dorsalis pedis and posterior tibial arteries.

• For each leg, use the higher ankle pressure divided by the higher brachial pressure.

What is the interpretation of ABI?

Interpretation

>1.4: Non-compressible arteries

1.0-1.4: Normal

0.91-0.99: Borderline

0.41-0.90: Mild-moderate PAD

How do you perform the intermittent claudation onset time?

Have patient walk at a steady pace (1 mph) on a level surface until the pain makes them stop. Important to record the time and the distance, which will be helpful in rehab and pushing/ stressing of the arterial system is what helps to build back some collateral circulation. This is testing ambulatory ischemic pain of the calf

What are the grades of the claudication onset time?

Grade 1- pain, discomfort, cramping or weakness with minimal exercise

Grade 2- moderate pain, discomfort, cramping or weakness with exercise

Grade 3- severe or intense pain, discomfort, cramping or weakness with exercise

Grade 4- excruciating or unbearable pain, discomfort, cramping or weakness with exercise

What is the Rutherford Classification for PAD?

0= Asymptomatic

1= Mild Claudication

2= Moderate Claudication (usually comes on at about 200 meters)

3= Severe Claudication

4= Rest Pain

5= Ischemia with ulcers on the digits

6= Severe ulcerations with gangrene

What is a Rooke Boot?

Lambs wool boot that is worn when a patient is dealing with arterial insufficiency - helps to create vasodilation

What is the goal of wound bed preparation?

Wound-bed preparation goal: remove or reduce bacteria, debris, and dead tissue while creating an environment that supports healing.

What is the difference between cleansing and disinfection?

Cleansing- helps optimize the healing environment and decrease wound bioburden. It loosens and washes away the debris

Disinfection: the irradiation or destruction of bacterial contamination - toxic to living tissue

What is bioburden?

Bioburden: the bacterial/contaminant burden in the wound that can interfere with healing. The lecture emphasizes reducing bioburden without unnecessarily damaging viable cells.

What are selection factors for a topical agent that we need to consider?

patient pain tolerance, method/pressure of delivery, amount of viable vs necrotic tissue, amount/nature of bioburden, and whether true infection is present.

What are examples of cytotoxic agents?

hydrogen peroxide, sodium hypochlorite/Dakin solution, povidone-iodine (Betadine), alcohol, and acetic acid.

What are examples of non-cytotoxic or more wound friendly agents?

normal saline, sterile water, surfactant cleansers (Saf-Clens), and hypochlorous-acid products like VASHE.

What is sodium hypochlorite and how does it help wounds?

A Dakin solution that is bactericidal; Technically household bleach but we want 0.005% solution is bactericidal but not cytotoxic; antimicrobial through chlorine release and can liquefy necrotic tissue, but stronger concentrations can damage viable tissue and may be used only when majority of wound is nonviable.

What is povidone-iodine/Betadine and how does it help wounds?

a bactericidal and active against organisms such as Staphylococcus aureus, but cytotoxic at commonly used concentrations and contraindicated over healthy granulation tissue. Betadine surgical scrub is for external skin preparation, not packing into a wound cavity.

What is the toxicity of betadine?

Toxicity of betadine: at 1% solution it is 100% toxic, 0.05% is 50 %, and at 0.001% is non-toxic

What is rubbing alcohol and how does it help wounds?

no routine role inside wounds (SHOULD NEVER BE USED ON WOUNDS); irritating and drying, with particular concern in patients who already have dry skin (ex: patients with DM). Should only be used for cleansing prior to the use of needles

What is acetic acid and how does it help wounds?

A bacteriostatic; Used at 0.25-0.5% solution and is nontoxic at a 0.003%; This is toxic to cultured human fibroblasts; Discussed as useful against Pseudomonas aeruginosa, but cytotoxic at commonly used concentrations; the lecture advises sparing/short-term use and avoiding it on clean granulating wounds or highly sensitive skin.

What is the difference between Bactericidal vs Bacteriostatic agents?

Bactericidal means kills while the bacteriostatic agent means stop replication of bacteria

Why do most people use hydrogen peroxide on a wound?

The bubbling effect of the solution makes it seem like it is beneficial but it is killing both the dead and healthy tissue/cells. This is VERY cytotoxic to healing tissue

What 2 non-cytotoxic cleansers are effective for most wounds and generally not contrindicated?

Water and Saline

Why use warm saline?

Warm saline is preferred because bringing the solution closer to body temperature reduces the cold stimulus /vasoconstriction that can occur when a wound is irrigated with cold fluid

What is the disadvantage of using water/saline?

Saline/water are gentle but do not work well against strongly adhered biofilm by themselves because they are a dense network on wounds

What are surfactants?

Surfactants are emulsifiers that help loosen and wash away debris; they can assist in freeing adhered biofilm for subsequent debridement. Surfactant cleansers are generally non-irritating and only slightly more cytotoxic than saline when low-toxicity products are selected.

What is hypochlorous acid?

Example: VASHE

described as non-cytotoxic, non-irritating, and useful as an irrigant/debriding and antimicrobial agent, including activity against resistant organisms such as VRE and MRSA.

What is the principle when selecting products?

do not choose a cleanser simply because it is on the formulary or heavily marketed; ask about toxicity data and choose the least cytotoxic product that can accomplish the clinical goal.

What is the goal of wound cleaning?

the goal is not to sterilize the wound; it is to reduce bioburden while preserving the viable cells needed for healing.

Rank these items from the least cytotoxic to the greatest

Restore

Biolex

Acedic Acid

Saline

Shur-Clens

Providone iodine

Puriclens

SAF-Clens

Cara-Klenz

0 - Saline, Shur-Cens, and Saline

10- Acedic Acid, Biolex, Cara-Klenz, Puriclens

100- Restore

1000- Povidone iodine

What is non-slective debridement?

mechanical removal of devitalized tissue without reliably isolating viable from nonviable tissue.

What are mechanical debridement advantages?

relatively inexpensive and requires less technical skill

What are mechanical debridement disadvantages?

non-selective, may traumatize viable tissue, can be painful, and historically may involve cytotoxic agents.

What are examples of mechanical debridement?

wet-to-dry dressings, hydrotherapy/whirlpool, forceful irrigation, and pulsatile lavage.

What are wet to dry dressings?

Highly non-selective, promote tissue desiccation (dries out the tissues), and can be very painful when adherent gauze is removed. Pain can be minimized with TENS but better to not use at all due to pain

What are disadvantages of wet to dry dressings?

Gauze can adhere to viable tissue and produce bleeding/ trauma during removal; loose fibers from the gauze may remain in the wound as foreign bodies and contribute to inflammatory response/granuloma formation. Packing a wound tightly with bulky gauze may physically stent the wound open and interfere with contraction.