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ACOLS > Chronic Venous Insufficiency and Lipedema > Flashcards

Chronic Venous Insufficiency and Lipedema Flashcards

1
Q

An advanced stage of venous disease in which the veins and muscle pump are incompetent, causing blood to pool in the feet and legs. Characterized by an increase in venous pressure during walking.

A

Chronic Venous Insufficiency - CVI

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2
Q

What causes Chronic Venous Insufficiency - CVI

A
  • repeated irritation to deep veins (DVTs)
  • varicosities
  • insufficient venous return
  • damage to venous valves (pathology, congenital)
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3
Q

How does Chronic Venous Insufficiency effect the Lymphatic System?

A
  • With a reduction in venous return there is an increase in blood capillary pressure and thus an increase in net-filtrate.
  • Lymphatic system will respond with Safety Factor (increase in frequency and amplitude of its lymph collectors)
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4
Q

What is the most common cause of CVI?

A

Post-Thrombotic Syndrome (PTS) - thrombus must be present (coagulation of blood in living tissue)

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5
Q

What are the signs on Post-Thrombotic Syndrome?

A
  • edema
  • pigmentation
  • superficial varicosis
  • ulceration
  • pain after ambulation
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6
Q

When do thrombus tend to form in PTS?

A
  • pregnancy
  • inactivity
  • hyper-coagulative states
  • post surgical
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7
Q

Characteristics of thrombus in PTS.

A
  • form behind valves as blood tends to swirl there
  • form when blood cells and fibrin stands clump together (platelets adhere to the wall)
  • clots form when the intima of the vein is rough
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8
Q

What is the term for when the body is able to overcome clots?

A

Re-canalization: blood can flow through small channels within the thrombus
- valves do not work
- collateral circulation

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9
Q

What are the acute symptoms of DVT?

A
  • heavy legs
  • pain with weight bearing
  • pain with coughing/sneezing
  • warm leg
  • swelling may not be obvious
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10
Q

Consideration of MLD with presence of DVT.

A

Contraindicated!

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11
Q

Consideration of MLD/CDT with presence of Thrombophlebitis.

A

Local Contraindication

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12
Q

The term for and cause of coagulation of blood and inflammation of the superficial veins.

A

Thrombophlebitis
- injury to vein (IV or Infusion) or irritation of varicosity

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13
Q

Symptoms of Thrombophlebitis.

A
  • redness
  • warmth
  • swelling in the area
  • palpable “cord”
  • fever
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14
Q

Treatment for Thrombophlebitis.

A
  • usually body will reabsorb within 1-2 weeks
  • not life threatening as no direct pathway to heart
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15
Q

Adequate venous return to the heart depends on what factors? (5)

A
  • effective muscle pump
  • competent valves
  • suction of the heart (diastole)
  • diaphragmatic breathing
  • pulsation of adjacent arteries
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16
Q

Why is the venous system called the capacity vessels?

A

It contains approximately 60% of the blood volume.

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17
Q

How and when does the venous blood from the superficial system reach the deep veins?

A

During the relaxation phase of the muscle pump via perforating veins (through the fascia).

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18
Q

What is the blood pressure at the venous capillaries and veins near the heart?

A

Capillaries - 0 mm/Hg
Veins near the heart - 1.5 - 4 mm/Hg

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19
Q

What is the venous pressure at the dorsum of the foot in the supine position?

A

~ 10 mm/Hg

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20
Q

Upon Orthostasis (standing) what happens to the veins and what is the venous pressure?

A

Veins dilate
Pressure is ~100 mm/Hg

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21
Q

What occurs to the circulating volume after standing for 10-15min?

A

Decreased by 15-20% due to venous pooling.

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22
Q

With ambulation the hydrostatic pressure of the veins changes to what mm/Hg and what occurs?

A

~30 mm/Hg
- if valves are functioning there is no venous pooling as the joint and muscle pump actions aid the venous return to the heart.
- in the presence of CVI ambulatory venous pressure increases

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23
Q

What is the term to refer to venous blood being forced distally into the superficial venous system via perforating veins in the presence of CVI?

A

Blow-out Syndrome or Ambulatory Venous Hypertension

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24
Q

How does CVI affect the Lymphatic System?

A

As abmulatory venous hypertension occurs there is an increase in capillary pressure resulting in an increase in net-filtration. The lymphatic system will use the safety factor to drain the addition amount of water (and protein).

25
Q

What is dynamic insufficiency of the lymphatic system?

A

With no treatment for CVI (compression, elevation) eventually the safety factor fails to compensate for the increased fluid and subsequent edema occurs.

26
Q

What is Lymphatic Mechanical Insufficiency?

A

CVI left untreated over time will cause damage to the lymphatic system and a reduction in the total capacity.

27
Q

Name the term and describe what occurs to the lymph anions during mechanical insufficiency.

A

Mural Insufficiency of the Lymphatic System:
High intra-lymphatic pressure causes proteins to seep into the lymph angion walls, which then become fibrotic. Causing further reduction of transport capacity.

28
Q

What is the term for insufficiency that includes both a reduced transport capacity and an increase in lymphatic loads?

A

Combined Insufficiency

29
Q

Name the 4 stages of Chronic Venous Insufficiency.

A

Stage 0 - Sub-clinical CVI Ambulatory
Stage 1 - Phlebo-lymphodynamic Insufficiency
Stage 2 - Phlebo-lymphostatic Insufficiency
Stage 3 - CVI Stage II with ulcerations

30
Q

Of the 7 million Americans who have CVI how many will develop an ulcer and what type?

A

Venous Ulcer - 14% (70-90%) of all ulcers
Combined Venous/Arterial Ulcer ~10-15%
Re-occurrence Rate of 13-18%

31
Q

At what stage of CVI is there venous pooling with ambulation as blood is pushed distally against valves but no swelling as the lymphatic system compensates.

A

Stage 0

32
Q

How does the lymph system respond to an increase in lymphatic load of water in Stage 0 of CVI?

A

Safety Factory
- Increases lymph formation
- Elevated contraction frequency in lymph collectors and trunks (lymphangiomotoricity)

33
Q

Treatment considerations for CVI Stage 0 and Stage I.

A

May see varicosities/edema at the end of the day for which light compression and elevation will help.
NO CDT as MLD can not increase transport capacity (lymphatic system is still healthy).

34
Q

What are the signs of CVI Stage I

A
  • Swelling at the end of the day, may be bi-lateral
  • edema recedes overnight
  • some mild pitting
  • Stemmer sign is negative
35
Q

What CVI stage struggles to manage the lymphatic water load and edema occurs during the course of the day (receding at night)?

A

Stage I or Phlebo-Lympho-Dynamic Insufficiency

36
Q

What are the signs of CVI Stage II? (6)

A
  • Stemmer sign positive
  • pitting present at early stage
  • swelling is asymmetrical
  • early in this stage, skin is soft
  • fibrotic tissue will eventually develop
  • swelling does not recede with elevation
37
Q

At what CVI Stage are the lymphatic vessels under constant hypertension, lymph seeps into walls of lymph collectors (fibrosis), there is both mural and valvular Insufficiency.

A

Stage II or Phlebo-Lympho-Static Insufficiency

38
Q

What type of insufficiency is CVI Stage II and why?

A

Combined Insufficiency due to damage and inflammatory response to the blood capillaries and lymph collectors (mechanical) as well as the elevated loads of water/protein (dynamic).

39
Q

What happens when the high pressure in the blood capillaries causes the space between the endothelial cells to widen?

A

plasma and blood cells escape into the interstitial tissues.

40
Q

What occurs when Erythrocytes escape into the skin due to high pressure in capillaries?

A

Hemosiderin Staining - Rusty Leg Syndrome
Small hemorrhages particularly in the ankle regions
Initially appear as red spots but as the iron deposits (in the erythrocytes) combine with oxygen will turn tissues brown.

41
Q

Treatment consideration for CVI Stage II.

A

Candidates for Complete Decongestant Therapy due to the accumulation of water and protein in the soft tissue. The lymphatic system is damaged (mechanical insufficiency).

42
Q

Explain the process that causes skin ulcerations in CVI Stage III.

A

Increased diffusion distance (swelling) and the interstitial fibrin cuff that forms as a result of plasma protein leakage. These both decrease the amount of oxygen and nutrients delivered to the tissues and lead to hypoxia and skin ulcerations.

43
Q

Characteristics of Venous Ulcers. (5)

A
  • Hemosiderin Staining
  • Medial aspect
  • distal 1/3 of lower leg,
  • usually heavy exudate
  • often large wound bed with irregular margins
44
Q

Characteristics of Artirieal Ulcers. (8)

A
  • elevation causes pain
  • located on toes, dorsum of foot
  • lateral malleolus
  • “punched out” lesion
  • pale, shiny skin
  • decreased (or absent) pulses
  • hair loss in the area
45
Q

How is the Ankle Brachial Index (ABI) derived and what does it indicate?

A

1) Take blood pressure in arms x2
2) Use the higher of the 2 systolic measures
3) Take blood pressure in both ankles x2
4) Use the higher of the 2 systolic measures
5) Divide each ankle by the highest brachial pressure
Indicates the degree of Peripheral Arterial Disease

46
Q

At what ABI measurement is it safe to compress?

A

Look for at least 0.7 - 0.8 to compress.

47
Q

What is a sign that an ulcer is of mixed etiology (venous/arterial).

A

Necrotic tissue in the wound bed.

48
Q

Why is complete decongestive therapy important in treatment of CVI Stage III.

A

CDT is required due to the presence of lymphedema. CDT will also greatly increase the tendency of venous stasis ulcers to heal.

49
Q

What disease is marked by bi-lateral and symmetrical swelling of the lower extremities caused by extensive deposits of subcutaneous fatty tissue?

A

Lipedema

50
Q

Where is lipedema most often found?

A

Between the iliac crest and ankles, feet are uninvolved though flaps of fatty tissue may overhand the ankles.
Occasionally present in the arms where the swelling will extend to the wrist area and a massive fold of fatty tissue is visible on the posterior upper arm.

51
Q

Characteristics of Lipedema.

A
  • most common in women
  • if in males most often associated with liver dysfunction
  • can be hereditary/hormonal disorders
  • “slim” from the waist up
  • no pitting and negative Stemmer sign
  • dorsum of the foot not involved
  • texture of skin is “orange peel”, rubbery, hard nodules
  • bruises easily (compromised blood capillaries)
  • varacosities
  • skin folds not generally deepened
52
Q

What is the term for painful lipedema?

A

Painful Lipodystrophy (Lipodystrophia dolorosa)

53
Q

What happens to the lymph system in Lipedema?

A
  • Proliferation of the fatty tissue compresses the lymph collectors of the superficial system
  • collectors become coiled “corkscrew-like”
  • resulting in a decreased transport capacity.
54
Q

What is the cause of edema in Lipedema?

A

Dynamic Insufficiency:
Diminished tissue resistance in fatty tissue causes ambulatory hypertension. This results in more water leaving capillaries increasing lymphatic load. This along with the increased fragility and permeability towards protein in the blood capillaries of the fatty tissue causes edema.

55
Q

Treatment options for Lipedema patients.

A

NOT CDT - solely compression is beneficial to manage the edema as long as no mechanical Insufficiency is present.

56
Q

What is the term for Lipedema if it progresses to include morphologic (seepage of protein into the walls of collectors) and functional damage to the lymph collectors?

A

Lipo-Lymphedema

57
Q

What are the characteristics of Lipo-Lymphedema?

A
  • total capacity drops below the normal lymphatic load
  • swelling is most often asymmetrical
  • Positive Stemmer sign
  • dorsum of foot involved
  • painful to pressure (not in pure lymphedema)
  • skin/tissue is more firm
  • natural skin folds are deepened
58
Q

Treatment consideration for Lipo-Lymphedema.

A
  • Complete Decongestive Therapy
  • Purpose is to remove lymphedema component
  • Lipedema (fatty tissue) component can not be reduced.
59
Q

What is the term if a venous disorder is present along with lymphedema and lipedema?

A

Phlebo-Lipo-Lymphedema

ACOLS (7 decks)

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