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#2 Derm > 14 - Common Ulcerations > Flashcards

14 - Common Ulcerations Flashcards

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Dermatology Board Prep flashcards
1
Q

Define ulceration

A
  • A lesion of the skin or mucous surface caused by superficial loss of tissue
  • Usually associated with necrosis and inflammation
  • There will be a wound where the epidermis and part of the dermis is absent
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2
Q

4 classification systems of wounds/ulcers

A
  • Wagner’s (diabetic)
  • University of Texas (wound)
  • Knighton
  • NPUAP (pressure ulcer)
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3
Q

Grading scale for Wagner’s diabetic ulcer classification system

A
  • Grade 0 = intact skin (signs of inflammation, irritation, pre-ulcerative)
  • Grade I = superficial (no sub Q involvement)
  • Grade II = extends to tendon, capsule, bone (tracks)
  • Grade III = associated with abscess, osteomyelitis, sepsis (clinical or radiographic signs of infection)
  • Grade IV = gangrene of the forefoot
  • Grade V = gangrene of the entire foot
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4
Q

Two components of a designation in the University of Texas wound classification system

A
  • Grade (indicates depth)

- Stage (indicates comorbidities)

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5
Q

Grade of ulcer for Texas system

A
  • Grade 0 = intact skin (pre- or post-ulcerative site)
  • Grade I = ulcers are superficial (wound through epidermis/dermis)
  • Grade II = through tendon or joint capsule
  • Grade III - through bone or into joint
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6
Q

Stage of ulcer for Texas system

A
  • Stage A = clean
  • Stage B = infection
  • Stage C = ischemia
  • Stage D = ischemia and infection
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7
Q

Knighton classification of ulcers

A
  • Grade I = partial thickness (through epidermis)
  • Grade II = full thickness (through dermis into sub Q)
  • Grade III = full thickness (to tendon, ligament, bone, joint)
  • Grade IV = full thickness (associated abscess or osteo)
  • Grade V = full thickness (necrosis)
  • Grade VI = full thickness (ulcer with gangrene)
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8
Q

NPUAP (National Pressure Ulcer Advisory Panel) staging system

A
  • Stage I = intact skin with non-blanchable redness of a localized area usually over a bony prominence. Darlky pigmented skin may not have visible blanching, its color may differ from the surrounding area.
  • Stage II = partial thickness loss of dermis presenting as a shallow open ulcer with a red pink wound bed, without slough. May also present as an intact or open/ruptured serum-filled blister.
  • Stage III = full thickness tissue loss. Subcutaneous fat may be visible but bone, tendon or muscle are not exposed. Slough may be present, but does not obscure the depth of tissue loss. May include undermining and tunneling.
  • Stage IV: full thickness tissue loss with exposed bone, tendon or muscle. Slough or eschar may be present on some parts of the wound bed. Often include undermining and tunneling.
  • Unstageable = full thickness tissue loss in which the base of teh ulcer is covered by slough (yellow, tan, gray, green or brown) and/or eschar (tan, brown or black) is present in the wound bed.
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9
Q

Common ulcerative foot disorders

A
  • Neuropathic
  • Venous (including lymphatic)
  • Arterial
  • Pressure (decubitus)
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10
Q

Neuropathic ulcerations and associated disease states

A
  • Diabetes
  • Peripheral nerve injury
  • Alcoholism
  • Anemia
  • Tabes dorsalis
  • Chemotherapy/radiation treatment
  • Spina bifida
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11
Q

Diabetic ulceration

A
  • Risk of amputation is 15-fold higher in diabetics

- Chronic foot ulcer is the leading cause of amputation in diabetic patients

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12
Q

TRIAD OF DIABETIC ULCERATION

A

Triad

  • Neuropathy
  • Ischemia
  • Infection

You will DEFINITELY see these 3 components in a diabetic ulcer

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13
Q

Etiology of a diabetic ulcer

skipped

A
  • Insulin is not required for glucose uptake in neurons
  • Therefore there tends to be an increased concentration of glucose in the neurons of diabetics
  • This prevents myoinositol by competitive inhibition
  • Low myoinositol concentration in neurons results in abnormal cell responses to receptor stimulation
  • Impaired Na/K ATPase activity and nerve dysfunction
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14
Q

Pathophysiology of a diabetic ulcer

barely talked about

A
  • Glycation products (AGEs) cause matrix overproduction, focal thrombosis and vasoconstriction
  • One study showed that there was 50% more large vessel disease in diabetic women and 25% more in diabetic med
  • Autonomic nueropathy also causes arteriovenous shunting and dry skin
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15
Q

Repetitive injuries in diabetics

barely talked about

A

Diabetics are at risk for developing repetitive injuries that do not heal well due to:

  • Ischemia
  • Painless
  • Low resistance to pathogenic organisms (includes poor inflammatory response, chemotaxis, bacterial-killing ability and amplified tissue necrosis)
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16
Q

Describe the characteristics of a neuropathic ulceration

A
  • Absence of pain
  • Ischemia (macrovascular and/or microvascular) which may or may not be present in the ulcer bed
  • If there is ischemia of the ulcer bed, it will alter its appearance
  • Usually located in a weight bearing or high pressure area
  • Usually well circumscribed
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17
Q

If you see granulation tissue in a neuropathic ulceration, what does that tell you?

A
  • If you see granulation tissue, it tells you that this part of the body is getting appropriate nutrition and oxygenation as part of the inflammatory process
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18
Q

What is “slough” found in a wound

A

A slime or film of “bio-burden”

  • Easily removable (like what you scraped away in clinic)
  • Bio-burden slows healing, so it needs to be removed
  • Removing the bio-burden decreases future infection risk because it is full of bacteria
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19
Q

Describe the etiology of neuropathic ulceration

A
  • Insensitivity and increased pressure allows for tissue breakdown
  • Repetative mechanical pressure or trauma under an area of weightbearing or bony prominences
  • Abnormal gait patterns (unstable)
  • Rocker bottom foot type
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20
Q

Clinical findings in neuropathic ulceration

A
  • Underlying bone pathology (rocker bottom, metatarsal deformity, sesamoid, hammertoe)
  • Tissue is usually warm with a zone of hypkeratotic tissue at the wound edges
  • NO PAIN
  • Depth (depends on location, length of wound, infection)
  • Base of ulceration has fibrous-granular tissue
  • If you see an ulcer in the midfoot, it is typically because they have Charcot or an arch collapse (biomechanical issue) and NOT typically due to a bony process
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21
Q

Slides 14-20

A

NEED TO KNOW THESE IMAGES

GO LOOK AT THEM

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22
Q

Treatment of neuropathic ulceration

skipped - “you already know this”

A

Multidisciplinary approach

  • Control of overall general health status (blood sugars, albumin)
  • Proper wound assessment
  • Perfusion (adequate circulation to heal - ABI, TCPO2, angiogram)
  • Debride devitalized tissue
  • Identify and control infection
  • Pressure relief
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23
Q

Venous ulceration etiology

A
  • Prolonged venous hypertension - KNOWN FACTOR*
  • Incompetent valves***
  • Superficial thrombophlebitis
  • DVT
  • Calf muscle dysfunction
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24
Q

What are two hypotheses which explain the cause of venous ulceration?

A
  • Fibrin cuff hypothesis

- White cell hypothesis

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25
Q

Fibrin cuff hypothesis

A
  • We see enlarged dermal capillaries, reduced capillary number, microvascular thrombosis, increased permeability of micro lymphatics
  • Increased capillary permeability leads to extravasation of plasma proteins like fibrinogen which forms an insoluble fibrin cuff
  • Hemosiderin is then able to deposit into the skin, causing a brown pigmentation
  • The “fibrin cuff” is a barrier to diffusion of oxygen and nutrients to overlying skin
  • If oxygen can’t get to the skin, there is cell death and therefore ulceration
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26
Q

White cell hypothesis

A
  • Adhering leukocytes degranulate and release potent enzymes and reactive oxygen species that damage he capillaries
  • This capillary damage causes increased permeability tissue damage
  • Macromolecules like albumin bind or trap growth factors and matrix materials, and are therefore unavailable for tissue maintenance or repair
  • They therefore don’t get to the areas they need to get to in order to maintain tissue in a healthy state
  • The tissue becomes unhealthy and ulceration can occur
27
Q

Manifestations of chronic venous insufficiency

A
  • Varicose veins
  • Superficial thrombophlebitis
  • Deep vein thrombosis
28
Q

Clinical presentation for venous ulceration

**KNOW THIS **

A
  • Usually present with presence of arterial flow
  • Usually have a granulating bed - “beefy red base” which looks similar to neuropathic ulcer if sufficient blood is present
  • Common location is by the medial malleolus (due to the larger vascular structures which are present here)
  • Associated with venous insufficiency (edema, hemosiderin deposition, induration)
  • Fair amount of pain is commonly associated, but not always
29
Q

Describe vericose veins

A
  • Dilated, tortuous superficial veins
  • Increased deep venous pressure (venous hypertension)
  • Increased distensibility of the venous walls
  • Development of venous lakes
  • Blue, purple, compressible papules which are actually dilated venules and capillaries
  • Superficial

LOOK AT PICTURE ON SLIDE 34 (not really what you would think)

30
Q

Thrombophlebitis

A
  • Effects greater and lesser saphenous veins
  • Presents as pain, swelling, warmth
  • Tender along involved vein
  • Often confused with cellulitis and infection
  • Chronic recurrent bouts of inflammation along vein secondary to incompetent superficial veins
31
Q

Sequence of events that occur with thrombophlebitis

A
  • Varicose veins
  • Thrombophlebitis
  • Deep venous thrombosis
  • Inoperative muscle pump
  • Development of eczematous plaque
  • Tissue hypoxia
  • Minor trauma (bump something, tight compression stockings, etc.)
  • Development of ulceration
32
Q

Clinical findings of thrombophlebitis

A
  • IRREGULAR BORDER WITH NO HYPERKERATOTIC RIM (this is the unique feature)***
  • Unilateral (medial ankle)
  • Can be bilateral if severe venous stasis, but won’t be symmetrical
  • Stasis pigmentation
  • Chronic edema
  • Fibrous-granular base (typically you can see granulation, but fibrosis occurs if it becomes chronic)
  • Variable size and depth
  • Variable amounts of pain
  • Serous drainage (leakage) from the wound or even seeping out of the skin
33
Q

Overall treatment of thrombophlebitis

A
  • Culture and biopsy the wound
  • TREAT UNDERLYING INFECTION with appropriate antibiotic therapy
  • Do a thorough exam and CHECK CIRCULATION to make sure you have adequate oxygenation
  • Elevate the extremity (this is KEY if you have incompetent valves)
34
Q

Treatment of the wound in thrombophlebitis

A
  • Regular debridement of the wound
  • Control on inflammation
  • COMPRESSION
35
Q

Describe regular debridement of the wound in thrombophlebitis

A
  • Can be very painful, so use topical lidocaine or a field block
  • This will decrease bacterial load on the surface of the ulcer
  • This also removes necrotic and fibrous tissues and stimulates bleeding (i.e. growth factors)
36
Q

Describe control of inflammation of the wound in thrombophlebitis

A
  • Cool, wet compression
  • Use Baron’s solution (aluminum subacetate dissolved in water)
  • Topicals: silvadene, iodosorb, calcium aginate dresings
37
Q

Describe compression therapy of the wound in thrombophlebitis

A
  • Compression therapy is KEY*
  • Key during wound care and often
  • Use unna boot (zinc oxide or calamine)
  • Need a minimum of 30 mmHg***
  • Can get an unna boot at 30 mmHg or a profore system at 40 mmHg
38
Q

Long term goals of thrombophlebitis

A
  • Patient education
  • Compression hose
  • Venous compression pumps
  • Vascular consult
39
Q

Ischemic ulceration due to arterial compromise

A
  • Signs of diminished circulation
  • Usually painful
  • Well circumscribed
  • Avascular wound bed
  • Any location on extremity (often where trauma has occurred)
40
Q

Two types of etiologies of ischemic ulceration

A
  • Occlusive peripheral arterial disease

- Diabetic microangiopathy

41
Q

Occlusive peripheral arterial disease as an etiology of ischemic ulceration

A

o Narrowing lumen, can be worsened by a sudden thrombus (ischemic pain, blue toe, showering emboli)
o Absent pedal pulses, bruits, temperature changes
o Trophic skin changes, muscle atrophy, tissue necrosis

42
Q

Diabetic microangiopahty as an etiology of ischemic ulceration

A

o Capillary basement membrane thickening
o Increased blood viscosity, Increased platelet aggregation
o Accelerated capillary endothelial cell aging

43
Q

Characteristics of ischemic ulcerations

A
  • Shallow with dark base, atrophic border, dry, xerotic, “lifeless” ulcer
  • Spontaneous ulcerations can start as a dark macule, then eschar, then further necrosis
  • Once the tissue becomes black, it is very difficult to determine the DEPTH of the wound
  • Remember wound is over necrotic tissue (base) which will be soft (contaminated and infected)
  • Make sure you are watching for signs of infection in ischemic ulcers
44
Q

How do you locally manage ischemic ulceration

A
  • Peripheral vascular consult, management of infection
  • Local wound care for light debridement: with gauze, wet to dry dressings
  • WE DO NOT USE SHARP DEBRIDEMENT
  • Surgical management (revascularization, amputation), medical management
45
Q

How do you medically manage ischemia?

A
  • Avoidance of vasoconstriction (caffeine and nicotine – AVOID THIS)
  • Exercising to tolerance
  • Dependent position of extremities – do NOT elevate
  • Pain will be much worse in elevation and it will further impede blood flow to extremity
  • Avoidance of tight socks and shoes
46
Q

Etiology of pressure ulcers

A
  • Prolonged pressure on a bony prominence – leads to shearing forces, friction, moisture
  • Deep tissue necrosis, compression of capillary circulation (blocks circulation)
  • External pressure causes venous and lymphatic obstruction then arterial occlusion
  • Tissue ischemia leads to toxic metabolites which cause pain
  • Muscle and subcutaneous tissues are more susceptible to pressure-induced injury than is the epidermis (i.e. deceptively minor skin defect with large zone of deep tissue necrosis)

PAINFUL

47
Q

Clinical presentation of pressure ulcers

A
  • Wide ulcer with peripheral undermining preceded by intense erythema
  • Depth usually extends to subcutaneous tissue, close to underlying bone
  • Trouble areas = Sacrum and Heels (from lying in bed – can use soft boots)
  • Due to repeated movement of the patient up and down in bed; friction and shearing
  • Underlying wound slow to heal
48
Q

Pressure ulcer prevention

A

VERY PREVENTABLE

  • Regular repositioning, pressure relief beds and boots, moisture barriers
  • Most preventable ulcer, should NOT occur
49
Q

Treatment of pressure ulcers

A

AVOID THEM
o Frequent rotation, movement of bedridden and wheelchair bound patients
o Lamb’s wool padding, pillows, heel protectors

If they occur…
o Local wound care (don’t be too aggressive)

50
Q

Other types of ulcers

A
  • Vasculitis ulcers
  • Radiation ulcers
  • Toxic drug ulcers
  • Sickle cell ulcers
  • Factitious ulcers
  • Hypertensive ulcers
  • Pyoderma gangrenosum
  • Inflammatory bowel disease
  • Marjolin’s
  • Trauma induced ulcers
51
Q

Vasculitis ulcer etiology

A 
Inflammatory vasculitis due to
o	Systemic lupus
o	Rheumatoid arthritis
o	Scleroderma
o	Sarcoidosis
o	Periarteritis nodosa

Elevated ESR, RF, ANA, lupus preparation, and cryoglobulinemia

52
Q

Treatment of vasculitis ulcer

A

Treat with prednisone!

53
Q

Radiation ulceration

A
  • Radiation ulcers form follow radiation therapy for cancer
  • Ulcers get larger and deeper over time
  • Treat with full-thickness excision of radiation ulcer
54
Q

What causes toxic drug ulcers?

A
  • IV chemotherapy (5-FU, doxyrubicin)

- Drugs of abuse

55
Q

Describe how IV chemotherapy causes a toxic drug ulcer

A

o If you have a chronic neuropathic ulceration of venous stasis ulceration, you can have a transition of tissue – transition to a squamous cell carcinoma (Marjolin’s ulcer)
o This is a tissue you would want to do a biopsy on, especially if it is not responding to tx
o You can then determine whether or not a squamous or basal cell carcinoma is present
o The interesting thing is that 5-FU can CAUSE this ulceration, but can also be the TREATMENT for it if it becomes squamous cell

56
Q

Treatment for toxic drug ulceration

A

Treat with debridement, grafts and HBO therapy

57
Q

Describe a sickle cell ulcer

A
  • Look VERY similar to venous stasis ulceration – develop spontaneously or after trauma
  • Hemozygous sickle cell anemia (Hbss) with leg ulcers in 8-10%
  • Sickling of red cells leads to vascular obstruction, increased venous and capillary pressures, secondary infection, local tissue hypoxia
  • Very painful ulcers, can be over medial and lateral malleoli = SIMILAR to venous stasis wound
  • Fibrosis, scarring, poor-granulation tissue, recur frequently

PAINFUL, LOOK LIKE VENOUS ULCER

58
Q

Factitious ulcer

A
  • Self-induced

- Treat the psyche and the wound

59
Q

Describe hypertensive ulcers

A

o Reddish patch, becomes cyanotic, gray bed, often symmetrical
o Anterolateral leg, jx of lower and middle 1/3 of leg
o Significant arterial HTN, good pulses, very painful
o Irregular, ragged edges, necrotic, cyanotic borders, poor granulation tissue

PAINFUL

60
Q

Etiology of hypertensive ulcers

A

Ischemia secondary to obliterating small arterioles

61
Q

Treatment of hypertensive ulcers

A

Do NOT debride these ulcers! – control their hypertension and enhance tissue perfusion

62
Q

Pyoderma gangrenosum

A
  • Associated with ulcerative colitis, starts as early pustule at a site of trauma
  • Turns rapidly to an ulcer – Purplish-blue undermined border, base has honey-comb appearance
  • Severe pain associated with them
  • EXTENSIVE DEBRIDEMENT IS DETRIMENTAL - Treat with high dose systemic steroids
63
Q

Marjolin’s ulceration

A

No specific criteria, need a biopsy

#2 Derm (13 decks)

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