ATHEROSCLEROSIS, ARTERIAL

INSUFFICIENCY, AND
ATHEROEMBOLIZATION

 Atherosclerosis obliterans (ASO), especially of the

lower extremities, is associated with spectrum of
cutaneous findings of slowly progressive ischemic
changes.
Symptoms range from intermittent claudication with
exertional muscle pain and fatigue to limb ischemia with
rest pain and tissue damage and acute ischemia.
Cutaneous findings range from dry skin, hair loss,
onychodystrophy, gangrene, and ulceration.

 Atheroembolism is the phenomenon of dislodgment of

atheromatous debris from a proximal affected artery or
aneurysm with centrifugal microembolization and
resultant acute ischemic and infarctive cutaneous
lesions.
More common with advanced age and invasive
procedures.
Manifestations are blue or discolored toes (blue toe),
livedo reticularis, and gangrene.

Atherosclerosis obliterans, early The great toe shows pallor and there
is mottled, livedoid erythema on the tip of the toe. In this 68-year-old
diabetic man, the iliac artery was occluded.

Atherosclerosis obliterans A. There is pallor of the forefoot and mottled erythema distally
with incipient gangrene on the great toe and the second digit. This is a female diabetic with
partial occlusion of the femoral artery. The patient was a smoker. B. More advanced
gangrene of the second to the fifth toe, the great toe is ebony white and will also turn black.

Atheroembolism after angiography A mottled (blue toe), violaceous,

vascular pattern on the forefoot and great toe. The findings were noted after
intravascular catheterization and angiography in an individual with ASO.

Atheroembolism with cutaneous infarction Violaceous discoloration and

cutaneous infarctions with a linear arrangement on the medial thigh of a 73year-old woman with atherosclerosis, heart failure, and diabetes.

THROMBOANGIITIS OBLITERANS
A rare inflammatory occlusive disease of medium sized
and small arteries and veins.
Predominantly in males, 2040 years of age.
Very strong association with smoking.
An angiitis clinically indistinguishable from TO
occurs in persons consuming cannabis.
Clinical manifestations
cold sensitivity;
ischemia: claudication of leg, foot, arm, or hand.
Peripheral cyanosis, ischemic ulcers, gangrene and superficial thrombophlebitis.
Therapy:
smoking cessation, analgesics, wound care; antiplatelet agents, prostacyclins,
pentoxyphylin, angioplasty, sympathectomy, amputation.
Synonym: Brger disease.

Thromboangiitis obliterans Infarctive necrosis on the great toe of

a 28-year-old man. The lesion is exquisitely painful. (The yellowishbrownish color is from iodine disinfection

THROMBOPHLEBITIS AND
DEEP VENOUS THROMBOSIS
Superficial phlebitis (SP) is an inflammatory thrombosis of a
superficial normal vein, usually due to infection or trauma from
needles and catheters.
Inflammatory thrombosis of varicose vein usually n the context of
the chronic venous insufficiency (CVI) syndrome.
Deep venous thrombosis (DV T) is due to thrombotic obstruction of
a vein with or without an inflammatory response.
Occurs due to slow blood flow, hypercoagulability, or changes in the
venous walls.
The most common causes are shown

Predisposing Factors in Deep Venous

Thrombosis
Common Factors
Major surgery
Oral contraceptives
Fractures
Malignancies
Congestive heart failure
Venous varicosities
Acute myocardial infarction
Previous history of venous thrombosis
Stroke
Leiden factor V mutation
Pregnancy and postpartum
Severe pulmonary insufficiency
Spinal cord injuries
Prolonged immobilization
Shock
Less Common Factors
Sickle cell anemia Antithrombin III deficiency
Homocystinuria Antiphospholipid antibodies
Protein C or S deficiency Ulcerative colitis

Superficial phlebitis and deep venous thrombosis A . A linear painful erythematous

cord extending from the popliteal fossa to the mid-calf in a 35-year-old man who had
moderate varicosities. Phlebitis occurred after a 15-h flight. B. The leg is swollen, pale, with
a blotchy cyanotic discoloration, and is painful. The episode occurred after abdominal
surgery (the circular marks are from a compression bandage).

CHRONIC VENOUS INSUFFICIENCY

Chronic venous insufficiency (CVI) results from failure of
centripetal return of venous blood and increased capillary
pressure.
The resultant changes include edema, stasis dermatitis,
hyperpigmentation, fibrosis of the skin and subcutaneous tissue
(lipodermatosclerosis) of the leg, and ulceration.
Venous ulcers are the most common chronic wounds in humans

Varicose veins A. There are meandering and convoluted irregular varicose veins
on the thigh of a 70-year-old man who also had lipodermatosclerosis and stasis
dermatitis on the lower legs. B. Starburst venectasias on the calf. This is an area
overlying an insufficient communicating vein.

Chronic venous insufficiency. Atrophie

blanche. An area of diffuse and mottled
pigmentation due to hemosiderin and
ivorywhite patches of atrophie blanche.
Such lesions are both itchy and painful.
Stasis dermatitis in CVI A patch of eczematous
dermatitis overlying venous varicosities on the
medial ankle in a 59-year-old woman. The lesion is
papular, scaly, and itching.

Chronic venous insufficiency and lipodermatosclerosis The ankle is relatively thin

and the upper calf edematous, creating a champagne bottle or piano leg
appearance. A. Varicose veins are embedded in pigmented, sclerotic tissue. There are
also areas of atrophie blanche. B. Varicose veins are less visible here but can be easily
palpated in the sclerotic plaque encasing the entire calf (groove sign). There is also
pigmentation and minor papular stasis dermatitis.

Venous insufficiency A. Two coalescing ulcers with a necrotic base in an area of

atrophie blanche, lipodermatosclerosis, and stasis dermatitis. Scratch marks indicate
itchiness of surrounding skin, while the ulcers are painful. B. A giant ulcer, well-defined
with scalloped borders and a beefy red base in a leg with lipodermatosclerosis.

MANAGEMENT
Prerequisite Compression dressings or stockings; Unna boot.
Atrophie Blanche
Avoid trauma to area involved.
Intralesional triamcinolone into painful lesions.
Compression.

Stasis Dermatitis
Topical gluscocorticoids (short term). Topical antibiotic treatments (e.g.,
mupirocin) when secondarily infected.
Culture for methicillin-resistant Staphylococcus aureus (MRSA).

Varicose Veins

Injection Sclerotherapy , such as tetradecyl sulfate , followed by prolonged

compression. Recurrence is common within 5 years.
Vascular Surgery Incompetent perforating veins are identified, ligated, and cut,
followed by stripping long and/or short saphenous veins out of the main trunk.
Residual perforating veins are the main cause of recurrences after surgery. In
patients with combined arterial and CVI, bypass or angioplasty may prove
beneficial.
Endovascular Techniques These new technologies encompass endoscopic
subfascial dissection of perforating veins (employed primarily in the elimination of
insufficient perforating veins in CVI); and endoscopic endovenous diode laser or
radiofrequency thermal heating, which leads to occlusion of varicose vein.

Livedoid vasculitis This is characterized by the triad of

livedo reticularis, atrophie blanche and small, painful,
crusted ulcers. This is clinically indistinguishable from
atrophie blanche seen in CVI except for the absence of
varicose veins.

Chronic lymphatic insufficiency: lymphedema Lower legs are thickened

of woody consistency and three is massive hyperkeratosis. The 60-yearold patient had had innumerable episodes of erysipelas and cellulitis.
There is also diabetes and therosclerotic arterial insufficiency.

LEG ULCERS

 Leg ulcers occur commonly in late middle and old age.

They arise in association with CVI, chronic arterial insufficiency, or
peripheral sensory neuropathy.
In some patients, a combination of these factors.
Particularly in diabetes leg ulcers are common. An estimated 2 million
persons in the United States have leg ulcers, with an estimated loss of 2
million workdays per year.
Leg ulcers are associated with significant longterm morbidity and often do
not heal unless the underlying problem(s) is (are) corrected.
Rarely squamous cell carcinoma can arise in chronic venous ulcers.

Squamous cell carcinoma in chronic venous ulcer

A venous ulcer had been present >10 years in an area of
lipodermatosclerosis and stasis dermatitis. Eventually the base of the ulcer
became elevated, hard, less painful. Deep biopsy (circular mark in the
center) revealed necrosis and at the base invasive squamous cell
carcinoma.

Chronic arterial insufficiency with a sharply defined,

punched out ulcer with irregular outlines. The
extremity was pulseless, and there was massive
ischemia on the toes.

Chronic arterial and venous insufficiency,

combined arterial and venous ulcers
Note pronounced lipodermatosclerosis and ulceration
on the supramalleolar lower leg (venous component)
and purple discoloration of forefoot and toes
with punched-out ulcer revealing tendon over
metatarsal site (arterial component).

MANAGEMENT
General Management
Factors such as anemia and malnutrition should be corrected to facilitate
healing.
Control hypertension, weight reduction in the obese, exercise
Mobilize patient
Correct edema caused by cardial, renal, or hepatic dysfunction.
Treatment of underlying disease. Arterial ulcers do not heal unless arterial
blood flow is corrected by endarterectomy to remove localized
atheromatous plaques or bypass of occluded areas

Local Treatment of Ulcer and Surrounding

Wet dressings in the acute exudative phase
Moderate to potent glucocorticoid ointment.
Debride necrotic material mechanically (surgically) or by enzymatic
debriding agents, including collagenase and papain
Antiseptics and antibiotics to counteract infection.
Hydrocolloid dressings.
Granulating but only slowly epithelializing ulcers are treated by surgical
procedures either by pinch grafts, split-thickness skin grafts, epidermal
grafts, cultured keratinocyte allografts, or composite grafts.

NECROBIOSIS LIPOIDICA

 Necrobiosis lipoidica (NL) is a cutaneous disorder often,

but not always, associated with diabetes mellitus.
The lesions are distinctive, sharply circumscribed,
multicolored plaques occurring on the anterior and
lateral surfaces of the lower legs.
Lesions may ulcerate.

Epidemiology and Etiology

Age of Onset Young adults, early middle age, but not uncommon in
juvenile diabetics.
Sex Female: male ratio 3:1 in both diabeticand nondiabetic forms.
Incidence From 0.33% of diabetic individuals.
NL may occur in individuals without manifest diabetes. Relationship to
diabetes : One-third of patients have clinical diabetes, one-third have
abnormal glucose tolerance only, one-third have normal glucose tolerance.
Etiology Unknown.
Precipitating Factors A history of preceding trauma to the site can be a
factor in the initial development of the lesions.

Pathogenesis

The arteriolar changes in the areas of necrobiosis of the collagen

have been thought by some to be precipitated by aggregation of
platelets.
The granulomatous inflammatory reaction is believed to be due to
alterations in the collagen.
The severity of NL is not related to the severity of diabetes.
Furthermore, control of the diabetes has no effect on the course of
NL.

Necrobiosis lipoidica diabeticorum A. A large, symmetric plaque with active tan-pink, yellow, welldemarcated, raised, firm border and a yellow center in the pretibial region of a 28-year-old diabetic
female. The central parts of the lesion are depressed with atrophic changes of epidermal thinning and
telangiectasis against yellow background. B. Late lesion after healed ulceration. A very extensive plaque
of necrobiosis lipoidica on the lower leg of a diabetic female. Apart from the features of necrobiosis
lipoidica there is extensive scarring and atrophic depressed scars.

PRESSURE ULCERS

Epidemiology

Age of Onset Any age, but the greatest prevalence of pressure

ulcers is in elderly, chronically bedridden patients.
Sex Equally prevalent in both sexes.
Prevalence Acute care hospital setting, 314%; long-term care
settings, 1525%; home-care settings, 712%; spinal cord units,
2030%.

Pathogenesis

Risk factors : inadequate nursing care, diminished sensation/immobility (obtunded

mental status, spinal cord disease), hypotension, fecal or urinary incontinence,
presence of fracture, hypoalbuminemia, and poor nutritional status.
The mean skin capillary pressure is approximately 25 mmHg.
External compression with pressures >30 mmHg occludes the blood vessels so that
the surrounding tissues become anoxic and eventually necrotic.
Amount of damage is proportional to extent and duration of pressure. Secondary
bacterial infection can enlarge the ulcer, extend to underlying structures
(osteomyelitis), and invade the bloodstream, with bacteremia and septicemia.
Infection also impairs or prevents healing.

 Pressure ulcers develop at body-support interfaces over bony

prominences as a result of external compression of the skin, shear
forces, and friction, which produce ischemic tissue necrosis.
Occur in patients who are obtunded mentally or have diminished
sensation (as in spinal cord disease) in the affected region.
Secondary infection results in localized cellulitis, which can extend
locally into bone or muscle or into the bloodstream.
Synonyms : Pressure sore, bed sore, decubitus ulcer.

Clinical Manifestation
Skin Lesions
Clinical Categories of Pressure Ulcers
Early change: localized erythema that blanches on pressure.

Stage I: Nonblanching erythema of intact skin.

Stage II: Necrosis, superficial or partial-thickness involving the epidermis
and/or dermis. Bullae necrosis of dermis (black) shallow ulcer.
Stage III: Deep necrosis, crateriform ulceration with full-thickness skin loss
(Fig. 16-17); damage or necrosis can extend down to, but not through,
fascia.
Stage IV: Full-thickness necrosis ( ulceration) with involvement of
supporting structures such as muscle and bone (Fig.16-18). May enlarge
to many centimeters. May or may not be tender. Borders of ulcers may be
undetermined.

Distribution
Occur over bony prominences:
sacrum (60%) > ischial tuberosities,
greater trochanter, heel > elbow,
knee, ankle, occiput.

General Examination
Fever, chills, or increased pain of ulcer suggests possible cellulitis or
osteomyelitis.

Pressure ulcer, stage III Well-demarcated crateriform

ulcer with full thickness skin loss extending down to fascia
over greater trochanteric region.

Pressure ulcer, stage IV Huge black necrosis over sacral

area in a patient who had been bedridden after a stroke. The
criss-cross marks in the necrotic area are from attempts to
mechanically debride necrotic tissue. Surgical debridement of
necrotic tissue under anesthesia revealed involvement of
fascia and bone.

Management
Prophylaxis in At-Risk
Patients Reposition patient every 2 h (more often if possible); massage areas prone to
pressure ulcers while changing position of patient; inspect for areas of skin
breakdown over pressure points.
Use interface air mattress to reduce compression.
Minimize friction and shear forces by using proper positioning, transferring, and
turning techniques.
Clean with mild cleansing agents, keeping skin free of urine and feces.
Minimize skin exposure to excessive moisture from incontinence, perspiration, or
wound drainage.
Maintain head of the bed at a relatively low angle of elevation (<30).
Evaluate and correct nutritional status; consider supplements of vitamin C and zinc.
Mobilize patients as soon as possible.

Stages I and II Ulcers

Topical antibiotics (not neomycin) under moist sterile gauze may be
sufficient for early erosions.
Normal saline wet to- dry dressings may be needed for debridement.
Hydrogels or hydrocolloid dressings.

Stages III and IV Ulcers

Surgical management: debridement of necrotic tissue, bony prominence
removal, flaps and skin grafts.
Infectious Complications
Prolonged course of antimicrobial agent depending on sensitivities, with surgical
debridement of necrotic bone in osteomyelitis.

Course and Prognosis

If pressure is relieved, some changes are reversible; intermittent periods of pressure
relief increase resistance to compression.
Osteomyelitis occurs in nonhealing pressure ulcers (3281%).
Septicemia is associated with a high mortality rate. Overall, patients with pressure
ulcers have a fourfold risk of prolonged hospitalization and of dying when compared
with patients without ulcers. With proper treatment,
Stages I and II ulcers heal in 14 weeks and stages III and IV ulcers heal in 6 to >12
weeks