Venous insufficiency

1. CHRONIC VENOUS
INSUFFICIENCY

2. Result of persistent
ambulatory venous
hypertension of the lower-
extremity venous system
leading to a spectrum of
clinical findings from
edema and tenderness to
venous ulceration
DEFINITION

3. Symptoms
● Leg fullness
● Aching discomfort
● Heaviness
● Nocturnal leg cramps
● Bursting pain on standing
Common Signs and Symptoms of Peripheral Venous
Disease

4. Common Signs and Symptoms of Peripheral Venous
Disease
Signs
● Very early
○ Tenderness to palpation
● Early
○ Edema, hyperpigmentation, stasis
dermatitis, varicose veins
● Late
○ Venous ulcers, atrophie blanche,
lipodermatosclerosis,
acroangiodermatitis of Mali,
postphlebitic syndrome

5. ● Extremely common; prevalence of 30% in adults
● Venous ulcers cause significant disability = 1% of adults
● Risk factors:
○ Heredity
○ Age
○ Female sex
○ Obesity
○ Pregnancy
○ Prolonged standing
EPIDEMIOLOGY
○ Phlebitis
○ Previous leg injury

6. ● Spectrum of clinical manifestations start with
telangectasias and reticular veins on one end
of the spectrum, and advanced chronic
venous insufficiency at the other end
● Findings of chronic venous insufficiency:
○ Dilated veins (varicose veins)
○ Edema
○ Leg pain
○ Cutaneous changes
● Earliest finding: Perimalleolar edema that
ascends up the leg, followed by soft tissue
tenderness
CLINICAL FINDINGS - Cutaneous Lesions

7. ● Varicose veins and smaller
varicosities appear about the
dorsum of the foot and ankle
○ Usually asymptomatic
○ Patient’s complaints: Aching,
cramping, itching, fatigue, and
swelling that worse with
prolonged standing
○ Superficial thrombophlebitis
can develop
CLINICAL FINDINGS - Cutaneous Lesions

8. ● Stasis dermatitis- occur during any
stage of chronic venous insufficiency
○ Erythema, scaling, pruritus,
erosions, crusting, and occasional
vesicles and serous drainage
○ Typical location: Medial
supramalleolar region
○ Overtime, lesions may lichenify
○ Evaluate for coexisting allergic
contact dermatitis
CLINICAL FINDINGS - Cutaneous Lesions

9. ● Lipodermatosclerosis (aka. Sclerosing panniculitis,
hypodermatitis sclerodermiformis)
○ Fibrosing panniculitis characterized by a bound down
plaque
○ Begins at the medial ankle and extends
circumferentially around the entire distal lower leg
○ As the fibrosis increases → constrict and strangle the
lower leg → impede venous and lymph flow →
brawny edema above and below the fibrosis (inverted
champagne bottle
○ Lack of response to oral antibiotics and a relapsing
nature = leads to its diagnosis
CLINICAL FINDINGS - Cutaneous Lesions

10. ● Atrophie blanche
○ Skin overlying areas of fibrosis appearing
in porcelain white and atrophic
○ Fully established: Irregular, smooth,
atrophic stellate plaques surrounded with
hyperpigmentation and telangectasias
○ Related to venous stasis; may be
associated with an underlying disorder of
hypercoagulation, livedoid vasculitis, or
autoimmune disease
CLINICAL FINDINGS - Cutaneous Lesions

11. ● Acroangiodermatitis
○ Has purple macules, nodules, or
verrucous plaques on the dorsal feet and
toes of patients with long standing venous
insufficiency
○ Mimics Kaposi sarcoma clinically and
histologically
● Venous ulcers
○ Ulcers occurring anywhere below the
knee
○ Tender, shallow, irregular, and have a red
base
○ Location: Medial ankle or along the line of
the long or short saphenous veins
CLINICAL FINDINGS - Cutaneous Lesions

12. • Recurrent ulceration
• Cellulitis
• Contact dermatitis
• Thrombi and venous
thrombosis
• Lymphatic impairment
• Elephantiasis nostras
COMPLICATIONS

13. A venous ulcer occurs after
failure of the calf muscle pump.
The heart pumps blood down to
the foot; the calf muscle pump
(when upright) returns venous
blood to the heart. Venous blood
from the skin and subcutis
collects in the superficial venous
system, including the greater and
lesser saphenous veins and its
tributaries, moves through the
fascia in a series of “perforating”
or “communicating” veins, and
fills the muscle-enveloped deep
venous system.
ETIOLOGY & PATHOGENESIS

14. In all patients with venous disease there
is failure of these one-way valves, and
this can result in varicose veins.
Any obstruction to venous return (eg,
thrombosis, radiation fibrosis) or
elevation of right atrial pressure (eg,
pulmonary hypertension, heart failure)
further compromises venous return.

15. The most common cause of venous
valvular failure is thrombosis. The
nidus for venous thrombosis is
typically the valve cusp, and when
the thrombus is lysed by plasmin,
valve function is often lost as well.
Calf muscle pump failure after
deep venous thrombosis is often
referred to as the postphlebitic
syndrome.

16. • High-pressure blood in the
deep system refluxes into
the unsupported veins of the
skin.
• Vascular leakage of
fibrinogen producing “fibrin
cuffs” that may interfere
with tissue nourishment
• Soft-tissue injury,
inflammation and fibrosis
• Subcutaneous fat is replaced
by scar, resulting in
lipodermatosclerosis.

17. DIAGNOSIS
Screening for Peripheral Arterial
Disease: The Ankle–Brachial
Index
● Measure systolic blood
pressure in the arms and
in the pedal pulses, using
Doppler ultrasound.
○ Normal ABI: greater
than or equal to 1
○ Less than 1 may indicate
PAD (the lower the ratio
the more severe the
arterial obstruction).

18. DIAGNOSIS

19. DIAGNOSIS

20. ● Skin biopsy- for diagnosis that in
doubt, tissue should be sent for
both histology and tissue culture.
○ Histologic signs of venous
hypertension:
■ Hemosiderin deposition
■ Lobular superficial
■ Deep dermal
neovascularization
■ Fibrosis of dermis and
subcutaneous tissue in
later stages
DIAGNOSIS

21. ● Functional testing of calf
muscle pump function and
venous valvular function
using plethysmography-
occasionally useful
● Duplex Doppler
ultrasonography- to document
valvular incompetence and to
evaluate patients for possible
sclerotherapy or surgery.
DIAGNOSIS

22. DIFFERENTIAL DIAGNOSIS

23. DIFFERENTIAL DIAGNOSIS

24. ● Excellent in the absence of comorbid illness.
● Uncomplicated chronic venous disease respond well to
ambulatory outpatient therapy.
● Permanent changes include hemosiderosis and fibrosis
that develop before therapy.
● Loss of valvular function is irreversible.
● Absence of continual lifelong cutaneous support in the
form of inelastic wraps or elastic stockings, skin and soft
tissue injury continues.
CLINICAL COURSE & PROGNOSIS

25. MANAGEMENT
Compression bandage using a zinc paste primary
layer (Unna boot) followed by Coban at full
stretch

26. MANAGEMENT
• Mechanical therapy - mainstay
of treatment
 Daily use of elastic compression
stockings:
 Reduces swelling in some patients
with postthrombotic syndrome
 Prevent worsening of established
postthrombotic syndrome
 Reduce recurrence of healed
venous ulcers

27. MANAGEMENT
• Diuretics -severe edema
• Aspirin- (300 to 325 mg/day)
• Pentoxifylline- improve healing of chronic
venous ulcers,
• Topical steroids and emollients- aid
resolution of stasis dermatitis
• Mupirocin- useful for folliculitis due to S.
aureus and streptococci
• Horse chestnut seed extract (Aesculus
hippocastanum L.)- 50 mg escin, short-term
treatment for leg pain and swelling

28. MANAGEMENT
 Continual hemodynamic support
 Graduated stockings (minimum of
30-40 mmHg) at the ankle- carefully
fitted
× elastic stockings on edematous limbs
 Compression bandaging- used until
all edema, inflammation, and
tenderness have resolved

29. MANAGEMENT
 Sclerotherapy or surgical
techniques
 Endovenous ablation- close
incompetent perforators and correct
the hemodynamic abnormalities that
lead to venous ulcer

30. ● Identify and treat patients at extra risk for
thrombosis.
● Venous thrombosis: Elastic compression
stockings- the only proven method to
reduce the risk of post thrombotic
syndrome.
● Supportive stockings- maternity can be
recommended since valvular failure may
develop during pregnancy
● Stockings are advisable for occupation or
lifestyle involving long periods of
immobility (long-distance flights).
PREVENTION