VENOUS AND LYMPHATIC

DISEASE

VENOUS FLOW: FACTORS

Upright position
Left ventricular force
( gravity )
( vis a tergo )
High volume, low Calf muscles
pressure circu- Venous valves in
lation
lower extremities
Intra-abdominal
Smooth muscles in
pressure
superficial veins

THE VASCULAR CONSULTATION

Painful extremity
Swollen extremity
Ulcerated leg

THE PAINFUL LOWER EXTREMITY

No characteristic pain in venous
disease
Aggravated by standing
Relieved by elevating leg and foot

PAIN
Varicose veins discomfort
Pulling
Burning
Pricking
Tingling
Superficial Thrombophlebitis
inflammation
Tenderness Warmth
Redness
Induration

PAIN
Venous thrombosis
- little or no pain
- moderate aching discomfort or
sensation of heaviness
- bursting pain uncommon
venous claudication

THE SWOLLEN LEG

High venous pressure
Cardiac
intrinsic
Venous obstruction
extrinsic

Gravitational pressure
- effect on incompetent valves

THE SWOLLEN LEG

Pressure
Protein
Permeability
Paresis
Pendency

EDEMA
Central / systemic
Pitting; no skin changes
Peripheral venous
Does not pit readily
Chronic brawny dermatitis
stasis dermatitis
gaiter distribution

EDEMA
Lymphedema
Diffuse
Spongy
Hypertrophic skin Elephantiasis

THE ULCERATED LEG

Stasis ulcer
Gaiter area around medial
malleolus
Mild pain relieved by elevation
Venous bleeding / oozing
Stasis dermatitis
Shallow, irregular with granulating
base

SUPERFICIAL THROMBOPHLEBITIS
Local inflammatory process
Usually aseptic
Etiology: acidic fluid infusion
prolonged cannulation
contrast injection
varicose veins
Treatment: bed rest, elevation
local heat
support hose / stockings

DEEP VENOUS THROMBOSIS

Virchow 1856
1. Stasis
2. Endothelial damage
3. Hypercoagulability

DEEP VENOUS THROMBOSIS: RISK

FACTORS

Pregnancy
Obesity
Malignancy
Trauma
Sepsis
Major surgery
Other disease states DIC, Polycythemia, Dysfibrinogenemia,
Anti-thrombin III deficiency

ORIGIN OF DVT
Usually from the lower extremity, starting at the calf
level going proximally; source of 80-90% of
pulmonary emboli
Pelvic veins
Renal veins
Inferior vena cava
Ovarian veins
Upper extremity and neck veins
Right atrium

DVT: CLINICAL MANIFESTATIONS

Classic clinical syndrome
Calf or thigh pain
Edema
Tenderness
(+)Homans sign
Nonspecific; associated with venographically proven DVT in only
50%
Conversely, 50% of those with DVT have
no associated physical findings

DEEP VENOUS THROMBOSIS

Pulmonary embolism is a common
presenting symptom in many patients
Need to rule out the presence of arterial
insufficiency

LOWER EXTREMITY DVT: CLINICAL

MANIFESTATIONS
Phlegmasia alba dolens
pain, pitting edema, blanching
pregnancy-related
Phlegmasia cerulea dolens
loss of sensory and motor function
cessation of arterial flow
venous gangrene

DEEP VENOUS THROMBOSIS: DIAGNOSIS

Radioactive-labelled fibrinogen
Doppler ultrasound
Impedance plethysmography
Venography
Venous duplex scan

TREATMENT OF DVT
PREVENTION !
- Identify risk factors
- Prophylaxis
Early ambulation
Anticoagulation heparin
Intermittent pneumatic
compression

TREATMENT OF DVT
Treatment
- Anticoagulation
Heparin Warfarin
Low molecular weight heparin
- Fibrinolysis
Urokinase / streptokinase
TPA
- Operative

OPERATIVE TREATMENT OF DVT

Thrombectomy
Vena caval interruption
Greenfield filter

PULMONARY EMBOLISM
Obstruction to blood flow in the pulmonary
arterial system due to thromboemboli
pulmonary hypertension, decreased cardiac
output, impaired gas exchange / oxygenation,
sudden death
One of MOST COMMON CAUSES OF
SUDDEN DEATH in hospitalized patients

PULMONARY EMBOLISM
Only around 10% are diagnosed PREMORTEM
> 90% of deaths occur within 2 hours of the
onset of symptoms
Associated with DVT in up to 40%; around
30% have no symptoms of DVT

PULMONARY EMBOLISM: RISK FACTORS

Pregnancy
Estrogen therapy
Obesity
Heart disease
Malignancy
Major trauma
Previous episode of PE
Varicose veins
Advanced age

PULMONARY EMBOLISM: SYMPTOMS

Classic signs only in 25%
Hemoptysis
Pleural friction rub
Gallop rhythm
Cyanosis
Common findings: tachycardia, tachypnea, dyspnea;
arrythmias; pulmonary effusion or infiltration
(infarction); hypoxemia on ABGs

Massive pulmonary embolism

Pulmonary infarction

CHF
Shock

PULMONARY EMBOLISM: DIAGNOSIS

Pulmonary radio-isotope scanning
Perfusion scan
Ventilation scan
Ventilation / perfusion scan
Pulmonary arteriography
Gold standard

PULMONARY EMBOLISM: MANAGEMENT

Cardiovascular support / critical care

Anticoagulation
Thrombolytic therapy
Pulmonary embolectomy

ANTICOAGULATION THERAPY: COMPLICATIONS

Major hemorrhage
Heparin-induced thrombocytopenia
Hemorrhage
Necrosis
Recurrent pulmonary embolism

VARICOSE VEINS
Primary
Familial
Favorable prognosis with medical or
surgical treatment
Secondary
Due to deep venous disease
Stasis dermatitis or ulceration

VARICOSE VEINS
Local pain and edema
Nonspecific ache or heaviness
Relieved by elevation of leg
Local inflammation
Local hemorrhage into surrounding tissues
Dilated superficial veins
Positive Trendelenburg test

VARICOSE VEINS
Diagnostic aids
Doppler ultrasound / duplex scan
Venous reflux plethysmography

VARICOSE VEINS: TREATMENT

Conservative unless:
Venous stasis
Dermatitis
Bleeding
Thrombosis / phlebitis
Superficial ulceration
Injection sclerotherapy
Surgery vein stripping
Endovenous procedures
Laser ablation
Radiofrequency ablation

CHRONIC VENOUS INSUFFICIENCY

Deep venous thrombosis
Post-thrombotic syndrome
Recanalization

Valve damage
Valve incompetence

CHRONIC VENOUS INSUFFICIENCY

Fluid, protein extravasation
Thickened, sclerotic subcutaneous tissues ( Brawny
edema )
Hemosiderin pigmentation
Skin atrophy, necrosis, stasis ulceration
Dermatitis, cellulitis
If no recanalization venous claudication

CHRONIC VENOUS INSUFFICIENCY

Compression tests
Trendeleburg
Perthes
Ochsner-Mahorner
Laboratory
Plethysmography
Duplex scanning

TREATMENT OF CVI
Supportive elastic stockings
frequent leg elevation
avoid prolonged
standing or sitting
Operative perforator vein ligation
venous reconstruction

LYMPHEDEMA
Swelling of one or more extremities caused by
lymphatic obstruction or insufficiency
Primary vs secondary

PRIMARY LYMPHEDEMA
Congenital present at birth
10% of cases
hereditary Milroys
disease
Lymphedema praecox from puberty;
most common type
Lymphedema tarda after 30s

SECONDARY LYMPHEDEMA

Malignancy
Radiation
Trauma
Inflammatory
Parasitic elephantiasis
Wuchereria bancrofti )

LYMPHEDEMA
Diagnosis confirmed by lymphangiogrphy
Treatment
- limb elevation, weight reduction,
salt restriction
- compressive stockings
- surgery: dermal flap
omental transposition
microsurgical anastomosis