unit 4 - venous history and physical

risk factors of DVT

age, surgery/trauma, immobilization, past history, coagulation disorders, malignancy, oral contraceptives, hormonal replacement therapy, , pregnancy, obesity, stroke, CHF, long-distance travel, varicose veins

3 causes for DVT (Virchow’s triad)

stasis, hypercoagulability, vessel wall injury

once thrombus is formed:

stabilize, propagate, embolize

stabalize

adhere to wall without changing location or propagating

propagate

grows in size and location, as it grows, will extend further down the vein

embolize

portion breaks free and travels elsewhere within vascular system

stasis

blood that remains stagnant for any period of time will clot with minimal stimulus, immobilization, obstruction, previous DVT, CHF

immobilization

surgery, acute stroke, acute paraplegic, prolonged bedrest, obesity

extrinsic compression

tumors, late trimester pregnancy, hematomas, trauma, paget-schroetter syndrome, may-thurner syndrome, nutcracker syndrome

paget-schrotter disease

AKA: effort thrombosis, venous side of thoracic outlet syndrome

may-thurners syndrome

left common iliac vein compression by the right common iliac artery

nutcracker syndrome

refers to the compression of the left renal vein between the SMA and Ao, renal venous hypertension, ruptured wall resulting in a hematoma

vein wall injury

there is an injury to the vein wall, the platelets attach to the wall and form a thrombus

hypercoagulability

sudden and significant increase in clotting factors and platelets

congenital hypercoagulability

decrease antithrombin III, MTHFR (methylenetetrahydrofolate reductase), protein C deficiency, protein S deficiency

acquired hypercoagulability

adenocarcinoma, estrogen replacements, oral contraceptives, pregnancy and postpartum, liver disease, smoking, nephrotic syndrome

signs and symptoms of superficial thrombophlebitis

local erythema, local inflammation, palpable subcutaneous cord

local erythema

reddish discoloration of the skin due to dilation of superficial blood vessels, secondary to inflammation

local inflammation

redness, warmth, pain in area of thrombus

palpable subcutaneous cord

feel area of vein that has thrombus in it

homan’s sign

dorsal flexion of the foot that causes pain in the calf, not very reliable

swelling

caused by obstruction of the venous circulation, due to increase venous volume and pressure, depends of collateral circulation and size of extent of clot

distended superficial veins

veins respond as collaterals and dilate in presence of significant DVT, commonly seen across the pelvis with iliofemoral DVT, upper extremity in anterior shoulder region with prox subclavian DVT

edema

begins distally at the level of the malleolus, can progress to mid-calf, worsens with dependency, relieved with lib elevation

venous claudication

intense burning or cramping in the calf with walking, caused by rapid increase in both superficial and deep venous pressure due to increased resistance to venous blood flow, patients with iliofemoral DVT and inadequate collaterals are most likely to experience this

signs and symptoms of PE

dyspnea, pleuritic chest pain, tachypnea, tachycardia, hemoptysis, right side heart failure, respiratory arrest leads to cardiac arrest

venous gangrene

chronic DVT, affecting deep tissue because of lack of blood flow - causes necrosis

hyperpigmentation

chronic DTV, brownish, discolored skin due to hemosiderin deposition, high venous pressure causes blood cells to be trapped in tissue

stasis dermatitis

chronic DVT, dry, flaky skin located along the inner aspect of the leg above the medial malleolus and may spread to entire leg, can become inflamed

lipodematosclerosis

chronic DVT, AKA: induration, hardening of skin

primary varicose veins

involves the superficial system only, hereditary, congenital absence or weakness of valves, caused by increase in intraluminal pressure

secondary varicose veins

DVT, congenital absence, involves both superficial and deep veins

lymphatic system

responsible for removing plasma proteins and fluis that has leaked out of the capillaries into the interstitial spaces due to obstruction, destruction, or hypoplasia of the lymph vessels, designed to return excess fluid and plasma proteins to the bloodstream

primary lymphedema

Congenital abnormal development of absence of lymphatic channels, classification is based on age of the patient and onset of disease, idiopathic

secondary lymphedema

caused by infection, inflammation, trauma, and malignant disease, usually accompanied by recurrent bouts of cellulitis

signs and symptoms of lymphedema

painless, firm swelling that progresses over time, rarely ulcerates, secondary lymphedema may develop recurrent bouts of cellulitis

cellulitis

fluid in the tissues caused by a bacterial infection involving the inner layers of the skin, dermis and subcutaneous fat

signs and symptoms of cellulitis

area of redness which increases in size over a couple of days, swollen skin, painful infection area