Venous system disorders - patho

chronic venoous insufficiency (CVI)

Impaired venous return from weakened valves

varicose veins

Visible, enlarged, twisted superficial veins

superficial thrombophlebitis

Clot-related inflammation of a superficial vein

Venous Thromboembolism (VTE)

Deep vein thrombosis (DVT) & pulmonary embolism (PE)

venous system

● Veins return deoxygenated blood to the right side of the heart — this is called venous return.

● Deep veins run within leg muscles; superficial veins sit in subcutaneous tissue; perforating veins connect the two.

● All veins contain bicuspid valves that keep blood flowing in one direction — toward the heart.

● When venous return is impaired, blood pools, tissue becomes irritated, veins enlarge, valves weaken further, and clots can form.

Chronic Venous Insufficiency (CVI) — Etiology

occurs when veins struggle to return blood from the legs to the heart, most often in the lower extremities where gravity works hardest against venous return.

Primary & Secondary Causes of Chronic Venous Insufficiency (CVI)

● Primary: often genetic — inherited weakness of vein/valve structure.

● Secondary: deep vein thrombosis (DVT) — the most common secondary cause.

● Damaged/incompetent valves that let blood flow backward.

● Venous obstruction, venous hypertension, external compression, or trauma to the vein lining.

risk factors of Chronic Venous Insufficiency (CVI)

● Family history, advancing age, female sex, pregnancy

● Obesity, sedentary lifestyle, tobacco use

● Prolonged sitting or standing (occupational risk!)

● Previous leg injury or history of DVT

Chronic Venous Insufficiency (CVI) - how it develops

● Incompetent valves allow reflux (backward flow) — blood pools and venous pressure rises.

● Increased pressure changes vein wall cells, triggering inflammation and increased vascular permeability → edema.

● The calf muscle pump (“second heart”) normally squeezes deep veins to push blood upward; weakness here worsens venous return.

● Virchow's Triad (endothelial injury, stasis, hypercoagulability) explains DVT as a secondary cause.

Chronic Venous Insufficiency (CVI) - clinical manifestations

● Leg heaviness, achiness, cramping, edema — improve with elevation early on.

● Telangiectasia (visible small vessels) and skin hyperpigmentation from leaked RBCs.

● Stasis dermatitis and lipodermatosclerosis — irreversible skin/tissue changes.

● Advanced disease: venous ulcers, typically around the ankles.

● CEAP classification grades severity from C0 (none) to C6 (active ulcer).

Chronic Venous Insufficiency (CVI) - diagnostic criteria

● Venous Doppler or duplex ultrasound — visualizes valve function and reflux.

● Reflux > 0.5 sec (superficial) or > 1.0 sec (deep) confirms incompetent valves.

● Air plethysmography — measures venous filling time with a BP cuff.

● Venography — invasive contrast imaging; rarely used due to risks.

Chronic Venous Insufficiency (CVI) - nursin management

● Graduated compression hose — tightest at ankle, mimics the calf muscle pump.

● Leg elevation ≥ 30 min, 3x daily to reduce venous stasis.

● Weight management, exercise (ankle dorsiflexion/plantar flexion), skin care.

● Advanced options: sclerotherapy, endovenous ablation, stents, or vein stripping.

Varicose Veins

_____ are visible, enlarged, twisted superficial veins — a complication of CVI. They are not curable, and even with treatment, they usually return.

Varicose Veins - Etiology & Risk Factors

● Incompetent valves in subcutaneous (superficial) veins — often the saphenous veins.

● Blood pools, pressure rises, vein walls stretch and weaken over time.

● Risk factors: female sex, multiparity, obesity, constipation, prior venous thrombosis.

● Prolonged standing/walking and increased intra-abdominal pressure (pregnancy, straining) contribute.

Varicose Veins - Pathophysiology: Arterialization

● Incompetent valves + high venous pressure → increased shear stress on vessel walls.

● Shear stress stimulates hyperplasia — vein tissue takes on thicker, artery-like characteristics.

● Result: dilated, twisted (“tortuous”) veins ≥ 3 mm in diameter.

Varicose Veins - manifestations

● Visible, cord-like or rope-like veins

● Leg heaviness

● Tenderness, cramping, burning pain

● Itchiness around the vein

● Worsens with prolonged sitting/standing

varicose veins - diagnosis

● Often visible on exam alone

● Color duplex ultrasound — evaluates valve function & flow direction

● Venogram — contrast dye + x-ray

● Pulse volume recording (PVR) — BP cuff + ultrasound for backward flow

varicose veins - management

● Exercise, weight control, leg elevation, low sodium intake

● Compression hose (OTC or prescription >20 mmHg)

● Sclerotherapy for smaller veins

● Phlebectomy (ligation/stripping) or endovascular thermal ablation for larger veins

Phlebitis

vein inflammation.

Thrombophlebitis

ein inflammation caused by a blood clot. When this occurs in a superficial vein, it's superficial thrombophlebitis

Superficial Thrombophlebitis: Etiology — Virchow's Triad in Action

● IV catheters are a leading cause — occurs in up to 20–80% of peripheral IV use.

● Endothelial injury: HTN, IV cannulation, varicose vein mechanical stress.

● Stasis: varicose veins, prolonged immobility.

● Hypercoagulability: inherited thrombophilia, pregnancy, malignancy, oral contraceptives

Superficial Thrombophlebitis - manifestiations and diagnosis

● Erythema tracking along the vein, induration (firmness), warmth, tenderness.

● May resemble a hematoma with well-defined edges.

● Significant edema is uncommon — if present, consider DVT instead.

● Compressive ultrasonography — confirms diagnosis AND rules out DVT.

● D-dimer may be elevated but is not definitive on its own.

Venous Thromboembolism (VTE)

______ begins when a thrombus forms inside a vein. It includes two related conditions: deep vein thrombosis (DVT) and pulmonary embolism (PE). VTE is a leading cause of preventable hospital death.

DVT Risk Factors (Virchow's Triad)

● Stasis: immobility, paralysis, long surgery, decreased cardiac output

● Endothelial injury: IV/central catheters, smoking, trauma, surgery

● Hypercoagulability: pregnancy, malignancy, inflammatory disease, inherited thrombophilias

● ~50% of DVT clients were hospitalized or had surgery within the prior 3 months

Inherited Thrombophilias

● Factor V Leiden: resists inactivation by activated protein C — up to 80x higher DVT risk (two copies).

● G20210A prothrombin mutation: excess prothrombin → more clot formation.

● Hyperhomocysteinemia: elevated homocysteine → oxidative stress & inflammation, raising clot risk

Deep Vein Thrombosis (DVT) - pathophysiology and manifestations

● Inflammation releases procoagulant mediators (cytokines, chemokines).

● Platelets, fibrin, RBCs, and WBCs form a solid thrombus that occludes/expands within the deep vein.

● Manifestations: pain, erythema, swelling, warmth, tenderness near the thrombus.

● Homan's sign is unreliable and should NOT be used to diagnose DVT.

Deep Vein Thrombosis (DVT) - diagnosis

● Step 1: D-dimer — if not elevated, DVT is unlikely.

● Step 2: Venous duplex ultrasound if D-dimer is elevated.

● Step 3: MR venography if ultrasound is negative but suspicion remains.

● Complication: post-thrombotic syndrome — chronic CVI-like changes.

Deep Vein Thrombosis (DVT) - medical management

● Anticoagulation: apixaban, rivaroxaban, warfarin (oral); IV heparin initially if hospitalized.

● Treatment typically continues 3–12 months — monitor for bleeding, INR (warfarin).

● IVC filter: for recurrent DVT or when anticoagulation is contraindicated.

● Goal: prevent clot growth/embolization while the body dissolves the thrombus.

Deep Vein Thrombosis (DVT) - nursing prevention

● Early ambulation after surgery — one of the most effective preventive actions.

● Foot and leg exercises for immobile or bedbound clients.

● Sequential compression devices (SCDs) — mimic the calf muscle pump.

● Administer prescribed anticoagulants; maintain hydration.

● Patient education on bleeding precautions and follow-up labs.

Pulmonary Embolism (PE)

_______ occurs when a thrombus — usually from a deep leg vein — dislodges and lodges in the pulmonary arteries, obstructing blood flow to the lungs

What Happens in the Lungs - Pulmonary Embolism (PE)

● Obstruction creates alveolar dead space — alveoli are ventilated but not perfused.

● Ventilation-perfusion (V/Q) mismatch → impaired gas exchange, hypoxia.

● Pulmonary vascular resistance rises → increased right ventricular workload.

● Can progress to right-sided heart failure and cardiogenic shock.

Pulmonary Embolism (PE) manifestations

● Sudden-onset dyspnea (most common), unilateral chest pain, cough, hemoptysis.

● Calf or thigh pain/swelling (from the originating DVT).

● Large PE: hypotension, tachycardia, hypoxia, tachypnea, diaphoresis, fever.

● Crackles on auscultation; new heart sounds (S3/S4).

Pulmonary Embolism (PE) - Diagnostic Criteria

● D-dimer: a negative result helps rule out PE; elevated is not confirmatory.

● CT pulmonary angiography (CTPA) — contrast CT; the definitive test.

● Ventilation-perfusion (V/Q) scan — alternative when contrast is contraindicated.

● PE carries a mortality rate of roughly 30% — rapid recognition saves lives.

Pulmonary Embolism (PE) - Management & Nursing Care

● Thrombolytic therapy for massive, life-threatening PE (bleeding risk — give within 48 hr of onset).

● Surgical embolectomy if unstable or thrombolysis fails/contraindicated.

● Nursing: continuous oxygenation & hemodynamic monitoring, watch for bleeding/neuro changes, emotional support.

● Prevention: SCDs, early ambulation, anticoagulation, hydration — same principles as DVT prevention.

CVI

Impaired venous return from weakened valves causes pooling, edema, and skin changes.

Varicose Veins

Arterialization of superficial veins from chronic reflux — visible, twisted, and recurrent

Superficial Thrombophlebitis

Clot-driven inflammation of a superficial vein; screen for DVT with ultrasound.

VTE (DVT & PE)

Virchow's Triad drives DVT; embolization to the lungs causes life-threatening PE.