Unit Three- Venous History and Physical/Pharmacology

Unit Three- Venous History and Physical/Pharmacology

DVT: Etiology

Virchow’s Triad

Virchow’s Triad (2)

• Causes of clot formation within the intact venous system

• “Discovered” by Rudolf Virchow in 1856

Virchow's Triad describes the 3 main factors that contribute to thrombosis:

• Stasis

• Vein wall injury

• Hypercoagulability

Why do we do venous testing? (4)

• Presence of thrombus

• Evaluate valve competence

• Vein Mapping

• Pre-Op AV Fistula

Presence of thrombus (3)

• R/O DVT

• R/O SVT

• Assess embolism risk

What does SVT stand for

Superficial Thrombophlebitis

ALL HISTORY AND PHYSICAL QUESTIONS RELATED TO DVT/VENOUS STUDIES SHOULD ALL REVOLVE AROUND THESE THREE THINGS!!

1. Stasis

2. Vein wall injury

3. Hypercoagulability

STASIS

Blood that remains stagnant for any period will clot with minimal stimulus

Examples of Stasis (4)

• Immobilization

• Obstruction/Extrinsic Compression

• Previous DVT History

• CHF

Stasis

Slowed Blood Flow

Hypercoagulability

Increased Clotting Tendency

Vein Wall Injury

Damage to Blood Vessel Lining

Immobilization (6)

• Surgery

• Acute Stroke

• Bedrest

• Obesity

• Paraplegic

• Etc.

Obstruction/Extrinsic Compression (7)

• Tumors

• Late Trimester Pregnancy

• Hematomas

• Trauma

• Paget-Schroetter Syndrome

• May-Thurner Syndrome

• Nutcracker Syndrome

PAGET-SCHROTTER DISEASE:

Effort Thrombosis

Effort Thrombosis Causes DVT Where?

Subclavian Vein

Paget-Schrotter Disease (4)

• Blood clot occurring in the Subclavian Vein under the Collarbone

• Extrinsic compression of the vein

• Annual Incidence: 1 and 2 out of 100,000

• Continuous flow would be demonstrated distally

Effort Thrombosis: Extrinsic compression of the vein

Aching, numbness, or tiredness with positional changes of the shoulder

MAY-THURNER SYNDROME:

Iliac Vein Compression Syndrome

Iliac Vein Compression Syndrome (3)

• The left Iliac Vein is compressed by the Right Common Iliac Artery

• Increased risk of endothelial injury to Iliac Vein

• Undetected until pathology is present

MTS

May-Thurner Syndrome

MTS: (2)

• *Endovenous stenting to treat MTS

• *Early thrombus removal would be beneficial in reducing the development of post thrombotic syndrome

VEIN WALL INJURY (3)

• Normal Venous Endothelium

• Luminal surface of these cells contain various substances in their membrane to prevent adhesion of platelets and clotting factors

• Mild to moderate injury can alter this

Normal Venous Endothelium

Intact single layer of non-thrombogenic cells

VEIN WALL INJURY DUE TO: (5)

• Indwelling catheters (most common in upper extremity)

• Venography

• Stretching or twisting injuries

• Blunt trauma

• Chemical injury

HYPERCOAGUABILITY

Increase in clotting factors and platelets/Condition that causes blood to clot more easily

HYPERCOAGUABILITY: Causes (2)

• Congenital

• Acquired

Congenital (5)

• Decreased antithrombin III

• Protein C Deficiency

• Protein S Deficiency

• Disorders of plasminogen and plasminogen activator

• Factor V Leiden

Acquired (7)

• Carcinoma (Cancer)

• Estrogen Replacements

• Oral Contraceptives

• Pregnancy and Postpartum

• Liver Disease

• Smoking

• Nephrotic Syndrome

Once Thrombus Has Formed… (3)

• Stabilize

• Propagate

• Embolize

STABILIZE

Adhere to wall without changing location or propagating

PROPAGATE

Growth in size and location

EMBOLIZE

A portion breaks free and travels elsewhere within vascular system

Signs and Symptoms of Acute DVT: (3)

• Non-specific symptoms

• Symptoms are NOT reliable (<50% chance)

• ASYMPTOMATIC!!

Symptoms are NOT reliable (<50% chance)

Pain, Swelling, Erythema

ASYMPTOMATIC

Due to the CAPACITANCE of the venous system and its ability to form collaterals around obstruction

Acute DVT: Pain and Tenderness (3) (most common)

• Most common symptom

• Ranges from mild to severe

• Does NOT necessarily correlate with size of the thrombus

Acute DVT: Swelling (4)

• Caused by obstruction of venous circulation

• Due to an increase in venous volume and pressure

• Ranges from mild to severe

• Dependent on collateral circulation and size/extent of clot

Acute DVT: Distended Superficial Veins (3)

• 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 proximal Subclavian DVT

CRITICAL ACUTE DVT: (2)

• Phlegmasia Cerulea Dolens

• Phlegmasia Alba Dolens

Phlegmasia Cerulea Dolens

Cyanosis (blue)

Phlegmasia Alba Dolens

Pallor (white)

PHLEGMASIA CERULEA DOLENS (5)

• Extensive lower extremity DVT

• Severe pain, swelling, cyanosis, and decreased limb temperature

• “Blue Leg”

• Arterial perfusion is also compromised

• May lead to VENOUS GANGRENE

Extensive lower extremity DVT

Deep and Superficial System

PHLEGMASIA ALBA DOLENS (4)

• Acute Iliofemoral Deep Vein Thrombosis

• Painful, swollen white leg

• “Milk Leg”

• Superficial Veins are still patent (deep system involved only)

Acute Iliofemoral Deep Vein Thrombosis; More common in which leg and why?

• Left leg

• Because of May-Thurner Anatomical Position

ACUTE DEEP VEIN THROMBOSIS: Complication

PULMONARY EMBOLISM/EMBOLUS (PE)

PULMONARY EMBOLISM/EMBOLUS (PE) (3)

• Complication from DVT

• Obstruction of pulmonary circulation from emboli

• Sudden onset

SIGNS AND SYMPTOMS OF PE: (7)

• Dyspnea

• Pleuritic chest pain

• Tachypnea

• Tachycardia

• Hemoptysis

• Right Side Heart Failure

• Respiratory Arrest → Cardiac Arrest

Dyspnea

Hard time breathing

Pleuritic chest pain

Chest pain in that area of your lungs

Tachypnea

Breathing really quickly

Tachycardia

Really fast heart rate

Hemoptysis

Coughing up blood

SVT Which vessels would this affect?! (Upper Extremity)

Superficial Vessels; Basilic and Cephalic

SVT Which vessels would this affect?! (Lower Extremity)

Superficial Vessels; Greater Saphenous Vein (GSV), Smaller Saphenous Vein (SSV) and Accessory Veins.

SVT (3)

• 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

CVI

Chronic Venous Insufficiency

General CVI Signs and Symptoms (8)

• Spider Veins

• Reticular Veins (Telangiectasias)

• Varicose Veins

• Edema

• Skin Changes (Hyperpigmentation)

• Ulceration (Wet/”Weepy”)

• Heaviness/tightness

• Achiness

Other CVI signs and symptoms

Heaviness, tension, achiness, burning or itching, tightness

Hyperpigmentation

Brownish, broany skin tone

Reticular Veins measure , while spider veins are less than in size; many texts say Reticular Veins=

1-3 mm; 1 mm; 2mm

CVI Causes: (4)

• “Post-Phlebotic Syndrome”- Recanalization!

• Chronic venous obstruction and/or venous valve insufficiency

• Frequency of symptoms in CVI is related to site of anatomic involvement and severity of the disease

• Pressure the greatest during muscle contraction

Symptoms and Cascade of Events

Venous Obstruction and/or Valvular Insufficiency

Venous Obstruction and/or Valvular Insufficiency (5)

• Venous HTN

• Capillary Distension

• Fibrin Deposition

• Lipodermatosclerosis

• Cell Death

Venous HTN

Normal: 90 mmHg when standing, 20-30 mmHg when walking

Capillary Distension (4)

• Edema

• Pain, Achy, Heaviness

• Venous Claudication

• Stasis Dermatitis

SWELLING (EDEMA) (4)

• Begins distally at level of the malleoli

• Can progress to mid calf

• Worsens with dependency

• Relieved with limb elevation

Pitting Edema

Apply pressure to swollen area with finger– it’s pitting edema if the depression stays

Achiness and/or Pain (3)

• C/O heaviness or achiness in the limb along with period of standing

• Relieved with walking or limb elevation

• Typically seen with patients with insufficiency of superficial system

Venous Claudication (3)

• Intense burning or cramping in the calf with walking

• Caused by rapid increase in both superficial and deep venous pressure due to increase resistance to venous flow

• Patients with Iliofemoral DVT and inadequate collaterals are most likely to experience venous claudication

What is claudication most often associated with?! (at least ___________)

peripheral artery disease ???

HYPERPIGMENTATION (3)

• Brownish, discolored skin due to VENOUS INSUFFICIENCY

• “Brawny” skin changes at the ankle

• High venous pressure causes blood cells to be trapped within the tissue

“Brawny” skin changes at the ankle

Most likely to represent CVI

Stasis Dermatitis (2)

• Dry, flakey skin located along the inner aspect of the leg above the medial malleolus, may spread to the entire leg

• May become inflamed

Lipodermatosclerosis (Induration) (2)

• Hardening of the skin

• Chronic inflammatory condition characterized by subcutaneous fibrosis and hardening of the skin of the lower legs

Varicose Veins (3)

• Due to increase venous pressure

• Elongated, tortuous, dilated, and thickened veins

• Two Types

Varicose Veins: Due to increase venous pressure (2)

• Chronic CVT

• Venous Insufficiency

Varicose Veins: Two Types (2)

• Primary

• Secondary

Primary Varicose Veins (3)

• Involves insufficiency of the Superficial Veins Only

• Hereditary

• Pressure

Primary Varicose Veins: Hereditary (2)

• Congenital absence or weakness of the valves

• Most common cause of CVI

Primary Varicose Veins: Pressure

Caused by increase in intraluminal pressure on veins: Pregnancy, prolonged standing, obesity

Secondary Varicose Veins (2)

• Develop secondary to a disease process

• Involves both superficial and deep veins

Develop secondary to a disease process (2)

• DVT

• Congenital Absence

Congenital Absence:

Klippel Trenaunay Syndrome (KTS)

Klippel Trenaunay Syndrome (KTS)

Absence or atresia of the deep veins

CEAP Classification: Used to classify patients:

C→ Clinical

E→ Etiologic

A→ Anatomic

P→ Pathophysiologic

CEAP– Clinical Classification (6)

• C0: no venous insufficiency signs or symptoms

• C1: telangiectasias and/or reticular veins (<3 mm in diameter)

  C2: varicose veins (≥3 mm in diameter)

• C3: edema

• C4: skin changes, presently subdivided into

  • C4A: minor skin changes

  • C4B: major skin changes such as lipodermatosclerosis

• C5: healed skin ulcers

• C6: open skin ulcers

CEAP- Etiological Classification (4)

• Ep: CVVI is the major cause of clinical manifestations.

• Es: CVI or CVVI is secondary to deep venous thrombosis or other pathology.

• Ec: CVI or CVVI has a congenital origin (venous malformation or lack of valves).

• En: unknown etiology, no venous etiology identified.

CEAP- Anatomical Classification (5)

• Ad: CVI or CVVI affects deep veins.

• As: CVI or CVVI affects superficial veins.

• Ap: CVI or CVVI affects perforating veins.

• Ads, Adp, Asp, and Adsp are multiple combinations.

• An: no venous anatomy identified.

CEAP- Pathophysiologic Classification (4)

• Pr: reflux or reverse venous flow

• Po: chronic venous obstruction

• Pro: a pathologic combination

• Pn: no venous pathophysiology identified

VENOUS STASIS ULCERS (2)

• Due to CVI!

• Most common type of ulcer you will see!

VENOUS STASIS ULCERS: Onset

Trauma

VENOUS STASIS ULCERS: Course

Chronic

VENOUS STASIS ULCERS: Pain

NONE (unless inflected)

VENOUS STASIS ULCERS: Location

Medial Leg/ankle “Gaiter Zone”

VENOUS STASIS ULCERS: Skin Temperature

Warm