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  1. Peripheral Venous (Anatomy) UE Deep Vns
    • -Deep Digital Vns: accompany Deep Palmar Vns(arch) & empty→Radial Vn
    • -Radial Vns: Paired vns coursing w/ corresponding Art on LAT forearm
    • -Ulnar Vns: Paired vns coursing w/ corresponding Art on MEDIAL forearm
    • *Both Radial & Ulnar unite @ Antecubital fossa to form Brachial Vn
    • -Brachial Vns: Paired vns couse SUP adj to Brachial Art & become Axillary Vn
    • -Axillary Vn: become Subc V @ 1st rib & confluence of Cephalic Vn
    • -Subc V: Unites w/ IJV to form Brachiocephalic (Innominate) Bilat
    • -External Jugular Vn (EJV): Located in the neck, courses INF fr head to join Subc V
    • -Inernal Jugular Vn (IJV): Located in the neck, ANT & LAT to Carotid Art joins Subc V to form Innominate (Brachiocephalic) Vn
  2. Deep Veins of Upper extremity fr fingers to the RT Atrium
    • 1. Confluence of the venules of Deep digital veins → Metacarpal vns
    • 2. Metacarpal vns→Deep venous arches→forearm vns
    • 3. Radial & Ulnar Vns join near the antecubital fossa in front of the elbow to form the Paired Brachial Vn
    • 4. Brachial Vns paired w/ BA joins the Basilic Vn to becomes Axillary Vn & it travels adj to Axillary Art and crosses the 1st rib to become the Subc Vn
    • 5. Subc Vn is inf/ant to Subc Art and courses Medially It joins IJV (Internal Jugular Vn) & forms & drains→Brachiocephalic/Innominate Vns
    • 6. RT & LT Innominate Vns unite to form SVC (Superior Vena Cava)
    • 7. SVC carries bl → RT atrium
  3. Peripheral Venous (Anatomy) UE Superficial Vns
    • -Superficial Digital Vns drain bl fr tissues→Deep Vns
    • -Superficial Digital Vns: form the Cephalic vn on LAT aspect of forearm & Basilic Vn on MEDIAL aspect
    • -Cephalic Vn: courses LAT aspect of arm (Radial side) & unites w/ Axillary Vn (below Clavicular level) where they become Subc V
    • -Basilic Vn: (Largest Vn in the UE) courses up MEDIAL aspect of arm (Ulnar side), unites with Brachial Vn & becomes Axillary Vn. Basilic can join dir→Axillary Vn
    • -Median Cubital Vn: connects Basilic & Cephalic Vns @ Antecubital fossa (bend of the elbow)
  4. Peripheral Venous (Anatomy) UE Collaterals
    • -UE & thorax have MULT extensive collaterals
    • -This is the reason there is LESS incidence for UE Venous disease
  5. Bl flow from Deep vns of the toes to the RT atrium
    • 1. Confluence of venules of the deep digital vns →Metatarsal vns
    • 2. Metatarsal vns →Deep venous arches = Tibial Vns
    • 3. Paired PTV + Paired Pero Vns drain →Tibioperoneal trunk 
    • 4. ANT Tibial + TibioPeroneal trunk and LSV = Pop V
    • 5. Pop V becomes Superficial Femoral Vn @ the Adductor hiatus (distal thigh)
    • 6. SFV becomes CFV w/c is medial to the CFA and is formed by the confluence of the SFV, DFV & GSV below the Inguinal Lig
    • 7. CFV becomes EIV above Inguinal Lig
    • 8. EIV unites w/ the IIV (Internal Iliac Vn) to form the Common Iliac Vn (CIV) 
    • 9. CIV's join to form IVC @ the level of the 5th lumbar vertebra to the RT atrium
  6. Peripheral Venous (Anatomy) LE Deep Vns
    • -Deep Digital Vns: form the Plantar Metatarsal Vns
    • -Metatarsals: connect→Dorsal Vns to form Deep Plantar arch
    • -Calf Vns: 
    • -Peroneal Vns: Paired Vs coursing along LAT aspect of the leg adj to fibula (Small bone) & its accompanying art.  Comes together w/ Tibial Vn to form Tibioperoneal Trunk
    • -PTV: Paired Vs coursing POST to Tibia. Comes together w/ PERO Art to form Tibioperoneal Trunk
    • -ATV: Paired Vs formed by Dorsalis Pedis Vs on the dorsum of the foot. Travels LAT to Tibia along Interosseous membrane to unite w/ Tibioperoneal Trunk to become POP Vn
    • -Gastrocnemius Vn: Paired Vs accompany Sural Art & terminate→POP Art. 'Dumb-bell appearance on grayscale imaging
    • -Soleal Vns: Reservoir lie w/in Soleal & Gastrocnemius muscles of the calf & emptyPERO & PTV Vs.  Spindle shaped channels drain bl when calf muscle pump is activated
    • -POP Vns: formed fr junction of ATV & Tibioperoneal Vs below level of the knee.  Courses up the back leg thru Adductor Hiatus (Hunter's canal) to become Femoral Vn
    • -SFV: aka Femoral Vn travels MEDIAL up the thigh to join Deep Femeral Vn & becomes CFV approx 1.5-2 cm below Inguinal Lig
    • -DFV: aka Profunda Femoris ff ADJ Art in thigh. Unites w/ FV to form CFV
    • -CFV: Conts beyond Inguinal Lig to become EIV. Lies w/in Femoral Triangle (Scarpa's triangle) MEDIAL to CFA
    • -EIV: Continuation of CFV. Begins POST to Inguinal Lig coursing SUP to join IIV to form CIV 
    • *Extrinsic Comp of the LT Iliac Vn as it passes under the RT Iliac Art Known as May Thurner Syndrome causes ↑ incidence of acute DVT of LT lower extremity
    • -IIV: aka Hypogastric Vn ascends POSTEROMEDIAL to its ADJ art. Joins w/ EIV to form CIV
    • CIV: Union of IIV & EIV. Joins w/ contralateral CIV to form the IVC
  7. Peripheral Venous (Anatomy) LE Superficial Vns
    • -GSV: aka Long Saphenous Vn or Great Saphenous is Longest Vn in body & Begins @ inner dorsum of the foot. It is ANT to the Medial Malleolus & courses MEDIAL aspect of leg. Terminates @ CFV (Saphenofemoral junction) NO companion ART. Approx 12 valves. Used for ART Bypass grafts
    • -LSV: aka Short Saphenous Vn or Small Saphenous begins @ outer dorsum of foot. Courses POST to the LATERAL Malleolus then ff Midline of the calf to POP space. Terminates @ POP Vn betw heads of Gastrocnemius muscle. Contains approx 6-12 valves
  8. Gastrocnemius Vns (Sural Vns)
    • -Paired Vns accompany Sural Art
    • -Terminates→POP A
    • -Have a 'dumb-bell' appearance on grayscale
  9. Soleal Veins (Sinuses)
    • -Reservoirs that lie w/in Soleal & gastrocnemius muscles of the calf
    • -Empties into the PTV or Pero Vns
    • -Spindle shaped channels drain bl when calf muscle pump is activated
  10. Peripheral Venous (Anatomy) LE Perforating Vs
    • -aka Communicating Vns
    • -Carry bl fr Superficial→Deep Vns
    • -Contains valves w/c assist in Venous emptying by preventing Bi-Dir flow
    • -Post Tibial+Greater Saphenous=Post Arch Vn
    • *Gaitor zone (near Medial Malleolus) an area where Venous Stasis Ulcers form due to Reverse flow↑ Po in Superficial Venous Sys
  11. Peripheral Venous (Anatomy) 3 important Peforators in LE
    • 1. DODD's: Connects GSV→SFV in Upper leg
    • 2. BOYD's: Connects GSV→POP V
    • 3. COCKETT's: Connects GSV→Deep Vns of calf
  12. 3 major perforating Vns in the lower extremity
    • 1. PTV's have 2 important perforators near medial malleolus.  
    • 2. Post comm branch of GSV in the medial lower calf is connected to a 3rd perforator
    • 3. Post arch vn provides superficial connection to 3 perforating vns @ the ankle level w/c are important in the development of venous stasis ulcers (Cockett perforators)
  13. Anatomic Variants of LE
    • -Duplicate SFV & POP Vns
    • -Trifurcation of Calf Vns (absence of Tibioperoneal Trunk)
    • -Duplicate GSV or LSV
    • -In up to 30% of indiv, LSV terminates @ the GSV, Giacomini Vn or SFV instead of POP V
    • -SVC: is formed fr union of RT + LT Brachiocephalic (Innominate) Vns in Upper chest & empties Bl fr head and UE→RT Atrium of the ♡
    • -IVC: is formed w/in the pelvis fr union of RT + LT CIV's & Rcvs bl fr the LE as well as numerous ABD branches.  Unites w/ SVC to empty Bl→RT Atrium of the ♡
    • 1. Consists of return Bl fr Viscera→liver, formed by confluence of the SMV+SV (Splenic Vn)
    • 2. Drains Bl fr Intestines, Spleen, Stomach, GB, & Pancreas
    • 3. MPV enter the liver @ the Porta Hepatis & Bif→RT & LT PV branches
    • 4. Normal Bl flow dir=HEPATOPETAL (flow →Liver) & Abnormal flow = HEAPTOFUGAL (flow out of the Liver)
    • 5. SV tributaries: Short gastric vn, Pancreatic vn, LT gastro-epiploc vn, IMV

    **Bl flow w/in Portal Sys DOES NOT drain dir→the IVC. It drains→LIVER
    • -SMV empties the Small Intestine & parts of the colon 
    • -Tributaries: RT gastro-epiploic vn, Pancreaticduodenal vn, Paraumbilical vn, LT/RT gastric vns, Cystic vn
    • -Empty bl fr Kidneys→IVC
    • -RT Renal Vn is shorter & has DIR route→IVC
    • -LT Renal Vn is longer & courses ANT to AO & POST to the SMA to Enter the IVC on its LAT aspect
    • -Drain Bl fr Liver→IVC
    • -Enlarges in Pts w/ CHF or any RT-side ♡ disease
    • -Normal Dir of flow=HEPATOFUGAL
    • -3 Wall Layers:
    • 1. Intima: Innermost, contact w/ bl
    • -Single layer of endothelial cells
    • -Venous Valves are Dir Ext of Intima in Vn
    • 2. Media: Middle, composed of smooth muscle
    • -Thinner than ART-allow walls to be collapsible
    • 3. Adventitia: Outermost, made of thin layer of Connective tissue
    • -Contains Vaso Vasorum (network of vessels that supply vessel walls w/ bl)
    • -aka SemiLunar Valves or Bicuspid Valves
    • -Dir Ext of Intimal layer, composed of cusps originating @ opposite sides of the vn & coapt in the middle
    • -Allows for Unidir flow→♡; prevents retrograde flow
    • -Valvular Sinuses are dilatations above origin of the valve=Where thrombus forms
    • -Valves are numerous DISTALLY in leg; Critical to Venomotor pump
  21. Upper Extremity Vns w/ OR w/o valves
    • W/O Valves:
    • Innominate Vns
    • Sup Vena Cava (SVC)

    • W/Valves:
    • Jugular Vn
    • Cephalic & Basilic Vns
  22. Lower Extremity Vns w/o valves
    • -Soleal Sinuses
    • -EIV: contains valves 25% of the time
    • -CIV
    • -IIV
    • -IVC
  23. Lower Extremity Vns w/ valves
    • GSV (most below knee) & LSV :4-12
    • Perforators: 1 ea
    • Pop & Femoral: 3-6
    • Calf Vs: 30-50 
    • CFV: 1 
    • EIV
  24. Risk Factors for Venous Disease (Predisposing)
    • -Age
    • -Cancer (malignancy)
    • -Pregnancy
    • -Hormones (estrogen)
    • -Oral contraceptives
    • -Recent Surgery
    • -Immobility (bed rest, long car or plane ride)
    • -Paraplegia
    • -Prior DVT
    • -Trauma
  25. Risk Factors for Venous Disease (Virchow's Triad)
    • -Primary factors contributing to development of DVT:
    • -Venous Stasis
    • -Vessel wall injury (damage endothelial layer)
    • -Hypercoagulability
  26. Mechanisms of Disease-ACUTE DVT
    • -Thrombosis w/in Deep venous sys originating in the Venous Valves or in Soleal Sinuses
    • -Thrombus due to Intimal Injury
    • -PROXIMAL thrombus in POP, FEM or ILIAC Vns = ↑ Risk for PE
    • -As Thrombus Propagates: Flow is restricted, Venous Po ↑ (Venous Hypertension), Walls dilate, Valves become damaged
  27. Mechanisms of Disease-CHRONIC DVT
    • -Obstructive Fibrous cord NOT at risk for embolization
    • -A site susceptible to Recurrent Acute DVT
    • -Vns may be Chronically obstructed, partially or completely Recanalized
    • -Abnormalities seen in Chronic DVT:
    • -Diffuse wall thickening
    • -Echogenic Intraluminal material
    • -Fibrous cord
    • -Valvular damage
  28. Mechanisms of Disease-Superficial Thrombophlebitis
    • -Thrombosis & inflammation of a Superficial Vn
    • -Characterized by: 
    • -Warmth/Local Erythema
    • -Tenderness/pain
    • -Palpable Subcutaneous hard 'cord'
  29. Mechanisms of Disease-Chronic Venous Insufficiency (CVI) Valvular Incompetence
    • -Damaged/absent valves allow for retrograde flow leading to Venous Hypertension
    • -Calf muscle pump NO longer adequate to pump bl→♡
    • -Stasis Pigmentation, Dermatitis & Ulcer
    • ation may occur
    • -Ambulatory Venous Hypertension: 
    • 1. ↑ in Venous Po when pt stands or walks
    • 2. Results fr Valvular Incompetence
    • 3. May result in edema, varicosities or ulcers
    • -VI w/in Deep vns force bl fr the Deep → Superficial Vns via Incompetent Perf Vns
  30. Chronic Venous Insufficiency-Stasis Pigmentation
    -May occur on the MEDIAL & less often the LAT aspect of ankle and Lower leg
  31. Chronic Venous Insufficiency-Stasis Dermatitis
    -Further complication involving erythem, mild scaling & brown (brawny) discoloration
  32. Chronic Venous Insufficiency-Stasis Ulceration
    • -May eventually occur
    • -Caused by Venous Hypertension due to CVI
    • -Ulcerations are shallow, moist, red & located above the Medial Malleolus
    • -Treatment includes:
    • 1. Keeping area clean & medicated
    • 2. Unna boot w/ provides Venous Compression
    • 3. Skin grafts can be attempted
  33. Mechanisms of Disease-Varicose Veins
    • -Dilated Superficial Vns caused by Venous Valvular Incompetency
    • -2 Etiologies:
    • 1. Primary Varicose Vns: Caused by Valvular incompetence of the Superficial Venous Sys
    • -Caused by: Hereditary, Congenital absence of valves, Venous Hypertension, Trauma, Inflammation
    • 2. Secondary: Related to Valvular damage ff DVT mainly fr the Deep Sys
    • -Incompetent valves=Excessive Transluminal Po causing Vns to dilate, stretch
    • -Can result fr Incompetency in: Perf vns, Superficial/Deep vns, Combination of all
    • -Pain during walking
  34. Mechanisms of Disease-Congenital
    • -Congenital absence of valves
    • -Hypercoagulability:
    • -Thrombophilia=Protein C & S deficiencies
  35. Mechanisms of Disease-Pulmonary Embolism (PE)
    -Part or entire thrombus breaks loose & travels fr site of DVT lodging in Pulmonary Art or its branches
  36. Signs & Sx: ACUTE DVT
    • -Clinical sx are unreliable: Sx are accurate in <50% of pts
    • -Most common clinical findings:
    • 1. Pain
    • 2. Warmth
    • 3. Redness (erythema)
    • 4. Swelling (edema)
    • -Phlegmasia Alba Dolens
    • -Phlegmasia Cerula Dolens
  37. Signs & Sx: ACUTE DVT (Phlegmasia Alba Dolens)
    • -Limb threatening condition fr advanced extensive Acute Iliofemoral thrombosis
    • -DIST Art spasms w/ ↓ pulses
    • -Characterized by: Pallor (whiteness) of LE, Swelling, Cool to touch
  38. Signs & Sx: ACUTE DVT (Phlegmasia Cerulea Dolens)
    • -Limb threatening condition fr advanced extensive Acute Iliofemoral thrombosis
    • -Results fr severely ↓ Venous Outflow, w/c ↓ Art Inflow
    • -Characterized by: Cyanosis (Blue), Sudden pain, Massive Ededma
  39. Signs & Sx: CHRONIC DVT
    • -Discoloration
    • -Hyperpigmentation: Brawny in lower leg → ankle area (gaitor zone)
    • -Peripheral edema (usually UNILAT)
    • -Sense of heaviness
    • -Ulcerations
    • -Varicosities
  40. Signs & Sx: Venous Ulceration/Stasis Ulcers (Chronic Venous Insufficiency)
    • -Sx are milder in Primary Varicose Vns than in Secondary 
    • -Secondary varicose vns can lead to brawny discoloration, edema, stasis & dermatitis
    • -Skin changes incl: Pitting edema (fl in subcutaneous tissue), Ulcerations
  41. Signs & Sx: Venous Ulcer/Stasis
    • -Tissue break down fr lack of O2 & nutrients
    • -Venous Stasis ulcers develop when 1 or all perforators that carry bl fr POST Arch→Deep Sys are Incompetent
    • -These Perf are located near the Medial Malleolus (inner ankle) where most venous ulcers develop
  42. Differentiation Betw VENOUS & ART Ulcers
    • Characteristics    Venous        Arterial
    • Location            Medial Mal    Tibial area, toes
    •                                         bony prominences
    • Pain                     Mild               Severe
    • Appearance    Shallow, irreg     Deep, reg
    • Bleeding        Venous ooze     Little bleeding
    • Other       Stasis Dermatitis    Trophic changes
    •                    (brawny)         shiny, loss of hair
    •                                          thickened toenails
  43. Non-Invasive Test for UE/LE Venous Thrombosis: Duplex Imaging (Capabilities)
    • -ID Venous thrombosis
    • -Differentiate betw Acute & Chronic
    • -Distinguish betw Extrinsic comp & Intrinsic obst
    • -Eval Non-occluding thrombus
    • -Eval Soft tissue masses
    • -Detect Venous Incompetence
    • -Map Superficial Vns prior to CABG (Coronary Art Bypass Graft), Hemodialysis Access, Venous Ablation, or Peripheral Vascular Reconstructive Surgery
  44. Non-Invasive Test for UE/LE Venous Thrombosis: Duplex Imaging (Limitations)
    • -Obesity/body habitus
    • -Bony structures/clavicle & ribs when Eval Subc & Innominate Vns
    • -Casts & bandages/recent surgery
    • -Edema
    • -Vessel depth, diameter, & tortuosity of vessel
  45. Non-Invasive Test for UE/LE Venous Thrombosis: Duplex Imaging (Pt positioning & Choice of Instrument)
    • -UE: Supine, arm resting @ side
    • -LE: Supine, head slightly elevated or Reverse Trendelenburg
    • *Pt sitting w/ legs dangling, can enhance visualization of Calf Vns
    • -Tx F:
    • UE/LE: 5 or 7.5 MHz Linear array Tx
  46. Non-Invasive Test for UE Venous Thrombosis: EXAM PROTOCOL
    • -TRV comp every 1-2 inch (grayscale)
    • *Verify anatomy, ID of bifid sys, Wall Comp
    • -Longitudinal Color
    • *ID occlusion, partial occlusion or recannalized vessel, ID anatomical landmarks
    • -Doppler waveforms w/ & w/o AUG
    • *Document Vessel patency, & venous incompetence
  47. Non-Invasive Test for Venous Thrombosis: Calf Anatomy EXAM PROTOCOL
    • -Imaging of Calf Vns is the accepted standard for venous assessment
    • 1. PTV (Paired)
    • 2. Pero V (Paired)
    • 3. ATV (Paired)
    • 4. Tib/Peroneal Trunk=PTV & PERO V confluence to form Tibioperoneal Trunk in the PROX calf
  48. Non-Invasive Test for Venous Thrombosis: Calf Anatomy (Pt Positioning & Technique)
    • -Pt Position:
    • -Create Calf Vn distention for optimal visualization
    • -10-15o Reverse Trendelenburg
    • -Leg dangling off the edge of table
    • -Tourniquet placement w/ gentle Po near knee
    • -Technique:
    • -Apply same as PROX LE compression, color & spectral Doppler techniques
  49. Non-Invasive Test for LE Venous Thrombosis: Duplex Imaging (Capabilities)
    • -CFV, Saphenofemoral Junction, PROX DFV, SFV, POP V Evaluated
    • -Same procedure as UE
    • *LSV-Popliteal junction, PTV, PERO, ATV, GSV & LSV s/b Evaluated if clinically indicated
  50. Non-Invasive Test for UE/LE Venous Thrombosis: 2-D Interpretation
    • Qualitative
    • -Normal:
    • -Vn completely compressible
    • -Anechoic lumen
    • -Competent Valves
    • -Abnormal:
    • -Vn does NOT compress completely
    • -Echogenic material w/in lumen
    • -Valve leaflets attached to wall
  51. Non-Invasive Test for UE/LE Venous Thrombosis: 2-D Interpretation (Acute Characteristics)
    • -Difficult to see (echogenicity similar to Bl)
    • -Can NOT be completely compressible (Vessel)
    • -Fresh Thrombus is Soft & easily compressible
    • -Hypoechoic/Homogenous (Clot)
    • -Smooth surface characteristics
    • -Poorly attached to wall (free floating)
    • -Spongy texture
    • -Dilated (larger than normal Vn)
    • -If partially obstructed-flow may be seen around thrombus
    • -If totally occluded-NO flow
    • -NO Collaterals evident
  52. Non-Invasive Test for UE/LE Venous Thrombosis: 2-D Interpretation (Chronic Characteristics)
    • -Highly Echogenic (Bright fibrous webs w/in vn)
    • -Can NOT be completely compressible (Vessel)
    • -Firm & Hard to compress (Clot)
    • -Hyperechoic vn walls (Varies w/ age of thrombus)
    • -Irreg surface characteristics
    • -Firmly attached to wall
    • -Rigid Texture
    • -Size is normal→moderately contracted
    • -Often evident due to Recanalization of native vn
  53. Non-Invasive Test for UE/LE Venous Thrombosis: Spectral Doppler Interpretation (NORMAL)
    • -Normal:
    • -Spontaneous Doppler signal
    • -Phasicity of doppler signal noted (may be absent of pt is supine)
    • -Flow ceases w/ VM
    • -Doppler signal AUG w/ Distal Comp
    • -Waveform is NON-PULSATILE
  54. Non-Invasive Test for UE/LE Venous Thrombosis: Spectral Doppler Interpretation (ABNORMAL)
    • -Abnormal:
    • -CONT Venous flow in Doppler or NO flow if obstructed
    • -↑ Pulsatility (LE only)
    • -Reflux of flow (LE only)
    • -NO Flow or ROULEAU flow (very sluggish flow)=PROXIMAL Obstruction
  55. Non-Invasive Test for UE/LE Venous Thrombosis: Color Doppler Interpretation
    • -ID presence/absence of flow in specific regions of the DEEP Vns that are not easily compressible
    • -Best utilized in Femoral Vn (Adductor canal), DIST POP & Calf Vns.
    • -Spectral Doppler s/b used in PROXIMAL Vns
    • *In SAG Color Doppler may obsucre a 'free floating thrombus'
    • -ID collaterals or recanalization in Chronic DVT
  56. Non-Invasive Test for UE/LE Venous Thrombosis: CW DOPPLER
    • -Capabilities:
    • -Detect obstructive thrombus in Iliac, Fem & Pop
    • -Detect VI in both Deep & Superficial Vns
    • Limitations:
    • -Technique is SUBJECTIVE
    • -Unable to detect Isolated Calf Vn Thrombi
    • -Nonobstructive thrombus in Vns may NOT be detected
    • -In well-collateralized vessels, Normal flow may be detected DIST to a thrombosed vessel
  57. Non-Invasive Test for UE/LE Venous Thrombosis: CW DOPPLER (Pt Positioning/Technique)
    • -Pt Position:
    • -Reverse Trendelenburg
    • -Leg externally rotated w/ hip & knee flexed
    • -Decub position to diminish extrinsic comp on IVC due to pregnancy, tumor or ascites
    • -Technique:
    • -Assess CFV, FEM, POP, PTV 
    • -Venous flow characteristics=Spontaneity, Phasicity w/ resp, AUG w/ both DIST/PROX comp, REFLUX w/ AUG maneuvers
  58. Non-Invasive Test for UE/LE Venous Thrombosis: CW Doppler (Normal Interpretation)
    • -Qualitative: Normal
    • -Spontaneity s/b heard @ all sites
    • -Spontaneous signal
    • *Normal PTV may NOT have spontaneous signal. Perform AUG to obtain signal
    • -Phasicity: LE=flow ↑ (EXP); ↓ INSP
    • UE= flow ↓ (EXP); ↑ (INSP)
    • -AUG w/ DIST Comp & PROX release
    • -Competence
  59. Non-Invasive Test for UE/LE Venous Thrombosis: CW Doppler (Abnormal Interpretation)
    • -Qualitative: Abnormal
    • -Continuous flow pattern
    • -Pulsatile flow w/ fl overload in CHF
    • -Lack of Phasicity indicate either a PROX thrombosis or Intrinsic/Extrinsic compression of Venous flow
    • -Absent signal: NO Flow
  60. Non-Invasive Test Procedures for CVI: Duplex imaging (Capabilities/Limitations/Pt Position)
    • -Capabilities:
    • -Detect Venous Incompetence
    • -Diff Superficial fr Deep Incomp
    • -ID incompetent PERF vns
    • -Limitiations:
    • -Obesity, Bony structures, Casts/bandages, Edema
    • -Pt Position:
    • UE: Supine, Arm resting @ side
    • LE: Supine, head slightly elevated, Reverse Trendelenburg
  61. Non-Invasive Test Procedures for CVI: Duplex imaging (VI Protocol in Deep Vs)
    • -R/o Acute or Chronic Venous Obst.
    • -Doppler Waveforms fr:
    • -a. CFV & PROX GSV during VM= Look for REFLUX

    -b. CFV, PROX GSV/SFV, LSV in POP Fossa w/ DIST AUG= Look for REFLUX upon Release

    • -c. DIST POP V w/ DIST & PROX AUG
    • *DIST AUG=Look 4 REFLUX upon Release
    • *PROX AUG=Look 4 REFLUX while Squeezing

    -Reflux lasting more than 0.75=Incompetent valves PROX to sample site
  62. Non-Invasive Test Procedures for CVI: Duplex imaging (Perforator Incompetence)
    • -Interrogate entire calf for Perforators
    • -Meas Diameter of any Perf seen (>3mm=incompetence)
    • -Augment limb, PROX/DIST to the Perf, Observing for Reflux (>1 s=Abnormal) 
    • -Normal flow in Perf s/b fr Superficial→Deep
    • -If reversed=Incompetent Valves
    • -Mark Perf w/ marker if needed
  63. Non-Invasive Test Procedures for CVI: Duplex imaging (Measurement techniques)
    • -Spectral Doppler Waveforms obtained w/ pt in a 10-150 Reverse Trendelenburg
    • -Reflux can be confirmed by repeating waveforms w/ PT standing
    • -Tourniquets used to eliminated flow in Superficial Vns
    • -Reflux can be quantified w/ Rapid Cuff inflator (for reliable & reproducible Aug)
    • -Technique:
    • 1. Pt. standing, wt off leg being examined
    • -Cuff size= Thigh=24 cm, Calf=12 cm, Foot=7cm
    • 2. Spectral Doppler Waveforms obtained @ CFV, SFJ, POP & SPJ using intermittent rapid cuff inflation/deflation
    • 3. Interpretation=ID presence/absence of Retrograde flow after deflation & Reflux (>0.5 sec=significant)
  64. Non-Invasive Test Procedures for CVI: Reflux Plethysmography (PPG)
    • -Eval presence & severity of Valvular Incompetence. Documents bl vol in subcutaneous tissue
    • -Limitations:
    • -Contraindicated in pts w/ known DVT
    • -Improper placement of PPG sensor=inaccurate signals
    • -Collaterals affect result
    • -Venous Stasis Ulcers in gaitor zone may limit exam
  65. Non-Invasive Test Procedures for CVI: Reflux Plethysmography (PPG) Technique
    • -Pt sitting, legs dangling, apply PPG sensor 5-10 cm above Medial Malleolus (bilat)
    • -Ask pt to Dorsiflex foot 5x to empty bl fr calf vns (stimulates calf muscle pump)
    • -Monitor PPG tracing for Venous Refill Time (VRT)
    • -VRT >20-25 sec=NORMAL
    • -VRT <20-25 sec=ABNORMAL indic rapid ret of bl to the calf via incompetent channels
    • -Apply Tourniquet to determine if competence is in DEEP or SUPERFICIAL Venous Sys.
  66. Non-Invasive Test Procedures for CVI: Reflux Plethysmography (PPG) Tourniquet Test
    • -Apply Po cuff on Lower thigh & inflate to 50mmHg (Occludes GSV but not Deep Vns)
    • -Repeat foot Dorsiflexions & monitor VRT
    • -If repeat VRT >20 sec=Superficial sys has Venous Icompetence
    • -If repeat VRT remains <20 sec=Deep sys is incompetent
  67. Non-Invasive Test Procedures for CVI: Reflux Plethysmography (APG) Capabilities/Limitations
    • -Capabilities:
    • Detects obstructive thrombus in Iliac, Fem, Pop Vns by measuring MVC & MVO
    • -Limitations:
    • -Can NOT detect Calf Vein Thrombosis
    • -Small thrombosis that does NOT obstruct bl flow=NOT detected
    • -False+ may occur in pts w/: CHF, Tricuspid Insuff, Severe Pulmonary problems, Art Insuff, Extrinsic obstruction (tumor, pregnancy, obesity, improp gauge placement)
  68. Non-Invasive Test Procedures for CVI: Reflux Plethysmography (APG) Position/Technique
    • -Position:
    • -Supine, head flat & calf raised above ♡ level for Venous drainage
    • -Knee slightly bent w/ leg externally rotated
    • -Technique:
    • -Tx is placed on calf to detect Vol changes as cuff is inflated & deflated
    • -Occluding cuff is placed above the knee & inflated above Venous Po but below Art Po (45mmHg) for 2 mins
    • -Baseline tracing should rise & reach a plateau=MVC (Max Venous Capacitance)
    • -Cuff is rapidly deflated & 3 sec outflow is measured=MVO (Max Venous Outflow)
  69. Non-Invasive Test Procedures for CVI: Reflux Plethysmography (APG) Interpretation
    • -Normal:
    • -Tracing falls to baseline w/in 3 sec of deflation
    • -Abnormal:
    • -If tracing fall to baseline >3 sec
    • -Repeat 3-5x to R/O False + result
  70. Correlative &/or Prior Imaging for Venous Study (Conventional Venography)
    • -Contrast agent is inj→Vn & visualized by radiography to assess patency of the vessel
    • -Pt position on an exam table tilted 600 upright
    • -It is the gold standard for diagnosis of DVT
  71. Correlative &/or Prior Imaging for Venous Study (Ascending Venography)
    • -Used to assess patency of the Deep Sys. 
    • -Assesses Acute DVT 
    • -IDs the presence and location of DVT  
    • -Venous puncture site is on the dorsum of the foot
    • -Capable of identifying filling defects consistent w/ an acute DVT, anatomic variations & development of collateral channels

    *This info may be helpful in determining if pt is a candidate for surgical intervention
  72. Correlative &/or Prior Imaging for Venous Study (Descending Venography)
    • -Used to assess leg for Valvular Incompetence/Insufficiency
    • -Contrast is inj in the Femoral Vn & watched to see if it Descends the leg=Valvular Incomp
  73. Correlative &/or Prior Imaging for Venous Study (Interpretation/Limitation)
    • -Interpretation:
    • -Venous thrombus can be seen as a filling defect w/in the vein
    • -Complete thrombosis is seen as a 'lack of filling of contrast agent' w/in the vein at its expected location
    • -Limitations:
    • -May be painful for pt
    • -Diff betw Acute & Chronic thrombus is hard
    • -Contrast material may injure Venous wall inducing clot formation (Thrombophlebitis)
  74. Correlative &/or Prior Imaging for Venous Study Magnetic Resonance Venography (MRV)
    • -Uses MRI to visualize the Vns
    • -NO Radiation
    • -Often used for imaging Veins of the ABD
  75. Correlative &/or Prior Imaging for Venous Study Computed Tomography Venography (CTV)
    • -Radiological imaging modality uses computer processing to generate an image (CT scan) of the Vns
    • -Used primarily for Pulmonary scanning
  76. Other Diagnostic Tests: Venous-Ventilation Perfusion Lung scan
    -Nuclear meds screening test to detect perfusion defects of the lung commonly attributed to PE secondary to LE DVT
  77. Other Diagnostic Tests: Venous-The d-Dimer assay
    • -Bl test used to R/O active bl clot formation
    • -Normal result: R/O possibility of Active thrombotic formation
    • -Elevated d-Dimer result: Does NOT necessarily mean Bl Clot is present; it means Add'l testing may be needed to see if bl clot exists
  78. Treatment for Venous Disease: Controlling Risk Factors of DVT
    • -Wear support hose/compression stockings
    • -Elevate legs
    • -Limit long periods of inactivity or bed rest
    • -Use intermittent pneumatic calf compression during & after surgery
  79. Treatment for Venous Disease: Anticoagulation (HEPARIN)
    • -IV or Subcutaneous injection
    • 1. Heparin
    • -Interferes w/ formation of bl clot
    • -Acts to prevent extension of clot
    • -Contraindications: Active or suspected bleeding (GI, Intracranial), Coagulation disorders (thrombocytopenia, hemophilia),
    • *Thrombocytopenia: ↓ in platelets
    • Causes bleeding complication (hematoma) in pts w/ heparin treatment
    • Post-op ophthalmic or neuro surg, Endocarditis
  80. Treatment for Venous Disease: Anticoagulation (LOVENOX)
    • -aka Enoxaparin
    • -Low Molecular wt Heparin
    • -Usually give w/ Coumadin or Aspirin (ASA)
  81. Treatment for Venous Disease: Anticoagulation (Oral)
    • -Warfarin (Coumadin)
    • -Most commonly used for long term oral theraphy
    • -Prolonged action time
    • -May be used after Heparin or thrombolytic therapy for: DVT, Art Thrombosis, A/V Graft failures, Valvular ♡ disease, Poor surgical candidates w/ Prosthetic ♡ valves, AF or Cerebrovascular disease
    • -Contraindication are same as Heparin
    • -Contraindicated in pregnancy
  82. How does Vitamin K influence anticoagulants?
    • -It hinders the effect of anticoagulant Coumadin
    • -Vitamin K laden foods (generally leafy green vegetables) and diuretics (↑ clotting factor concentration) reduce the anticoagulant effect and ↓ the turnover of clotting factors.
  83. Treatment for Venous Disease: Antiplatelet Agents
    • -Aspirin, Persantine, Ticlopidine (anti-inflammatory drugs)
    • -↓ risk of platelt aggregation & thrombus formation
    • -Contraindications incl: Pts w/ gastric ulcers, Pregnancy, Sensitivity to the drugs
  84. Treatment for Venous Disease: Thrombolytic Therapy
    • -Urokinase, Streptokinase, tissue plasminogen activators (tPA)
    • -Used to break down existing clot (thrombolysis)
    • -Indications: Coronary Art Occl, Acute Art Occl, PE, Central Venous catheter Occl, Recent extensive DVT, Acute Stroke
    • -Contraindications: Recent surgical procedures, Recent invasive non-surgical procedures (biopsy, lumbar puncture), Pregnancy, Recent Trauma, Uncontrolled Hypertension
  85. Treatment for Venous Disease: Percutaneous IVC filters
    • -Used to prevent PE in pts who can NOT be subjected to Anticoagulant therapy
    • -Using fluoroscopy, Filter is placed in the IVC via either the Jugular or Femoral Vn
    • -It attaches DIST to the Renal Vns to catch any thrombus that may have broken off from the LE
  86. Treatment for Venous Disease: SURGERY
    • -For CVI: 
    • -Ligation of Incompetent Peft vns.
    • -Radio f/laser ablation of Incompetent Saphenous Vns.
    • -For Varicose Veins:
    • -Stripping or local excision of varicosities
    • -Sclerotherapy for venous 'closure' of GSV, LSV & small varicosities
  87. IF pulsatile flow is seen in Vns
    • -Indicates venous or pulmonary HTN, CHF, or the presence of an AVF 
    • -If Bilat =Systemic Venous HTN
    • -(EXCEPT: Flow in JUGULAR, SUBC & INNOM is pulsatile due to close proximity to the heart)
    • -SUBC VN will usually Augment w/ Inspiration
  88. CWD Venous assessment
    • -Venous incompetence or Valvular incompetence can be assessed w/ handheld CW doppler
    • -Nonspontaneous flow seen in PTVs or GSV is common in pts that are nervous and/or cold & therefore, Vasoconstricted (less flow in venous side due to closed down arterioles)
  89. Venous Flow Characteristics
    • -Spontaneity: flow is immediately seen when probe is placed over vessel
    • -Phasicity: related to respiration
    • -During inspiration venoussignals stop, during expiration venous signals return in an augmented state.
    • -Augmentation w/ distal compression & proximal release
    • -Patency: open vessel throughout
Card Set:
2015-07-16 01:23:07
Peripheral Venous
Venous Arterial RVS
Peripheral Venous/ART
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