Unit 2: LEV Pathophysiology

deep vein thrombosis (DVT)

• coagulates blood clot within a deep vein

• most common serious sequelae (consequence of prev. disease/injury) is a pulmonary embolism (PE) that originated from a lower extrem. DVT

• PE has significant morbidity and mortality if not recognized and/or treated early

risk factors:

• age

  • women >60yr

  • remains stable for males across age groups

• previous VTE (DVT and/or PE)

• hereditary hypercoagulable conditions

• acquired hypercoagulable conditions

• blood stasis conditions

venous thromboembolism (VTE)

• consists of DVT in conjunction w/ obstruction to flow to a pulm. artery or branch (PE) from thrombotic emboli

—

• 90% of pts. w DVT involve lower extremities

• 79% of pts. w/ a PE have evidence of DVT in their legs

• up to 50% of pts. w/ DVT may develop PE

LEV DVT

• usually originates from calf veins and propagates up into thigh

• affects only lone leg at a time

  • bilateral LEV exams are rare, if both legs are swollen u/s is ordered for whichever leg is worse

• rarely clinically important if isolated to calf veins

  • less likely to dislodge and travel up the smaller vessels

• very clinically important if left untreated and propagates up into larger deep veins

blood

blood composition:

• 55% plasma

  • liquid component

  • mix of water, sugar, fat, proteins, enzyme nutrients, hormones, gases, and salts

  • maintains body’s fluid balance

• 45% hematocrit

  • 3 types of blood cells:

    • RBC, WBC, platelets

plasma composition:

• large contributor to blood viscosity

• contributes to osmotic pressure

• albumin

  • dec. lvls lead to fluid accumulation in body (hypoalbuminemia)

    • causes edema

• fibrinogen

  • essential to blood clotting

  • dec. lvls lead to inc. risk of bleeding

  • inc. lvls can cause clot formation

red blood cells:

• aka erythrocytes

• transports O2 to tissue, and CO2 to lungs

COMMON DISORDERS

• anemia

  • dec # of RBCs to carry O2 to tissues » reduces blood viscosity

• sickle cell anemia

  • malformed and elongated RBCs » causes clumping of RBCs which leads to clot formation

• polycythemia

  • elevated RBCs » inc. blood viscosity

platelets:

• aka thrombocytes

• small cell fragments

• assists in clotting (coagulation)

COMMON DISORDERS

• thrombocytopenia

  • dec. # of thrombocytes » can cause excessive bleeding » lowers blood viscosity

• thrombocytosis

  • inc. # of thrombocytes » causes unnecessary clotting » inc. blood viscosity

clot formation

normal setting:

1. triggered by injured blood vessel

2. vasospasm

3. platelets form a temporary plug at site of injury (primary hemostasis)

4. series of rxns known as coagulation cascade

   1. activates clotting factors

   2. thrombin converts fibrinogen into sticky fibrin strands

   3. fibrins strands weave a mesh » trapping more platelets and RBCs

   4. forms a stable fibrin clot that seals injury and stops bleeding

intravascular thrombus formation:

1. triggered by endothelial injury or inflammatory signals (ie. surgery, cancer, stasis)

2. leads to platelet adhesion proteins and cluster to form a primary plug

3. series of rxns known as coagulation cascade

   1. results in a clot that obstructs blood flow

—

• clot formation itself can cause irritation to the intima layer, triggering inflammation

  • phlebitis: inflammation of a the vein

  • thrombophlebitis: inflammation of the vein due to a presence of clot

virchow’s triad

• DVT etiology

• named after German physician Rudolf Virchow

• describes 3 primary conditions that lead to thrombosis:

—

1. hypercoagulability = conditions that inc. blood viscosity and stickiness

2. venous stasis = conditions that promotes slow moving/stagnant blood flow

3. endothelial damage = conditions that activate the coagulation casacde

hereditary hypercoagulable conditions

• protein C and S deficiencies (antithrombin deficiencies)

• factor V leiden » most common inherited hypercoagulable disorder

• elevated plasminogen activator inhibitor-1

  • PAI-1: inhibits fibrinolysis (process of breaking down clots)

• non-O blood group » higher lvls of von Willebrand factor

• inc. lvls of clotting factor proteins (II, VII, IX, X, XI)

• primary hyperhomocysteinemia: impairs the balance of clotting factors

• antiphospholipid antibody syndrome: immune system mistakenly produces antibodies that makes blood more likely to clot

• myeleodysplasia: elevated lvls of pro-clotting cells, inflammation, and a genetic pre-desposition to clotting

• hyperviscosity syndromes

acquired hypercoagulable conditions

• malignant cancer: tumours can directly make blood more viscous/sticky

• chemotherapy: can dec. body’s natural proteins that thin the blood; some cancer drugs can cause more viscous/sticky blood

• heparin-induced thrombocytopenia: body produces antibodies against heparin (which is a natural coagulant)

• inflammatory bowel disease: chronic inflammation activates clotting factors, inc. platelets, and impairs fibrinolysis

• obesity: promotes continuous, low-grade inflammatory state

• pregnancy, oral contraceptive use, or hormonal replacement therapy: elevated lvls of clotting proteins and dec. lvls of proteins that prevent clotting

• polycythemia vera: overproduction of RBCs » making blood thicker

blood stasis conditions

• immobilization

• post surgery <3 months

  • highest risk <2wks post-op

  • most DVT are small and isolated to calf veins

  • ~50% of cases spontaneously resolved within 72hrs

• slow flow conditions

  • congestive HF

  • liver disease

• extrinsic compression

  • pregnancy (compression on iliofemoral region)

  • trauma (hematoma)

  • May-Thurner syndrome » compression of lt. CIV by the rt. CIA

clinical findings with DVT

• + D-dimer test » indicated thrombus formation somewhere in body

  • D-dimer lvls only remain elevated for ~7days post-thrombus formation, so not as useful for chronic thrombosis

  • >500µg/mL indicates +D-dimer

  • usually highly sensitive

    • less sensitive w/ small clots isolated in calf veins » results in low lvls of D-dimer

  • low specificity, could be (+) from other conditions..

    • mild bruising/hematoma, hemorrhage, cancer, sepsis

  • a (-) D-dimer is highly predictive for rling out DVT

—

signs and symp:

• swelling from edema

• pain and tenderness (often focal)

• redness & inc. warmth

• symptoms inc. when walking & subside w/ rest

• pain in buttocks and/or groin (w. iliofemoral DVT)

• superficial thrombophelbitis

  • more common than deep vein thrombophlebitis, and the affected vein can feel like a tender palpable cord near skin’s surface; skin may be red or warm to touch

• homan’s sign: discomfort in calf muscles on forced dorsiflexion of the foot w/ knee straight

  • non-specific, but presents in 1/3rd of DVT pts.

wells criteria

challenges w/ DVT signs and symp:

• up to 50% of pts. are asymp.

• up to 50% of pts. w/ “classic” DVT symptoms don’t have any DVT

—

• to help w/ the symptoms being non-specific nor sensitive, we have the Wells scoring to help determine probability of the presence of DVT

  • =/>3 points = high

  • 1-2 points = intermediate

  • =/<0 points = low

• continuous flow seen in CFV findings for DVT

compressions:

• main criterion for diagnosing presence of venous thrombosis is the inability to fully collapse a vein w/ compression

• if DVT is evident by 2D, compressions should be done gently and w/ caution to avoid dislodging the clot

rouleaux flow:

• can mimic thrombus

• may indicate higher risk for thrombosis (venous stasis)

• smoky appearance, shifts or moves w/ respiration or pressure

colour doppler:

• partial (some blood flow) = non-occlusive DVT

• complete (no blood flow) = occlusive

spectral findings:

ABOVE DVT SITE (above image)

• continuous flow lacking phasicity (blocks relfections from diaphragm movement)

  • if continuous flow seen in CFV unilaterally » consider iliac vein obstruction

  • if continuous flow seen in CFV bilaterally » consider IVC obstruction

BELOW DVT SITE (below image)

• calf compression/augmentation will not yield an increase in flow on the spectral tracing (in the absence of collaterals)

acute vs. chronic DVT

acute DVT:

• expands vein (vein size > artery size)

• anechoic - slightly hypo

• collaterals can develop quickly

• may be free floating or adherent to walls

chronic DVT:

• more echogenic and retracts in size

• more eccentric and focal

• adherent to walls

• can lead to “frozen” valves, synechia, calcification

• partial recanalization of the lumen may be observed in 60-80% of DVT pts.

• veins may collapse and fibrose (scar)

• serpiginous collaterals

• can lead to venous insufficiency from valvular damage

recurrent/new DVT

• new areas of thrombus compared to prev. exam

• >2mm inc. in vessel diameter during compression maneuvers

• this is where careful mapping of baseline DVT is important

  • need to document length

  • distance to landmarks or deep/superficial system

  • non-occlusive vs. occlusive?

superficial thrombophlebitis

• if thrombus is found in a superficial vein, it’s important to document its relationship to the deep venous sys.

• thrombus within 3cm of the deep sys. is an indication for anticoagulation therapy

treatment for DVT

heparin:

• intravenous anti-coagulant

• gold standard for DVT treatment

• permits fibrinolysis and prevents additional thrombus formation

• contraindications..

  • active, uncontrollable bleeding

vitamin K antagonist (VKA):

• type of anticoagulant medication that prevents blood clotting by interfering w/ the action of vitamin K (which is essential to produce certain clotting factors)

• oral warfarin is the most widely prescribed VKA

• taken in addition to heparin (usually over 5 days)

thrombolysis:

• not commonly used as it comes w/ higher risk of bleeding

• used for more serious extensive thrombus (ie. iliofemoral region) where there’s risk for post-thrombotic syndrome

compression therapy:

• treatment for post-thrombotic syndrome NOT during active thrombus

• wearing compression stocking (often 30-40mmHg) during the day can help prevent venous distension

sequelae of DVT

• in most pts. w/ post DVT, the thrombosed vein shows at least partial recanalization over a period of months » allowing for adequate venous return

  • despite recanalization, venous valves can be permanently damaged in up to 60% cases

post-thrombotic syndrome (PTS)

• long-term complication that can develop post-DVT

• affects 20-50% of pts. post-DVT diagnosis

• DVT may cause permanent damage to venous valves leading to..

  • venous reflux and blood pooling in veins

  • chronic swelling and leg pain

    • chronic leg swelling & reflux can result in ulceration of the gaiter zone (just above the ankle)

      • ulceration can develop spontaneously or post-trauma

      • underlying pathophysiology is complex and not entirely clear

  • poor circulation

  • skin changes (darkening, itchiness, dryness)

  • prolonged venous reflux leads to blood flow backup, ultimately to arterial side » resulting in diminished oxygenated blood to tissue

  • varicose veins

    • abnormally dilated & tortuous superficial veins

    • primary: develops in absence of coexisting DVT

    • secondary: associated w/ presence of DVT

critical forms of DVT

• acute massive venous thrombosis that occludes major venous channels (iliofemoral)

• can cause critical limb ischemia

• may progress to limb loss

• three stages

phlegmasia alba dolens:

• stage 1

• painful white inflammation (aka milk leg)

• venous drainage is dec. but still present

• patent small venous collateral channels

phlegmasia cerulea dolens:

• stage 2

• painful blue inflammation

• venous obstruction is segmental and includes collateral channels

• significant reduction in arterial inflow (cyanosis)

venous gangrene:

• stage 3

• ischemia leads to infarction & necrotic tissue

• primarily affects toes and foot

Which of the following best describes the findings in this ultrasound images?

Acute DVT in the popliteal vein

Which of the following can contribute to edema accumulation?

Hypoalbuminemia

venous insufficiency

aka..

• chronic venous insufficiency (CVI)

• chronic venous valvular insufficiency (CVVI)

• venous valvular insufficiency (VVI)

• postphlebotic syndrome

—

• the failure of the venous sys to provide adequate circulation (venous return to the heart), esp. from the lower extremity

• occurs from venous valvular incompetence in the superficial, deep, perforating and/or the non-saphenous veins of the lower limb

• distal superficial valve incompetence is more common than prox. incompetence

• can also be found in pelvic veins

• produces inc. ambulatory venous press.

varicose veins

• distended, lengthened and tortuous superficial veins secondary to valve incompetence

• superficial veins will distend outside of fascia where soft tissue doesn’t offer any external support

• varicosities don’t affect deep veins bcuz fascia contains and provides external support to the deep sys

• lower limb varicose veins are most often found along trunk of GSV

• most are large (>4mm in diameter), palpable, and tortuous

chronic venous insufficiency (CVI)

• affects ~40-50% of pop.

• remains poorly understood

• 80% of pts. w/ CVI have reflux alone

• clinical findings often not easily distinguishable from venous thrombosis

pathophysiology of venous insufficiency in lower limbs

• venous valves are present in the deep, superficial, and perforating veins

• greatest # of valves are in the calf

• resting venous pressure ~90mmHg when standing (height dependent)

• ambulation (walking) propels venous blood forward in the lower limbs

hemodynamics in a normal setting (competent valves)

valves:

• open valves promote flow return to heart

• brief flow reversal promotes valve closure

• normal vein valve closure depends on..

  • reversal of blood flow to force valve leaflets to coapt

  • blood flow reversal exceeding 30cm/s

  • velo. of retrograde flow is related to external pressure applied to vein

calf muscle contraction:

• distal valves and perforating valves clpse

• venous press. in foot is reduced to 20-30mmHg

calf muscle relaxation:

• venous sys is slowly refilled from arterial flow

• calf venous pressure still remains low

• blood flows from superficial to deep system via perforating veins

hemodynamics w incompetent valves

valves:

• reflux is often secondary to vein wall weakening » vein wall dilation » valves no longer able to connect/coapt when closed

• reflux occurs when valves are incompetent and a significant transvalvular PG is present:

  • during calf contraction and relaxation

  • performing valsalva

  • manual compression above or below incompetent valves

    • compression above will mimic diaphragm descent

    • compression below will mimic calf contraction and relaxation

calf muscle contraction:

• blood moves from deep to superficial veins (reflux)

calf muscle relaxation:

• blood can still move in a retrograde direction (reflux)

—

summary:

• incompetent valves results in an uninterrupted column of blood under the influence of gravitational and hydrostatic pressure

  • leads to persistent elevation of venous pressure at rest and during exercise = venous HTN

etiology of venous insufficiency

primary venous insuffiency:

• unrelated to venous obstruction

ETIOLOGY..

• hereditary

• congenital absence of valves

• venous HTN

• trauma

• inflammation

secondary venous insufficiency:

• damage secondary to obstruction/thrombosis

• found in..

  • perforating, superficial, deep veins

sequelae of DVT

w/ recanalization:

DVT » recanalization (partial or complete) » permanent vein valve damage (60% of cases) » immobile leaflets fixed to wall » venous reflux when upright » post-thrombotic syndrome (PTS)

no recanalization:

• DVT » no recanalization » chronic obstruction » post-thrombotic syndrome (PTS)

anatomical location of venous insufficiency

superficial:

• reflux limited to superficial venous sys. alone

• competent perforators

  • ie. GSV, SSV, superficial varicosities

deep:

• usually sequela of previous DVT (secondary insufficiency)

• deep valves damages post DVT

• competent superficial and perforator veins

superficial & deep:

• usually post DVT

• involves both deep and perforator or superficial veins

risk factors for venous insufficiency

• hx of DVT

• inc. age

• female

• family hx

• pregnancy

• obesity

• smoking

• occupations that require long periods of standing or sitting (no calf contractions)

clinical findings of early stage venous insufficiency

edema & pain

• ankle edema and leg pain that’s relieved by ambulation and/or limb elevation

  • relief w/ walking = reflux, pain w/ walking = obstruction/thrombus

• limb pain (heaviness and achiness, worse when upright for long periods)

superficial vein dilation

• dilated superficial or cutaneous calf veins

• most commonly seen medial lower calf and ankle

• aka varicose or spider veins (telangiectasia, reticular veins)

telangiectasia

• broken capillaries appearing as small linear blood vessels

reticular veins

• small visible blue-green veins

clinical findings of chronic stages of venous insufficiency

edema & pain

• dilated calf veins become more prominent and tortuous

• pitting edema (residual indent after pressing) that extends to mid-calf lvl

• persistent venous pressure elevation promotes leakage of protein-rich fluid and RBCs thru capillary walls into intercellular spaces

chronic interstitial leakage

• can lead to..

  • statis dermatitis

  • lipodermatosclerosis (LDS)

  • atrophie blanche

  • corona phlebectatica

statis dermatitis

• aka varicose eczema or venous eczema

• inflammation, redness, scaling, itching, and in severe cases » ulcers

• results in brown (brawny) skin discoloration (aka stasis pigmentation or hemosiderin staining)

lipodermatosclerosis (LDS)

• chronic skin inflammation w/ subcutaneous fibrosis

• assoc. w/ slow-healing wounds

• acutely

  • painful, red, warm to touch

  • often mistaken for cellulitis

• chronically

  • thickening and hardening (induration)

  • hyperpigmentation

  • “inverted champagne bottle” or “bowling pin” appearance

atrophic blanche

• porcelain white, stellate (star-shaped), and thin distinct scars from prev. healed venous ulcers

corona phlebectatica

• fan-shaped dilated red and blue cutaneous veins

ankle ulceration

• aka stasis ulceration

• reduced tissue O2 intake » malnutrition/hypoxia

• 20% of pts. w/ CVI develop venous ulcers

• recurrence common even after treatment

• pts. have 3-4 incompetent segments involving the deep and superficial venous systems (segmental venous valve incompetence)

venous vs. arterial ulcerations

venous:

• near medial malleolus

• mild discomfort

• shallow and irregular

• venous ooze and likely to bleed

• may also see..

  • statis dermatitis

  • brawny discolouration

  • varicosities

arterial:

• near tibial areas, toes, bony prominences

• severe discomfort

• deep and regular shape

• less likely to bleed

• may also see..

  • shiny skin

  • loss of hair

  • thickened toenails

basics of ultrasound in venous insufficiency

role:

• defining anatomical lvl and source(s) of incompetence

• determining if pathological process involves both valve incompetence and/or venous obstruction

  • initial assessment to rule out thrombus should be performed

• primarily focused on superficial veins, major tributaries, and perforating veins

pt. position:

• standing on a platform 18-24in in height surrounded in railing

• avoid bearing weight on examined leg during exam

• if pt. can’t remain standing, they should be supine in an exaggerated reverse Trendelenburg position

anatomy assessed:

• CFV

• femoral vein(s)

• SFJ

• GSV and its tributaries

• SSV

• pop v

varicosities in pelvis and thigh:

• assess these if varicosities are found..

  • IVC

  • pelvic veins

  • common and external iliac veins

normal sonographic findings (no insufficiency)

• gradual dec. in venous diameter distally

• full opening of valves and complete coaptation

GSV:

• lies within saphenous compartment b/w echogenic superficial and muscular fascia » “Egyptian eye” in TRV

• “terminal valve” present near saphenofemoral junction (SFJ), and a preterminal valve is freq. seen ~2cm below SFJ

  • superficial circumflex iliac vein, superficial inferior epigastric vein, and superficial & deep pudendal veins join the GSV b/w these two valves

  • these tributaries are often source of reflux if the terminal GSV valve is incompetent

SSV:

• normally ends above popliteal crease

• usually joins Pop V laterally @ saphenopopliteal junction (SPJ)

• may alternatively join a thigh extension vein (Giacomini vein) and join the GSV or deep veins

thigh extension (TE) vein:

• found in ~95% of pop.

• often considered the prox. extension of SSV into thigh

  • giacomini vein (GV) usually refers to part of TE that communicates the SSV w/ GSV

• TE may be source of reflux from more prox. veins

• may terminate into GSV, posterior thigh muscle veins, femoral vein, or branches of the iliac vein

perforator veins:

• perforator diameter <1mm

• may be duplicated or have a accompanying artery

• four main groups:

  • posterior, anterior, medial, lateral

doppler findings:

• spontaneous, antegrade flow that’s phasic w/ respiration (above calf)

• flow that’s augmented in cephalad direction w/ distal manual compression or foot flexion and flow cessation post-compression

• flow arrest w/ valsalva that returns to cephalad flow w/ release

abnormal sonographic findings (venous insufficiency)

2D:

• veins >7mm diameter » inc. incidence of reflux

• GSV..

  • dilation commonly seen at entry point of an incompetent tributary

  • dec. in size commonly seen distal to entry point of an incompetent tributary

• perforator veins..

  • 2mm = 50% chance of dysfunction

  • >3mm = confirms dysfunction

doppler:

• prominent retrograde flow when distal compression is released

  • can be seen in both colour and spectral

• retrograde flow w/ proximal manual compression (abdo or upper limb)

• retrograde flow during deep inspiration

• prominent retrograde flow during Valsalva

• prolonged duration of reflux (documented along spectral timeline)

  • clinically significant superficial or deep reflux - >0.5-1s

  • significant perforator reflux =/>0.35s

  • longer the reflex = more severe

treatment options for venous insufficiency

compression stockings:

• only treatment available for deep vein valve incompetence

• conservative treatment to help promote appropriate valve function

transilluminated powered phlebectomy (TIPP):

• uses illuminated endoscope to visualize varicose veins

• removes varicose veins w/ powered suction device thru small incisions

phelbectomy:

• aka surgical saphenectony or vein avulsion

• via a small surgical incision, a wire is used to pull out and disconnect the incompetent vein

endovenous ablation:

• non-surgical method for chronic valvular incompetence

• vein segments are ablated by either..

  • heat (laser or radiofrequency)

  • chemical (aka sclerotherapy)

  • glue

• causes veins to close off and scar over time

endovenous therapy advantages

• performed using local anesthesia

• minimally invasive

• reduced risk of post-op scarring or infection

• shorter procedure duration

• less post-procedure discomfort compared w/ vein stripping or avulsion

• majority of pts. can resume normal activity within days of procedure

ultrasound and treatment for venous insufficiency

pre-procedure:

• determine incompetent valve sites, diameter, and depth of veins, detect tortuous sites, detect anatomical variations

• can use skin markers to note location incompetent perforating veins and varicosities to help identify secondly by doppler & to reassess at time of treatment

procedure:

• help guide wire and catheter placement

• venous ablation occurs when RF or laser energy is applied to endothelial surface of vein wall and..

  • causes heating and vaporization of venous blood

  • results in carbonization and thermal destruction of the vein wall

  • seen on u/s as vasospasm followed by formation of thrombus

  • coagulation usually seen within 10-20s of applying RF or laser energy

post-op:

IMMEDIATELY

• pt. scanned to confirm ablation and then compression bandages applied

DAYS LATER

• confirm successful ablation of superficial and perforating veins

• confirm continued patency of CFV and prox. FVs

• rule out thrombus prox. to terminal GSV valve at SFJ

• successful ablation appears as heterogeneous echoes throughout ablated vein lumen

• may see arterialized spectral waveforms along vein walls, assoc. w/ intraluminal neovascularization

EXTENDED TIME LATER

• veins will become retracted and non-compressible w/ thickened walls and an echogenic, cord-like appearance

• should be no evidence of flow

Venous incompetence in the distal leg is more common than in the proximal leg.

true

Which of the following is NOT true with varicose veins?

Deep veins will distend outside the deep muscular fascia.

Which of the following symptoms is NOT consistent with lower extremity venous insufficiency?

Increase in pain with ambulation.

Match the following:

Telangiectasia = Superficial red linear vessels

—

Reticular veins = Superficial blue-green veins

—

Lipodermatosclerosis = Hyperpigmentation

Which of the following statements is NOT true for performing a duplex examination of the lower limbs to assess for venous insufficiency?

Reflux is primarily demonstrated by the Valsalva maneuver.

arterial stenosis/occlusion

may see significant plaque in lower extremity arteries

• typical stenosis u/s findings

• pre-stenosis » higher resistance flow

• at stenosis » high velocities and turbulence

• post-stenosis » turbulence

• distal to stenosis » tradus parvus flow

—

occlusion = absence of flow

popliteal artery aneurysm

• most common peripheral artery aneurysm

• can be mistaken for Baker’s cyst by 2D alone

pseudoaneurysm

• often seen as complication post-percuatenous arterial catheterization

• seen in groin area w/ typical PSA u/s findings..

  • neck with to-and-fro flow

  • cystic mass w/ yin-yang colour flow & possible internal debris/thrombus

• treated w/ ultrasound guided thrombin injection

  • most common treatment method

  • resolution is quick

soft tissue edema

• common cause of limb swelling

• bilateral leg swelling is more common w/ venous congestion (rt HF)

• excessive inc. in venous transmural pressure = dec. PG b/w arterioles & venules = dec. capillary perfusion = inc. filtration of fluids into tissue (edema)

etiology:

• DVT

• venous HTN

  • venous insufficiency

  • HF » venous congestion

  • extrinsic venous compression/obstruction

• fluid overload

  • renal failure

  • iatrogenic over-hydration

2D findings:

• marbled, reticulated pattern when found in subcut. fat

• small fluid collections may be seen within superficial tissues

• can obstruct ultrasound’s signals and make visualization of deeper structures more challenged (inc. attenuation)

doppler findings:

• extrinsic venous compression/obstruction:

  • continuous non-phasic flow below obstruction

• HF » venous congestion

  • inc. transmission of cardiac phasic changes in peripheral veins

  • waveforms are even more pulsatile than usual in upper leg veins w/ more prominent bidirectional venous

—

pulsatile venous flow v. arterial flow:

• venous patterns are less periodic than typical triphasic flow

• venous flow direction is primarily still towards heart

• venous flow pattern is affected by Valsalva

lymphadema

• caused by obstruction in lymph channels » resultings in excess fluid in the interstitial tissue

• may present as uni or bilateral leg swelling and pitting edema

• swelling os often recurrent, less in the morning & more severe later in the day

etiology:

• malignancy, radiation, infection, trauma, surgery

two types:

• primary

  • less common

  • inherited; occurs independently

• secondary

  • secondary to disease or other condition

sono findings:

• relatively thick subcutaenous tissue w/ “ant farm” appearance

• grainy appearance of subcutaneous tissue

• degraded image quality » inc. attenuation

• app. is typically indistinguishable from soft tissue edema

• may or may not see enlarged lymph nodes

lymphatic system

• lymph nodes are commonly seen in groin area, neck, and axillary regions

• typically, <1cm in AP diameter & enlarge w/ inflammatory or malignant infiltration

• inflamed lymph nodes are tender and can be the cause of lower limb pain

• adenopathy = enlarged lymph nodes

  • can cause swelling if associated w/ lymphatic or venous obstruction

• should be assessed for any abnormal characteristics

normal sono app:

• hypoechoic mantle of peripheral tissue surrounding central hyperechoic hilum containing fat & feeding vessels

• feeding vessels have low resistance arterial flow (doesn’t matter is benign or malignant)

benign appearance:

• almond-shaped or kidney shaped

• echogenic central hilum maintained

• SAX diameter = <1/2 LAX diamater

• maintains normal feeding vessels

  • extended from periphery to central hilum

  • well organized

malignant appearance:

• abnormal architecture & more rounded than oblong

• SAX diameter = >1/2 LAX diameter

• central hilum may be replaced by tumour

  • dec. echogenicity

• altered vascularity

  • irregular vessels follow disorganized pattern

cellulitis

• diffuse soft tissue inflammation of the skin & subcutaneous tissues

  • usually caused by bacterial infection post-break in the skin from trauma, surgery, or bite

• limb presents w/ redness, warmth, & shiny stretched skin app.

• may also see skin thickening, edema, & swelling of subcutaneous tissues

• often a clinical diagnosis that requires differential DVT diagnosis exclusion

sono findings:

• mimics soft tissue edema

• hyperemesis

lymphangitis

• bacterial infection in the lymphatic vessels

• presents as painful red streaks below skin surface

• potentially serious

  • can rapidly spread to bloodstream (sepsis)

  • potentially fatal

sono findings:

• mimics cellulitis & soft tissue edema

abscess

• implies enclosed collection of pus

• caused by bacterial infection

• presents w/

  • focal swelling, skin erythema, pain, tenderness

sono findings:

• may be well-circumscribed or ill-defined borders

• fluid collection within soft tissues containing complex fluid & echogenic internal debris (that may or may not include shadowing from tiny gas bubbles)

• may see surrounding hyperemic tissue

hematoma

• blood accumulation within tissue post-injury

• may present w/ focal or diffuse leg swelling

• injury is accompanied initially by bleeding, then inflammation

• can cause compression on surrounding veins

• MRI is superior for viewing soft tissue contrast and extent of hematoma

assoc. with:

• trauma

• vigorous exercise or abrupt straining

• prior injury/intervention

sono findings:

• focal mass; can be cystic, complex, or solid

• hyperechoic, and then either homo or hetero

• 7 days post-injury: intermediate to low lvl echogenicity & heterogeneous » persists for 3wks

• area is often focal & fusiform

• appears to “split” muscle strata

• tends to spread cephalocaudal in the facial planes

• absence of internal vascularity

• may initially present w irregular borders

• over time, mass will retract & becomes more well-defined and ovoid

• comparison w/ contralateral anatomy can help highlight abnormal variations in muscular tissue

baker’s cyst

• aka popliteal cyst or synovial cyst

• results from fluid collections in the gastrocnemius-semimembranous bursa (an extension of the knee joint)

• focal fluid collections along the pop fossa space, typically posteromedial to knee joint

• seen posterior to the medial femoral condyle in b/w the tendons and gastrocnemius muscles

• as these cysts enlarge, they may dissect thru the tissue planes and extend down into calf musculature

• prone to spontaneous rupture

• presents w/..

  • pain, tenderness, swelling, and similar symp. to DVT

• typically in pts. >50-6oyrs

etiologies:

• congenital

• trauma

• inflammation

• local degenerative changes

usually related to inflammation or irritation

& assoc. w/ multiple conditions..

• arthritis, trauma, infection, dialysis, hemophilia

differentials:

• hematoma, abscess, tumour

• soft tissue edema

• popliteal artery aneurysm, popliteal vein aneurysm (2x inc. in size)

• rare, associated w/ thromboembolic disease

sono findings:

CLASSIC

• seen along posterior-medial aspect of joint, adj. to head of gastrocnemius muscle

• simple cystic appearance w/ no internal echoes & well-defined walls

RUPTURED

• irregular margins, heterogeneous contents and/or echogenic debris, & extension into calf

joint effusion

• results from inflammation, infection, or trauma

• may cause pain & swelling

• distension of joint capsule w/ fluid

sono findings:

• fluid collects laterally, medially, & superiorly to patella

• fluid remains close to joint

• fluid may be simple or complex

soft tissue tumours

• unlikely cause of leg swelling and tenderness

• solid soft tissue masses must be distinguished from superficial or deep vein thrombosis

• large masses may be benign or malignant

• better defined w/ CT or MRI

benign examples:

• lipoma » most common benign lesion

• fibroma

• leiomyoma

• desmoid tumour

• neurofibromatosis

• soft tissue hemangioma

malignant examples:

• sarcoma

• lymphoma

• leukemia

sono findings:

• variable appearance

• may be solid or complex, depending on degree of necrosis

• high velocity, low resistance arterial flow

Which of the following lower extremity venous Doppler findings is consistent with right heart failure?

Bilateral increased venous pulsatility and biphasic flow.

What is this ultrasound image showing?

Enlarged lymph nodes

The following patient presents to the ultrasound department with calf swelling and pain. Visual examination reveals obvious swelling, but no redness or warmth to the touch. 

Large calf hematoma