Venous Disease

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Venous Disease
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ANATOMY

• A clear understanding of the anatomy of the
  venous system in the legs is essential to
  understanding pathophysiology as well as
  treatment. Venous drainage of the legs is the
  function of two parallel and connected systems
  the deep and the superficial systems connected
  by perforators .

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Superficial Venous System

• The superficial veins of the sole form a network
  that connects to the superficial dorsal veins of
  the foot and the deep plantar veins. The dorsal
  venous arch, into which empty the dorsal
  metatarsal veins, is continuous with the greater
  saphenous vein medially and the lesser saphenous
  vein laterally .
• The greater saphenous vein, in close proximity to
  the saphenous nerve, ascends anterior to the
  medial malleolus, crosses, and then ascends
  medial to the knee. It ascends in the superficial
  compartment and empties into the common femoral
  vein after entering the fossa ovalis.
• Before its entry into the common femoral vein, it
  receives medial and lateral accessory saphenous
  veins, as well as small tributaries from the
  inguinal region, pudendal region, and anterior
  abdominal wall. The posterior arch vein drains
  the area around the medial malleolus, and as it
  ascends up the posterior medial aspect of the
  calf, it receives medial perforating veins,
  termed Cocketts perforators, before joining the
  greater saphenous vein at or below the knee.
• The lesser saphenous vein arises from the dorsal
  venous arch at the lateral aspect of the foot and
  ascends posterior to the lateral malleolus, and
  it empties into the popliteal vein after
  penetrating the fascia. The exact entry of the
  lesser saphenous vein into the popliteal vein is
  variable.

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Deep Venous System

• The plantar digital veins in the foot empty into
  a network of metatarsal veins that comprise the
  deep plantar venous arch. This continues into the
  medialand lateral plantar veins that then drain
  into the posterior tibial veins. The dorsalis
  pedis veins on the dorsum of the foot form the
  paired anterior tibial veins at the ankle.The
  paired posterior tibial veins, adjacent to and
  flanking the posterior tibial artery, run under
  the fascia of the deep posterior compartment.
  These veins enter the soleus and join the
  popliteal vein, after joining with the paired
  peroneal and anterior tibial veins. There are
  large venous sinuses within the soleus musclethe
  soleal sinusesthat empty into the posterior
  tibial and peroneal veins.
• The popliteal vein enters a window in the
  adductor magnus, at which point it is termed the
  femoral vein. The femoral vein ascends and
  receives venous drainage from the profunda
  femoris vein, or the deep femoral vein, and after
  this confluence, it is called the common femoral
  vein. As the common femoral vein crosses the
  inguinal ligament, it is called the external
  iliac vein.

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Perforating veins

• Perforating veins connect the superficial venous
  system to the deep venous system at various
  points in the legthe foot, the medial and
  lateral calf, the mid- and distal thigh .

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Venous Function

• The venules, the smallest veins ranging from 0.1
  to 1 mm, contain mostly smooth muscle cells,
  whereas the larger extremity veins contain
  relatively few smooth muscle cells. These larger
  caliber veins have limited contractile capacity.
• The venous valves prevent retrograde flow, and it
  is the failure of the valves that leads to reflux
  and associated symptoms. Venous valves are most
  prevalent in the distal lower extremity, whereas
  as one proceeds proximally, the number of valves
  decreases to the point that in the superior and
  inferior vena cava, no valves are present.
• The return of the blood to the heart from the
  lower extremity is facilitated by the muscle pump
  function of the calfa mechanism whereby the calf
  muscle, functioning as a bellows during exercise,
  compresses the gastrocnemius and soleal sinuses
  and propels the blood toward the heart. The
  normally functioning valves in the venous system
  prevent retrograde flow it is when one or more
  of these valves become incompetent that symptoms
  of venous insufficiency can develop. During calf
  muscle contraction, the venous pressure of the
  foot and ankle drop dramatically. The pressures
  developing in the muscle compartments during
  exercise range from 150 to 200 mm Hg, and when
  there is failure of perforating veins, these high
  pressures are transmitted to the superficial
  system.

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Varicose Veins terms

• The term varicose veins is, in the common
  parlance, a term that encompasses a spectrum of
  venous dilation that ranges from minor
  telangiectasia to severe dilated, tortuous
  varicose veins. As stated earlier, for a proper
  categorization, as well as for appropriate
  treatment options to be considered, certain
  definitions must be agreed on.
• Varicose veins refer to any dilated, tortuous,
  elongated vein of any caliber.
• Telangiectasias are intradermal varicosities that
  are small and tend to be cosmetically unappealing
  but not symptomatic in and of themselves.
• Reticular veins are subcutaneous dilated veins
  that enter the tributaries of the main axial or
  trunk veins.
• Trunk veins are the named veins, such as the
  greater or lesser saphenous veins or their
  tributaries.
• The end result of CVI can range from aching,
  heaviness, pain, and swelling with prolonged
  standing or sitting in the case of symptomatic
  varicose veins, to severe lipodermatosclerosis
  with edema and ulceration in the patient with
  severe CVI.

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Risk Factors

• A combination of risk factors, rather than any
  one specific risk factor, is a better predictor
  of the likelihood of a given patient developing
  symptomatic varicose veins.
• Heredity undoubtedly plays a significant role in
  the development of varicose veins.
• Valvular dysfunction and insufficiency
• Female sex, gravitation hydrostatic force, and
  hydrodynamic forces due to muscular contraction.
• Hormonal Influence
• Venous function is undoubtedly influenced by
  hormonal changes. In particular, progesterone
  liberated by the corpus luteum stabilizes the
  uterus bycausing relaxation of smooth muscle
  fibers. This effect directly influences venous
  function. The result is passive venous dilation,
  which, in many instances, causes valvular
  dysfunction. Although progesterone is implicated
  in the first appearance of varicosities in
  pregnancy, estrogen also has profound effects. It
  produces the relaxation of smooth muscle and a
  softening of collagen fibers. Further, the
  estrogen-progesterone ratio influences venous
  distensibility. This ratio may explain the
  predominance of venous insufficiency symptoms on
  the first day of a menstrual period when a
  profound shift occurs from the progesterone phase
  of the menstrual cycle to the estrogen phase.

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Pathogenesis

• Defects in the strength and characteristics of
  the venous wall enter into the pathogenesis of
  varicose veins.
• Furthermore, communicating veins connecting the
  deep with the superficial compartment may have
  valve failure.
• Pressure studies show that two sources of venous
  hypertension exist. The first is gravitational
  and is a result of venous blood coursing in a
  distal direction down linear axial venous
  segments. This is referred to as hydrostatic
  pressure and is the weight of the blood column
  from the right atrium.
• The second source of venous hypertension is
  dynamic. It is the force of muscular contraction,
  usually contained within the compartments of the
  leg. If a perforating vein fails, high pressures
  (ranging from 150 to 200 mm Hg) developed within
  the muscular compartments during exercise are
  transmitted directly to the superficial venous
  system. Here, the sudden pressure transmitted
  causes dilation and lengthening of the
  superficial veins. Progressive distal valvular
  incompetence may occur.

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Pathogenesis Changes occur at the cellular
level.

• In the distal liposclerotic area, capillary
  proliferation is seen and extensive capillary
  permeability occurs as a result of the widening
  of interendothelial cell pores. Transcapillary
  leakage of osmotically active particles, the
  principal one being fibrinogen, occurs. The
  extravascular fibrin remains to prevent the
  normal exchange of oxygen and nutrients in the
  surrounding cells.However, little proof exists
  for an actual abnormality in the delivery of
  oxygen to the tissues. An other factor is the
  protolytic enzymes from the extravasated
  leukocytes

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VENOUS INSUFFICIENCY

• The C-E-A-P classification is a recent scoring
  system that stratifies venous disease based on
  clinical presentation, etiology, anatomy, and
  pathophysiology.
• C Clinical signs (grade 06 , supplemented by A
  for asymptomatic and S for symptomatic
  presentation
• E Etilogic classification (congential, primary,
  secondary)
• A Anatomic distribution (superficial, deep, or
  perforator, alone or in combination)
• P Pathophysiologic dysfunction (reflux or
  obstruction, alone or in combination)

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Clinical Classification of Chronic Lower
Extremity Venous Disease

• Class 0 No visible or palpable signs of venous
  disease
• Class 1 Telangiectasia, reticular veins,
  malleolar flare
• Class 2 Varicose veins
• Class 3 Edema without skin changes
• Class 4 Skin changes ascribed to venous disease
  (e.g., pigmentation, venous eczema,
  lipodermatosclerosis)
• Class 5 Skin changes as defined above with healed
  ulceration
• Class 6 Skin changes as defined above with active
  ulceration

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• Etiologic Classification of Chronic Lower
  Extremity Venous Disease
• Congenital (EC ) Cause of the chronic venous
  disease present since birth
• Primary (EP ) Chronic venous disease of
  undetermined cause
• Secondary (ES ) Chronic venous disease with an
  associated known cause (post-thrombotic,
  post-traumatic, other)
• ANATOMIC CLASSIFICATION (AS , AD , or AP )
• The anatomic site(s) of the venous disease should
  be described as superficial (AS ), deep (AD ), or
  perforating (AP ) vein(s). One, two, or three
  systems may be involved in any combination. For
  reports requiring greater detail, the involvement
  of the superficial, deep, and perforating veins
  may be localized by use of the anatomic segments.
• PATHOPHYSIOLOGIC CLASSIFICATION (PR,O )
• Clinical signs or symptoms of chronic venous
  disease result from reflux (PR ), obstruction (PO
  ), or both (PR,O ).

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Symptoms

• The patient with symptomatic varicose veins
  relates, most often, symptoms of aching,
  heaviness, discomfort, and sometimes pain in the
  calf of the affected limb.
• This is particularly worse at the end of the day,
  most likely due to prolonged sitting or standing
  that results in venous distention and associated
  pain. The symptoms are typically reduced or
  absent in the morning owing to the fact that the
  limb has not been in a dependent position through
  the night.
• In the case of women, the symptoms are often most
  troubling and exacerbated during the menstrual
  period, particularly during the first day or two.
  
• Primary varicose veins consist of elongated,
  tortuous, superficial veins that are protuberant
  and contain incompetent valves.
• Primary varicose veins merge imperceptibly into
  more severe CVI.
• Swelling ,edema is moderate to severe, an
  increased sensation of heaviness occurs with
  larger varicosities, and early skin changes of
  mild pigmentation and subcutaneous induration
  appear.
• When CVI becomes severe, marked swelling and calf
  pain occur after standing, sitting, or walking.
• Multiple dilated veins are seen associated with
  various clusters and heavy medial and lateral
  supramalleolar pigmentation.

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• Many causes of leg pain are possible, and most
  may coexist. Therefore, defining the precise
  symptoms of venostasis is necessary. Discomfort
  usually occurs during warm temperatures and after
  prolonged standing. The pain is
  characteristically dull, does not occur during
  recumbency or early in the morning, and is
  exacerbated in the afternoon, especially after
  long standing. The discomforts of aching,
  heaviness, fatigue, or burning pain are relieved
  by recumbency, leg elevation, or elastic support.
• Cutaneous itching is also a sign of venostasis
  and is often the hallmark of inadequate external
  support. It is a manifestation of local
  congestion and may precede the onset of
  dermatitis. This, and nearly all the symptoms of
  stasis disease, can be explained by the
  irritation of superficial nerve fibers by local
  pressure or accumulation of metabolic end
  products with a consequent pH shift.
• External hemorrhage may occur as superficial
  veins press on overlying skin within this
  protective envelope.

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DIAGNOSTIC EVALUATION OF VENOUS DYSFUNCTION

• Clinical examination of the patient in good light
  provides nearly all the information necessary. It
  determines the nature of the venostasis disease
  and ascertains the presence of intercutaneous
  venous blemishes and subcutaneous protuberant
  varicosities, the location of principal points of
  control or perforating veins that feed clusters
  of varicosities, the presence and location of
  ankle pigmentation and its extent, and the
  presence and severity of subcutaneous induration.
  
• Visual examination can be supplemented by noting
  a downward-going impulse on coughing.
• Tapping the venous column of blood also
  demonstrates pressure transmission through the
  static column to incompetent distal veins.
• The modified Perthes test for deep venous
  occlusion .
• Brodie-Trendelenburg test ,and multible
  tornicheat test of axial reflux
• Those testes have been replaced by in-office use
  of the continuouswave, handheld Doppler
  instrument supplemented by duplex evaluation.The
  handheld Doppler instrument can confirm an
  impression of saphenous reflux, and this, in
  turn, dictates the operative procedure to be
  performed in a given patient. And it is used in
  specific locations to determine incompetent
  valves of perforators.
• Duplex technology more precisely defines which
  veins are refluxing by imaging the superficial
  and deep veins.

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Treatment

• Indications for treatment are pain, easy
  fatigability, heaviness, recurrent superficial
  thrombophlebitis, external bleeding, and
  appearance.
• Nonoperative Management
• The cornerstone of therapy for patients with CVI
  is external compression.
• A triple-layer compression dressing, with a zinc
  oxide paste gauze wrap in contact with the skin,
  is utilized most commonly from the base of the
  toes to the anterior tibial tubercle with snug,
  graded compression.
• In general, snug, graded-pressure triple-layer
  compression dressings effect more rapid ulcer
  healing than compression stockings alone.

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Venous Ablation Sclerotherapy

• Cutaneous venectasia with vessels smaller than 1
  mm in diameter do not lend themselves to surgical
  treatment. Dilute solutions of sclerosant (e.g.,
  0.2 sodium tetradecyl) can be injected directly
  into the vessels of the blemish. Care should be
  taken to ensure that no single injection dose
  exceeds 0.1 mL but that multiple injections
  completely fill all vessels contributing to the
  blemish.
• Venules larger than l mm and smaller than 3 mm in
  size can also be injected with sclerosant of
  slightly greater concentration (e.g., 0.5 sodium
  tetradecyl), but limiting the amount injected to
  less than 0.5 mL.
• If their cause is saphenous or tributary venous
  incompetence, these conditions can be treated
  surgically.
• Surgery is not indicated for the treatment of
  venous insufficiency in limbs with deep venous
  incompetence .

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Surgical Management

• Surgical treatment may be used to remove clusters
  with varicosities greater than 4 mm in diameter.
  Ambulatory phlebectomy may be performed using the
  stab avulsion technique with preservation of the
  greater and lesser saphenous veins, if they are
  unaffected by valvular incompetence

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• When greater or lesser saphenous incompetence is
  present, the removal of clusters is preceded by
  limited removal of the saphenous vein
  (stripping).
• Stripping techniques are best done from above
  downward to avoid lymphatic and cutaneous nerve
  damage.

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Subfascial endoscopic perforator vein surgery

• perforating vein division using laparoscopic
  instrumentation. Initial data suggested that
  perforator interruption produced rapid ulcer
  healing and a low rate of recurrence.
• Direct Venous Reconstruction ??

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DEEP VENOUS THROMBOSIS

• Acute deep venous thrombosis (DVT) is a major
  cause of morbidity and mortality in the
  hospitalized patient, particularly in the
  surgical patient. The triad of venous stasis,
  endothelial injury, and hypercoagulable state
  first posited by Virchow has held true a century
  and a half later.
• The thrombotic process initiating in a venous
  segment can, in the absence of anticoagulation or
  in the presence of inadequate anticoagulation,
  propagate to involve more proximal segments of
  the deep venous system, thus resulting in edema,
  pain, and immobility.
• The most dreaded sequel to an acute DVT is that
  of pulmonary embolism, a condition of potentially
  lethal consequence.
• The late consequence of DVT, particularly of the
  iliofemoral veins, can be CVI due to valvular
  dysfunction in the presence of luminal
  obstruction.
• For these reasons, understanding the
  pathophysiology, standardizing protocols to
  prevent or reduce DVT, and instituting optimal
  treatment promptly all are critical to reducing
  the incidence and morbidity of this unfortunately
  common condition.

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Etiology

• Stasis
• Soleal sinuses are the most common sites for
  initiation of venous thrombosis. The stasis may
  contribute to the endothelial cellular layer
  contacting activated platelets and procoagulant
  factors, thereby leading to DVT.
• The Hypercoagulable State
• Should any of these conditions be identified, a
  treatment regimen of anticoagulation is
  instituted for life, unless specific
  contraindications exist.
• Following major operations, large amounts of
  tissue factor may be released into the
  bloodstream from damaged tissues. Tissue factor
  is a potent procoagulant .Increases in platelet
  count, adhesiveness, changes in coagulation
  cascade, and endogenous fibrinolytic activity all
  result from physiologic stress such as major
  operation or trauma and have been associated with
  an increased risk of thrombosis.
• Venous Injury
• It has been clearly established that venous
  thrombosis occurs in veins that are distant from
  the site of operation for instance, it is well
  known that patients undergoing total hip
  replacement frequently develop contralateral
  lower extremity DVT.
• There were multiple microtears noted within the
  valve cusps that resulted in the exposure of the
  subendothelial matrix. The exact mechanism by
  which this injury at a distant site occurs, and
  what mediators, whether cellular or humeral, are
  responsible is not clearly understood but that
  the injury occurs and occurs reliably is evident
  from these and other studies.

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Hypercoagulable States

• Factor V Leiden mutation
• Prothrombin gene mutation
• Protein C deficiency
• Protein S deficiency
• Antithrombin III deficiency
• Antiphospholipid syndrome

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Incidence

• Venous thromboembolism occurs for the first time
  in approximately 100 persons per 100,000 This
  incidence increases with increasing age with an
  incidence of 0.5 per 100,000 at 80 years of age.
• More than two thirds of these patients have DVT
  alone, and the rest have evidence of pulmonary
  embolism.
• The recurrence rate with anticoagulation has been
  noted to be 6 to 7 in the ensuing 6 months.
• Aside from pulmonary embolism, secondary CVI
  (that resulting from DVT) is significant in terms
  of cost, morbidity, and lifestyle limitation.
• If the consequence of DVT, in terms of pulmonary
  embolism and CVI, is to be prevented, the
  prevention, diagnosis, and treatment of DVT must
  be optimized.

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Clinical Diagnosis

• The diagnosis of DVT requires, to use an overused
  phrase, a high index of suspicion.
• Most are familiar with Homans sign, which refers
  to pain in the calf on dorsiflexion of the foot.
  It is certainly true that although the absence of
  this sign is not a reliable indicator of the
  absence of venous thrombus, the finding of a
  positive Homans sign should prompt one to
  attempt to confirm the diagnosis.
• Certainly, the extent of venous thrombosis in the
  lower extremity is an important factor in the
  manifestation of symptoms. For instance, most
  calf thrombi may be asymptomatic unless there is
  proximal propagation.
• Only 40 of patients with venous thrombosis have
  any clinical manifestations of the condition.
• Major venous thrombosis involving the iliofemoral
  venous system results in a massively swollen leg
  with pitting edema, pain, and blanching, a
  condition known as phlegmasia alba dolens. With
  further progression of disease, there may be such
  massive edema that arterial inflow can be
  compromised. This condition results in a painful
  blue leg, the condition called phlegmasia cerulea
  dolens. With this evolution of the condition,
  unless flow is restored, venous gangrene can
  develop.

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Investigation

• Duplex Ultrasound.
• The modern diagnostic test of choice for the
  diagnosis of DVT is the duplex ultrasound, a
  modality that combines. Real time B-mode
  ultrasonography with color-flow imaging has
  improved the sensitivity and specificity of
  ultrasound scanning. With color-flow duplex
  imaging, blood flow can be imaged in the presence
  of a partially occluding thrombus. The probe is
  also used to compress the vein A normal vein
  should be easily compressed, whereas in the
  presence of a thrombus, there is resistance to
  compression. Magnetic Resonance Venography.
• With major advances in technology of imaging,
  magnetic resonance venography has come to the
  forefront of imaging for proximal venous disease.
  The cost and the issue of patient tolerance due
  to claustrophobia limit the widespread
  application, but this is changing. It is a useful
  test for imaging the iliac veins and the inferior
  vena cava, an area where duplex ultrasound is
  limited in its usefulness.

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Prophylaxis

• The patient who has undergone either major
  abdominal surgery, major orthopedic surgery, has
  sustained major trauma, or has prolonged
  immobility (gt3 days) represents a patient who has
  an elevated risk for the development of venous
  thromboembolism.
• The methods of prophylaxis can be mechanical or
  pharmacologic.
• The simplest method is for the patient to be able
  to walk. Activation of the calf pump mechanism is
  an effective means of prophylaxis.
• A patient who is expected to be up and walking
  within 24 to 48 hours is at low risk of
  developing venous thrombosis. The practice of
  having a patient out of bed into a chair is one
  of the most thrombogenic positions that one could
  order a patient into. Sitting in a chair with the
  legs in a dependent position causes venous
  pooling, which in the postoperative milieu could
  be easily a predisposing factor in the
  development of thromboembolism.
• The most common method of prophylaxis in the
  surgical universe has traditionally revolved
  around sequential compression devices, which
  periodically compress the calves and essentially
  replicate the calf bellows mechanism. This has
  clearly reduced the incidence of venous
  thromboembolism in the surgical patient.

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Heparin

• Minidose heparin the dose traditionally used is
  5000 units of unfractionated heparin every 12
  hours. When subcutaneous heparin is used on an
  every-8-hour dosing, rather than every 12 hours,
  there is a reduction in the development of venous
  thromboembolism.
• More recently, fractionated low-molecular-weight
  heparin (LMWH) for prophylaxis and treatment of
  venous thromboembolism.
• LMWH inhibits factors Xa and IIA activity, with
  the ratio of antifactor Xa to antifactor IIA
  activity ranging from 11 to 41.
• LMWH has a longer plasma half-life and has
  significantly higher bioavailability. There is
  much more predictable anticoagulant response than
  heparin. No laboratory monitoring is necessary
  because the partial thromboplastin time (PTT) is
  unaffected. LMWH results less bleeding
  complications.
• In short, LMWH should be considered the optimal
  method of prophylaxis in moderate and high-risk
  patients.

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TREATMENT

• Traditionally, the treatment of DVT centers
  around heparin treatment to maintain the PTT at
  60 to 80 seconds, followed by warfarin therapy to
  obtain an International Normalized Ratio (INR) of
  2.5 to 3.0.
• A widely used regimen is 80 U/kg bolus of
  heparin, followed by a 15 U/kg infusion. The PTT
  should be checked 6 hours after any change in
  heparin dosing.
• Warfarin is started the same day. If warfarin is
  initiated without heparin, the risk of a
  transient hypercoagulable state exists, because
  proteins C and S levels fall before the other
  vitamin Kdependent factors are depleted.
• With the advent of LMWH, it is no longer
  necessary to admit the patient for intravenous
  heparin therapy. It is now accepted practice to
  administer LMWH to the patient as an outpatient,
  as a bridge to warfarin therapy.
• A minimum treatment time of 3 months is advocated
  in most cases.
• If, however, the patient has a known
  hypercoagulable state or has experienced episodes
  of venous thrombosis, then lifetime
  anticoagulation is required, in the absence of
  contraindications.
• The accepted INR range is 2.0 to 3.0.
• Oral anticoagulants are teratogenic and thus
  cannot be used during pregnancy. In the case of
  the pregnant woman with venous thrombosis, LMWH
  is the treatment of choice, and this is continued
  through delivery and can be continued postpartum
  if needed.

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Thrombolysis

• The advent of thrombolysis has resulted in
  increased interest in thrombolysis for DVT. The
  purported benefit is preservation of valve
  function with subsequently lesser chance of
  developing CVI. However, to date, little
  definitive, convincing data exist to support the
  use of thrombolytic therapy for DVT.
• One exception is the patient with phlegmasia in
  whom thrombolysis is advocated for relief of
  significant venous obstruction. In this
  condition, thrombolytic therapy probably results
  in better relief of symptoms and less long-term
  sequelae than heparin anticoagulation alone.
• The alternative for this condition is surgical
  venous thrombectomy.
• No matter which treatment is chosen, long-term
  anticoagulation is indicated.
• The incidence of major bleeding is higher with
  lytic therapy.

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Vena Caval Filter

• The most worrisome and potentially lethal
  complication of DVT is pulmonary embolism.
• The symptoms of pulmonary embolism, ranging from
  dyspnea, chest pain, and hypoxia to acute cor
  pulmonale are nonspecific and require a vigilant
  eye for the diagnosis to be made.
• The gold standard remains the pulmonary
  angiogram, but increasingly this is being
  displaced by the computed tomographic angiogram.
• Adequate anticoagulation is usually effective in
  stabilizing venous thrombosis, but if a patient
  should develop a pulmonary embolism in the
  presence of adequate anticoagulation, a vena cava
  filter is indicated. The modern filters are
  placed percutaneously over a guide wire. The
  Greenfield filter, with the most extensive use
  and data, has a 95 patency rate and a 4
  recurrent embolism rate.
• This high patency rate allows for safe suprarenal
  placement if there is involvement of the inferior
  vena cava up to the renal veins or if it is
  placed in a woman of childbearing potential.
• The device-related complications are wound
  hematoma, migration of the device into the
  pulmonary artery, and caval occlusion due to
  trapping of a large embolus. In the latter
  situation, the dramatic hypotension that
  accompanies acute caval occlusion can be mistaken
  for a massive pulmonary embolism. The distinction
  between the hypovolemia of caval occlusion versus
  the right heart failure from pulmonary embolism
  can be arrived at by measuring filling pressures
  of the right side of the heart. The treatment of
  caval occlusion is volume resuscitation.

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Indications for a Vena Cava Filter

• Recurrent thromboembolism despite adequate
  anticoagulation
• Deep venous thrombosis in a patient with
  contraindications to anticoagulation
• Chronic pulmonary embolism and resultant
  pulmonary hypertension
• Complications of anticoagulation
• Propagating iliofemoral venous thrombus in
  anticoagulation

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Pulmonary Thromboembolism

• DVT is most common source of PE lt10 of PE
  cases cause pulmonary infarction
• Symptoms and signs include dyspnea and chest
  pain (present in 75) tachycardia, tachypnea,
  altered mental status classic triad of dyspnea,
  chest pain, and hemoptysis in only 15 pleural
  rub and S1Q3T3 rarely found
• V? /Q? scan has sensitivity and specificity of
  90, but 67 of studies are inconclusive spiral
  computed tomography is more accurate
• Differential Diagnosis
• Other causes of chest pain and hypoxia, such as
  pneumonia
• Treatment
• Stabilize initially with pressors and
  ventilatory support start heparin or
  low-molecular-weight heparin quickly
• Surgery consider IVC filter if risk of embolus
  is ongoing and anticoagulation
• is risky
• Open surgical thrombectomy (Trendelenburg
  procedure) high mortality, rarely clinically
  useful for massive saddle embolus
• Prevention DVT prophylaxis in perioperative
  period

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Superficial Thrombophlebitis

• Can occur spontaneously in varicose veins, post
  traumatic, pregnant or postpartum women,
  thromboangiitis obliterans, Behçet disease
  superficial migratory phlebitis (Trousseau)
  suggests abdominal carcinoma
• Symptoms and signs include local extremity pain,
  redness indurated, erythematous, tender areas
  indicate thrombosed superficial veins well
  localized over superficial vein
• Differential Diagnosis
• Ascending lymphangitis
• Cellulitis
• Treatment
• Primary treatment includes nonsteroidal
  anti-inflammatory drugs, heat, elevation, support
  stockings, elastic wrap ambulation is encouraged
• Surgery excise vein if condition persists gt2
  weeks or recurs ligate and resect vein at
  saphenofemoral or cephalic-subclavian junction
• Prognosis uncomplicated superficial
  thrombophlebitis responds well to conservative
  therapy extension into DVT may be associated
  with PE

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Leg ulcer

• An ulcer is defined as an area of discontinuity
  of the surface epithelium.
• Pain suggests ischaemia or infection.
• Neuropathic ulcers occur over points of
  pressure and trauma.
• Marked worsening of a chronic ulcer suggests
  malignant change.
• Several precipitating causes may coexist (e.g.
  diabetes, PVD and neuropathy).
• Venous ulcers
• Venous hypertension secondary to DVT or
  varicose veins ulceration on the medial side of
  the leg, above the ankle, any size, shallow with
  sloping edges, bleeds after minor trauma, weeps
  readily, surrounded by pigmentation associated
  dermatoliposclerosis.
• Arterial ulcers
• Occlusive arterial disease painful ulcers, do
  not bleed, nonhealing, lateral ankle, heel,
  metatarsal heads, tips of the toes, associated
  features of ischaemia, e.g. claudication, absent
  pulses, pallor. Elderly patients may present with
  blue toe syndrome.
• Diabetic ulcers
• Ischaemic same as arterial ulcers.
• Neuropathic deep, painless ulcers, plantar
  aspect of foot or toes, associated with
  cellulitis and deep tissue abscesses, warm foot,
  pulses may be present.

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• Malignant ulcers
• Squamous cell carcinoma may arise de novo or
  malignant change in a chronic ulcer or burn
  (Marjolins ulcer). Large ulcer, heaped up,
  everted edges. Lymphadenopathy highly
  suspicious.
• Basal cell carcinoma uncommon on the leg,
  rolled edges, pearly white.
• Malignant melanoma lower limb is a common
  site, consider malignant if increase in size or
  pigmentation, bleeding, itching or ulceration.
• Miscellaneous ulcers
• Trauma may be caused by minor trauma.
  Predisposing factors are poor circulation,
  malnutrition or steroid treatment.
• Vasculitis (rare), e.g. rheumatoid arthritis,
  SLE.
• Infections (rare) syphilis, TB, tropical
  infections.
• Pyoderma gangrenosum multiple necrotic ulcers
  over the legs that start as nodules. Seen with
  ulcerative colitis and Crohns disease.

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