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Thrombophlebitis and Occlusive Arterial Disease

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Mild cases can be treated with warm compresses, ... T/F Pt with political aneurysm frequently have abdominal aortic aneurysm and contra lateral political aneurysm. – PowerPoint PPT presentation

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Title: Thrombophlebitis and Occlusive Arterial Disease


1
Thrombophlebitis and Occlusive Arterial Disease
  • October 6th, 2005
  • George Filiadis D.O.

2
Thrombophlebitis
  • Formation of a venous clot depends on the
    presence of of at least of one of Virchows triad
    factors -venous stasis -injury to
    vessel wall -hypercoagulable state

3
Clinical risk factors for deep vein thrombosis
  • Trauma, travel
  • Hypercoagulable, hormone replacement
  • Recreational drugs(IV drugs)
  • Old (age gt60y)
  • Malignancy
  • Birth control, blood group A
  • Obesity, obstetrics
  • Surgery, smoking
  • Immobilization
  • Sickness

4
Pathophysiology
  • Most common cause of hereditary hemophilia is
    factor V Leiden
  • See Table 59.2 for other hypercoagulable states
  • Thrombi usually form at the venous cusps of deep
    veins where altered or static blood flow causes
    clot formation
  • Alternatively, clots form from intimal defects
  • Clots are composed from fibrin, red cells and
    platelets and cause partial/complete obstruction
    of vein

5
Pathophysiology
  • Postphlebitic syndrome (PPS) may develop after
    the resolution of a DVT
  • PPS is due valvular incompetence, persistent
    outflow obstruction and abnormal microcirculation.

6
Superficial Thrombophlebitis
  • Thrombosis can occur in any superficial vein
    primarily the saphenous vein and its tributaries
  • Local pain, redness, and tenderness are
    characteristic findings.
  • Mild cases can be treated with warm compresses,
    analgesia and elastic supports
  • Severe cases can be debilitating and should be
    managed by bed rest, elevation of extremity,
    support stockings, and analgesia.
  • Antibiotics and anticoagulants are useful in
    septic thrombophlebitis

7
Superficial Thrombophlebitis
  • Incidence of DVT from extension of a superficial
    clot is 3.
  • Most clots in great saphenous vein will extend
    into a deep vein system in a week or so thus a
    follow-up US is guaranteed
  • Definite treatment is ligation and excision of
    affected vein.

8
Deep Vein Thrombosis
  • Clinical exam is unreliable for detection or
    exclusion of a DVT
  • Pain, redness, swelling, and warmth are present
    in less than half the patients with confirmed
    DVT.
  • Pain in calf with dorsiflexion of ankle with the
    leg straight (Homans sign) is unreliable
  • See table 59.3 for predictors of deep vein
    thrombosis

9
Deep Vein Thrombosis
  • Symptomatic DVT will be in popliteal or more
    proximal veins more than 80
  • Nonextending calf DVT rarely cause PE
  • Uncommon presentations of DVT include phlegmasia
    cerulea dollens and phlegmasia alba dollens
  • In phlegmasia cerulea dollens, patients present
    with extensive swollen and cyanotic leg due to
    massive ileofemoral thrombosis which can lead to
    venous gangrene.

10
Deep Vein Thrombosis
  • In phlegmasia alba dolens, the leg is white due
    to arterial spasm secondary to massive
    iliofemoral thrombosis, often mistaken for
    arterial occlusion.
  • PPS can be difficult to differentiate from
    recurrent DVT due to pain, swelling and
    ulceration of the skin.
  • Up to to one third of the patients with DVT can
    develop PPS.

11
Deep Vein Thrombosis-Diagnosis
  • All patients with any signs or symptoms
    suggestive DVT should undergo an objective
    diagnostic evaluation
  • Venography was the historical gold standard for
    detection of DVT with 100 sensitivity and
    specificity but it is invasive and can cause
    contrast-related reactions, phlebitis and DVT
    (3).

12
Deep Vein Thrombosis-Diagnosis
  • Choice of test to identify DVT is ultrasound
  • Ultrasound has 97 and 94 sensitivity and
    specificity respectively for detecting proximal
    DVT
  • Ultrasound is less sensitive for pelvic DVT and
    has sensitivity of 73 for a calf DVT.
  • Impedance plethysmography is portable and
    inexpensive but less sensitive than US
  • IP measures changes in electrical resistance in
    response to changes in calf volume due to
    obstruction

13
Deep vein thrombosis-Diagnosis
  • Radioisotopes have been used to diagnose DVT but
    are not particularly useful in ED
  • MRI is being used with increased frequency and
    can detect a filling defect in entire extremity
    (including calf and pelvic veins)
  • D-Dimer fragments which are degradation products
    of fibrin can be used to as an indicator for the
    presence or absence of DVT or PE.
  • The ELISA based D-Dimer has sensitivity 97 and
    specificity 35

14
Deep Vein Thrombosis-Diagnosis
  • When D-Dimer is less than 500ng/ml, the
    likelihood of DVT is less than 1.
  • The latex agglutination assay D-Dimer is less
    sensitive than the ELISA essay.
  • Sepsis, surgery, trauma, hemorrhage, pregnancy,
    cardiovascular diseases, collagen vascular
    disease, liver disease, cancer are associated
    with elevated d-dimer value.

15
Clinical Approach to Establishing the Diagnosis
16
Treatment
  • Bed rest, leg elevation and elastic stockings are
    of unproven benefit in the management of DVT.
  • Aggressive anticoagulation will prevent extension
    of the clot.
  • Early ambulation after adequate anticoagulation
    is a safe approach
  • Primary objective of treating DVT is the
    prevention of pulmonary embolus

17
Treatment
  • Patients with negative ultrasound can safely have
    a repeat ultrasound in a week without
    anticoagulation
  • Risk of PE in these patients is near 0 and risk
    of forming a DVT is 1.
  • Anticoagulation is recommended for patients with
    calf DVT who had PE/DVT, immobile, have
    hypercoagulable state

18
Treatment
  • Patients with proximal DVT require
    anticoagulation
  • Preferred treatment is LMWH over UFH because of
    the ease of administration, more predictable
    anticoagulant effect, lack of need to monitor the
    anticoagulation effect, lower incidence of major
    bleeding and HIT
  • LMWH has a preferentially inhibitory effect on
    factor Xa.

19
Treatment
  • Because of LMWH is cleared by the kidneys, it
    should be avoided in outpatients with Cr gt2.03
  • One need not to wait for the creatinine result
    before initiating LMWH therapy.
  • The ability to discharge patients from the ED
    after initial dose of LMWH is cost-effective,
    safe, practical and acceptable practice as long
    as there is a secured 24 hr follow up with PCP.

20
Treatment
  • Indications for admission include inability to
    ambulate, poor social support, unreliable
    follow-up, difficulty with education with drug
    administration, need for lysis or invasive
    therapy, and an alternative serious diagnosis
    under investigation or that requires
    treatment(arterial ischemia, cellulitis, pelvic
    mass)

21
Treatment
  • If LMWH is contraindicated, use UFH as 80
    units/kg bolus and then 18 units/kg/hr
  • Serious bleeding from LMWH cannot be completely
    reversed with protamine which has been associated
    with hypotension and anaphylactoid reactions.
  • If a patient has contraindication to heparin like
    in pt with HIT, you can use a thrombin inhibitor
    like lepirudin

22
Treatment
  • In pregnant pt who cannot have heparin, danaproid
    should be used.
  • It is acceptable to start coumadin and LMWH
    simultaneously.
  • Warfarin is contraindicated in pregnancy, active
    bleeding, recent major surgery (thoracoabdominal,
    nervous system, spine, eye)
  • LMWH does not interfere with the work up of a
    possible hypercoagulable state compared with UFH.

23
Treatment
  • Initial hematological testing at follow-up
    includes factor V leiden, prothrombin molecular
    tests, screening for antiphospholipid
    anticoagulants and a fasting homocysteine level.
  • Upon completion of the anticoagulation , further
    testing includes antithrombin III, protein C,
    protein S, and factor VIII level

24
Treatment
  • Thrombolysis for DVT is indicated for extensive
    iliofemoral thrombosis and upper extremity DVT in
    patients with low risk for bleeding.
  • IVC filter is indicated for when anticoagulation
    therapy is contraindicated, there is embolization
    of DVT after 1-2 weeks of anticoagulation

25
Treatment
  • Thrombectomy is only indicated with ischemic leg
    secondary to a massive venous clot like in
    phlegmasia cerulea dolens.
  • In ED , pt adequately anticoagulated who present
    with new thrombus or propagation should receive
    LMWH
  • If the fail LMWH or there is a free-floating
    thrombus an IVC should emergently inserted.

26
Pelvic Vein Thrombosis
  • Usually its an extension of a clot from the
    femoral vein.
  • An isolated pelvic vein thrombosis is rare and
    can be a complication in the postpartum period,
    after pelvic surgery or trauma.
  • Septic pelvic vein thrombophlebitis is a
    life-threatening condition after post-partum
    endometritis and is usually diagnosed with CT or
    MRI.

27
Axillary and Subclavian Vein thrombosis
  • 2-4 of DVTs occur in axillary or subclavian vein
  • Risks include recent central venous catheters or
    pacemakers, IV drug use, malignancy,
    hypercoagulable states and excessive or unusual
    exercise, chronic compression(cervical rib,
    scalene or web)
  • PE occurs in 5-10 of cases involving axillary or
    subclavian DVT
  • Treatment includes anticoagulation alone or
    preceded by thrombolysis.

28
OCCLUSIVE ARTERIAL DISEASE
  • Acute limb ischemia secondary to thrombosis or
    embolus is true emergency.
  • Mortality is 25 and risk of amputation is 20.
  • 11-27of elderly have peripheral arterial disease
  • Smoking, diabetes, hyperlipidemia, hypertension
    and homocysteinemia are significant risk factors
  • At least half of the patients with coronary or
    cerebrovascular disease have PVD

29
Pathophysiology
  • Acute limb ischemia leads to cell death and
    irreversible tissue damage.
  • After prolonged arterial obstruction, reperfusion
    may not be fully attainable due to distal edema
    and thrombi forming in the microcirculation.
  • Peripheral nerves and skeletal muscle are very
    sensitive to ischemia and irreversible damage can
    occur within 6 h of anoxia
  • Non-embolic ischemia is due to atherosclerosis of
    the vessels

30
Pathophysiology
  • Progression of ischemic injury can occur through
    several mechanisms i)propagation of clot to
    include collateral vessels ii)ischemia-rela
    ted distal edema leading to high compartment
    pressures iii)fragmentation of clot in the
    microcirculation iv)edema of the
    microvasculature cells

31
Etiology
  • Thrombotic occlusion is significantly more common
    cause of acute limb ischemia than is embolism.
  • Emboli originate from the heart in 80-90 with
    atrial fibrillation being the cause in two thirds
    of all peripheral emboli.
  • Mural thrombus in the ventricle after recent
    myocardial infarction is the second most common
    cause.

32
Etiology
  • Other causes of emboli include atrial myxomas,
    vegetations from valve leaflets, and parts of
    prosthetic devices such as mechanical valves.
  • Noncardiac causes include thrombi from aneurysms
    and atheromatous plaques.
  • Iatrogenic embolization can happen during
    angiograhic procedures of the aorta and larger
    vessels

33
Etiology
  • Thrombosis unrelated to atherosclerotic disease
    can occur at an area of vessel injury during
    invasive studies.
  • Peripheral arterial supply can be obstructed by
    vasospastic or inflammatory conditions like
    Raynaud disease and Thromboangitiis obliterans
    (young smokers)
  • Limb ischemia can also seen with central causes
    like thoracic aortic dissection and Takayasu
    arteritis.

34
Etiology
  • Low cardiac output states like cardiogenic or
    hypovolemic shock may also present with limb
    ischemia
  • Cardiac tamponade, ischemic cardiomyopathy,
    valvular heart disease can impair left ventricle
    function and lead to leg ischemia in patients
    with existing peripheral vascular disease.

35
Clinical features
  • 6 Pspain, pallor, polar (for cold),
    pulselessness, paresthesias, and paralysis.
  • Despite the belief that the limb salvage is
    possible within 4-6h, tissue loss can occur with
    significantly shorter occlusion times.
  • Chronic peripheral arterial insufficiency is
    characterized by intermittent claudication with
    activity that is relieved at rest.
  • Shiny, hyperpigmented skin with hair loss and
    ulceration, thickenend nails, poor pulses are
    hallmarks of chronic disease

36
Diagnosis
  • Clinical evaluation is the most useful diagnostic
    tool.
  • Capillary refill is not reliable alone
  • A hand held Doppler can detect the presence or
    absence of a pulse.
  • If a pulse is detected, then the ankle-brachial
    index (ABI) and segmental leg pressures should be
    checked
  • An ABIlt0.5 indicates acute arterial obstruction
  • If time permits, do a duplex ultrasound

37
Treatment
  • Goals of therapy include restoration of blood
    flow, preservation of limb and life, and
    prevention of recurrent thrombosis
  • Current practice includes UFH to prevent clot
    extension, venous thrombosis, the appearance of
    thrombi distal to the obstruction, and
    reocclusion.
  • Fluid resuscitation and treatment of heart
    failure and dysrhythmias are sometimes necessary
    to improve limb perfusion.
  • Definite treatment includes surgery or
    thrombolysis

38
Upper Extremity Ischemia
  • Upper extremity arterial occlusion is less
    common.
  • There is a well-developed collateral circulation
    around the shoulder and elbow, thus arterial
    occlusion is better tolerated.
  • Usual causes are vasospasm, arteritis, trauma,
    hypercoagulable state, plaque rupture, thoracic
    outlet syndrome, aneurysms.
  • Treatment includes heparinization and surgical
    thrombectomy.

39
Aneurysms of the extremity
  • Incidence of aneurysms in lower extremities
    appears to be increasing due to the aging
    population.
  • Femoral and popliteal aneurysms are the most
    common.
  • Symptoms include local pain, limb edema, and
    ischemic complications
  • For femoral aneurysms (majority are false), US,
    CT or MRI can confirm the diagnosis

40
Aneurysms of the extremity
  • In patients with popliteal aneurysm there is 37
    chance of abdominal aortic aneurysm and 50
    chance of coexisting popliteal aneurysm on the
    contralateral leg.
  • Subclavian artery aneurysms can produce central
    neurologic findings or upper extremity iscemia
    and are due to atherosclerosis, trauma, thoracic
    outlet obstruction, syphilis or cystic medial
    necrosis.

41
Questions
  • 1.Regarding superficial thrombophlebitis, all of
    the following are correct except
  • A)treatment includes bedrest, elevation, support
    stockings, and analgesia.
  • B)antibiotics and anticoagulants are of no proven
    benefit.
  • C)incidence of DVT from superficial thrombus is
    30
  • D)all of the IV drug users with superficial DVT
    should receive antibiotics

42
Questions
  • 2.T/F Calf DVT usually extend proximally and are
    a common case of PE
  • 3.T/F Occlusive arterial disease is usually due
    to a thrombosis event rather than embolic
  • 4. T/F Pt with political aneurysm frequently have
    abdominal aortic aneurysm and contra lateral
    political aneurysm.

43
Questions
  • 5.Which of the following statements is true
  • A)Diagnosis of a DVT can be based on clinical
    exam
  • B)Test of choice for diagnosis of DVT is
    ultrasound.
  • C)Venography is the gold standard diagnostic
    modality given its low complications rate
  • D)Ultrasound has higher sensitivity for detecting
    calf DVT than proximal DVT
  • Answers 1)c, 2)F, 3)T, 4)T, 5)B
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