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Venous Thromboembolism
Including Pulmonary
Embolism
• Pulmonary embolism (PE) occurs when clotted blood enters the
pulmonary arterial circulation.
• Most PEs result from deep vein thrombosis (DVT) in the legs, arms, or
pelvis and occasionally from the jugular vein or inferior vena cava.
• The term venous thromboembolism (VTE) includes PE and DVT
PATHOPHYSIOLOGY
• Blood clots occur when coagulation exceeds the removal by
fibrinolysis.
• Thrombophilias are conditions that tip the balance of coagulation-
fibrinolysis toward excessive clotting
• Most guidelines categorize VTE as provoked or unprovoked (also
called idiopathic).
• Provoked VTEs are a consequence of a triggering risk factor for clots,
such as recent surgery, trauma, or any condition associated with limb
or body immobility; active cancer can be a persistent provoking factor
for VTE.
• Most VTEs diagnosed in the ED are unprovoked.
• Patients with unprovoked VTE have a 15% chance of recurrence in
the next year compared with 5% for those with a provoked episode.
• At least one third of patients with DVT have concomitant PE, even
when the patient lacks symptoms of PE.
• Although 75% to 80% of hospitalized patients with PE have image-
demonstrated DVT, only 40% of ambulatory ED patients with PE
• Patients with PE generally die from one of the following two
mechanisms:
1. Abrupt near-total pulmonary artery occlusion that leads to pulseless
electrical activity or asystole from ischemic effect on the His-Purkinje
conduction system.
2. Progressive right heart failure and circulatory shock, which occurs
over hours to days.
CLINICAL FEATURES OF PULMONARY EMBOLISM
• The hallmark of PE is dyspnea unexplained by auscultatory findings,
ECG changes, and without a clear alternative diagnosis on chest
radiograph.
• Chest pain with pleuritic features is the second most common
symptom of PE, although about one half of all patients diagnosed
with PE in the ED have no chest pain.
• The classic PE pain is in the thorax between the clavicles and the
costal margin that increases with cough or breathing; it is not
substernal and emanating from the skin or muscle.
• Pulmonary infarction (lung tissue destruction) can inflict severe focal
pain, usually occurring 1 to 3 days after the embolic event.
• Pulmonary infarction in basilar lung segments can refer pain to either
shoulder, or it can mimic biliary or ureteral colic.
• Proximal PE without infarction can also cause pleuritic chest pain
without focal pain.
PULSE OXIMETRY, CHEST RADIOGRAPH, AND ECG
• Pulse oximetry, chest radiograph, and ECG obtained in the ED
generally demonstrate nonspecific findings in patients with PE
• Spontaneously breathing patients with PE also demonstrate a lower
end-tidal carbon dioxide compared with healthy individuals
• Most patients with PE have a chest radiograph with one or more
abnormalities, - cardiomegaly,
-basilar atelectasis,
-infiltrate, or
-pleural effusion; all are nonspecific for PE
• In <5% of patients, a wedgeshaped area of lung oligemia (called
Westermark’s sign—usually from complete lobar artery obstruction)
• or peripheral dome-shaped dense opacification (Hampton’s hump—
indicative of pulmonary infarction) exists.
• Findings of acute pulmonary hypertension on ECG increase the
probability of PE
• ECG finding of PE
- heart rate >100 bpm(Sinus tachycardia most common feacher)
-T-wave inversion in leads V1 to V4,
-incomplete or complete right bundle branch block, and
-the S1-Q3-T3 pattern
CLINICAL FEATURES OF DEEP VEIN THROMBOSIS
• Patients with DVT complain of extremity pain, swelling, or cramping.
• A difference of ≥2 cm between right and left leg diameter at 10 cm
below the tibial tubercle doubles the likelihood of DVT.
• Calf vein thrombosis may cause Homan’s sign, which is calf pain that
occurs with passive foot dorsiflexion; this test has such low sensitivity
and specificity that it has no predictive value.
• Phlegmasia alba dolens is a swollen, painful, and pale or white limb
with a proximal venous thrombosis, whereas a limb
• phlegmasia cerulea dolens is a swollen, painful and a dusky or blue
color with a proximal venous thrombosis .
• Either condition poses the threat of limb loss, demanding aggressive
treatment that can include clot disruption.
DIAGNOSTIC TESTING FOR VENOUS
THROMBOEMBOLISM
• The key is generating a clinical gestalt first; if low, then use the PE
rule-out criteria to guide testing
• Other PE and DVT prediction tools exist
-Wells’ score
-Charlotte and
-the simplified, revised Geneva score
•The Wells’ rule has a subjective component—clinical judgment of the
likelihood of an alternative diagnosis.
d-DIMER TESTING
• The d-dimer assay is the only useful blood test to exclude VTE,
working on the principle that clots contain fibrin that is degraded
naturally through the action of plasmin.
• For PE and DVT, the diagnostic sensitivity of automated quantitative
d-dimer assays ranges from 94% to 98%, and the specificity ranges
from 50% to 60%.
• The d-dimer has a half-life of approximately 8 hours and can be
elevated for at least 3 days after symptomatic VTE.
CHEST CT ANGIOGRAPHY
• Chest CT angiography is the most common imaging modality for PE,
identifying a clot as a filling defect in contrast-enhanced pulmonary
arteries
• The diagnostic sensitivity and specificity are both approximately 90%.
-Clot identification
-exclude alternate dx(pnemonia)
• interobserver agreement for subsegmental clots is poor
PLANAR VENTILATION–PERFUSION LUNG
SCANNING
• A V/Q scan with homogeneous scintillation throughout the lung in
the perfusion portion is nearly 100% sensitive in excluding PE,
regardless of the appearance of the ventilation portion.
• sensitivity of 96% and a specificity of 97%.
• V/Q single-photon emission CT detects subsegmental perfusion
defects
MAGNETIC RESONANCE IMAGING
• MRI is a zero-radiation option for imaging the pulmonary vasculature
that may have utility in pregnant patients.
• sensitivity of 75% with specificity of 80%
LUNG US
• Lung US is an adjunctive modality to help diagnose and exclude PE at
the bedside
• lung US has a sensitivity of 85% and specificity of 83% .
VENOUS US
• Venous US is the imaging test of choice in DVT; it can be done quickly.
• When performed by experienced ultrasonographers, compression
venous US has a diagnostic sensitivity of 96% and a specificity of 96%
for DVT;
• it also has a sensitivity of about 40% as a surrogate method to
diagnose PE
INTEGRATED APPROACH TO
DIAGNOSIS AND TREATMENT
STEP ONE
• For a patient to enter a PE testing regimen, he or she should have
atleast one physiologic manifestation of PE.
STEP TWO
• After finding a physiologic manifestation of PE, the next step is to ask,
“Do I have more than a low initial suspicion for PE?” Low suspicion
means that the physician’s gestalt interpretation of the overall clinical
picture is PE likelihood of <15%.
• If the answer to this question is yes, then a diagnostic test is needed.
• If the answer is no, then it remains possible that PE can be excluded
using the PE rule-out criteria rule.
• If all eight criteria of the PE rule-out criteria rule are met in the
setting of a gestalt-based low suspicion, then no further testing is
necessary.
• In general, if any one of the eight criteria is not met or if a prominent
finding exists, order a diagnostic test for PE.
• STEP THREE
• If PE cannot be excluded with the PE rule-out criteria rule, choose a
diagnostic test result that can produce a posttest probability of
<2.0%.
• An age-adjusted quantitative d-dimer assay is the best diagnostic test
in patients for whom clinical suspicion is low or moderate based on
either gestalt estimation, a Wells’ or simplified revised Geneva score
of ≤4, or a “safe” designation according to the PE rule-out criteria rule
• STEP FOUR
• Test further only those with a positive d-dimer result or a high pretest
probability; base the choice of the next test on patient and facility
factors.
TREATMENT OF PULMONARY EMBOLISM
AND DEEP AND SUPERFICIAL EXTREMITY
THROMBOSES
• Treatment of VTE requires systemic anticoagulation to prevent further
clot formation and allow endogenous fibrinolysis to proceed/
• Patients with DVT diagnosed in the ED are typically discharged
afterreceiving the first dose of low-molecular-weight heparin,
apixaban, or rivaroxaban,
• The two most common options are unfractionated heparin or a Initial
anticoagulation treatment for VTE can also include oral apixaban or
rivaroxaban.
• Indications for admission in patients with DVT are primarily
dependent upon
-social determinants,
-comorbid conditions, and
-presence of iliofemoral DVT with signs of phlegmasia
• Current data favor the use of low-molecular-weight heparins over
unfractionated heparin for treatment of both PE and DVT in terms of
composite outcomes (bleeding and death) and cost.
• In patients with severe renal insufficiency and acute DVT or PE, most
experts recommend unfractionated heparin over low-molecular-
weight heparin.
• Treat upper extremity DVT the same as lower extremity DVT, and
consider removing any indwelling catheters associated with clot.
• Do not delay unfractionated heparin for thrombophilia testing.
• Most DVT can be treated with anticoagulation, but iliofemoral DVT
that causes phlegmasia cerulea dolens requires rapid action to reduce
the venous pressure.
• In addition to initiating anticoagulation,
-place the affected limb at a neutral level;
- remove constrictive clothing, cast, or dressing; and
- arrange for vascular consultation and consultant delivered
catheter-directed thrombolysis
• consider systemic fibrinolytics if there are no absolute
contraindications
TREATMENT FOR SUPERFICIAL
THROMBOPHLEBITIS
• Treatment for localized superficial thrombophlebitis is an oral NSAID
or topical diclofenac gel until symptoms resolve; there is no need for
systemic anticoagulation.
• For extensive superficial vein involvement, full-dose anticoagulation is
recommended.
• Compression stockings may provide some relief in selected individuals
TREATMENT FOR ISOLATED CALF VEIN
THROMBOSIS
• There are no universally accepted treatment guidelines for
thromboses isolated to the calf veins (soleal or gastrocnemius) or the
saphenous vein, although many use 3 months of oral anticoagulation.
• Alternatives include no acute treatment, with repeat US in 1 week to
identify progression of clot, or outpatient treatment with low-
molecular weight heparin .
• Patients with a history of VTE or risk factors for VTE should receive 3
months of full-dose anticoagulation when calf thrombosis exists
unless contraindications are present
OUTPATIENT TREATMENT OF PULMONARY
EMBOLISM
• Patients with PE and a low risk of death plus adequate home support
can qualify for outpatient anticoagulation.
• Select low-risk patients using either the modified Hestia criteria or
the Simplified PE Severity Index criteria
• If low risk, assess the patient’s wishes and ability to comply; if no
highrisk features exist (elevated troponin, a B-type natriuretic peptide
>100 picograms/mL, pulmonary arterial hypertension on ECG, or
bleeding risks, outpatient care after an ED stay (up to 23 hours) is an
option; otherwise, short-term hospitalization is a good choice.
FIBRINOLYSIS FOR PULMONARY EMBOLISM
• PE is classified into three categories based on severity: massive,
submassive, and less severe PE.
• Massive PE patients have a systolic blood pressure of <90 mm Hg for
>15 minutes, a systolic blood pressure of <100 mm Hg with a history
of hypertension, or a >40% reduction in baseline systolic blood
pressure.
• Submassive PE patients have normal or near normal blood pressure,
but with other evidence of cardiopulmonary stress
• All other PE cases are “less severe.” Patients with low-risk PE should
not receive fibrinolysis.
•massive and submassive PE benefit from fibrinolysis.
indication SYSTEMIC FIBRINOLYSIS
 cardiac arrest;
 hypotension (any systolic blood pressure >90 mm Hg);
 respiratory failure, evidenced by severe hypoxemia (pulse ximetry
reading <90%) despite oxygen administration, together with vidence
of increased work of breathing; or
evidence of right-sided heart strain on echocardiography or elevated
levels of troponin T or I, orboth
Major contraindications to thrombolytic therapy include
intracranial disease,
uncontrolled hypertension at presentation,
recent major surgery or trauma (past 3 weeks), and
 metastatic cancer.
head injury
ISOLATED SUBSEGMENTAL PULMONARY
EMBOLISM
• Isolated subsegmental PE is a filling defect seen in one small
pulmonary artery, usually <3 mm in diameter and in the absence of
DVT.
• The author’s choice is to treat subsegmental PE as an outpatient with
apixaban or rivaroxaban and check a d-dimer in 1 month and, if
normal, stop anticoagulation.
CANCER PATIENTS WITH VENOUS
THROMBOEMBOLISM
• Current data and guidelines recommend treatment of patients with
active cancer with low-molecular-weight heparin for at least 6
months.
• One randomized trial suggested that rivaroxaban can be used in
patients with active cancer, with a reduction in VTE recurrence but
increased risk of bleeding
END??

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VTE AND PE.pptx

  • 2. • Pulmonary embolism (PE) occurs when clotted blood enters the pulmonary arterial circulation. • Most PEs result from deep vein thrombosis (DVT) in the legs, arms, or pelvis and occasionally from the jugular vein or inferior vena cava. • The term venous thromboembolism (VTE) includes PE and DVT
  • 3. PATHOPHYSIOLOGY • Blood clots occur when coagulation exceeds the removal by fibrinolysis. • Thrombophilias are conditions that tip the balance of coagulation- fibrinolysis toward excessive clotting • Most guidelines categorize VTE as provoked or unprovoked (also called idiopathic). • Provoked VTEs are a consequence of a triggering risk factor for clots, such as recent surgery, trauma, or any condition associated with limb or body immobility; active cancer can be a persistent provoking factor for VTE.
  • 4. • Most VTEs diagnosed in the ED are unprovoked. • Patients with unprovoked VTE have a 15% chance of recurrence in the next year compared with 5% for those with a provoked episode. • At least one third of patients with DVT have concomitant PE, even when the patient lacks symptoms of PE. • Although 75% to 80% of hospitalized patients with PE have image- demonstrated DVT, only 40% of ambulatory ED patients with PE
  • 5. • Patients with PE generally die from one of the following two mechanisms: 1. Abrupt near-total pulmonary artery occlusion that leads to pulseless electrical activity or asystole from ischemic effect on the His-Purkinje conduction system. 2. Progressive right heart failure and circulatory shock, which occurs over hours to days.
  • 6. CLINICAL FEATURES OF PULMONARY EMBOLISM • The hallmark of PE is dyspnea unexplained by auscultatory findings, ECG changes, and without a clear alternative diagnosis on chest radiograph. • Chest pain with pleuritic features is the second most common symptom of PE, although about one half of all patients diagnosed with PE in the ED have no chest pain.
  • 7. • The classic PE pain is in the thorax between the clavicles and the costal margin that increases with cough or breathing; it is not substernal and emanating from the skin or muscle. • Pulmonary infarction (lung tissue destruction) can inflict severe focal pain, usually occurring 1 to 3 days after the embolic event. • Pulmonary infarction in basilar lung segments can refer pain to either shoulder, or it can mimic biliary or ureteral colic. • Proximal PE without infarction can also cause pleuritic chest pain without focal pain.
  • 8. PULSE OXIMETRY, CHEST RADIOGRAPH, AND ECG • Pulse oximetry, chest radiograph, and ECG obtained in the ED generally demonstrate nonspecific findings in patients with PE • Spontaneously breathing patients with PE also demonstrate a lower end-tidal carbon dioxide compared with healthy individuals • Most patients with PE have a chest radiograph with one or more abnormalities, - cardiomegaly, -basilar atelectasis, -infiltrate, or -pleural effusion; all are nonspecific for PE
  • 9. • In <5% of patients, a wedgeshaped area of lung oligemia (called Westermark’s sign—usually from complete lobar artery obstruction) • or peripheral dome-shaped dense opacification (Hampton’s hump— indicative of pulmonary infarction) exists.
  • 10. • Findings of acute pulmonary hypertension on ECG increase the probability of PE • ECG finding of PE - heart rate >100 bpm(Sinus tachycardia most common feacher) -T-wave inversion in leads V1 to V4, -incomplete or complete right bundle branch block, and -the S1-Q3-T3 pattern
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  • 13. CLINICAL FEATURES OF DEEP VEIN THROMBOSIS • Patients with DVT complain of extremity pain, swelling, or cramping. • A difference of ≥2 cm between right and left leg diameter at 10 cm below the tibial tubercle doubles the likelihood of DVT. • Calf vein thrombosis may cause Homan’s sign, which is calf pain that occurs with passive foot dorsiflexion; this test has such low sensitivity and specificity that it has no predictive value.
  • 14. • Phlegmasia alba dolens is a swollen, painful, and pale or white limb with a proximal venous thrombosis, whereas a limb • phlegmasia cerulea dolens is a swollen, painful and a dusky or blue color with a proximal venous thrombosis . • Either condition poses the threat of limb loss, demanding aggressive treatment that can include clot disruption.
  • 15. DIAGNOSTIC TESTING FOR VENOUS THROMBOEMBOLISM • The key is generating a clinical gestalt first; if low, then use the PE rule-out criteria to guide testing • Other PE and DVT prediction tools exist -Wells’ score -Charlotte and -the simplified, revised Geneva score •The Wells’ rule has a subjective component—clinical judgment of the likelihood of an alternative diagnosis.
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  • 19. d-DIMER TESTING • The d-dimer assay is the only useful blood test to exclude VTE, working on the principle that clots contain fibrin that is degraded naturally through the action of plasmin. • For PE and DVT, the diagnostic sensitivity of automated quantitative d-dimer assays ranges from 94% to 98%, and the specificity ranges from 50% to 60%. • The d-dimer has a half-life of approximately 8 hours and can be elevated for at least 3 days after symptomatic VTE.
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  • 21. CHEST CT ANGIOGRAPHY • Chest CT angiography is the most common imaging modality for PE, identifying a clot as a filling defect in contrast-enhanced pulmonary arteries • The diagnostic sensitivity and specificity are both approximately 90%. -Clot identification -exclude alternate dx(pnemonia) • interobserver agreement for subsegmental clots is poor
  • 22. PLANAR VENTILATION–PERFUSION LUNG SCANNING • A V/Q scan with homogeneous scintillation throughout the lung in the perfusion portion is nearly 100% sensitive in excluding PE, regardless of the appearance of the ventilation portion. • sensitivity of 96% and a specificity of 97%. • V/Q single-photon emission CT detects subsegmental perfusion defects
  • 23. MAGNETIC RESONANCE IMAGING • MRI is a zero-radiation option for imaging the pulmonary vasculature that may have utility in pregnant patients. • sensitivity of 75% with specificity of 80% LUNG US • Lung US is an adjunctive modality to help diagnose and exclude PE at the bedside • lung US has a sensitivity of 85% and specificity of 83% .
  • 24. VENOUS US • Venous US is the imaging test of choice in DVT; it can be done quickly. • When performed by experienced ultrasonographers, compression venous US has a diagnostic sensitivity of 96% and a specificity of 96% for DVT; • it also has a sensitivity of about 40% as a surrogate method to diagnose PE
  • 25. INTEGRATED APPROACH TO DIAGNOSIS AND TREATMENT STEP ONE • For a patient to enter a PE testing regimen, he or she should have atleast one physiologic manifestation of PE. STEP TWO • After finding a physiologic manifestation of PE, the next step is to ask, “Do I have more than a low initial suspicion for PE?” Low suspicion means that the physician’s gestalt interpretation of the overall clinical picture is PE likelihood of <15%. • If the answer to this question is yes, then a diagnostic test is needed.
  • 26. • If the answer is no, then it remains possible that PE can be excluded using the PE rule-out criteria rule. • If all eight criteria of the PE rule-out criteria rule are met in the setting of a gestalt-based low suspicion, then no further testing is necessary. • In general, if any one of the eight criteria is not met or if a prominent finding exists, order a diagnostic test for PE.
  • 27. • STEP THREE • If PE cannot be excluded with the PE rule-out criteria rule, choose a diagnostic test result that can produce a posttest probability of <2.0%. • An age-adjusted quantitative d-dimer assay is the best diagnostic test in patients for whom clinical suspicion is low or moderate based on either gestalt estimation, a Wells’ or simplified revised Geneva score of ≤4, or a “safe” designation according to the PE rule-out criteria rule
  • 28. • STEP FOUR • Test further only those with a positive d-dimer result or a high pretest probability; base the choice of the next test on patient and facility factors.
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  • 32. TREATMENT OF PULMONARY EMBOLISM AND DEEP AND SUPERFICIAL EXTREMITY THROMBOSES
  • 33. • Treatment of VTE requires systemic anticoagulation to prevent further clot formation and allow endogenous fibrinolysis to proceed/ • Patients with DVT diagnosed in the ED are typically discharged afterreceiving the first dose of low-molecular-weight heparin, apixaban, or rivaroxaban, • The two most common options are unfractionated heparin or a Initial anticoagulation treatment for VTE can also include oral apixaban or rivaroxaban.
  • 34. • Indications for admission in patients with DVT are primarily dependent upon -social determinants, -comorbid conditions, and -presence of iliofemoral DVT with signs of phlegmasia
  • 35. • Current data favor the use of low-molecular-weight heparins over unfractionated heparin for treatment of both PE and DVT in terms of composite outcomes (bleeding and death) and cost. • In patients with severe renal insufficiency and acute DVT or PE, most experts recommend unfractionated heparin over low-molecular- weight heparin. • Treat upper extremity DVT the same as lower extremity DVT, and consider removing any indwelling catheters associated with clot. • Do not delay unfractionated heparin for thrombophilia testing.
  • 36. • Most DVT can be treated with anticoagulation, but iliofemoral DVT that causes phlegmasia cerulea dolens requires rapid action to reduce the venous pressure. • In addition to initiating anticoagulation, -place the affected limb at a neutral level; - remove constrictive clothing, cast, or dressing; and - arrange for vascular consultation and consultant delivered catheter-directed thrombolysis • consider systemic fibrinolytics if there are no absolute contraindications
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  • 38. TREATMENT FOR SUPERFICIAL THROMBOPHLEBITIS • Treatment for localized superficial thrombophlebitis is an oral NSAID or topical diclofenac gel until symptoms resolve; there is no need for systemic anticoagulation. • For extensive superficial vein involvement, full-dose anticoagulation is recommended. • Compression stockings may provide some relief in selected individuals
  • 39. TREATMENT FOR ISOLATED CALF VEIN THROMBOSIS • There are no universally accepted treatment guidelines for thromboses isolated to the calf veins (soleal or gastrocnemius) or the saphenous vein, although many use 3 months of oral anticoagulation. • Alternatives include no acute treatment, with repeat US in 1 week to identify progression of clot, or outpatient treatment with low- molecular weight heparin . • Patients with a history of VTE or risk factors for VTE should receive 3 months of full-dose anticoagulation when calf thrombosis exists unless contraindications are present
  • 40. OUTPATIENT TREATMENT OF PULMONARY EMBOLISM • Patients with PE and a low risk of death plus adequate home support can qualify for outpatient anticoagulation. • Select low-risk patients using either the modified Hestia criteria or the Simplified PE Severity Index criteria • If low risk, assess the patient’s wishes and ability to comply; if no highrisk features exist (elevated troponin, a B-type natriuretic peptide >100 picograms/mL, pulmonary arterial hypertension on ECG, or bleeding risks, outpatient care after an ED stay (up to 23 hours) is an option; otherwise, short-term hospitalization is a good choice.
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  • 42. FIBRINOLYSIS FOR PULMONARY EMBOLISM • PE is classified into three categories based on severity: massive, submassive, and less severe PE. • Massive PE patients have a systolic blood pressure of <90 mm Hg for >15 minutes, a systolic blood pressure of <100 mm Hg with a history of hypertension, or a >40% reduction in baseline systolic blood pressure. • Submassive PE patients have normal or near normal blood pressure, but with other evidence of cardiopulmonary stress
  • 43. • All other PE cases are “less severe.” Patients with low-risk PE should not receive fibrinolysis. •massive and submassive PE benefit from fibrinolysis.
  • 44. indication SYSTEMIC FIBRINOLYSIS  cardiac arrest;  hypotension (any systolic blood pressure >90 mm Hg);  respiratory failure, evidenced by severe hypoxemia (pulse ximetry reading <90%) despite oxygen administration, together with vidence of increased work of breathing; or evidence of right-sided heart strain on echocardiography or elevated levels of troponin T or I, orboth
  • 45. Major contraindications to thrombolytic therapy include intracranial disease, uncontrolled hypertension at presentation, recent major surgery or trauma (past 3 weeks), and  metastatic cancer. head injury
  • 46. ISOLATED SUBSEGMENTAL PULMONARY EMBOLISM • Isolated subsegmental PE is a filling defect seen in one small pulmonary artery, usually <3 mm in diameter and in the absence of DVT. • The author’s choice is to treat subsegmental PE as an outpatient with apixaban or rivaroxaban and check a d-dimer in 1 month and, if normal, stop anticoagulation.
  • 47. CANCER PATIENTS WITH VENOUS THROMBOEMBOLISM • Current data and guidelines recommend treatment of patients with active cancer with low-molecular-weight heparin for at least 6 months. • One randomized trial suggested that rivaroxaban can be used in patients with active cancer, with a reduction in VTE recurrence but increased risk of bleeding
  • 48. END??

Editor's Notes

  1. FIGURE 56-2. Proposed algorithm for evaluation of suspected pulmonary embolism. Begin with the pulmonary embolism rule-out criteria (PERC) rule—diagnostic algorithm for pulmonary embolism (PE). * Some physicians prefer to start with a clinical decision rule such as the Wells’ score (where <2, 2–6, and >6 are used instead of <15%, 15% to 40%, and >40%, respectively). Note: Determine renal function by clinical picture (healthy, no risk factors for reduced glomerular filtration rate [GFR]) or calculated GFR. Nondiagnostic ventilation–perfusion (V. /Q . ) scan findings require confirmation from results of another test, such as CT pulmonary angiography (CTPA), if benefits outweigh risks. + = positive for PE; – = negative for PE; Bilat LE CUS = bilateral lower extremity compression US; Cr = creatinine; FEU = fibrinogen equivalent units; High = high-probability scan findings; LMWH = low-molecular-weight heparin; Nondiagnostic = any reading other than normal or high probability; quant = quantitative; SPECT = single-photon emission CT; sRGS = simplified, revised Geneva score; V. /Q . = ventilation/perfusion ratio.
  2. Alteplase (tissue plasminogen activator) is the only currently approved agent for PE, dosed at 100 milligrams IV over 2 hours. Either enoxaparin (1 milligram/kg SC) or unfractionated heparin (80 units/kg IV bolus followed by 18 units/kg/h) is the anticoagulant, with the activated partial thromboplastin time kept at <120 seconds for unfractionated heparin. Heparin or low-molecular-weight heparin is typically started after the thrombolytic infusion. Use of 50 mg of alteplase may reduce bleeding risk with similar outcomes as 100 mg of alteplase, although the safety and effi_x0002_cacy of this approach remain controversial.81,82 For further discussion of fibrinolytic agents,