Pulmonary embolism ms

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MAGDI AWAD SASI 2013 PULMONARY EMBOLISM AND DVT
Pulmonary Embolism
MAGDI AWAD SASI

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Pulmonary embolism (PE) is a common and potentially lethal condition. Most patients
who succumb to pulmonary embolism do so within the first few hours of the event. In
patients who survive, recurrent embolism and death can be prevented with prompt
diagnosis and therapy. Unfortunately, the diagnosis is often missed because patients
with pulmonary embolism present with nonspecific signs and symptoms. If left
untreated, approximately one third of patients who survive an initial pulmonary embolism
die from a subsequent embolic episode.
The most important conceptual advance regarding pulmonary embolism over the last
several decades has been the realization that pulmonary embolism is not a disease;
rather, pulmonary embolism is a complication of venous thromboembolism, most
commonly deep venous thrombosis (DVT). Virtually every physician who is involved in
patient care (eg, internist, family physician, orthopedic surgeon, gynecologic surgeon,
urologic surgeon, pulmonary subspecialist, cardiologist) encounters patients who are at
risk for venous thromboembolism, and therefore at risk for pulmonary embolism.
DEFINITION:
PE is the obstruction of the pulmonary artery or one of its branches by a
thrombus (or thrombi) that originates somewhere in the venous system or in
the right side of the heart .
Definition for Massive PE
Acute PE with with at least 1 of the following:
1. Sustained hypotension
SBP <90 mmHg for at least 15 minutes or requiring inotropic support, not
due to a cause other than PE, such as arrhythmia, hypovolemia, sepsis, or LV
dysfunction, drugs,etc.
2. Pulselessness
3. Persistent profound bradycardia
Heart rate <40 bpm with signs or symptoms of shock
Definition for Submassive PE
Acute PE without systemic hypotension (SBP >90 mm Hg) but with either RV
dysfunction or myocardial necrosis.

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• RV dysfunction means the presence of at least 1 of the following:
– Echo: RV dilation (apical 4-chamber RV diameter divided by LV
diameter >0.9), or RV systolic dysfunction
•
– CT: RV dilation (4-chamber RV diameter divided by LV diameter >
0.9)
– BNP > 90 pg/mL or N-terminal pro-BNP > 500 pg/mL
– ECG changes: New complete or incomplete RBBB, anteroseptal ST
elevation or depression, or anteroseptal T-wave inversion
• Myocardial necrosis is defined as either of the following:
– Troponin I > 0.4 ng/mL, or Troponin T > 0.1 ng/mL
Definition for Low-Risk PE
Acute PE and the absence of the clinical markers of adverse prognosis that
define massive or submassive PE.

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PREVALENCE
PE is estimated to cause 200,000 deaths each year in the United States .
The 2nd
leading cause of death among hospitalized patients, unexpected,
nontraumatic death.
Most cases are not recognized antemortem, and LESS THAN 10% of
patients with fatal emboli have received specific treatment for the
condition.
Management demands a vigilant systematic approach to diagnosis and an
understanding of risk factors so that appropriate preventive therapy can
be given.
The incidence of PE in USA is 650-900,000 per year.
AETIOLOGY
Many substances can embolize to the pulmonary circulation, including
1. AIR (during neurosurgery, from central venous catheters)
2. AMNIOTIC FLUID(during active labor), fat (long bone fractures)
3. FOREIGN BODIES (talc in injection drug users)
4. PARASITE EGGS (schistosomiasis)
5. SEPTIC EMBOLI (acute infectious endocarditis)
6. TUMOR CELLS(renal cell carcinoma).
7. RED EMBOLUS (DVT, atrial fibrillation)
The most common embolus is thrombus, which may arise anywhere in the
venous circulation or heart but most often originates in the deep veins of the
lower extremities. Thrombi confined to the calf rarely embolize to the
pulmonary circulation. However, about 20% of calf vein thrombi propagate
proximally to the popliteal and ileofemoral veins, at which point they may break
off and embolize to the pulmonary circulation.((50%asymptomatic DVT)).
Pulmonary emboli will develop in 50–60% of patients with proximal deep
venous thrombosis (DVT); half of these embolic events will be asymptomatic.
DEEP VEIN THROMBOSIS:
50% of all patients with venous thrombosis of the lower extremities have no
symptoms. Approximately 50–70% of patients who have symptomatic
pulmonary emboli will have lower extremity DVT when evaluated.

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Obstruction of the deep veins of the legs produces edema and swelling of the
extremity because the outflow of venous blood is inhibited. The amount of
swelling can be determined by measuring extremity circumference at various
levels with a tape measure. The skin over the affected leg may become warmer,
and superficial veins may become more prominent. Tenderness, which usually
occurs later, is produced by inflammation of the vein wall and can be detected by
gentle palpation by the extremity. Homan’s Signs, pain in the calf after sharp
dorsiflexion of the foot, is not specific for deep venous thrombosis because it can
be elicited in any painful condition of the calf. In some cases, signs of a
pulmonary embolus are the first indication of a deep venous thrombosis. -
Thrombosis of superficial veins produces pain or tenderness, redness, and
warmth of the involved area. The risk of dislodgment and embolization of
superficial venous thrombi is very low because the majority of them undergo
spontaneous lysis; thus, condition can be treated at home with rest, extremity
elevation, analgesics, and possibly anti-inflammatory agents.
CAUSES:
1. Thrombus 2. Embolism
3. Trauma 4. Surgery
5. Hypercoaguability 6. Heart failure
7. Pregnancy (increase coaguability of BLOOD)
8. Older than 50 years 9. Arial fibrillation
RISK FACTORS:
PE and DVT are two
manifestations of
the same disease.
((DVT))
► It commonly
affects the
leg veins,
such as the
femoral vein
or the
popliteal vein
or the deep
veins of the
pelvis.

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SIGNS AND SYMPTOMS
Pain,
Swelling
Redness of
the leg and
dilatation of
the surface
veins
Shinning skin
with redness
Hotness and
tenderness
Pedal edema
may occur.
Pathogenesis:
The risk factors for PE are the risk factors for thrombus formation within the
venous circulation.

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1. Venous stasis OR turbulence(Venous flow disturbance):
o Immobility leads to local venous stasis by accumulation of clotting
factors and fibrin, resulting in thrombus formation.
o The risk of pulmonary embolism increases with prolonged bed rest
or immobilization of a limb in a cast.
o Paralysis increases the risk of DVT.
o V. stasis leads to accumulation of platelets and thrombin in veins
Bed rest—especially postoperative, Hip replacement, knee replacement,
caesarian operation, post delivery, comatose patient in ICU, Fracture of
long bones, sitting for hours in work or long trip by car or airplane or bus
with out activity, CCU admission, obesity, stroke, comatose patient).
Intra-pelvic or intra-abdominal mass impairing venous return from the
lower limbs ( ovarian mass, cervix cancer , uterine tumors , prostate
cancer , sigmoid cancer).
2. Hypercoagulable state(hyperviscosity)
a. The complex and delicate balance between coagulation and
anticoagulation is altered by many diseases, by obesity, after
surgery, or by trauma.
b. Concomitant hypercoagulability may be present in disease states
where prolonged venous stasis or injury to veins occurs.

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Congenital –((inherited gene defects-Protein defects))
 Factor (V) Leiden ( 20-40%)
G to A mutation at base pair 1691 results in amino acid 506,Glu instead of Arg
 Prothrombin 20210 (6%)(G to A)
 Defect or deficiency of protein C (4%) (outozomal dominant)
 Defect or deficiency of Protein S (3-4%) ( outozomal dominant)
pregnancy and estrogens reduced protein S
 Dysfibrinogenemia ( 3% )
 Antithrombin deficiency ( 1% ) (outozomal dominant ) acquired deficiency
of it happened in sever obesity , liver disease , chronic renal failer , using
oral contraceptive ,immature neonates
 Dysplasminogenemia ( <1% )
 Reduced Heparin cofactor II
 Elevation of PAI-1
 Elevation of Coagulation factors VII,VIII,IX,X,XI and II
 Reduction of protein Z
Acquired— Hematologic diseases :
 DIC(disseminated intravascular thrombocytopenia),thrombocytosis
 HIT(heparin induced thrombocytopenia), leukemia
 Anti phospholipid syndrome
 TTP(thrombocytopenic thrombotic purpura)
 HUS(hemolytic uremic syndrome)
Thrombocytosis, leukemia , nephrotic syndrome, Oral contraceptives and
estrogen replacement, antiphospholipid syndrome, Homocysteinemia .
o Malignancy has been identified in 17% of patients with venous
thromboembolism.
o The neoplasms most commonly associated with pulmonary
embolism, in descending order of frequency, are pancreatic
carcinoma; bronchogenic carcinoma; and carcinomas of the
genitourinary tract, colon, stomach, and breast.

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3. Endothelial injury
INJURY TO ENDOTHELIUM CAN BE CAUSED BY
1. ATHEROSCLEROSIS
2. HYPERTENSION
3. HYPERCHOLESTEROLEMIA
4. RADIATION INJURY
5. SMOKING
6. Thrombophlebitis -Vascular disease
7. -Foreign bodies (IV/central venous catheters)
Risk factors for venous thrombosis
 Age
 Prolonged immobility
 Obesity
 Neurological disease
 Cardiac disease
 Pregnancy
 Oral contraceptive (ocp) if the patient has
the factor ( V ) leiden mutation the risk is
increased 28-fold
 Surgery
 Malignancy
Pathophysiology
 When a thrombus completely or partially obstructs a pulmonary
artery(massive embolus) or its branches in diseased lung or heart,
 The alveolar dead space is increased. The area, although continuing to be
ventilated, receives little or no blood ﬂow. Thus, gas exchange is impaired
or absent in this area.
 Regional blood vessels and bronchioles constrict.

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 More than 50% of the vascular bed has to be occluded before PAP
becomes substantially elevated
 In patients without cardiopulmonary disease, occlusion of 25-30 % of the
vascular bed .
 Causes an increase in pulmonary vascular resistance. Impaired gas
exchange
A . Ventilation/perfusion mismatch
B. Release of inflammatory mediators leads to surfactant dysfunction,
atelectasis, alveolar hemorrhage ,Intrapulmonary shunting
 PVR from 1. The regional vasoconstriction
2. Reduced size of the pulmonary vascular bed.
 An increase in pulmonary arterial pressure
 An increase in right ventricular work to maintain pulmonary blood ﬂow.
 When obstruction approaches 75%, the RV must generate systolic
pressure in excess of 50mmHg to preserve pulmonary circulation.
 When the work requirements of the right ventricle exceed its capacity,
right ventricular failure occurs, leading to a decrease in cardiac output
followed by a decrease in systemic blood pressure and the development
of shock.(fatigue , syncopy, dizziness).

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SYMPTOMOLOGY:
Clinical clues cannot make the diagnosis of PE; their main value lies in
suggesting the diagnosis.
The symptoms are quite variable according to the heart and lung situation
whether they are healthy or diseased and degree of damage.
Most of the cases are missed as no specific symptom that the symptoms
can be explained by other diagnosis by most of doctors which can lead to
lose of the patients.
Signs and symptoms are highly variable, nonspecific, and common in
patients without PE.
 Fatal PE typically leads to death within one to two hours of the event.
 Small PE in healthy pt= asymptomatic.
 Dyspnea (80%) – usually
acute onset
 Pleuritic chest pain (44%)
 Calf pain/swelling (41-44%)
 Orthopnea (28%)
 Wheezing (21%)
 Cough (20%)
 Syncope (14%)
 Hemoptysis (7%)
 1.Dyspnea is the most frequent symptom; all of a SUDDEN in high risk
patients , while in bed or moving from resting state, NEVER GRADUAL,
The duration and intensity of the dyspnea depend on the extent of
embolization ,heart and lung status.

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 2. Chest pain is common and is usually sudden and pleuritic. It may be
substernal and misdiagnosed with angina pectoris or a myocardial
infarction. It is severe from the first minute in high risk patient.
 3. All chest symptoms may occur and all of sudden onset in absence of
other possibilities(( acute pneumothorax , acute left ventricular failure,
acute dissection of ascending aorta)).
 97% with PE have at least one of the following:
1. Dyspnea
2. Tachypnea
3. Pleuritic pain
 Presence of DVT should trigger initial suspicion.
OTHERS may present with low cardiac out put symptoms such as dizziness,
syncopy, profuse sweating, sudden fatigability in suspected high risk patient
with dyspnea mimicking vasovagal attacks.
OTHERS may present with sudden vomiting with epigastric pain and
diarrhea with fatigue and right hypochondrial discomfort or heaviness due
to right side congestion in massive/submassive P.E. WITH HYPOTENSION.
Other symptoms include anxiety, fever, tachycardia, apprehension, cough,
diaphoresis, hemoptysis, unexplained fatigue or palpitation/shivering.
SIGNS:
 Tachypnea (53%) Tachycardia (24%)
 Rales (18%) Decreased breath sounds (17%)
 Accentuated P2 (15%) JV distension (14%)
 Signs of DVT

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Physical examination findings are quite variable in pulmonary embolism and, for
convenience, may be grouped into 4 categories as follows:
Massive pulmonary embolism
o The patient in SHOCK. (( systemic hypotension, poor perfusion of
the extremities, tachycardia, and tachypnea , drowzy)).
o Additionally, signs of pulmonary hypertension such as palpable P2
second left intercostal space, loud P2, right ventricular S3 gallop,
and (tricuspid regurgitation) may be present.
Acute pulmonary infarction
o These patients have decreased excursion of the involved
hemithorax, palpable or audible pleural friction rub, and even
localized tenderness.
o Signs of pleural effusion, such as dullness to percussion and
diminished breath sounds, may be present.
Acute embolism without infarction
o These patients have nonspecific physical signs that may easily be
secondary to another disease process.
o Tachypnea and tachycardia frequently are detected, pleuritic pain
sometimes may be present, crackles may be heard in the area of
embolization, and local wheeze may be heard rarely.
Multiple pulmonary emboli or thrombi
o Physical signs of pulmonary hypertension and cor pulmonale.
o Patients may have elevated jugular venous pressure, right
ventricular heave, palpable P2 , right ventricular S3 gallop, TR,
hepatomegaly, ascites, and dependent pitting edema.
o These findings are not specific for pulmonary embolism and require
a high index of suspicion for pursuing appropriate diagnostic
studies.
LUNG EXAMINATION- collapse, consolidation where there is 2ry
pneumonia which may delay the diagnosis, elevation of diaphragm,
cavitating lung cavity with missed diagnosis mimicking lung abscess,
pleural effusion , pleural rub , localized wheezing ,basal inspiratory fine
crepiataion .

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Assessment and Diagnostic Findings:
 No single noninvasive test is sufficiently sensitive or specific to diagnose
or exclude PE in all patients.
 No single test can reliably rule out PE.
 Yep, that includes CT Angio (right?)
THEY ARE HELPFUL IN MASSIVE /SUBMASSIVE PE NOT SMALL .
 The clinical priorities in the investigation of patients with suspected PE
include:
1. Diagnosis of extensive PE
2. Diagnosis of PE in patients with severe symptoms and/or poor
cardiopulmonary reserve
3. Diagnosis of any PE when associated with symptomatic or
asymptomatic proximal DVT
4. Diagnosis in patients presenting with possible recurrent PE
1.ABG-arterial blood gases:
 pO2 pCO2
 Increased A-a gradient

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2.D-dimer:
 This blood screening test relies on the principle that most patients with
PE have ongoing endogenous fibrinolysis that is not effective enough to
prevent PE but that does break down some of the fibrin clot to d-dimers .
 Although elevated plasma concentrations of d-dimers are sensitive for the
presence of PE, they are not specific.
 patients with a low clinical probability of PE who had negative d-dimer
results, additional diagnostic testing was not necessary
 Different assays have different sensitivities
 PE in low-risk patients with a negative D-dimer…
o Thrombus formation >72 hrs before blood draw (circulating dimer
t1/2 = 8 hrs)
o Subsegmental PE
 False-positives = age >70, pregnancy, active malignancy, recent surgery,
liver disease, RA, infections, trauma
 False-negatives = Coumadin use, symptoms >5days, small clots or
infarction, isolated calf vein thrombosis.
 Therefore, the plasma d-dimer assay is ideally suited for outpatients or
emergency department patients who have suspected PE but no coexisting
acute systemic illness OR history of venous thromboembolism and whose
symptoms are of short duration.
 This test is generally not useful for acutely ill hospitalized inpatients
because their D-dimer levels are usually elevated. A normal d-dimer assay
appears to be as diagnostically useful as a normal lung scan to exclude PE.
 D-dimer test should not be used when the clinical probability of
pulmonary embolism is high, because the test has low negative predictive
value in such cases.

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3.Electrocardiographic Signs:
Sinus tachycardia( THE COMMENEST )
Incomplete or complete right bundle branch block
Right-axis deviation
T wave inversions in leads III and aVF or in leads V1-V4
S wave in lead I and a Q wave and T wave inversion in lead III (S1Q3T3)
QRS axis greater than 90 degrees or an indeterminate axis
Atrial fibrillation or atrial flutter

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4.Chest Radiography:
A near-normal radiograph in the setting of severe respiratory compromise
is highly suggestive of massive PE.(AHA)
Major chest radiographic abnormalities are uncommon.
Focal oligemia (Westermark sign) indicates massive central embolic
occlusion.
A peripheral wedge-shaped density above the diaphragm (Hampton
hump) usually indicates pulmonary infarction.
Subtle abnormalities suggestive of PE include enlargement of the
descending right pulmonary artery, elevated diaphragm,collapse.
The vessel often tapers rapidly after the enlarged portion. PE.

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5.Echocardiographic Signs:
 Right ventricular enlargement or hypokinesis, especially free wall
hypokinesis, with sparing of the apex (the McConnell sign).
Interventricular septal flattening and paradoxical motion toward the left
ventricle, resulting in a D-shaped left ventricle in cross section.
 Tricuspid
regurgitation.
 Pulmonary
hypertension with a
tricuspid regurgitant
jet velocity
>2.6 m/sec.
 Loss of respiratory-
phasic collapse of the
inferior vena cava
with inspiration.
 Dilated inferior vena
cava without
physiologic
inspiratory collapse.
 Direct visualization of thrombus (more likely with transesophageal
echocardiography)
Overview of Imaging Modalities for Pulmonary Embolism:
 Lower extremity venous ultrasonography
 Multidetector helical CT pulmonary angiography
 MRI
 Ventilation-perfusion scintigraphy (V/Q scan)

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6. Computed Tomography
1. Size, location, and extent of thrombus
2. Other diagnoses that may coexist with PE or explain PE symptoms:
Pneumonia, Atelectasis, Pericardial effusion, Pneumothorax, abscess,
Left ventricular enlargement
3. Pulmonary artery enlargement === pulmonary hypertension
Age of thrombus: acute, subacute, chronic
4. Location of thrombus: pulmonary arteries , deep leg veins,
5.Right ventricular enlargement
6.Contour of the interventricular septum: whether it bulges toward
the left ventricle, thus indicating right ventricular pressure overload
7.Incidental masses or nodules in lung

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7. CT pulmonary Angiography
CT angiography (CTA) is the initial imaging modality of choice for stable
patients with suspected pulmonary embolism(low risk).
Sensitivity/Specificity ~90%
withholding anticoagulation after negative pulmonary CTA results
appears to be safe.
CTPA use increased 10-fold from 1998-2006
Incidence increased 81% from 1998-2006 (112/100,000) with only 3%
mortality reduction
o Increased in-hospital antigcoagulation complications during that
same time period
8. Spiral CT- can visualize main, lobar, and segmental pulmonary emboli
with a reported sensitivity of greater than 90%.
Spiral CT scanning can help detect emboli as small as 2 mm that are
affecting up to the seventh border division of the pulmonary artery.
A further benefit of spiral CT scanning is that the results may suggest
an alternative diagnosis in up to 57% of patients.
A significant limitation of spiral CT scanning is that small subsegmental
emboli may not be detected.
o The technique is as follows:
 Spiral CT examination is performed immediately after infusion
of 150-200 mL of 30% contrast material.
 Scanning is performed from the level of the aortic arch to
approximately 2 cm below the level of the inferior pulmonary
vein while the patient is holding his or her breath at full
inspiration.
 If the patient is not able to hold his or her breath for 20-30
seconds, scanning may be performed during gentle breathing.
Positive findings on CT imaging include a central intravascular filling
defect within the vessel lumen, eccentric tracking of contrast material
around a filling defect, and complete vascular occlusion. Smooth filling

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defects making an obtuse angle with a vessel wall may represent
chronic thrombi or recent recanalization. In the lung parenchyma, signs
of pulmonary embolism include oligemia, pulmonary hemorrhage
(ground-glass attenuation), and pulmonary infarction (peripheral
wedge-shaped pleural-based opacification.
9. Ventilation-perfusion (V/Q) scanning of the lungs:
This is an important diagnostic modality for establishing the diagnosis of
pulmonary embolism.
However, V/Q scanning should be used only 1.when CT scanning is not
available or 2. If the patient has a contraindication to CT scanning or
intravenous contrast material.
New criteria for V/Q scanning diagnosis of pulmonary embolism, from the
Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED) II
trial:
High probability criteria are as follows:
Two large (>75% of a segment) segmental perfusion defects
without corresponding ventilation or chest x ray defects.
One large segmental perfusion defect and 2 moderate (25-
75% of a segment) segmental perfusion defects without
corresponding ventilation or radiographic abnormalities.
Four moderate segmental perfusion defects without
corresponding ventilation or chest radiographic abnormalities

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Intermediate probability criteria are as follows:
One moderate to fewer than 2 large segmental perfusion
defects without corresponding ventilation or chest
radiographic abnormalities
Corresponding V/Q defects and radiographic parenchymal
opacity in lower lung zone
Single moderate matched V/Q defects with normal chest
radiographic findings
Corresponding V/Q and chest radiography small pleural
effusion
Difficult to categorize as normal, low, or high probability
Low probability criteria are as follows:
Multiple matched V/Q defects, regardless of size, with
normal chest radiographic findings
Corresponding V/Q defects and radiographic parenchymal
opacity in upper or middle lung zone
Corresponding V/Q defects and large pleural effusion
Any perfusion defects with substantially larger radiographic
abnormality
Defects surrounded by normally perfused lung (stripe sign)
More than 3 small (<25% of a segment) segmental perfusion
defects with normal chest radiographic findings
Nonsegmental perfusion defects (cardiomegaly, aortic
impression, enlarged hila)
Very low criterion is 3 small (<25% of a segment) segmental
perfusion defects with normal chest radiograph findings.

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Advantage
1. a normal V/Q scan rules out PE
>99% negative predictive value
2. the radiation dose is low
3. iodine-based contrast is not used
other investigations:
1.MRI
2.PULMONARY ANGIOGRAPHY
3. Multidetector helical CT pulmonary angiography

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Simplified Revised Geneva
Score
 Age >65
 Previous history of PE or DVT
 Sx or Fx within 1 month
 Active malignancy
 HR 75-94
 HR >95
 Unilateral leg edema
 Unilateral leg pain
 Hemoptysis
Points
1
1
1
1
1
2
1
1
1
Risk factors
Clinical
signs
Symptoms
Wicki J, Perneger TV, Junod AF, et al. Assessing clinical probability of pulmonary embolism in the emergency ward.
Arch Intern Med. 2001;161:92-97.
0-2 = PE unlikely , 3-7 = PE likely
Prevention
 Prevent deep venous thrombosis.
1. Active leg exercises
2. The intermittent pneumatic leg compression device ( venous stasis).
3. Use of elastic compression stockings
4. Anticoagulant therapy
Medical Management
• General measures to improve respiratory and vascular status
• Anticoagulation therapy
• Thrombolytic therapy
• Surgical intervention

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GENERAL MANAGEMENT
Oxygen therapy is administered to correct the hypoxemia, relieve the
pulmonary vascular vasoconstriction, and reduce the pulmonary
hypertension.
Thrombolytics
 Evidence of circulatory/respiratory insufficiency
 Hypotension (SBP <90)
 Hypoxia (SpO2 <95%)
 Evidence of RV dysfunction
 RV dilation/hypokinesis
 Elevated troponin-I (>0.4) or proBNP (>900)
 EKG changes
FDA-recommended dose: Alteplase 100mg over 2hrs
Fibrinolysis Contraindications
Relative
 Age > 75
 Current anticoagulation use
 Pregnancy
 Noncompressible vascular punctures
 Traumatic or prolonged CPR >10 min
 Recent surgery/bleeding w/in 2-4 wks
 Poorly controlled HTN >180/110
 Dementia
 Recent Ischemic CVA > 3 months
Absolute
 Prior ICH
 Known intracranial CV disease (AVM)
 Malignant intracranial neoplasm
 CVA within 3 months
 Suspected aortic dissection
 Active bleeding
 Recent surgery of spinal cord/brain
 Recent closed-head trauma with brain
injury

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 Therapeutic anticoagulation with subcutaneous LMWH, intravenous or
subcutaneous UFH with monitoring, unmonitored weight-based
subcutaneous UFH, should be given to patients with objectively
confirmed PE and no contraindications to anticoagulation.
 UFH=Weight-based dosing (nomogram)
IV bolus – 80mg/kg IV bolus, then 18mg/kg/hr
Monitor PTT (1.5-2.0 x), CBC
Continue 4-5d and therapeutic on Warfarin for 2d (INR>2.0)
LMWH
 Alternative regimen Lovenox – 1mg/kg SC q12h
 Better bioavailability, longer half-life, more predictable effect
 No monitoring of PTT (follow CBC)
 Contraindications: renal failure (CrCl<30), weight extremes
Warfarin
 Start when therapeutic on Heparin
 Monitor INR daily
 Goal: INR 2.0-3.0 for 3-6 months
 Identified precipitant 3 mos
 First idiopathic episode 6 mos
 Prolonged/indefinite:
 2 thrombotic episodes
 1 spont. life-threatening episode
 Anti-phospholipid antibody syndrome, ATIII deficiency

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 Catheter embolectomy
 Surgical embolectomy
 Reasonable for…
 Massive PE if still unstable after fibrinolysis
 Massive/Submassive PE if fibrinolysis is contra-indicated or there is
evidence of adverse prognosis
o Three General Categories of Percutaneous Intervention
Aspiration thrombectomy
Thrombus fragmentation
Rheolytic thrombectomy

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Probabilityof PE above treatmentthreshold
Submassive withoutRV
Strain(Low risk PE)
Submassive withRV strain
(Abnormal echo orbiomarkers)
Systolicblood pressure
<90 mmHgfor >15 min
HeparinAnticoagulation
Assess forevidence ofincreased severity that suggests
potential forbenefitof fibrinolysis
1. EVIDENCEOF SHOCK ORRESPIRATORY FAILURE:
• Any hypotension (SBP<90 mm Hg) OR
• Shock index >1.0 OR
• Respiratory distress (SaO2 <95% with Borg score >8,or
altered mental status, or appearance of suffering)
2. EVIDENCEOF MODERATE TO SEVERERV STRAIN:
• RVdysfunction (RV hypokinesis or estimated RVSP> 40
mmHg) OR
• Clearly elevated biomarker values (e.g., troponin above
borderline value, BNP >100 pg/mL or pro-BNP >900 pg/mL)
Nocontraindicationstofibrinolysis
Alteplase 100 mg over 2 h IV
HeparinAnticoagulation HeparinAnticoagulation

Pulmonary embolism ms

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