PULMONARY EMBOLISM

DR. ISEKO I.I

HEMATOLOGY POSTGRADUATE SEMINAR
 INTRODUCTION
• This humour…immediately congeals not only
outside the body but actually contained in its
own surroundings: and this congealing of
itself, we see terminate in the thrombus for by
this term the Greeks name the congealed
blood.
• Galen, C Black bile. Corpus medicorum Graecorum
Quae Exstant V: 106, Leipzig, Cnoblock, 1823
 INTRODUCTION
• Pulmonary embolism (PE) refers to exogenous
or endogenous material that travels to the
lungs through the pulmonary circulation,
causing a potential spectrum of
consequences.

• Thrombus from the deep veins of the lower

extremities is by far the most common
material to embolize to the lungs
 INTRODUCTION
Many substances can embolize to the
pulmonary circulation, including ;
– Air (during neurosurgery, from central venous
catheters)
– Amniotic fluid (during active labor)
– Fat (long bone fractures)
– Foreign bodies (talc in injection drug users)
– Parasite eggs (schistosomiasis)
– Septic emboli (acute infectious endocarditis)
– Tumor cells (renal cell carcinoma)
 INTRODUCTION
• Majority of cases are not recognized antemortem

• Fewer 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 NIGERIAN EXPERIENCE
Cent Afr J Med. 1992 Nov;38(11):432-5.
Pulmonary embolism in Ibadan, Nigeria: five years autopsy report.
Awotedu AA, Igbokwe EO, Akang EE, Aghadiuno PO.

• Pulmonary embolism occurred in 3.8% of all autopsied patients during this

period. There was a male to female ratio 1.4:1
• average age was 47 years.
• Malignant neoplasms, infections and cardiac failure were the leading
predisposing factors to PE identified.
• The ante-mortem clinical features consisted largely of non-specific respiratory
symptoms of dyspnoea, cough, chest pain and haemoptysis.
• Of these patients, 15.6% were diagnosed ante-mortem as having PE.
• Pulmonary infarction occurred in 13.3% of the cases and was commoner in
females and in patients with underlying cardiac diseases
 AETIOLOGY
• Genetic and acquired factors contribute to the
likelihood of VTE.

• However, only a minority of patients with VTE

have identifiable predisposing genetic factors.

• The majority of patients with predisposing

genetic factors will not develop clinical evidence
of clotting
NORMAL PATHWAY(simplified)
 AETIOLOGY
• Pulmonary embolism and DVT are two
manifestations of the same disease
• VENOUS STASIS
– Venous stasis increases with immobility (bed rest—
especially postoperative—obesity, stroke), hyperviscosity
(polycythemia), and increased central venous pressures
(low cardiac output states, pregnancy).

• INJURY TO THE VESSEL WALL

– Vessels may be damaged by prior episodes of thrombosis,
orthopedic surgery, or trauma
 AETIOLOGY
HYPERCOAGULABILITY

• Hypercoagulability can be caused by

– Medications (oral contraceptives, hormonal replacement therapy)
– Disease (malignancy, surgery)
– Inherited gene defects
Most common inherited cause in white populations is resistance
to activated protein C, also known as Factor V Leiden
• Other major risks for hypercoagulability include the
following:
– Deficiencies or Dysfunction of protein C, protein S, and
– Antithrombin III;
– Prothrombin gene mutation;
– Antiphospholipid antibodies (lupus anticoagulant and anticardiolipin
antibody).
 AETIOLOGY
MAJOR ACQUIRED RISK FACTORS
• Advancing age
• Arterial disease including carotid and coronary disease
• Obesity
• Cigarette smoking
• Chronic obstructive pulmonary disease
• Personal or family history of venous thromboembolism
• Recent surgery, trauma, or immobility including stroke
• Acute infection
• Long-haul air travel
• Cancer Pregnancy, oral contraceptive pills, or hormone replacement therapy
• Pacemaker, implantable cardiac defibrillator leads, or indwelling central
venous catheters
AETIOLOGY
AETIOLOGY
 AETIOLOGY

MAJOR THROMBOPHILIAS ASSOCIATED WITH VTE

• Inherited Factor V Leiden resulting in activated protein C resistance
• Prothrombin gene mutation 20210
• Antithrombin III deficiency
• Protein C deficiency
• Protein S deficiency
• Acquired Antiphospholipid antibody syndrome
• Hyperhomocysteinemia
AETIOLOGY
AETIOLOGY
 PATHOPHYSIOLOGY
EMBOLIZATION :

• About half of patients with pelvic vein thrombosis or

proximal leg DVT develop PE, which is usually asymptomatic.

• Isolated calf vein thrombi pose a much lower risk of PE, but
they are the most common source of paradoxical embolism.

• With increased use of chronic indwelling central venous

catheters, permanent pacemakers and internal cardiac
defibrillators, upper extremity venous thrombosis is
becoming a more common problem. These thrombi rarely
embolize and cause PE.
 PATHOPHYSIOLOGY
EMBOLIZATION :
• Other less common sources of pulmonary embolism
include
– Deep pelvic veins,
– Renal veins,
– Inferior vena cava,
– Right side of the heart, and
– Axillary veins.
– Upper extremity deep vein thrombosis also may lead to
pulmonary embolism
• Most clinically important pulmonary emboli arise
from proximal deep vein thrombosis of the leg.
PATHOPHYSIOLOGY
 PATHOPHYSIOLOGY
• The most common gas exchange abnormalities are
hypoxemia (decreased arterial PO2) and an increased
alveolar-arterial O2 tension gradient.

• Anatomic dead space increases because breathed

gas does not enter gas exchange units of the lung.

• Physiologic dead space increases because ventilation

to gas exchange units exceeds venous blood flow
through the pulmonary capillaries.
Other pathophysiological abnormalities include:

• Increased pulmonary vascular resistance due to vascular obstruction or

platelet secretion of vasoconstricting neurohumoral agents such as serotonin.

• Impaired gas exchange due to increased alveolar dead space

• Alveolar hyperventilation due to reflex stimulation of irritant receptors

• Increased airway resistance due to constriction of airways distal to the

bronchi

• Decreased pulmonary compliance due to lung edema, lung hemorrhage, or

loss of surfactant
Right Ventricular Dysfunction
 CLINICAL FEATURES
• The clinical diagnosis of pulmonary
thromboembolism is notoriously difficult for two
reasons

• First, the clinical findings depend on both the size of

the embolus and the patient's preexisting
cardiopulmonary status

• Second, common symptoms and signs of pulmonary

emboli are not specific to this disorder
 CLINICAL FEATURES
Symptoms      
• Dyspnea
• Respirophasic chest pain
• Cough
• Legpain
• Hemoptysis
• Palpitations
• Wheezing
• Anginal pain
 CLINICAL FEATURES
Signs
• Respiratory rate >20/min
• Crepitations   
• Heart rate > 100/min
• Fourth heart sound (S4)
• Accentuated pulmonary component of second heart sound
(P2)   
• T >37.5 °C - 38.5 °C
• Homans' sign
• Pleural friction rub
• Third heart sound (S3)
• Cyanosis
 CLINICAL FEATURES
Indeed, no single symptom or sign or
combination of clinical findings is
specific to pulmonary
thromboembolism
CLINICAL PRESENTATION
  Clinical Decision Rule

WELLS VTE PREDICTION SCORE:   

Score Points
• DVT symptoms or signs 3
• An alternative diagnosis is less likely than PE 3
• HR > 100/min 1.5
• Immobilization or surgery within 4 wk 1.5
• Prior DVT or PE 1.5
• Hemoptysis 1
• Cancer treated within 6 mo or metastatic 1
• Wells VTE prediction score:
– Total score:
• <2.0 low pretest probability
• 2.0-6.0 intermediate pretest probability
• >6.0 high pretest probability
– Dichotomized score:
• ≤ 4.0 PE unlikely
• >4.0 PE likely
 DIFFERENTIAL DIAGNOSIS.

Myocardial infarction
Pericarditis
Heart failure
Pneumonia
Asthma
Chronic obstructive pulmonary disease
Pneumothorax
Pleurodynia
Pleuritis from connective tissue disease
Thoracic herpes zoster (“shingles”)
Rib fracture
Musculoskeletal pain
Primary or metastatic intra thoracic cancer
Infra diaphragmatic processes (e.g., acute cholecystitis, splenic infarction)
Hyperventilation syndrome
 Clinical Syndromes of Pulmonary Embolism
• Classification of Acute Pulmonary Embolism :
Classification Presentation Therapy
Massive PE Systolic BP ≤ 90 mm Hg Thrombolysis
or poor tissue perfusion or embolectomy
or multisystem organ failure or IVC filter
plus plus
rt or lt PA thrombus anticoagulation
or “high clot burden”
Submassive PE Hemodynamically stablebut Addition of thrombolysis,
mod. or sev.RVdysfunction embolectomy or filter
or enlargement remains controversial

Small to mod.PE Normal hemodynamics and Anticoagulation

normal RV size and function
 Clinical Syndromes of Pulmonary Embolism

• PULMONARY INFARCTION.
Caused by a tiny peripheral pulmonary embolism
Tissue infarction usually occurs 3 to 7 days after embolism.
Pleuritic chest pain, often not responsive to narcotics
Low-grade fever
Pleural rub
Occasional scant hemoptysis
Leukocytosis
• PARADOXICAL EMBOLISM.
small DVT that embolizes to the arterial system, usually through a
patent foramen ovale.
 Clinical Syndromes of Pulmonary Embolism

NONTHROMBOTIC PULMONARY EMBOLISM:

include fat, tumor, air, and amniotic fluid

-Fat embolism syndrome is most often observed after blunt trauma

complicated by long-bone fractures.

-Air embolus can occur during placement or removal of CVC

- Amniotic fluid embolism may be catastrophic and is characterized by

respiratory failure, cardiogenic shock, and DIC.

-Intravenous drug abusers sometimes self-inject hair, talc, and cotton

that contaminate the drug they have acquired
INVESTIGATIONS
NONIMAGING DIAGNOSTIC MODALITIES
PLASMA d-DIMER ASSAY:
• D-dimer is a unique degradation product produced by plasmin-mediated
proteolysis of cross-linked fibrin. D-dimer is measured by latex
agglutination or by an enzyme-linked immunosorbent assay (ELISA) and a
test result is considered positive if the level is greater than 500 ng/mL.
• Latex agglutination tests are notoriously unreliable, with a historical
sensitivity of only 50-60% for DVT and PE.
• The ELISA test is more sensitive than the latex agglutination test, with a
sensitivity of 96-98%.
• The challenge is that the test is nonspecific and results may be positive in
patients with infection, cancer, trauma, or other inflammatory states.
• A D-dimer screen is best used in conjunction with a clinical assessment of
the patient's probability of pulmonary embolism
NONIMAGING DIAGNOSTIC MODALITIES
PLASMA d-DIMER ASSAY:
• Quantitative plasma D-dimerenzyme-linked immunosorbent assay (ELISA)
rises in the presence of DVT or PE .
• The D-dimer is a useful "rule out" test. It is normal (<500 ng/mL) in more
than 95% of patients without PE.
• In patients with low clinical suspicion of DVT, it is normal in more than
90% without DVT.
• Levels increase in pts with MI, pneumonia, sepsis, cancer, the
postoperative state, and 2nd or 3rd trimester of pregnancy.
• Therefore, it rarely has a useful role among hospitalized patients
because their D-dimers are frequently elevated due to some systemic
illness
NONIMAGING DIAGNOSTIC MODALITIES

• Elevated Cardiac Biomarkers :

-Serum troponin levels increase in RV microinfarction.

-Myocardial stretch often results in elevation of BNP or NT-pro- BNP

-Elevated cardiac biomarkers predict an increase in major

complications and mortality from PE
 ELECTROCARDIOGRAM.
-Sinus tachycardia

- Incomplete or complete
RBBB
- 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 >90 degrees or an

indeterminate axis
-AF or Atrial flutter
NONINVASIVE IMAGING MODALITIES
CHEST RADIOGRAPHY :
• A normal or near-normal CXR in a dyspneic patient
often occurs in PE.
• Well-established abnormalities include
– focal oligemia ( Westermark's sign),
– a peripheral wedged-shaped density above the diaphragm
(Hampton's hump),
– an enlarged right descending pulmonary artery ( Palla's
sign).
– Small pleural effusion may be seen sometimes
Chest radiograph shows bilateral pleural effusion and long
linear bands of atelectasis (Fleischner lines) (arrows).
NONINVASIVE IMAGING MODALITIES
CHEST CT
• CT of the chest with IV contrast is the principal imaging test
for the diagnosis of PE.
• Multi detector-row spiral CT acquires all chest images with 1
mm. This CT scanners can image small peripheral emboli.
• The CT scan also obtains excellent images of the RV and LV
and can be used for a risk stratification as well as a diagnostic
tool.
• In patients without PE, the lung parenchymal images may
establish alternative diagnoses not apparent on chest x-ray
that explain the presenting symptoms and signs, such as
pneumonia, emphysema, pulmonary fibrosis, pulmonary
mass, or aortic pathology.
CT demonstrate wedge-shaped, nonenhancing pulmonary
infarction in the anterior and posterior basal segment. Clot
is visible in anterior and posterior basal segment arteries
(arrows). Right pleural effusion is also present.
NONINVASIVE IMAGING MODALITIES
LUNG SCANNING
• Lung scanning is now a second-line diagnostic test for PE.
• It is mostly used for patients who cannot tolerate intravenous
contrast.
• Small particulate aggregates of albumin labeled with a
gamma-emitting radionuclide are injected IV and are trapped
in the pulmonary capillary bed.
• The perfusion scan defect indicates absent or decreased
blood flow, possibly due to PE.
• Ventilation scans, obtained with radiolabeled inhaled gases
such as xenon or krypton, improve the specificity of the
perfusion scan.
NONINVASIVE IMAGING MODALITIES
LUNG SCANNING
• Abnormal ventilation scans indicate abnormal non ventilated
lung, thereby providing possible explanations for perfusion
defects other than acute PE, such as asthma or COPD.
• A high probability scan for PE is defined as having two or more
segmental perfusion defects in the presence of normal
ventilation.
• The diagnosis of PE is very unlikely in patients with normal
and near-normal scans but is about 90% certain in patients
with high-probability scans.
• As many as 40% of patients with high clinical suspicion for PE
and "low-probability" scans do, in fact, have PE at
angiography.
NONINVASIVE IMAGING MODALITIES
MAGNETIC RESONANCE (MR)
• MR utilizes gadolinium contrast agent, which, unlike iodinated
contrast agents used in venography or CT angiography, is not
nephrotoxic.

• MR imaging should be considered for suspected DVT or PE

patients with renal insufficiency or contrast dye allergy.

• MR pulmonary angiography detects large proximal PE but is

not reliable for smaller segmental and sub segmental PE.
NONINVASIVE IMAGING MODALITIES
ECHOCARDIOGRAPHY
• Echocardiography is not a reliable diagnostic imaging tool for
acute PE.
• Transthoracic echo rarely images thrombus directly.
• The best-known indirect sign of PE on transthoracic echo is
– McConnell's sign: hypokinesis of the RV free wall with
normal motion of the RV apex.
• Transesophageal echo should be considered when CT
scanning facilities are not available or when a patient has
renal failure or severe contrast allergy. This imaging modality
can directly visualize large proximal PE.
NONINVASIVE IMAGING MODALITIES
VENOUS ULTRASONOGRAPHY
• The primary diagnostic criterion for DVT is loss of vein
compressibility. Normally, the vein collapses completely when gentle
pressure is applied to the skin overlying it.

• When PE is suspected, venous ultrasonography is useful if it

demonstrates DVT because DVT can be considered a surrogate for PE.

• However, at least half of patients with PE have no imaging evidence

of DVT.

• Therefore if clinical suspicion of PE is moderate or high, patients

without evidence of DVT should undergo further investigation for PE.
NONINVASIVE IMAGING MODALITIES
• The white blood cell (WBC) count may be
normal or elevated. A WBC count as high as
20,000 is not uncommon in patients with PE.
• Clotting study results are normal in most
patients with pulmonary thromboembolism.
– Prolongation of the prothrombin time (PT), activated
partial thromboplastin time (aPTT), or clotting time
have no prognostic value in the diagnosis of PE.
– DVT and PE can and often do recur in patients who
are fully anticoagulated.
 INVASIVE DIAGNOSTIC MODALITIES
PULMONARY ANGIOGRAPHY :
-Chest CT with contrast has virtually replaced invasive pulmonary
angiography as a diagnostic test.
- Reserved for patients with technically unsatisfactory chest CTs
or for those in whom an interventional procedure such as
catheter-directed thrombolysis or embolectomy is planned.
- A definitive diagnosis of PE depends upon visualization of an
Intraluminal filling defect in more than one projection.
- Secondary signs of PE include abrupt occlusion ("cut-off") of
vessels, segmental oligemia or avascularity, a prolonged arterial
phase with slow filling, or tortuous, tapering peripheral vessels
Multiple intravascular filling defects in the right pulmonary
artery on angiogram.
 INVASIVE DIAGNOSTIC MODALITIES
• CONTRAST PHLEBOGRAPHY

Venous ultrasonography has virtually replaced contrast

phlebography as the diagnostic test for suspected DVT.
INTEGRATED DIAGNOSTIC APPROACH
MANAGEMENT
MANAGEMENT
Risk Stratification
 Predictors of Increased Mortality

• Clinical
Systolic blood pressure less than or equal to 100 mm Hg
Age older than 70 years
Heart rate higher than 100 beats/min
Congestive heart failure ,Chronic lung disease ,Cancer

• Cardiac Biomarkers and Imaging

Elevated troponin I or troponin T
Elevated BNP or pro-BNP
Right ventricular hypokinesis on echocardiogram
Right ventricular enlargement on chest CT
 Anticoagulation
Unfractionated heparin (UFH) prevents additional thrombus formation and
permitting endogenous fibrinolytic mechanisms to lyse clot that has
already formed.
• UFH is dosed to achieve a target (aPTT) that is 2–3 times the upper limit of
the laboratory normal. This is usually equivalent to an aPTT of 60–80 s.
• For UFH, a typical IVbolus is 5000–10,000 units followed by a continuous
infusion of 1000–1500 units/h.
• The most popular nomogram utilizes an initial bolus of 80 units/kg,
followed by an initial infusion rate of 18 units/kg per hour.

• The major advantage of UFH is that it has a short half-life.

• The major disadvantage of UFH is that achieving the target aPTT can be
difficult and may require repeated blood sampling and heparin dose
adjustment every 4–6 h.
– UFH molecules possessing anticoagulant activity
constitute approximately one-third by weight of
commercial heparin products
– The natural anticoagulant effect of AT is
potentiated resulting in the accelerated binding
and inactivation of serine proteases, in general,
and factor Xa and thrombin, in particular
Anticoagulation
 Raschke Nomogram

Variable Action

Initial IV heparin bolus 80 U/kg bolus, then 18 U/kg/hr

aPTT <35 seconds (<1.2 × control) 80 U/kg bolus, then increase by

4 U/kg/hr
aPTT 35 - 45 seconds (1.2 -1.5 c) 40 U/kg bolus, then by 2 U/kg/hr

aPTT 46 - 70 seconds (1.5 to 2.3 c) No change

aPTT 71 - 90 seconds (2.3 to 3 c ) infusion rate by 2 U/kg/hr

aPTT >90 seconds (>3 c) Hold infusion 1 hr, then decrease

infusion rate by 3 U/kg/hr
• Low Molecular Weight Heparins:

exhibit less binding to plasma proteins and endothelial cells and

consequently have greater bioavailability, a more predictable dose
response, and a longer half-life than UFH.

-No monitoring or dose adjustment is needed unless the patient is markedly

obese or has renal insufficiency.

• Enoxaparin 1 mg/kg twice daily and tinzaparin 175 units/kg once daily have
received FDA approval for treatment of patients who present with DVT.

• The weight-adjusted doses must be adjusted downward in renal

insufficiency because the kidneys excrete LMWH
• Fondaparinux:
-Fondaparinux, an anti-Xa pentasaccharide, is administered by once-daily
subcutaneous injection and has been approved by the FDA to treat DVT
and PE.

-No laboratory monitoring is required.

-Patients weighing <50 kg receive 5 mg,

50–100 kg receive 7.5 mg, and
>100 kg receive 10 mg.

-The dose must be adjusted downward for patients with renal dysfunction
because the drug is excreted by the kidneys.
 Warfarin
• This vitamin K antagonist prevents carboxylation activation of coagulation
factors II, VII, IX, and X.

• The full effect of warfarin requires at least 5 days.

• If warfarin is initiated as monotherapy a paradoxical exacerbation of

hypercoagulability can increase the likelihood of thrombosis rather than
prevent it.

• Overlapping UFH, LMWH, or fondaparinux with warfarin for at least 5

days can counteract the early procoagulant effect of unopposed warfarin.
Warfarin
 Warfarin

• Dosing
- In an average-sized adult, warfarin is usually initiated in a dose of 5 mg.

-Doses of 7.5 or 10 mg can be used in obese or large-framed young

patients who are otherwise healthy.

- Patients who are malnourished or who have received prolonged courses

of antibiotics are probably deficient in vitamin K and should receive smaller
initial doses of warfarin, such as 2.5 mg.

-The prothrombin time is standardized with the INR.

-The target INR is usually 2.5, with a range of 2.0–3.0

 OTHERS
• Melagatran
– This oral thrombin inhibitor undergoing phase III trials seems to
be well tolerated, with few clinically significant bleeding
problems, in patients with venous thromboembolism.
– Ximelagatran has the advantage that it does not require
anticoagulant monitoring and dose titration in the individual
patient.
• Hirudin and direct thrombin inhibitors
– Hirudin, a 65 amino acid residue anticoagulant peptide from the
leech Hirudo medicinalis, binds thrombin with high specificity and
sensitivity.
– Hirulog and argatroban among the best developed.
 Optimal Duration of Anticoagulation

• Clinical Setting Recommendation

• 1ST provoked PE/proximal leg DVT 6 mo

First provoked upper extremity DVT 3 mo

or isolated calf DVT

Second provoked VTE 12 mo

or indefinite duration

Third VTE Indefinite duration

Cancer 6 mo
or indefinite duration

Unprovoked VTE Consider indefinite duration

 Optimal Duration of Anticoagulation

• CLINICAL SETTING RECOMMENDATION

• Idiopathic event (no identifiable 6 months at least

risk factor)

• Idiopathic event (with known Indefinite

hypercoagulable risk factor)

• Recurrent idiopathic events Indefinite

 RICHARD M. NIXON

While generally healthy, he was on lifelong warfarin

anticoagulant therapy after multiple episodes of deep vein
thrombosis and pulmonary embolism starting in 1965 (these
conditions would later contribute to his fatal stroke).
 SIDE EFFECTS OF ANTICOAGULANT THERAPY

BLEEDING
• Bleeding is the most common side effect of anticoagulant
therapy.
• Bleeding can be classified as major or minor according to
standardized international criteria.
– Major bleeding is defined as clinically overt bleeding resulting in a
decline of hemoglobin of at least 2g/dl, transfusion of at least 2 U
of packed red cells, or bleeding that is retroperitoneal or
intracranial.
– The rates of major bleeding in clinical trials of initial therapy with
intravenous heparin, LMW heparin, or fondaparinux are 1 to 2
percent.
 SIDE EFFECTS OF ANTICOAGULANT THERAPY

• HEPARIN-INDUCED THROMBOCYTOPENIA
– Heparin or LMW heparin may cause
thrombocytopenia.
– In large clinical studies of acute venous
thromboembolism treatment, thrombocytopenia
occurred in fewer than 1 percent of more than 2000
patients treated with unfractionated heparin or
LMW heparin.
– High rate of limb loss and a high mortality when it
occurs
 SIDE EFFECTS OF ANTICOAGULANT THERAPY

• HEPARIN-INDUCED OSTEOPOROSIS
– Osteoporosis may occur as a result of long-term
treatment with heparin or LMW heparin (usually
after more than 3 months).
– The earliest clinical manifestation of heparin-
associated osteoporosis usually is nonspecific low
back pain primarily involving the vertebrae or the
ribs.
– Patients also may present with spontaneous
fractures.
 SIDE EFFECTS OF ANTICOAGULANT THERAPY

• Additional rare side effects of heparin include

– Hypersensitivity and
– Skin reactions, such as necrosis, alopecia,
– Hyperkalemia occurring as a result of
hypoaldosteronism.
• Ximelagatran treatment may cause elevated
liver transaminase enzyme levels
 Inferior Vena Caval Filters

• The indications for insertion of an IVC filter are

(1) active bleeding that precludes anticoagulation, and
(2) recurrent venous thrombosis despite intensive anticoagulation

• Prevention of recurrent PE in patients with Rt. heart failure who are not
candidates for fibrinolysis or prophylaxis of extremely high-risk patients are
"softer" indications for filter placement.

• The filter itself may fail by permitting the passage of small to medium-sized
clots.
• Large thrombi may embolize to the pulmonary arteries via collateral veins that
develop.
• A more common complication is caval thrombosis with marked bilateral leg
swelling
 Inferior Vena Caval Filters

• Retrievable filters can now be placed for patients with

-an anticipated temporary bleeding disorder or
-for patients at temporary high risk of PE

• The filters can be retrieved up to several months following insertion,

unless thrombus forms and is trapped within the filter.

• The retrievable filter becomes permanent if it remains in place or if, for

technical reasons such as rapid endothelialization, it cannot be removed
 Maintaining Adequate Circulation

• For patients with massive PE and hypotension, the most common initial
approach is administration of 500–1,000 ml of normal saline.

• However, fluids should be used with extreme caution.

• Excessive fluid administration exacerbates RV wall stress, causes more

profound RV ischemia, and worsens LV compliance and filling by causing
further IVS shift toward the LV.

• Dopamine and dobutamine are first-line inotropic agents for treatment

of PE-related shock.
 FIBRINOLYSIS

• Thrombolysis usually
(1) dissolves much of the obstructing pulmonary arterial thrombus
(2) prevents the continued release of serotonin and other neurohumoral
factors that exacerbate pulmonary hypertension and
(3) dissolves much of the source of the thrombus in the pelvic or
deep leg veins, thereby decreasing the likelihood of recurrent PE.

• The preferred fibrinolytic regimen is 100 mg of recombinant tissue

plasminogen activator (tPA) administered as a continuous peripheral IV
infusion over 2 h.

• Patients appear to respond to fibrinolysis for up to 14 days after the PE

has occurred.
FIBRINOLYSIS
FIBRINOLYSIS
 FIBRINOLYSIS
• Contraindications to fibrinolysis include intracranial disease, recent
surgery, or trauma.

• The overall major bleeding rate is about 10%, including a 1–3% risk of
intracranial hemorrhage.

• Indication for PE fibrinolysis is massive PE.

• For patients with preserved systolic blood pressure and submassive PE,
guidelines recommend individual patient risk assessment of the
thrombotic burden versus bleeding risk
FIBRINOLYSIS
 MANAGEMENT
• Pulmonary Embolectomy

-The risk of intracranial hemorrhage with fibrinolysis has prompted

the renaissance of surgical embolectomy for acute PE
- At Brigham and Women's Hospital, 47 patients with massive PE
underwent emergency surgery in 53 months, with a 94% survival rate

• Alternative to open surgical embolectomy is catheter embolectomy

 PULMONARY THROMBO ENDARTERECTOMY
• Chronic thromboembolic pulmonary hypertension is caused by vascular
obstruction at the capillary level, not direct thromboembolic occlusion

• Patients severely impaired with dyspnea due to chronic thromboembolic

PHTN should be considered for pulmonary thromboendarterectomy,
which, if successful, can markedly reduce and at times even cure PHTN.

• The two most common complications are

(1) "pulmonary steal," where blood rushes from previously perfused

areas to newly revascularized areas of the lung; and

(2) reperfusion pulmonary edema

PREVENTION
PREVENTION
 PREVENTION
Low Medium High
Ambulatory with no other CHF COPD / Pneumonia Elective LE arthroplasty
risk factors. Same day or Most Medical Patients Most Hip/pelvic fx
minor surgery Gen Surg Patients Acute SCI w/ paresis
Everybody Else Multiple major trauma
Abd / pelvic CA surgery

Early ambulation UFH 5000 units q 8 h (5000 Enox 30 mg q 12 h

units q 12 h if > 75 or or Enox 40 q day
weight <50 kg) or Other LMWH
LMWH Enox 40 mg q day Or Fondaparinux 2.5 mg q
Other LMWH day
CONSIDER add IPC or Warfarin INR 2-3
AND MUST HAVE IPC
Prevention of VTE
Olikoye Ransome-Kuti
• REFERENCES:

1. Gregory Y H Lip et al, Abc Of Antithrombotic Therapy 2003

2. Awotedu AA, Akang EE, et al. Pulmonary embolism in Ibadan, Nigeria: five years autopsy
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