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PULMONARY EMBOLISM
PREPARED BY:
DR. IBRAHIM AYOUB
DR. SUHAIL KHOJAH
INTRODUCTION
Acute pulmonary embolism (PE) is a common
and often fatal disease. Mortality can be reduced
from 30% to up to 2-8% by prompt diagnosis
and therapy.
Unfortunately, the clinical presentation of PE is
variable and nonspecific, making accurate
diagnosis difficult.
CLASSIFICATION
PE can be classified as acute or chronic
-Patients with acute PE typically develop
symptoms and signs immediately after
obstruction of pulmonary vessels.
-In contrast, patients with chronic PE tend to
develop slowly progressive dyspnea over a
period of years due to pulmonary hypertension.
Acute PE can be further classified as massive or submassive:
-Massive PE causes hypotension, defined as:
a systolic blood pressure <90 mmHg
or
a drop in systolic blood pressure of ≥40 mmHg from
baseline for a period >15 minutes.
It should be suspected anytime there is hypotension
accompanied by an elevated central venous pressure (or
neck vein distension), which is not otherwise explained by
acute myocardial infarction, tension pneumothorax,
pericardial tamponade, or a new arrhythmia.
-All acute PE not meeting the definition of massive PE are
considered submassive PE.
RISK FACTORS
PE is a common complication of deep vein thrombosis (DVT), occurring
in more than 50% of cases confirmed to have DVT.
So, factors that promote the development of DVT also increase the risk
for PE. These include:
-immobilization
-surgery within the last three months
-stroke, paresis, paralysis
-history of venous thromboembolism
-malignancy
-central venous instrumentation within the last three months
-chronic heart disease.
-Additional risk factors identified in women include
obesity (BMI ≥29 kg/m2)
heavy cigarette smoking (>25 cigarettes per day)
hypertension.
SYMPTOMS
The most common symptoms are:
-dyspnea at rest or with exertion (73%)
-pleuritic pain (44%)
-cough (34%)
->2-pillow orthopnea (28%)
-calf or thigh pain (44%)
-calf or thigh swelling (41%)
-wheezing (21%).
*The onset of dyspnea was usually within seconds
(46%) or minutes.
SIGNS
The most common signs are:
-tachypnea (54%)
-tachycardia (24%)
-rales (18%)
-decreased breath sounds (17%)
-loud P2 (15%)
-jugular venous distension (14%)
DIFFERENTIAL DIAGNOSES
Acute coronary syndrome
Tention pneumothorax
Cardiac tamponade
Aortic dissection
Esophageal disorder
INVESTIGATIONS
Routine laboratory findings (non-specific):
-leukocytosis
-increased erythrocyte sedimentation rate (ESR)
-elevated serum LDH or AST (SGOT)
-normal serum bilirubin
ABG: usually reveal hypoxemia, hypocapnia, and
respiratory alkalosis.
The typical ABG findings are not always seen. As an
example, massive PE with hypotension and respiratory
collapse can cause hypercapnia and a combined
respiratory and metabolic acidosis (the latter due to lactic
acidosis). In addition, hypoxemia can be minimal or
absent.
TROPONIN: Serum troponin I and troponin T are elevated in 3050% of patients who have a moderate to large pulmonary embolism.
presumed mechanism is acute right heart overload.
ECG: ECG abnormalities are also common in patients without PE,
limiting the diagnostic usefulness of the ECG.
ECG abnormalities historically considered to be suggestive of PE
-S1Q3T3 pattern
-right ventricular strain
-new incomplete right bundle branch block
ECG changes are infrequent during acute PE. However, they are
common among patients with massive acute PE and cor pulmonale.
CXR:
-Atelectasis (69%)
-Pleural effusion (47%)
-Normal (12%)
V/Q SCAN: Diagnostic accuracy is greatest when the V/Q scan is
combined with clinical probability.
Ultrasound: used to diagnose DVT which is the most common cause
of PE.
D-dimer: have good sensitivity and negative predictive value, but
poor specificity and positive predictive value.
Angiography: Pulmonary angiography is the definitive diagnostic
technique or "gold standard" in the diagnosis of acute PE.
Spiral CT: spiral (helical) CT scanning with intravenous contrast (ie,
CT pulmonary angiography or CT-PA) is being used increasingly as
a diagnostic modality for patients with suspected PE.
Initial reports suggested that 98% of patients with PE were detected
by CT-PA.
RECOMMENDED DIAGNOSTIC
APPROACH
When PE is suspected (eg, in a patient with
sudden onset of dyspnea, deterioration of
existing dyspnea, or onset of pleuritic
chest pain without another apparent
cause), the clinician should determine
which diagnostic modalities are available
and how much the hospital is experienced
in performing and interpreting spiral CT
(CT-PA)
When PE is suspected, the modified Wells criteria should be applied to
determine if PE is unlikely (score <4) or likely (score >4).
The modified Wells Criteria include the following:
Clinical symptoms of DVT (leg swelling, pain with palpation)
3.0
Other diagnosis less likely than pulmonary embolism
3.0
Heart rate >100
1.5
Immobilization (3 days) or surgery in the previous four weeks
1.5
Previous DVT/PE
1.5
Hemoptysis
1.0
Malignancy
1.0
Probability
Score
Traditional clinical probability assessment
High
>6.0
Moderate
2.0 to 6.0
Low
<2.0
Simplified clinical probability assessment
PE likely
PE unlikely
>4.0
< or = 4.0
Patients classified as PE unlikely should undergo
quantitative D-dimer testing. If the D-dimer level
is <500 ng/mL, the diagnosis of PE can be
excluded.
Patients classified as PE likely and patients
classified as PE unlikely who have a D-dimer
level >500 ng/mL should undergo CT-PA. A
positive CT-PA confirms the diagnosis of PE.
Alternatively, a negative CT-PA excludes the
diagnosis of PE.
Modified wells criteria
PE unlikely
PE likely
Quantitative D-dimer test
<500 ng/ml
Exclude PE
>500 ng/ml
CT-PA
In case you are working in CT inexperienced hospital or the
patieng can’t undergo CP-PA (e.g. renal insufficiency or
morbid obecity), a ventilation-perfusion (V/Q) scan is
then performed, with the following combinations of
outcomes possible:
-Normal V/Q scan plus any clinical probability excludes PE.
-Low probability V/Q scan plus low clinical probability
excludes PE.
-High probability V/Q scan plus high clinical probability
confirms PE.
Any other combination of V/Q scan result plus clinical
probability should prompt either a pulmonary angiogram
or serial lower extremity venous ultrasound exams.
A reasonable alternative approach for patients with a low or
intermediate clinical probability of PE is to obtain a Ddimer. A negative D-Dimer by the SimpliRed assay
excludes PE.
MANAGEMENT
RESUSCITATION:
Respiratory support:
-oxygen supplement
-severe hypoxemia or respiratory failure
Intubation
Hemodynamic support (If the patient presents with systemic
hypotension):
-IVF
-if not resolved: -norepinephrine
-dopamine
-combined norepinephrine and dobutamine
ANTICOAGULANT THERAPY:
Anticoagulant therapy reduces mortality and is considered primary
therapy for PE. The goal of anticoagulation is to decrease mortality
by preventing recurrent PE.
For patients in whom there is a high clinical suspicion of PE and no
excess risk of bleeding, empiric anticoagulation should be initiated
immediately and continued during the diagnostic evaluation.
Heparin:
Dose :loading: 80U/Kg IV
:maintenance :18U/Kg/h
T ½ : 90m
Route of administration: IV/SC
Duration :7-10 d
Reversal :stop heparin
protamine sulphate :1U neutralize 100 IU heparin
No FFP
• LMWH:
-Dose :brand dependent
-Mechanism of action :anti-X > anti-II
-Route of administration :IV or S/C
-Monitoring : not indicated
-Indication for monitoring : pregnancy ,morbid obesity , sever renal or
liver derangement
-Duration : 7-10 d
-Reversal :stop heparin
protamine sulphate :un-predictable response
Warfarin:
-Route of administration: P.O
-Monitoring :INR
-Desired target INR:2.5
Further management:
-Thrombolysis.
-IVC filter.
-Embolectomy