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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.
      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
       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:
-surgery within the last three months
-stroke, paresis, paralysis
-history of venous thromboembolism
-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)
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.
The most common signs are:
-tachypnea (54%)
-tachycardia (24%)
-rales (18%)
-decreased breath sounds (17%)
-loud P2 (15%)
-jugular venous distension (14%)

Acute coronary syndrome
Tention pneumothorax
Cardiac tamponade
Aortic dissection
Esophageal disorder
 Routine laboratory findings (non-specific):
-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
 TROPONIN: Serum troponin I and troponin T are elevated in 30-
 50% 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.

-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.
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
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                                                         >4.0
      PE unlikely                                                     < 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

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      >500 ng/ml

Exclude PE                          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 D-
   dimer. A negative D-Dimer by the SimpliRed assay
   excludes PE.
   Respiratory support:
-oxygen supplement
-severe hypoxemia or respiratory failure   Intubation

    Hemodynamic support (If the patient presents with systemic
-if not resolved: -norepinephrine
                  -combined norepinephrine and dobutamine
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.

  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
-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

-Route of administration: P.O
-Monitoring :INR
-Desired target INR:2.5
Further management:
-IVC filter.

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