Discussion - PE

The diagnosis of pulmonary embolism is suspected on the basis of the medical history, current physical findings, imaging and the ECG findings. The CXR with some atelectasis does not explain a significant and refractory hypoxia. The timing is right for an embolus and the pelvic operation is frequently associated with thrombosis in the pelvis. A CT angiogram of the chest showed saddle pulmonary embolism and the ECG showed the expected S1Q3T3 pattern with right ventricular strain.

Pulmonary embolism is a common condition, it is also potentially lethal in all age groups. Prompt diagnosis and treatment can reduce the morbidity and mortality but diagnosis is difficult as the symptoms are often vague and nonspecific.

After traveling to the lung, large thrombi may lodge at the bifurcation of the main pulmonary artery or the lobar branches with haemodynamic effects. However, small thrombi occlude smaller peripheral vessels and so must be very numerous to cause haemodynamic changes. Peripheral emboli tend to produce pleuritic chest pain because the occluded area which is adjacent to the parietal pleura undergoes an inflammatory reaction. Lwer lobes are more commonly involved.

The incidence of pulmonary embolism varies greatly depending on the population (outside V in hospital). Both sexes are equally affected. Recurrent thromboembolic disease is more common in men, and venous thromboembolism and pulmonary embolism are commoner in the elderly.

The presentation of pulmonary embolism varies from a slowly progressive dyspnoea to a syndrome of catastrophic abrupt haemodynamic collapse with sudden death or syncope. Its signs are so subtle that a diagnosis of pulmonary embolism should be entertained in any patient with respiratory symptoms unexplained by a clear alternate diagnosis. A detailed assessment of risk factors is required. Pulmonary embolism can be categorized in abruptness and severity to:

  1. Massive pulmonary embolism:
    1. Large emboli
    2. sufficient compromise of pulmonary circulation
    3. circulatory collapse, shock and reduced cardiac output
    4. Symptoms
      1. hypotension
      2. tachycardia
      3. weakness
      4. pallor
      5. sweating
      6. oliguria
      7. altered consciousness.
  2. Acute pulmonary infarction:
    1. occluded pulmonary artery
      1. lung infarction
      2. symptoms
        1. acute-onset pleuritic chest pain (but may mimic acute coronary syndrome.)
        2. SOB
        3. haemoptysis
  3. Acute embolism without infarction:
    1. non-specific symptoms
      1. unexplained SOB
      2. retrosternal discomfort
      3. atypical/pleuritic chest pain.

Commonly pulmonary embolism causes (in order) dyspnoea (73%), pleuritic chest pain (66%), cough (37%), and hemoptysis (13%).

The ECG shows

  1. sinus tachycardia (rate > 100 beats/min)
    1. very common, and a clue to the presence of PE if no other cause is forthcoming
  2. S1Q3T3 pattern
    1. prominent S-wave in lead I
    2. prominent Q-wave in lead III
    3. biphasic T wave in lead III
  3. right bundle branch block
    1. usually a new finding
  4. P-wave pulmonale
  5. right-axis deviation

These findings are neither sensitive or specific for the diagnosis by ECG alone.

The patient's postoperative state and the presence of malignancy are associated with pulmonary embolus. Fatal PE is 4 times more likely in cancer patients. Peri-operative mortality is also 4 times more likely in cancer patients. Other risk factors include oral contraceptives (especially in young females), immobilization, prolonged travel, and pregnancy. There are also hypercoagulable states resulting from Factor V Leiden mutation, and acquired deficiencies in protein C, protein S, and antithrombin III.

The diagnosis of pulmonary embolism takes thought based on Bayesian estimations of pretest probability. In a patient with a low pretest probability of pulmonary embolism, a NEGATIVE D-dimer test will exclude PE. Patients with a suspected PE should have a CT angiography if stable. An acceptable alternative where there is not CT is a ventilation-perfusion (V/Q) scan. While an US of the legs has excellent sensitivity and specificity DVT, it cannot diagnose PE in patients with DVT, much less in patients without symptoms of DVT.

All patietns with suspected PE require immediate and successful anticoagulation. Investigations should not delay empirical anticoagulation. Anticoagulation is started with heparin and an oral anticoagulant (warfarin) at the time of diagnosis. The heparin is ceased when the INR is >2.0 for 1 day, when 5 days of warfarin has been delivered. Warfarin therapy should persist for at least 3 months in the first instance. Treatment for longer than 6 months is indicated in patients with recurrence or a persistent risk factor. Inferior vena caval (IVC) filters are indicated for patients who have an absolute contraindication to anticoagulant therapy (eg, recent surgery, hemorrhagic stroke, significant active or recent bleeding), those with have survived one massive pulmonary embolism but probably not a second, and those who are anticoagulated but still have objective recurrent venous thromboembolism.

Thrombolysis is indicated for haemodynamically unstable patients. Patients remained hypotensive despite these treatments may proceed to pulmonary embolectomy. Historically this was a high risk procedure (50-80% mortality) during or after arrest. Newer data has indicated a lower mortality rate especially without arrest.

Unless otherwise stated, the content of this page is licensed under Creative Commons Attribution-NonCommercial-NoDerivs 3.0 License