Pulmonary embolism natural history, complications and prognosis
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Pulmonary embolism Microchapters
Natural History, Complications and Prognosis
Pulmonary embolism natural history, complications and prognosis On the Web
Pulmonary embolism can be acutely complicated by the development of cardiogenic shock, pulseless electrical activity and sudden cardiac death and chronically by the development of pulmonary hypertension. The medical management of pulmonary embolism often requires the administration of potent parenteral anticoagulants and fibrinolytics and massive bleeding can be a complication of their administration. If left untreated almost one-third of patients with pulmonary embolism die, typically from recurrent pulmonary embolism. However, with prompt diagnosis and treatment, the mortality rate is approximately 2–8%. The true mortality associated with pulmonary embolism may be underestimated as two-thirds of all pulmonary embolism cases are diagnosed by autopsy.
- Atrial flutter
- Heart failure or shock
- Pulmonary hypertension
- Pulseless Electrical Activity
- Sudden cardiac death
- Chronic thromboembolic hypertension (rare - 1%)
- Pulmonary hypertension
- Recurrent pulmonary embolism
Complications of Firbrinolytic Therapy for Pulmonary Embolism
- Severe bleeding can occur as a complication of fibrinolytic treatment:
If left untreated, almost one-third of the patients die, typically from recurrent PE. However, with prompt diagnosis and treatment, the mortality rate is approximately 2–8%. Unfortunately, two-thirds of all PE cases are diagnosed by autopsy.  Pulmonary embolism causes death in approximately 16% of hospitalized patients.
A 26% mortality rate associated with untreated pulmonary embolism is often cited based upon a trial published in 1960 by Barrit and Jordan which compared anti-coagulation against placebo for the management of pulmonary embolism. Barritt and Jordan performed their study in the Bristol Royal Infirmary in 1957. This study is the only placebo controlled trial ever to examine the efficacy of anticoagulants in the treatment of pulmonary embolism. The results of this were so convincing that the trial has not been repeated. On the other hand, the reported mortality rate of 26% in the placebo group may underestimate the true mortality insofar as the sensitivity and specificity of diagnostic technology in 1957 may have only allowed the detection of massive pulmonary emboli.
Risk Stratification in Assessing Prognosis
The prognosis in a patient with pulmonary embolism depends upon:
- The extent of the pulmonary vasculature that is occluded
- Co-existence of other medical conditions (i.e. the patient's comorbidities)
Clinical correlates of mortality among patients with pulmonary embolism are listed below.
Observational studies such as the International Co-operative Pulmonary Embolism Registry (ICOPER) and the Management and Prognosis in Pulmonary Embolism Trial (MAPPET) have shown that shock and hypotension are principal high risk markers of early death in acute PE. The MAPPET study demonstrated that systemic shock was associated with mortality of 24.5% where as hypotension (but not shock) was associated with the mortality of 15.2%.
A post-hoc analysis of the ICOPER study demonstrated that the 90-day all-cause mortality rate was 52.4% (95% CI,43.3–62.1%) among patients with a systolic blood pressure less than 90 mm Hg compared to 14.7% (95% CI, 13.3–16.2%) among patients with a normal blood pressure.
Markers of Right Ventricular Dysfunction (RVD) 
The presence of right ventricular dysfunction (RVD) on echocardiography has been associated with a higher mortality in the setting of pulmonary embolism.
|Study||Year||Patients (n)||Blood pressure||Echocardiographic criteria||RVD(present) vs. RVD(absent): Mortality percentage(%)|
|Goldhaber et al.||1993||101||Normotensive||RV hypokinesis and dilatation||4.3% vs. 0%|
|Ribeiro et al. ||1997||126||Normotensive and hypotensive||RVD||12.8% vs. 0%|
|Kasper et al.||1997||317||Normotensive and hypotensive||RV >30 mm or TI >2.8 m/s||13% vs. 0.9%|
|Grifoni et al.||2000||162||BP ≥ 100 mmHg|| Atleast one of the following
||4.6% vs. 0%|
|Kucher et al.||2005||1035||BP ≤ 90 mmHg||RVD||16.3% vs. 9.4%|
Abbreviations Used: RV , right ventricle; TI, tricuspid insufficiency; LV, left ventricle; AcT, ACceleration Time of right ventricular ejection; TIPG, tricuspid insufficiency peak gradient.
Brain Natriuretic Peptide
In patients with a pulmonary embolism, elevated plasma levels of natriuretic peptides (brain natriuretic peptide and N-terminal pro-brain natriuretic peptide) have been associated with higher mortality. Levels of N-terminal pro-brain natriuretic peptide greater than 500 ng/L serve as an indicator of the burden of PE and are associated with death.
Elevated serum troponin levels are associated with an increased risk of death among pulmonary embolism patients. The elevation of troponin in patients with a massive pulmonary embolism does not reflect epicadial coronary artery disease but rather transmural RV infarctions on autopsy. 
Hyponatremia at the time of presentation is associated with increased mortality and hospital readmission
- Atrial arrhythmias
- Right bundle branch block
- Q-waves in the inferior leads
- Precordial T-wave inversion and ST-segment changes.
- Development of a QR wave in lead V1 is identified as an independent risk factor for an adverse prognosis.
ESC 2008 Guidelines for Prognostic Assessment (DO NOT EDIT)
|"1. Initial risk stratification of suspected and/or confirmed PE based on the presence of shock and hypotension is recommended to distinguish between patients with high and non-high-risk of PE-related early mortality. (Level of Evidence: B) "|
|"1. In non-high-risk PE patients, further stratification to an intermediate- or low-risk PE subgroup based on the presence of imaging or biochemical markers of RVD and myocardial injury should be considered.(Level of Evidence: B) "|
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