Pulmonary Embolism
Disease Details
Family Health Simplified
- Description
- Pulmonary embolism is a blockage in one of the pulmonary arteries in the lungs, usually due to blood clots traveling from the legs or other parts of the body.
- Type
- Pulmonary embolism is primarily a vascular disease caused by the blockage of one or more arteries in the lungs, usually due to blood clots that travel from the legs or other parts of the body. It is not typically classified under genetic diseases with a specific mode of genetic transmission. However, certain genetic factors, such as inherited thrombophilias (e.g., Factor V Leiden mutation, Prothrombin gene mutation), can increase the risk of developing blood clots and thus elevate the risk of pulmonary embolism.
- Signs And Symptoms
- Symptoms of pulmonary embolism are typically sudden in onset and may include one or many of the following: dyspnea (shortness of breath), tachypnea (rapid breathing), chest pain of a "pleuritic" nature (worsened by breathing), cough and hemoptysis (coughing up blood). More severe cases can include signs such as cyanosis (blue discoloration, usually of the lips and fingers), collapse, and circulatory instability because of decreased blood flow through the lungs and into the left side of the heart. About 15% of all cases of sudden death are attributable to PE. While PE may present with syncope, less than 1% of syncope cases are due to PE.On physical examination, the lungs are usually normal. Occasionally, a pleural friction rub may be audible over the affected area of the lung (mostly in PE with infarct). A pleural effusion is sometimes present that is exudative, detectable by decreased percussion note, audible breath sounds, and vocal resonance. Strain on the right ventricle may be detected as a left parasternal heave, a loud pulmonary component of the second heart sound, and/or raised jugular venous pressure. A low-grade fever may be present, particularly if there is associated pulmonary hemorrhage or infarction.As smaller pulmonary emboli tend to lodge in more peripheral areas without collateral circulation, they are more likely to cause lung infarction and small effusions (both of which are painful), but not hypoxia, dyspnea, or hemodynamic instability such as tachycardia. Larger PEs, which tend to lodge centrally, typically cause dyspnea, hypoxia, low blood pressure, fast heart rate and fainting, but are often painless because there is no lung infarction due to collateral circulation. The classic presentation for PE with pleuritic pain, dyspnea, and tachycardia is likely caused by a large fragmented embolism causing both large and small PEs. Thus, small PEs are often missed because they cause pleuritic pain alone without any other findings and large PEs are often missed because they are painless and mimic other conditions often causing ECG changes and small rises in troponin and brain natriuretic peptide levels.PEs are sometimes described as massive, submassive, and nonmassive depending on the clinical signs and symptoms. Although the exact definitions of these are unclear, an accepted definition of massive PE is one in which there is hemodynamic instability. This is a cause of obstructive shock, which presents as sustained low blood pressure, slowed heart rate, or pulselessness.
- Prognosis
- Fewer than 5 to 10% of symptomatic PEs are fatal within the first hour of symptoms.There are several markers used for risk stratification and these are also independent predictors of adverse outcomes. These include hypotension, cardiogenic shock, syncope, evidence of right heart dysfunction, and elevated cardiac enzymes. Some ECG changes including S1Q3T3 also correlate with a worse short-term prognosis. There have been other patient-related factors such as COPD and chronic heart failure thought to also play a role in prognosis.Prognosis depends on the amount of lung that is affected and on the co-existence of other medical conditions; chronic embolisation to the lung can lead to pulmonary hypertension. After a massive PE, the embolus must be resolved somehow if the patient is to survive. In thrombotic PE, the blood clot may be broken down by fibrinolysis, or it may be organized and recanalized so that a new channel forms through the clot. Blood flow is restored most rapidly in the first day or two after a PE. Improvement slows thereafter and some deficits may be permanent. There is controversy over whether small subsegmental PEs need treatment at all and some evidence exists that patients with subsegmental PEs may do well without treatment.Once anticoagulation is stopped, the risk of a fatal pulmonary embolism is 0.5% per year.Mortality from untreated PEs was said to be 26%. This figure comes from a trial published in 1960 by Barrit and Jordan, which compared anticoagulation against placebo for the management of PE. 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 place of anticoagulants in the treatment of PE, the results of which were so convincing that the trial has never been repeated as to do so would be considered unethical. That said, the reported mortality rate of 26% in the placebo group is probably an overstatement, given that the technology of the day may have detected only severe PEs.
- Onset
- The onset of a pulmonary embolism can be sudden and severe. Symptoms often appear abruptly and may include shortness of breath, chest pain that may become worse when you breathe deeply or cough, rapid heart rate, and dizziness or fainting. In some cases, symptoms may develop more gradually.
- Prevalence
- Pulmonary embolism (PE) affects approximately 60 to 70 per 100,000 people annually in the general population. The prevalence can vary based on factors like age, with higher rates observed in older adults.
- Epidemiology
- There are roughly 10 million cases of pulmonary embolisms per year. In the United States, pulmonary embolisms are the primary cause of at least 10,000 to 12,000 deaths per year and a contributing cause in at least 30,000 to 40,000 deaths per year. True incidence involving pulmonary embolisms is unknown because they often go undiagnosed or unnoticed until autopsy. From 1993 to 2012, there have been an increased number of admissions in hospitals due to pulmonary embolisms, jumping from 23 cases per 100,000 people to 65 cases per 100,000 people. Despite this increase, there has been a decrease in mortality during that same time period due to medical advances that have occurred.Venous thromboembolism (VTE), a common risk factor, is present at much higher rates in those over the age of 70 (three times higher compared to those aged 45 to 69). This is likely due to there being a generally lower level of activity among the elderly, resulting in higher rates of immobility and obesity. VTE has a large, and continuously rising, case fatality rate. This rate is roughly 10% after 30 days, 15% after three months and up to 20% after one year. Pulmonary embolisms alone (when resulting in hospitalizations) have a case fatality rate of about 5% to 10% so VTE can play a large factor in the severity of the embolisms.When looking at all cases, the rate of fatal pulmonary emboli has declined from 6% to 2% over the last 25 years in the United States. In Europe, an average of approximately 40,000 deaths per year with pulmonary embolism as the primary cause were reported between 2013 and 2015, a conservative estimate because of potential underdiagnosis.
- Intractability
- Pulmonary embolism (PE) is not inherently intractable. Treatability can vary based on factors like the size and location of the embolism, the patient's overall health, and how quickly treatment is initiated. Effective interventions include anticoagulant medications, thrombolytic therapy, and sometimes surgical procedures. Prompt medical attention is crucial for improving outcomes.
- Disease Severity
- Pulmonary embolism severity can vary widely depending on the size and location of the clot, as well as the overall health of the individual. It can range from minor symptoms to life-threatening conditions.
- Healthcare Professionals
- Disease Ontology ID - DOID:9477
- Pathophysiology
- Pulmonary embolism (PE) occurs when a blood clot, typically from deep veins in the legs (deep vein thrombosis), travels to the pulmonary arteries in the lungs. This obstructs blood flow, leading to increased pressure in the right ventricle of the heart and decreased oxygen levels in the blood. The obstruction can cause lung tissue damage, decreased oxygenation of the blood, and can strain the heart, potentially leading to heart failure if untreated.
- Carrier Status
- Carrier status is not applicable to pulmonary embolism. Pulmonary embolism is a condition in which one or more arteries in the lungs become blocked by a blood clot. It is not a genetic disorder with a carrier status but rather a medical emergency related to cardiovascular health and other risk factors such as prolonged immobility, surgery, certain medications, and underlying health conditions.
- Mechanism
-
Pulmonary embolism (PE) occurs when a blood clot, typically originating from the deep veins of the legs (a condition known as deep vein thrombosis or DVT), travels through the bloodstream and lodges in the pulmonary arteries, obstructing blood flow to part of the lung. This obstruction can lead to impaired gas exchange, decreased oxygen levels, and potential damage to lung tissue.
**Molecular Mechanisms:**
1. **Thrombus Formation:** The process begins with the formation of a thrombus (blood clot) in the deep veins. This involves the interplay of platelets, coagulation factors, and endothelial cells. Platelet activation and aggregation form a platelet plug, while the coagulation cascade leads to the generation of thrombin, which converts fibrinogen to fibrin, stabilizing the clot.
2. **Virchow's Triad:** There are three main factors contributing to thrombogenesis, collectively known as Virchow’s triad:
- **Endothelial Injury:** Damage to the vascular endothelium can expose subendothelial collagen and tissue factor, initiating the coagulation cascade.
- **Hypercoagulability:** An increase in coagulation propensity due to genetic factors (e.g., Factor V Leiden mutation) or acquired conditions (e.g., cancer, pregnancy).
- **Stasis of Blood Flow:** Reduced blood flow, often due to prolonged immobility or certain medical conditions, increases the risk of clot formation.
3. **Embolization:** Once a thrombus is formed, parts of it can dislodge and travel through the venous system. The embolus passes through the right side of the heart and into the pulmonary arteries.
4. **Pulmonary Artery Occlusion:** The embolus lodges in the pulmonary arteries, creating a mechanical blockage. The size and location of the embolus determine the extent of the hemodynamic impact.
5. **Inflammatory Response:** The lodged embolus can trigger an inflammatory response involving cytokines and other mediators, which may further contribute to pulmonary artery constriction and tissue damage.
6. **Secondary Effects:** The obstruction can lead to increased pulmonary vascular resistance, elevated right ventricular afterload, reduced right ventricular function, and subsequent cardiovascular compromise.
Understanding the molecular mechanisms underlying PE helps in developing targeted therapies and preventive measures to manage and reduce the risk of this potentially life-threatening condition. - Treatment
- Anticoagulant therapy is the mainstay of treatment. Acutely, supportive treatments, such as oxygen or analgesia, may be required. People are often admitted to hospital in the early stages of treatment, and tend to remain under inpatient care until the INR has reached therapeutic levels (if warfarin is used). Increasingly, however, low-risk cases are managed at home in a fashion already common in the treatment of DVT. Evidence to support one approach versus the other is weak.
- Compassionate Use Treatment
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Compassionate use treatments, off-label, and experimental treatments for pulmonary embolism (PE) may include:
1. **Compassionate Use Treatment**:
- **Thrombolytics**: In severe cases where conventional treatments fail or are not an option, high-dose thrombolytics (e.g., recombinant tissue plasminogen activator) might be used.
2. **Off-Label Treatments**:
- **Direct Oral Anticoagulants (DOACs)**: While typically used for treatment and prevention of PE, certain specific DOACs may be used off-label in populations not explicitly covered by clinical trial data.
- **Low Molecular Weight Heparin (LMWH)**: Although used commonly, certain administration routes or combinations with other therapies could be considered off-label.
3. **Experimental Treatments**:
- **Catheter-Directed Thrombolysis (CDT)**: This involves directly delivering thrombolytic drugs to the site of the clot via a catheter and is being studied for safety and efficacy.
- **Novel Anticoagulants**: Newer anticoagulants in the phase of research trials that might offer better safety profiles or efficacy.
- **Extracorporeal Membrane Oxygenation (ECMO)**: Used in life-threatening cases of PE where conventional treatments have failed, often as part of clinical trial protocols.
It's important to consult with a healthcare provider for the most current and individualized treatment approach. - Lifestyle Recommendations
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Lifestyle recommendations for pulmonary embolism primarily involve reducing risk factors and managing overall health. These include:
1. **Physical Activity**: Engage in regular exercise to improve blood circulation and overall cardiovascular health.
2. **Healthy Weight**: Maintain a healthy weight to decrease pressure on veins and reduce the risk of clot formation.
3. **Diet**: Eat a balanced diet rich in fruits, vegetables, lean proteins, and whole grains. Limit intake of saturated fats, trans fats, and excessive sugars.
4. **Hydration**: Stay adequately hydrated to help maintain proper blood viscosity.
5. **Smoking Cessation**: Avoid smoking, as it can damage blood vessels and increase clot risk.
6. **Moderate Alcohol Intake**: Limit alcohol consumption to reduce adverse cardiovascular effects.
7. **Medication Adherence**: If prescribed anticoagulants or other medications, take them as directed to manage clotting risks.
8. **Compression Stockings**: Use compression stockings if recommended by a healthcare provider to improve blood flow in the legs.
9. **Avoid Prolonged Immobility**: Stand up, stretch, and move around regularly, especially during long periods of sitting, such as during travel or desk jobs.
10. **Regular Check-ups**: Schedule routine medical appointments to monitor and manage any underlying conditions that may contribute to clot formation.
These recommendations can significantly lower the risk and aid in preventing the recurrence of pulmonary embolism. - Medication
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Medications used for pulmonary embolism typically include:
1. **Anticoagulants:** These are the mainstay of treatment and include:
- Heparin (unfractionated or low molecular weight)
- Warfarin
- Direct oral anticoagulants (DOACs) such as rivaroxaban, apixaban, and dabigatran
2. **Thrombolytics:** Used in severe cases to dissolve clots, such as:
- Tissue plasminogen activator (tPA)
3. **Analgesics:** For pain relief, such as:
- Acetaminophen or opioids (if needed) - Repurposable Drugs
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For pulmonary embolism, some repurposable drugs include:
1. **Rivaroxaban**: Traditionally used as an anticoagulant for deep vein thrombosis, now also used for pulmonary embolism.
2. **Apixaban**: Another anticoagulant initially used for atrial fibrillation, now also for pulmonary embolism treatment.
3. **Dabigatran**: Originally for atrial fibrillation, this anticoagulant is now repurposed for treating pulmonary embolism.
4. **Warfarin**: Though an old drug for preventing clots in general, it continues to be used for pulmonary embolism management.
These medications help prevent further clotting and reduce the risk of complications associated with pulmonary embolism. - Metabolites
-
Pulmonary embolism (PE) is associated with various metabolic changes. Key metabolites that can be significant in the context of PE include:
1. **Lactate**: Elevated lactate levels may indicate tissue hypoxia due to impaired blood flow.
2. **D-dimer**: This fibrin degradation product is often elevated in the presence of thrombus formation and degradation.
3. **Cardiac troponins**: These proteins may be elevated if the PE has caused significant strain on the heart, leading to myocardial injury.
4. **Brain Natriuretic Peptide (BNP) or N-terminal proBNP (NT-proBNP)**: These markers are often elevated in response to cardiac strain and heart failure, which can be secondary to a significant PE.
These metabolites can be crucial in the diagnosis, assessment of severity, and management of pulmonary embolism. - Nutraceuticals
- Nutraceuticals are not typically considered a primary treatment for pulmonary embolism (PE). PE is a serious medical condition that requires prompt medical treatment, such as anticoagulants, thrombolytics, or surgical intervention, to prevent severe complications or death. Nutraceuticals may offer general health benefits but are not a substitute for standard medical treatment for PE. Always consult with a healthcare provider for appropriate diagnosis and treatment recommendations.
- Peptides
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Pulmonary embolism (PE) refers to a blockage in one of the pulmonary arteries in the lungs, usually caused by blood clots that travel to the lungs from deep veins in the legs. Specific peptides such as B-type natriuretic peptide (BNP) and N-terminal pro-BNP (NT-proBNP) can be elevated in patients with PE due to the strain on the heart. These biomarkers can help in risk stratification but are not specific to PE alone.
Regarding "nan" (which could refer to nanotechnologies), advancements in nanotechnology are being researched for the diagnosis and treatment of PE. This includes the development of nanoparticles for targeted drug delivery to dissolve clots, improving both the efficacy and safety of treatments. Additionally, nanoscale imaging techniques are being explored to enhance the detection and characterization of emboli in the pulmonary arteries.