Acute unexplained dyspnea is often the presenting symptom of PE. The most frequently encountered physical finding is tachypnea, with a respiratory rate at rest greater than 16 per minute. Sinus tachycardia often accompanies dyspnea and can be a clue to the diagnosis of PE.
Unexplained pallor, fatigue, apprehension can be other associated symptoms. The diagnosis of PE in this group of patients is many a times missed and requires a high index of suspicion in potential clinical situation.Pulmonary infarction or hemorrhage is an uncommon presentation of PE. These patients present with pleural pain, haemoptysis, dyspnea, cough and fever. These cases can often be confused as having chest infection, pneumonia or other form of lung disease. Crepitations in lungs and pleural rub are often present in this group of patients.
Acute right ventricular failure can be a presentation in patients with massive occlusion of pulmonary arterial tree. This group usually presents as an emergency. These patients present either with chest pain, syncope, acute dyspnea or in a state of shock with all its signs (pallor,tachypnea, tachycardia, cyanosis, hypotension, gallop rhythm and other features of circulatory failure). This group of patients may die suddenly, develop refractory shock or improve if provided with necessary medical assistance. In this group of patients the initial differential diagnosis may be a cardiogenic shock secondary to myocardial infarction.Differential diagnosis of PE is broad and covers a spectrum from life- threatening disease such as acute myocardial infarction to innocuous anxiety states.
Investigations
1)X-ray chest
The chest x-ray is a useful investigation but may not provide a diagnostic information. The x-ray is often helpful in excluding lung disease like pneumonia as a cause of acute dyspnea.The chest x-ray can be helpful in establishing the diagnosis of pulmonary infarction by demonstrating pleural effusion, an infiltrate, atelectasis, or an elevated hemidiaphragm.However, it should be emphasized that a normal chest x-ray does not rule out diagnosis of PE.
2)Electrocardiogram (ECG)
The ECG is a simple and useful test but may not provide diagnostic information in each and every case. A normal electrocardiogram does not exclude PE.The presence of right ventricular abnormality, as demonstrated by S1Q 3T3, right bundle branch block, right axis deviation, or atrial abnormality, are seen in only 26 per cent of patients with PE. Atrial fibrillation, supraventricular arrhythmias and ST–T changes in anterior and inferior leads are also seen.
3)Arterial Blood Gases (ABG)
Analysis of ABG is helpful in supporting the diagnosis of PE. Finding of low PO 2 , low CO 2 and respiratory alkalosis are pointers to the diagnosis of PE in a patient with risk factors for its development. It should be remembered that conditions which mimic PE like pneumonia,severe chest infections or chronic obstructive lung disease (COPD) can also cause low PO 2 .Pulse oxymetry is extremely insensitive in making a diagnosis of PE and can be normal in many patients.
4)Echocardiography
Echocardiography is insensitive for the visualization of thrombi in pulmonary circulation but is a rapid, practical and sensitive technique for detection of right ventricular overload among patients with established and large PE. Echocardiographic detection of right ventricular dysfunction at the time of presentation with PE is useful for risk stratification and prognostication. For those patients in whom transthoracic imaging is unsatisfactory,transesophageal echocardiography may be useful.
5)Ventilation Perfusion Lung Scan (VQ scan)
The VQ scan used to be considered an important investigation for many years. However,the availability of computed tomography (CT) has reduced its utility. At present if facilitiesare available, CT is usually preferred for diagnosis. The use of VQ scan is reserved for patients in whom motion artifact or poor right heart function limit the quality of CT examination and those with contraindication to intravenous radiography contrast.In pulmonary embolism, the ventilation is normal and perfusion in the affected segments is reduced and there is ventilation perfusion mismatch. Certain VQ scan readings are of substantial utility. A normal perfusion scan virtually excludes the diagnosis of PE. On the other hand, presence of multiple perfusion defects strongly favour a diagnosis of PE. The
low and intermediate probability scans are non-diagnostic and need further investigation.
6)Pulmonary Angiography
Standard contrast pulmonary angiography has been considered the gold standard for accurate in vivo diagnosis or exclusion of PE. With availability of digital subtraction angiography, nonionic contrast media, improved techniques and experience, it can be performed expeditiously and safely in most patients. Angiography is most useful when a diagnostic dilemma persists despite the use of non-invasive tests. This situation is most common when the diagnostic test results are negative or ambiguous in the presence of high clinical suspicion for PE. Pulmonary angiography is obviously also required when interventions are planned such as suction catheter embolectomy, mechanical clot fragmentation, or catheter-directed thrombolysis.Diagnosis of PE is entertained by demonstrating filling defects (clots), abrupt cut off or tapering of pulmonary arteries and by ancillary findings such as webs, dilated main and branch pulmonary arteries. Pulmonary artery (PA) pressure should also be recorded during angiography. Elevation of PA pressure further supports the diagnosis of PE.
7)D-dimer Assay
D-dimer is a blood test which can be rapidly performed and is utilized these days as a screening test for venous thromboembolism (deep venous thrombosis, or PE). D-dimer is a fibrin specific degradation produce that detects cross- linked fibrin resulting from endogenous fibrinolysis. In the presence of an acute thrombo-embolic event (like DVT or PE) the simultaneous activation of coagulation factors and fibrinolytic enzymes leads to increased concentration of D-dimer.Normal values of this protein have high negative predictive value, i.e. a patient whose D- dimer is less than 500 micrograms is unlikely to have PE. On the other hand, elevated D- dimer levels do not necessarily indicate PE and can be elevated in DVT, infections, inflammation, necrosis, trauma, and cancer, etc.
8)Computed Tomographic (CT) Pulmonary Angiography (PA)
Unexplained pallor, fatigue, apprehension can be other associated symptoms. The diagnosis of PE in this group of patients is many a times missed and requires a high index of suspicion in potential clinical situation.Pulmonary infarction or hemorrhage is an uncommon presentation of PE. These patients present with pleural pain, haemoptysis, dyspnea, cough and fever. These cases can often be confused as having chest infection, pneumonia or other form of lung disease. Crepitations in lungs and pleural rub are often present in this group of patients.
Acute right ventricular failure can be a presentation in patients with massive occlusion of pulmonary arterial tree. This group usually presents as an emergency. These patients present either with chest pain, syncope, acute dyspnea or in a state of shock with all its signs (pallor,tachypnea, tachycardia, cyanosis, hypotension, gallop rhythm and other features of circulatory failure). This group of patients may die suddenly, develop refractory shock or improve if provided with necessary medical assistance. In this group of patients the initial differential diagnosis may be a cardiogenic shock secondary to myocardial infarction.Differential diagnosis of PE is broad and covers a spectrum from life- threatening disease such as acute myocardial infarction to innocuous anxiety states.
Investigations
1)X-ray chest
The chest x-ray is a useful investigation but may not provide a diagnostic information. The x-ray is often helpful in excluding lung disease like pneumonia as a cause of acute dyspnea.The chest x-ray can be helpful in establishing the diagnosis of pulmonary infarction by demonstrating pleural effusion, an infiltrate, atelectasis, or an elevated hemidiaphragm.However, it should be emphasized that a normal chest x-ray does not rule out diagnosis of PE.
2)Electrocardiogram (ECG)
The ECG is a simple and useful test but may not provide diagnostic information in each and every case. A normal electrocardiogram does not exclude PE.The presence of right ventricular abnormality, as demonstrated by S1Q 3T3, right bundle branch block, right axis deviation, or atrial abnormality, are seen in only 26 per cent of patients with PE. Atrial fibrillation, supraventricular arrhythmias and ST–T changes in anterior and inferior leads are also seen.
3)Arterial Blood Gases (ABG)
Analysis of ABG is helpful in supporting the diagnosis of PE. Finding of low PO 2 , low CO 2 and respiratory alkalosis are pointers to the diagnosis of PE in a patient with risk factors for its development. It should be remembered that conditions which mimic PE like pneumonia,severe chest infections or chronic obstructive lung disease (COPD) can also cause low PO 2 .Pulse oxymetry is extremely insensitive in making a diagnosis of PE and can be normal in many patients.
4)Echocardiography
Echocardiography is insensitive for the visualization of thrombi in pulmonary circulation but is a rapid, practical and sensitive technique for detection of right ventricular overload among patients with established and large PE. Echocardiographic detection of right ventricular dysfunction at the time of presentation with PE is useful for risk stratification and prognostication. For those patients in whom transthoracic imaging is unsatisfactory,transesophageal echocardiography may be useful.
5)Ventilation Perfusion Lung Scan (VQ scan)
The VQ scan used to be considered an important investigation for many years. However,the availability of computed tomography (CT) has reduced its utility. At present if facilitiesare available, CT is usually preferred for diagnosis. The use of VQ scan is reserved for patients in whom motion artifact or poor right heart function limit the quality of CT examination and those with contraindication to intravenous radiography contrast.In pulmonary embolism, the ventilation is normal and perfusion in the affected segments is reduced and there is ventilation perfusion mismatch. Certain VQ scan readings are of substantial utility. A normal perfusion scan virtually excludes the diagnosis of PE. On the other hand, presence of multiple perfusion defects strongly favour a diagnosis of PE. The
low and intermediate probability scans are non-diagnostic and need further investigation.
6)Pulmonary Angiography
Standard contrast pulmonary angiography has been considered the gold standard for accurate in vivo diagnosis or exclusion of PE. With availability of digital subtraction angiography, nonionic contrast media, improved techniques and experience, it can be performed expeditiously and safely in most patients. Angiography is most useful when a diagnostic dilemma persists despite the use of non-invasive tests. This situation is most common when the diagnostic test results are negative or ambiguous in the presence of high clinical suspicion for PE. Pulmonary angiography is obviously also required when interventions are planned such as suction catheter embolectomy, mechanical clot fragmentation, or catheter-directed thrombolysis.Diagnosis of PE is entertained by demonstrating filling defects (clots), abrupt cut off or tapering of pulmonary arteries and by ancillary findings such as webs, dilated main and branch pulmonary arteries. Pulmonary artery (PA) pressure should also be recorded during angiography. Elevation of PA pressure further supports the diagnosis of PE.
7)D-dimer Assay
D-dimer is a blood test which can be rapidly performed and is utilized these days as a screening test for venous thromboembolism (deep venous thrombosis, or PE). D-dimer is a fibrin specific degradation produce that detects cross- linked fibrin resulting from endogenous fibrinolysis. In the presence of an acute thrombo-embolic event (like DVT or PE) the simultaneous activation of coagulation factors and fibrinolytic enzymes leads to increased concentration of D-dimer.Normal values of this protein have high negative predictive value, i.e. a patient whose D- dimer is less than 500 micrograms is unlikely to have PE. On the other hand, elevated D- dimer levels do not necessarily indicate PE and can be elevated in DVT, infections, inflammation, necrosis, trauma, and cancer, etc.
8)Computed Tomographic (CT) Pulmonary Angiography (PA)
CTPA has gained acceptance as a first – line imaging study in cases of suspected acute PE, replacing traditional V/Q scintigraphy at many institutions. CTPA has also reduced the need for invasive pulmonary angiography. CTPA provides visualization of the pulmonary arterial system in the axial plane, and multiplanar and three dimensional reconstructions can be generated from raw data to enhance diagnostic accuracy. The cardinal sign of acute PE on CTPA is an intravascular filling defect in a pulmonary artery that partially or completely occludes the vessel and is often associated with increased diameter of the affected vessel. The most specific sign of acute PE is a filling defect that forms acute angles with the vessel wall.Even spiral CT can diagnose PE. The other advantage of spiral CT technique is its ability to diagnose or exclude other lung disorders which can mimic PE. A reliable diagnosis of lung consolidation, collapse, effusion, abscess, tumors and pneumothorax can be made by CT scan technique.
9)Magnetic Resonance (MR) Pulmonary Angiography
This technique has developed significantly in the last 10 years. However, there are still several problems including acquisition of good images in breathless patients. At the present time CTPA is considered superior to MR angiography.
Management
1)General
Depending on the clinical presentation the patient needs to be treated either in intensive care unit, hospital wards or advanced referral hospitals. Those patients of PE who present with marked symptoms or are hemodynamically unstable (low blood pressure, cyanosis or shock) need to be treated in an intensive care unit. In sick patients, the aim of treatment is to provide symptomatic relief, maintain oxygenation, ventilation and provide inotropic support.Patients who are hypoxic require oxygen and may need ventilatory support.Dobutamine, a beta adrenergic agonist with positive inotropic and pulmonary vasodilating effects should be considered a first line agent to treat right sided heart failure and cardiogenic shock. The use of diuretics, intravenous fluids and dopamine should be individualized. Sedation should be avoided if patient is showing arterial hypoxemia.
2)Anticoagulation
Anticoagulant therapy has been the mainstay of treatment for VTE. Treatment of patients with uncomplicated PE or DVT involves similar anticoagulant regimens, in part because asymptomatic PE occurs frequently in patients with symptomatic proximal DVT, and vice versa. Treatment of VTE involves initiation of anticoagulant therapy with either UFH or LMWH and considering long term initiation of oral anticoagulation (Warfarin therapy).
The utility of UFH or LMWH in treatment of VTE have been documented in large number of studies. Both these heparins are effective, safe, provide symptomatic benefit and reduce the mortality and morbidity due to this disease. The incidence of PE, its recurrence and the long term sequale of this illness are reduced by use of heparin. UFH has been in clinical use for over 100 years, is safe and comparatively cheap. LMWH has become popular during the last decade and is gradually replacing the UFH. The primary difference between these two heparins relates to their pharmacological properties and cost. The main side effects of both the heparins is minor or major bleeding. The treatment by either heparin is usually given for 5 to 7 days. Oral anticoagulation is started either simultaneously or soon after depending on patient profile. Before initiating anticoagulation therapy, proper history should be obtained to rule out any history of bleeding (piles, peptic ulcer, hemorrhagic stroke) or related disorders.
Monitoring of the activated partial thromboplastin time (aPTT) is needed and therapeutic range of aPTT ratio (patient/control) of 1.5 to 2.5 is generally recommended. The UFH can be administered intravenously (IV) by infusion or by subcutaneous (SC) route. However, the bioavailability of SC UFH is less than that of IV UFH and larger initial doses of SC heparin are needed to achieve a therapeutic anticoagulant effect. Due to this, intravenous infusion is preferred.Oral anticoagulation therapy using warfarin or any other agent is advocated in majority of patients for variable duration. The duration of long term anticoagulation is to be individualized depending on risk factors. For patients with VTE associated with a major transient risk factor such as recent surgery, anticoagulation therapy is usually recommended for 3 months. For patients with unprovoked VTE, stopping anticoagulant therapy after 6 or more months of treatment is associated with a high risk of recurrent VTE and justifies long term anticoagulation for such patients. The argument favouring long term therapy is stronger if the unprovoked episode was PE; if a second or subsequent episode of unprovoked VTE occurs; or any hypercoaguable state is diagnosed. Regular monitoring of blood test called as prothrombin time and International Normalized Ratio (INR) is mandatory while administering oral anticoagulation. An INR of 2 to 2.5 is generally recommended. Inferior Vena Cava (IVC) filters are advocated to prevent further episodes of VTE in selected patients and particularly in those with contraindication to long term anticoagulation.There are newer direct thrombin inhibitors agents like hirudin, hirulog or oral ximelagatran which are investigational at present and may become available in near future as substitute to existing anticoagulants.
3)Thrombolysis
Systemic IV infusion of thrombolytic agents have been proven superior to anticoagulation for treatment of PE. Compared with heparin in hemodynamically stable patients with large PE, systemic thrombolytic therapy reduced mortality (11 per cent versus 4.7 per cent) and recurrent PE (18.7 per cent versus 7.7 per cent, P = 0.016) but was associated with higher rates of bleeding complications. In view of the higher incidence of bleeding thrombolysis is not indicated in all patients with large PE.The use of thrombolysis should be reserved for following category of patients:
9)Magnetic Resonance (MR) Pulmonary Angiography
This technique has developed significantly in the last 10 years. However, there are still several problems including acquisition of good images in breathless patients. At the present time CTPA is considered superior to MR angiography.
Management
1)General
Depending on the clinical presentation the patient needs to be treated either in intensive care unit, hospital wards or advanced referral hospitals. Those patients of PE who present with marked symptoms or are hemodynamically unstable (low blood pressure, cyanosis or shock) need to be treated in an intensive care unit. In sick patients, the aim of treatment is to provide symptomatic relief, maintain oxygenation, ventilation and provide inotropic support.Patients who are hypoxic require oxygen and may need ventilatory support.Dobutamine, a beta adrenergic agonist with positive inotropic and pulmonary vasodilating effects should be considered a first line agent to treat right sided heart failure and cardiogenic shock. The use of diuretics, intravenous fluids and dopamine should be individualized. Sedation should be avoided if patient is showing arterial hypoxemia.
2)Anticoagulation
Anticoagulant therapy has been the mainstay of treatment for VTE. Treatment of patients with uncomplicated PE or DVT involves similar anticoagulant regimens, in part because asymptomatic PE occurs frequently in patients with symptomatic proximal DVT, and vice versa. Treatment of VTE involves initiation of anticoagulant therapy with either UFH or LMWH and considering long term initiation of oral anticoagulation (Warfarin therapy).
The utility of UFH or LMWH in treatment of VTE have been documented in large number of studies. Both these heparins are effective, safe, provide symptomatic benefit and reduce the mortality and morbidity due to this disease. The incidence of PE, its recurrence and the long term sequale of this illness are reduced by use of heparin. UFH has been in clinical use for over 100 years, is safe and comparatively cheap. LMWH has become popular during the last decade and is gradually replacing the UFH. The primary difference between these two heparins relates to their pharmacological properties and cost. The main side effects of both the heparins is minor or major bleeding. The treatment by either heparin is usually given for 5 to 7 days. Oral anticoagulation is started either simultaneously or soon after depending on patient profile. Before initiating anticoagulation therapy, proper history should be obtained to rule out any history of bleeding (piles, peptic ulcer, hemorrhagic stroke) or related disorders.
Monitoring of the activated partial thromboplastin time (aPTT) is needed and therapeutic range of aPTT ratio (patient/control) of 1.5 to 2.5 is generally recommended. The UFH can be administered intravenously (IV) by infusion or by subcutaneous (SC) route. However, the bioavailability of SC UFH is less than that of IV UFH and larger initial doses of SC heparin are needed to achieve a therapeutic anticoagulant effect. Due to this, intravenous infusion is preferred.Oral anticoagulation therapy using warfarin or any other agent is advocated in majority of patients for variable duration. The duration of long term anticoagulation is to be individualized depending on risk factors. For patients with VTE associated with a major transient risk factor such as recent surgery, anticoagulation therapy is usually recommended for 3 months. For patients with unprovoked VTE, stopping anticoagulant therapy after 6 or more months of treatment is associated with a high risk of recurrent VTE and justifies long term anticoagulation for such patients. The argument favouring long term therapy is stronger if the unprovoked episode was PE; if a second or subsequent episode of unprovoked VTE occurs; or any hypercoaguable state is diagnosed. Regular monitoring of blood test called as prothrombin time and International Normalized Ratio (INR) is mandatory while administering oral anticoagulation. An INR of 2 to 2.5 is generally recommended. Inferior Vena Cava (IVC) filters are advocated to prevent further episodes of VTE in selected patients and particularly in those with contraindication to long term anticoagulation.There are newer direct thrombin inhibitors agents like hirudin, hirulog or oral ximelagatran which are investigational at present and may become available in near future as substitute to existing anticoagulants.
3)Thrombolysis
Systemic IV infusion of thrombolytic agents have been proven superior to anticoagulation for treatment of PE. Compared with heparin in hemodynamically stable patients with large PE, systemic thrombolytic therapy reduced mortality (11 per cent versus 4.7 per cent) and recurrent PE (18.7 per cent versus 7.7 per cent, P = 0.016) but was associated with higher rates of bleeding complications. In view of the higher incidence of bleeding thrombolysis is not indicated in all patients with large PE.The use of thrombolysis should be reserved for following category of patients:
A) Patients with massive PE presenting as a life threatening emergency.
B) Patients with sub-massive PE and demonstration of right ventricular dysfunction on echocardiography.
C) Patients who develop recurrent PE despite treatment with heparin. In some centers thrombolytic agents are directly injected into pulmonary arteries (catheter directed thrombolysis) to facilitate clot lysis.
4) Newer interventional and surgical treatment
There are patients who fail to improve despite all available treatment. For these patients interventional (catheter directed thrombolysis, clot fragmentation or thrombus aspiration) techniques used in catheterization laboratories or surgical techniques such as embolectomy are indicated. These techniques are available in some advanced tertiary care hospitals.The indications for use of these interventions are: 1) Persistent arterial hypotension (systolic blood pressure < 90 mmHg or a rapid decrease of > 40 mmHg). 2) Systemic hypoperfusion and hypoxemia. 3) Need for cardiopulmonary resuscitation. 4) Severe right ventricular failure. 5)Contraindication to anticoagulation or thrombolysis.
B) Patients with sub-massive PE and demonstration of right ventricular dysfunction on echocardiography.
C) Patients who develop recurrent PE despite treatment with heparin. In some centers thrombolytic agents are directly injected into pulmonary arteries (catheter directed thrombolysis) to facilitate clot lysis.
4) Newer interventional and surgical treatment
There are patients who fail to improve despite all available treatment. For these patients interventional (catheter directed thrombolysis, clot fragmentation or thrombus aspiration) techniques used in catheterization laboratories or surgical techniques such as embolectomy are indicated. These techniques are available in some advanced tertiary care hospitals.The indications for use of these interventions are: 1) Persistent arterial hypotension (systolic blood pressure < 90 mmHg or a rapid decrease of > 40 mmHg). 2) Systemic hypoperfusion and hypoxemia. 3) Need for cardiopulmonary resuscitation. 4) Severe right ventricular failure. 5)Contraindication to anticoagulation or thrombolysis.
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