Pulmonary Embolism Essay
INTRODUCTION :
I hereby present to you a case study on pulmonary embolism( PE), in which includes details of the patient , current problems and management taken place while caring for the patient .
Present compalints:
A 65 year old female with chest pain, acute shortness of breath, cough and swelling on the surgical limb.
Detail history of presenting complaints:
Mrs Blue, a 65 year old female who presents with chest pain and shortness of breath, underwent bilateral total knee replacement under general anesthesia , had video laryngoscope for intubation and was initially admitted in intensive care for close observation. The surgeon ordered to withhold DVT prophylaxis until the next day due to high volumes of haemoserous output …show more content…
to the handyvac drain. Following day, the patient was discharged to the ward with no complications. On early morning of post op day 3, the staff noticed Mrs Blue was getting breathless while she was resting in bed and complained that it is associated with sharp pain on the chest exacerbated by breathing. The night staff reported that she had persistent cough throughout the shift. The patient reported to staff that she experienced chest pain for one hour but she thought it would subside eventually but instead it got worse. Mrs Blue’s observations were as follows, respiratory rate:28 breaths /min, oxygen saturation:84% on non-rebreather mask, heart rate:104-120 beats/min, blood pressure:98/52mmHg .
The history-taking process is integral to making a diagnosis and is a way to accumulate information about the patient and the events leading up to that presentation (Seidel et al, 2003). The primary aim is to find out the actual problem for the patient and also to identify if any other problems that may occur later on. Mrs Blue was not understanding what was going on with her and I had to reassure the patient that she would be transferred back to the Intensive Care Unit and a cardiologist would be involved in her care. Considering all the symptoms, chances of pulmonary embolism was high at this stage on the list of differential diagnosis. However, a diagnosis of pulmonary embolism based on clinical signs and history is difficult and inaccurate and can rarely confirm or refute the diagnosis with any particularly certainty (Iles et al, 2002). Torbicki et al (2008) suggest that more than 90% of patients with pulmonary embolism show tachypnea ,chest pain and tachycardia. It is difficult to point out pulmonary embolism with patient with cardiac issues or respiratory problems with the given symptoms mentioned.
Evidence based literature supports clinical scoring systems such as the revised Geneva score (Le Gal et al,2006) and Wells score (Wells et al, 2000). These scoring tools are used along with diagnostic tests that can confirm or exclude the diagnosis of PE. For Mrs blue the revised Geneva score indicates 15, which mean high clinical probability of pulmonary embolism, and with Wells score it scores 4, which means moderate probability to PE.
Past medical history and risk factors :
Past history of Mrs Blue is hypertension, hyperlipidemia, obesity with BMI of 33 and asthma. She takes ramipril and atacand for hypertension, simvastatin 40mg once daily for high cholesterol and ventolin and seretide puffers for asthma.
The past medical history should include any illness, operations, serious injuries, recent travel and general health prior to this episode (Seidel et al, 2003). Going through the past history of the patient also helps us to assessing the current complaints and risk factors of other disease conditions. Thomson and Hales (2012) states that chronic cardiac disease, autoimmune disease, high body mass index (BMI) of ≥29, hypertension and smoking more than 25 cigarettes per day are the risk factors for PE. Mrs blue has hypertension and obesity which are contributing risk factors to pulmonary embolism.
Other risk factors that are setting or environment- related such as prolonged bed rest due to medical conditions such as heart failure or acute respiratory failure, recent major surgery, chemotherapy, insertion of a central venous line, immobility due to prolonged periods of sitting such as car or air travel or prolonged bed rest of more than 3 days for any other reason (Torbicki et al, 2008). Mrs Blue had bilateral total knee replacement which is a major surgery, she was immobile for two post operative days because of swelling and pain in both legs which was aggravated by the weight imposed onto the affected limbs on every attempt to ambulate which are the risk factors to PE. The risk of pulmonary embolism increases with age and 65% of pulmonary embolism patients are above the age of 60 (Torbicki et al, 2008). The age of Mrs Blue which was 65 years old is considered a risk factor.
DEFINITION :
Pulmonary embolism is the sudden occlusion of blood flow to the lungs by a blood clot that has usually arisen from a deep vein thrombosis (DVT) (Simon et al, 2002)
PATIENT COMPARISON WITH BOOK PICTURE :
Pathophysiology
A blood clot or a thrombus forming into a pulmonary emboli arises from the venous system of the lower extremities.
It could also come from the upper extremity veins or from the renal or pelvic areas in few instances. Pulmonary emboli are often times, multiple which could affect the lower lobes than the upper lobes of the lung. Deep vein thrombosis are blood clots developing in deep veins of the lower limbs can disintegrate and are carried by the circulation to the heart and eventually to the lung arteries which would result to blockage of the pulmonary artery which can be fatal. Clots is smaller form could also be found in the smaller vessels of the lung periphery which could often times cause pleuritic chest pain from the inflammatory changes in the pleura.
Clots ( eg : from deep vein thrombosis of the leg )travels through the heart to the pulmonary arteries.
The obstruction of pulmonary artery, which can be acute or chronic, is caused by three major factors such as local trauma to the vessel wall, hypercoagulability, and stasis of blood, which is commonly called as Virchow’s triad( Jarreau et al,2008) . Acute symptoms can be differentiate from chronic depending upon the onset of symptoms . For acute PE, the onset of symptoms is sudden whereas chronic PE symptoms can take place over a period of time ( Thompson and Hales,2012). Almost 75% of patients who develop PE have experienced DVT as mostly the thrombus arises from the lower limbs.( Kearon,2003).
Clinical Manifestations …show more content…
:
The classic triad signs and symptoms of PE include hemoptysis, dyspnea and chest pain. These symptoms only occurs in less than 20% of patients with pulmonary embolism because these symptoms could also be manifested as other symptoms aside from pulmonary embolism(Feied and Handler, 2006) .From the statement provided, Mrs blue had dyspnea and chest pain .
Diagnosis :
Diagnosis of Pulmonary embolism can be started by taking history from the patient (present and past history). Finding out the present complaints of the patient
A detailed history should be carried out which includes complaints of chest or leg discomfort, difficulty of breathing; lightheadedness and it should also take into account patients past and family histories.
. Unfortunately, the individual clinical features of both DVT and pulmonary embolism have low predictive value (about 15%) (Wells et al, 1997).
Electrocardiogram: ECG abnormalities occur in patients without pre-existing cardiovascular disease in the context of pulmonary embolism. ECG changes considered to be suggestive of pulmonary embolism are an S1Q3T3 (S I, Q III, T III) pattern. right ventricular strain, new incomplete right bundle branch block, T wave inversion and ST segment changes in the precordial leads suggesting right ventricular dysfunction, inferior Q waves and atrial arrhythmias
(Thompson and Hales, 2011).
Chest X-ray : The chest X-ray may initially be normal. However, after a period of time (approximately 24–72 hours) a third of patients go on to develop infiltrates, which are difficult to distinguish from infectious pneumonia (Feied and Handler, 2006).
Troponin
The routine bloodwork requested on the patient presenting with chest pain would generally include a cardiac troponin I or T test. Troponin is released from cardiac muscle following ischaemia and infarction and subsequent myocardial cell death and this troponin rise can be used in the diagnosis of myocardial infarction (Agewall et al, 2011). A raised troponin is seen in 30–50% of patients with moderate to large pulmonary embolism (Thompson and Hales, 2011). The reason for troponin release with acute pulmonary embolism is unclear but may be due to hypoxia and hypoperfusion including in the coronary arteries (Agewall et al, 2011). It has also been shown that a rise in troponin is associated with a higher risk of death and poor prognosis in pulmonary embolism (Agewall et al, 2011). The elevation time is also shorter in pulmonary embolism with the level resolving within 40 hours after the onset of the event.
D-dimer test: D-dimer is a clot dissolving substance released when the body is attempting to break down a clot. The D-dimer test is considered useful in that a negative test provides strong evidence against the presence of an embolism. Elevated values, however, are less reliable as they can be raised as a result of age, inflammation and cancer (Kearon, 2003).
CT scanning: A computed tomography (CT) scan of the chest will directly identify clots blocking the pulmonary vessels
Mrs. Blue had axial CT angiogram has been performed of the pulmonary arteries with multiplanar and MIP reconstructions. The report says there is non-occlusive pulmonary embolus within the right lower lobe pulmonary artery extending into the segmental branches. In addition, there is a small amount of non-occlusive embolus within the middle lobe artery however this does not extend into the segmental branches. There is no other pulmonary embolus and there is no pulmonary embolus on the left.
Dependent changes are present in the lung bases bilaterally associated with minimal atelectasis. There is no pleural and pericardial effusion. There are no end bronchial lesions.
Non-occlusive middle lobe and right lower lobe pulmonary emboli.
TREATMENT:
The British Thoracic Society (BTS) guidelines (2003) suggest two different approaches for the treatment of pulmonary embolism, depending on whether the presentation is massive or no massive pulmonary embolism. Massive pulmonary embolism is defined as a thrombus occluding more than 50% of the lung vasculature. Any amount of occlusion less than this is classed as nonmassive (Shaunessy, 2007). A massive pulmonary embolism causes symptoms of hypotension with a systolic blood pressure of less than 90 mmHg or a drop of more than 40 mmHg from baseline for 15 minutes or longer (Moores et al, 2011. For massive pulmonary embolism, the BTS (2003) suggest a 50 mg bolus of alteplase if cardiac arrest is imminent. For nonmassive pulmonary embolism, heparin is given to prevent existing blood clots from enlarging and additional clots from forming. Heparin is given intravenously to achieve a rapid effect, and while it does nothing to dissolve a clot that has developed already, it remains the single most important treatment that can be provided, because the greatest contribution to the mortality rate is the ongoing embolization of new thrombi (Feied and Handler, 2006). Prompt effective anticoagulation has been shown to reduce the overall mortality rate from 30% to less than 10% (BTS, 2003). After the initial effective anticoagulation, a long-term blood-thinning agent should be commenced in a form of warfarin, which will be continued for a minimum period of three months (Longmore et al, 2001).
There are two ways of treating pulmonary embolism. This includes comprises initial stabilization and anticoagulation. Hemodynamic stabilization should be the first and foremost focus of treatment for patients with pulmonary embolism. Symptomatic treatment is advised for patients with hypoxemia such as provision of supplemental oxygen. Whereas for patients with low blood pressure are given fluid boluses and thereafter giving vasopressor agents, such as metaraminol, noradrenaline, adrenaline and vasopressin. Patients with high chances of pulmonary embolism (PE), the core treatment is giving anticoagulants such as heparin. While patients with confirmed diagnosis PE or with high chances of getting PE without any contraindications are given anticoagulation therapy with low-molecular weight heparin eg: clexane. Anticoagulants inhibit the clots to become bigger by dissolving the fibrin, a protein involved in blood clot formation or it acts to cease the growth of clots and formation of new clots. The treatment of PE with thrombolytic agents taking into consideration the bleeding risks is outlined in the American Heart Association and Amercian College of Chest Physicians guidelines. The mechanism of action of thrombolytic agents specially in acute pulmonary embolism includes hastening the clot lysis thereby improving both respiratory and hemodynamic functioning.
REFERENCES
1)Kearon C, Kahn SR, Agnelli G, Goldhaber S, Raskob GE, Comerota AJ;American College of Chest Physicians. Antithrombotic therapy for venous thromboembolic disease: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Chest. 2008;133(6 suppl):454S-545S.
2) Jaff MR, McMurtry S, Archer SL, et al; American Heart Association
Council on Cardiopulmonary, Critical Care, Perioperative and Resuscitation; American Heart Association Council on Peripheral Vascular Disease; American Heart Association Council on Arteriosclerosis, Thrombosis and Vascular Biology. Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association [published correction appears in Circulation. 2012;125(11):e495]. Circulation. 2011;123(16):1788-1830
3) Horlander KT, Mannino DM, Leeper KV. Pulmonary embolism mortalityin the United States, 1979-1998: an analysis using multiple-cause data.Arch Intern Med. 2003;163:1711-1717.
4)Agewall S, Giannitsis E, Jernberg T, Katus H (2011) Troponin elevationin coronary vs non-coronary disease. Eur Heart J 32: 404-11
5)Iles S, Hodges AM, Darley JR, Frampton C, Epton M, Beckert LE, Town
6)GI (2003) Clinical experience and pre-test probability scores in the diagnosis of pulmonary embolism. QJM 96: 211–5
7)Jarreau T, Hanna E, Rodriguez F 3rd, Romero J, Martinez J, Lopez FA(2008) Massive pulmonary embolism: A case report and review of literature. J La State Med Soc 160: 189–94
8)Kearon C (2003) Diagnosis of pulmonary embolism.
CMAJ 168:183-94
9)Le Gal G, Righini M, Roy P et al (2006) Prediction of pulmonary embolism in the emergency department: the revised Geneva score. Ann Intern Med 144: 165–71
10)Moores LK, King CS, Holley AB (2011) Current approach to the diagnosisof acute nonmassive pulmonary embolism. Chest 140: 509–18
11)National Clinical Guideline Centre (2012) Venous Thromboembolic Diseases: The Management of Venous Thromboembolic Disease and the Role of Thrombophilia Testing. Clinical Guideline. Methods, Evidence and Recommendations. [Full version of NICE ClinicalGuideline 144].
12)National Institute for Health and Clinical Excellence (2010) VenousThromboembolism: Reducing the Risk. [Clinical guideline 92]. NICE: London
13) Seidel HM, Ball JW, Dains JE, Benedict GW (2003) Mosby’s Guide to Physical Examination. 5th edn. Mosby, St Louis
14) Torbicki A, Perrier A, Konstantinides S et al (2008) Guidelines on the diagnosis and management of acute pulmonary embolism. The Taskforce for the Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology. Eur Heart J 29:
2276–315
15) Wells PS, Anderson DR, Rodger M et al (2000). Derivation of a simple model to categorize patients probability of pulmonary embolism: Increasing the model’s utility with the SimpliRED D-dimer. ThrombHaemost 83: 416–20
16) Stein PD, Matta F, Musani MH, Diaczok B (2010) Silent pulmonary embolism in patient with deep vein thrombosis: a systematic review.Am J Med 123: 426–31
17) Thompson BT, Hales CA (2012) Overview of acute pulmonary embolism.
18) Sharma S (2006) Pulmonary embolism. eMedicine www.emedicine.com/med/topic1958.htm (accessed 23 May 2008)
19) Longmore M, Wilkinson I, Torok E (2001) Oxford Handbook of Clinical Medicine. 5th edn. Oxford University Press, Oxford
20) British Thoracic Society (2003) British Thoracic Society Guidelines for the management of suspected acute pulmonary embolism. Thorax 58: 470–484
21)Feied C, Handler JA (2006) Pulmonary embolism. eMedicine http://www.emedicine.com/emerg/ topic490.htm (accessed 23 May 2008)
22)Goldhaber SZ, Fanikos J (2004) Prevention of deep vein thrombosis and pulmonary embolism.Circulation 110: 445–447
23)Gossage JR (2002) Early intervention in massive pulmonary embolism: A guide to diagnosis and triage for the critical first hour. Postgrad Med 111: www.postgradmed.com/issues/2002/03_02/gossage1.shtml (accessed 23 May 2008)
24) Simon C, Everitt H, Birtwistle J, Stevenson B (2002) Oxford Handbook of General Practice. Oxford, Oxford University Press
I hereby present to you a case study on pulmonary embolism( PE), in which includes details of the patient , current problems and management taken place while caring for the patient .
Present compalints:
A 65 year old female with chest pain, acute shortness of breath, cough and swelling on the surgical limb.
Detail history of presenting complaints:
Mrs Blue, a 65 year old female who presents with chest pain and shortness of breath, underwent bilateral total knee replacement under general anesthesia , had video laryngoscope for intubation and was initially admitted in intensive care for close observation. The surgeon ordered to withhold DVT prophylaxis until the next day due to high volumes of haemoserous output …show more content…
to the handyvac drain. Following day, the patient was discharged to the ward with no complications. On early morning of post op day 3, the staff noticed Mrs Blue was getting breathless while she was resting in bed and complained that it is associated with sharp pain on the chest exacerbated by breathing. The night staff reported that she had persistent cough throughout the shift. The patient reported to staff that she experienced chest pain for one hour but she thought it would subside eventually but instead it got worse. Mrs Blue’s observations were as follows, respiratory rate:28 breaths /min, oxygen saturation:84% on non-rebreather mask, heart rate:104-120 beats/min, blood pressure:98/52mmHg .
The history-taking process is integral to making a diagnosis and is a way to accumulate information about the patient and the events leading up to that presentation (Seidel et al, 2003). The primary aim is to find out the actual problem for the patient and also to identify if any other problems that may occur later on. Mrs Blue was not understanding what was going on with her and I had to reassure the patient that she would be transferred back to the Intensive Care Unit and a cardiologist would be involved in her care. Considering all the symptoms, chances of pulmonary embolism was high at this stage on the list of differential diagnosis. However, a diagnosis of pulmonary embolism based on clinical signs and history is difficult and inaccurate and can rarely confirm or refute the diagnosis with any particularly certainty (Iles et al, 2002). Torbicki et al (2008) suggest that more than 90% of patients with pulmonary embolism show tachypnea ,chest pain and tachycardia. It is difficult to point out pulmonary embolism with patient with cardiac issues or respiratory problems with the given symptoms mentioned.
Evidence based literature supports clinical scoring systems such as the revised Geneva score (Le Gal et al,2006) and Wells score (Wells et al, 2000). These scoring tools are used along with diagnostic tests that can confirm or exclude the diagnosis of PE. For Mrs blue the revised Geneva score indicates 15, which mean high clinical probability of pulmonary embolism, and with Wells score it scores 4, which means moderate probability to PE.
Past medical history and risk factors :
Past history of Mrs Blue is hypertension, hyperlipidemia, obesity with BMI of 33 and asthma. She takes ramipril and atacand for hypertension, simvastatin 40mg once daily for high cholesterol and ventolin and seretide puffers for asthma.
The past medical history should include any illness, operations, serious injuries, recent travel and general health prior to this episode (Seidel et al, 2003). Going through the past history of the patient also helps us to assessing the current complaints and risk factors of other disease conditions. Thomson and Hales (2012) states that chronic cardiac disease, autoimmune disease, high body mass index (BMI) of ≥29, hypertension and smoking more than 25 cigarettes per day are the risk factors for PE. Mrs blue has hypertension and obesity which are contributing risk factors to pulmonary embolism.
Other risk factors that are setting or environment- related such as prolonged bed rest due to medical conditions such as heart failure or acute respiratory failure, recent major surgery, chemotherapy, insertion of a central venous line, immobility due to prolonged periods of sitting such as car or air travel or prolonged bed rest of more than 3 days for any other reason (Torbicki et al, 2008). Mrs Blue had bilateral total knee replacement which is a major surgery, she was immobile for two post operative days because of swelling and pain in both legs which was aggravated by the weight imposed onto the affected limbs on every attempt to ambulate which are the risk factors to PE. The risk of pulmonary embolism increases with age and 65% of pulmonary embolism patients are above the age of 60 (Torbicki et al, 2008). The age of Mrs Blue which was 65 years old is considered a risk factor.
DEFINITION :
Pulmonary embolism is the sudden occlusion of blood flow to the lungs by a blood clot that has usually arisen from a deep vein thrombosis (DVT) (Simon et al, 2002)
PATIENT COMPARISON WITH BOOK PICTURE :
Pathophysiology
A blood clot or a thrombus forming into a pulmonary emboli arises from the venous system of the lower extremities.
It could also come from the upper extremity veins or from the renal or pelvic areas in few instances. Pulmonary emboli are often times, multiple which could affect the lower lobes than the upper lobes of the lung. Deep vein thrombosis are blood clots developing in deep veins of the lower limbs can disintegrate and are carried by the circulation to the heart and eventually to the lung arteries which would result to blockage of the pulmonary artery which can be fatal. Clots is smaller form could also be found in the smaller vessels of the lung periphery which could often times cause pleuritic chest pain from the inflammatory changes in the pleura.
Clots ( eg : from deep vein thrombosis of the leg )travels through the heart to the pulmonary arteries.
The obstruction of pulmonary artery, which can be acute or chronic, is caused by three major factors such as local trauma to the vessel wall, hypercoagulability, and stasis of blood, which is commonly called as Virchow’s triad( Jarreau et al,2008) . Acute symptoms can be differentiate from chronic depending upon the onset of symptoms . For acute PE, the onset of symptoms is sudden whereas chronic PE symptoms can take place over a period of time ( Thompson and Hales,2012). Almost 75% of patients who develop PE have experienced DVT as mostly the thrombus arises from the lower limbs.( Kearon,2003).
Clinical Manifestations …show more content…
:
The classic triad signs and symptoms of PE include hemoptysis, dyspnea and chest pain. These symptoms only occurs in less than 20% of patients with pulmonary embolism because these symptoms could also be manifested as other symptoms aside from pulmonary embolism(Feied and Handler, 2006) .From the statement provided, Mrs blue had dyspnea and chest pain .
Diagnosis :
Diagnosis of Pulmonary embolism can be started by taking history from the patient (present and past history). Finding out the present complaints of the patient
A detailed history should be carried out which includes complaints of chest or leg discomfort, difficulty of breathing; lightheadedness and it should also take into account patients past and family histories.
. Unfortunately, the individual clinical features of both DVT and pulmonary embolism have low predictive value (about 15%) (Wells et al, 1997).
Electrocardiogram: ECG abnormalities occur in patients without pre-existing cardiovascular disease in the context of pulmonary embolism. ECG changes considered to be suggestive of pulmonary embolism are an S1Q3T3 (S I, Q III, T III) pattern. right ventricular strain, new incomplete right bundle branch block, T wave inversion and ST segment changes in the precordial leads suggesting right ventricular dysfunction, inferior Q waves and atrial arrhythmias
(Thompson and Hales, 2011).
Chest X-ray : The chest X-ray may initially be normal. However, after a period of time (approximately 24–72 hours) a third of patients go on to develop infiltrates, which are difficult to distinguish from infectious pneumonia (Feied and Handler, 2006).
Troponin
The routine bloodwork requested on the patient presenting with chest pain would generally include a cardiac troponin I or T test. Troponin is released from cardiac muscle following ischaemia and infarction and subsequent myocardial cell death and this troponin rise can be used in the diagnosis of myocardial infarction (Agewall et al, 2011). A raised troponin is seen in 30–50% of patients with moderate to large pulmonary embolism (Thompson and Hales, 2011). The reason for troponin release with acute pulmonary embolism is unclear but may be due to hypoxia and hypoperfusion including in the coronary arteries (Agewall et al, 2011). It has also been shown that a rise in troponin is associated with a higher risk of death and poor prognosis in pulmonary embolism (Agewall et al, 2011). The elevation time is also shorter in pulmonary embolism with the level resolving within 40 hours after the onset of the event.
D-dimer test: D-dimer is a clot dissolving substance released when the body is attempting to break down a clot. The D-dimer test is considered useful in that a negative test provides strong evidence against the presence of an embolism. Elevated values, however, are less reliable as they can be raised as a result of age, inflammation and cancer (Kearon, 2003).
CT scanning: A computed tomography (CT) scan of the chest will directly identify clots blocking the pulmonary vessels
Mrs. Blue had axial CT angiogram has been performed of the pulmonary arteries with multiplanar and MIP reconstructions. The report says there is non-occlusive pulmonary embolus within the right lower lobe pulmonary artery extending into the segmental branches. In addition, there is a small amount of non-occlusive embolus within the middle lobe artery however this does not extend into the segmental branches. There is no other pulmonary embolus and there is no pulmonary embolus on the left.
Dependent changes are present in the lung bases bilaterally associated with minimal atelectasis. There is no pleural and pericardial effusion. There are no end bronchial lesions.
Non-occlusive middle lobe and right lower lobe pulmonary emboli.
TREATMENT:
The British Thoracic Society (BTS) guidelines (2003) suggest two different approaches for the treatment of pulmonary embolism, depending on whether the presentation is massive or no massive pulmonary embolism. Massive pulmonary embolism is defined as a thrombus occluding more than 50% of the lung vasculature. Any amount of occlusion less than this is classed as nonmassive (Shaunessy, 2007). A massive pulmonary embolism causes symptoms of hypotension with a systolic blood pressure of less than 90 mmHg or a drop of more than 40 mmHg from baseline for 15 minutes or longer (Moores et al, 2011. For massive pulmonary embolism, the BTS (2003) suggest a 50 mg bolus of alteplase if cardiac arrest is imminent. For nonmassive pulmonary embolism, heparin is given to prevent existing blood clots from enlarging and additional clots from forming. Heparin is given intravenously to achieve a rapid effect, and while it does nothing to dissolve a clot that has developed already, it remains the single most important treatment that can be provided, because the greatest contribution to the mortality rate is the ongoing embolization of new thrombi (Feied and Handler, 2006). Prompt effective anticoagulation has been shown to reduce the overall mortality rate from 30% to less than 10% (BTS, 2003). After the initial effective anticoagulation, a long-term blood-thinning agent should be commenced in a form of warfarin, which will be continued for a minimum period of three months (Longmore et al, 2001).
There are two ways of treating pulmonary embolism. This includes comprises initial stabilization and anticoagulation. Hemodynamic stabilization should be the first and foremost focus of treatment for patients with pulmonary embolism. Symptomatic treatment is advised for patients with hypoxemia such as provision of supplemental oxygen. Whereas for patients with low blood pressure are given fluid boluses and thereafter giving vasopressor agents, such as metaraminol, noradrenaline, adrenaline and vasopressin. Patients with high chances of pulmonary embolism (PE), the core treatment is giving anticoagulants such as heparin. While patients with confirmed diagnosis PE or with high chances of getting PE without any contraindications are given anticoagulation therapy with low-molecular weight heparin eg: clexane. Anticoagulants inhibit the clots to become bigger by dissolving the fibrin, a protein involved in blood clot formation or it acts to cease the growth of clots and formation of new clots. The treatment of PE with thrombolytic agents taking into consideration the bleeding risks is outlined in the American Heart Association and Amercian College of Chest Physicians guidelines. The mechanism of action of thrombolytic agents specially in acute pulmonary embolism includes hastening the clot lysis thereby improving both respiratory and hemodynamic functioning.
REFERENCES
1)Kearon C, Kahn SR, Agnelli G, Goldhaber S, Raskob GE, Comerota AJ;American College of Chest Physicians. Antithrombotic therapy for venous thromboembolic disease: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Chest. 2008;133(6 suppl):454S-545S.
2) Jaff MR, McMurtry S, Archer SL, et al; American Heart Association
Council on Cardiopulmonary, Critical Care, Perioperative and Resuscitation; American Heart Association Council on Peripheral Vascular Disease; American Heart Association Council on Arteriosclerosis, Thrombosis and Vascular Biology. Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association [published correction appears in Circulation. 2012;125(11):e495]. Circulation. 2011;123(16):1788-1830
3) Horlander KT, Mannino DM, Leeper KV. Pulmonary embolism mortalityin the United States, 1979-1998: an analysis using multiple-cause data.Arch Intern Med. 2003;163:1711-1717.
4)Agewall S, Giannitsis E, Jernberg T, Katus H (2011) Troponin elevationin coronary vs non-coronary disease. Eur Heart J 32: 404-11
5)Iles S, Hodges AM, Darley JR, Frampton C, Epton M, Beckert LE, Town
6)GI (2003) Clinical experience and pre-test probability scores in the diagnosis of pulmonary embolism. QJM 96: 211–5
7)Jarreau T, Hanna E, Rodriguez F 3rd, Romero J, Martinez J, Lopez FA(2008) Massive pulmonary embolism: A case report and review of literature. J La State Med Soc 160: 189–94
8)Kearon C (2003) Diagnosis of pulmonary embolism.
CMAJ 168:183-94
9)Le Gal G, Righini M, Roy P et al (2006) Prediction of pulmonary embolism in the emergency department: the revised Geneva score. Ann Intern Med 144: 165–71
10)Moores LK, King CS, Holley AB (2011) Current approach to the diagnosisof acute nonmassive pulmonary embolism. Chest 140: 509–18
11)National Clinical Guideline Centre (2012) Venous Thromboembolic Diseases: The Management of Venous Thromboembolic Disease and the Role of Thrombophilia Testing. Clinical Guideline. Methods, Evidence and Recommendations. [Full version of NICE ClinicalGuideline 144].
12)National Institute for Health and Clinical Excellence (2010) VenousThromboembolism: Reducing the Risk. [Clinical guideline 92]. NICE: London
13) Seidel HM, Ball JW, Dains JE, Benedict GW (2003) Mosby’s Guide to Physical Examination. 5th edn. Mosby, St Louis
14) Torbicki A, Perrier A, Konstantinides S et al (2008) Guidelines on the diagnosis and management of acute pulmonary embolism. The Taskforce for the Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology. Eur Heart J 29:
2276–315
15) Wells PS, Anderson DR, Rodger M et al (2000). Derivation of a simple model to categorize patients probability of pulmonary embolism: Increasing the model’s utility with the SimpliRED D-dimer. ThrombHaemost 83: 416–20
16) Stein PD, Matta F, Musani MH, Diaczok B (2010) Silent pulmonary embolism in patient with deep vein thrombosis: a systematic review.Am J Med 123: 426–31
17) Thompson BT, Hales CA (2012) Overview of acute pulmonary embolism.
18) Sharma S (2006) Pulmonary embolism. eMedicine www.emedicine.com/med/topic1958.htm (accessed 23 May 2008)
19) Longmore M, Wilkinson I, Torok E (2001) Oxford Handbook of Clinical Medicine. 5th edn. Oxford University Press, Oxford
20) British Thoracic Society (2003) British Thoracic Society Guidelines for the management of suspected acute pulmonary embolism. Thorax 58: 470–484
21)Feied C, Handler JA (2006) Pulmonary embolism. eMedicine http://www.emedicine.com/emerg/ topic490.htm (accessed 23 May 2008)
22)Goldhaber SZ, Fanikos J (2004) Prevention of deep vein thrombosis and pulmonary embolism.Circulation 110: 445–447
23)Gossage JR (2002) Early intervention in massive pulmonary embolism: A guide to diagnosis and triage for the critical first hour. Postgrad Med 111: www.postgradmed.com/issues/2002/03_02/gossage1.shtml (accessed 23 May 2008)
24) Simon C, Everitt H, Birtwistle J, Stevenson B (2002) Oxford Handbook of General Practice. Oxford, Oxford University Press