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Normalization of Sweat Chloride Concentration and Clinical Improvement With Ivacaftor in a Patient With Cystic Fibrosis With Mutation S549N
CHEST
Postgraduate Education Corner ULTRASOUND CORNER
A 44-Year-Old Man With Progressive Shortness of Breath and Left-Sided Pleuritic Chest Pain Sandeep Khosa, MD; Grace Dosanjh, MD; Vidya Krishnan, MD; and Ziad Shaman, MD, FCCP
CHEST 2013; 144(4):e1–e4
man presented to our ED with proA44-year-old gressive shortness of breath and left-sided pleuritic
chest pain. His history was remarkable for alcohol and tobacco abuse. On examination, his vital signs were stable except for sinus tachycardia (119 beats/min). Laboratory values for cardiac markers were within normal limits, and chest roentgenogram was notable for a wedge-shaped infiltrate (Fig 1). Acute pulmonary embolism (PE) was suspected, and CT pulmonary angiography (CTPA) was performed. The CTPA showed multiple PEs in segmental branches and wedge-shaped infarcts in the bilateral lower lobes (Fig 2). In addition, a mass was noted near the periphery of the right hepatic lobe, suspicious for a malignancy (Fig 3). The patient was treated for acute PE with heparin and transitioned to warfarin. In addition, investigations were undertaken to further characterize the liver mass. Biopsy of the liver mass was deferred because of the immediate need for anticoagulation and was scheduled to be obtained as an outpatient. The patient was discharged with improvement in his symptoms. Three weeks later, the patient returned to the ED because of sudden onset of chest pain and shortness of breath. The patient had been compliant with his anticoagulation, and records indicated international norManuscript received April 21, 2013; revision accepted August 20, 2013. Affiliations: From the Division of Pulmonary, Critical Care, and Sleep Medicine (Drs Khosa, Krishnan, and Shaman), MetroHealth Medical Center, Case Western Reserve University, Cleveland, OH; and the Department of Gastroenterology and Hepatology (Dr Dosanjh), Mayo Clinic, Rochester, MN. Correspondence to: Sandeep Khosa, MD, Division of Pulmonary, Critical Care, and Sleep Medicine, Bell-Greve Third Floor, MetroHealth Medical Center, Case Western Reserve University, Cleveland, OH; e-mail: [email protected] © 2013 American College of Chest Physicians. Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details. DOI: 10.1378/chest.13-0803
Figure 1. Chest roentgenogram showing a left lower lobe opacity, suspicious for pulmonary infarct. A, Posteroanterior. B, Lateral.
malized ratios in the therapeutic range. His BP was 134/83 mm Hg, heart rate was 115 beats/min, respiratory rate was 24 breaths/min, temperature was 36.6°C, and pulse oximetry was 90% on room air. ECG showed sinus tachycardia with T-wave inversions in the anterior leads, and his troponin I level was elevated at 0.39 ng/mL (normal , 0.21 ng/mL). A repeat CTPA was performed, showing an interval increase of PE at the segmental and subsegmental pulmonary arterial branches bilaterally. Given the concern for impending hemodynamic instability, the patient was admitted
Figure 2. CT pulmonary angiography. A, The axial image shows filling defects in the segmental pulmonary arteries. B, There is also evidence of pulmonary infarction in the left lower lobe on the sagittal view, corresponding to the opacity seen in Figure 1.
journal.publications.chestnet.org
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Figure 3. Upper abdominal cross-sectional slices of the CT pulmonary angiography showing a heterogeneous mass at the periphery of the right hepatic lobe, suspicious for malignancy.
to our medical ICU, and a bedside, goal-directed ultrasound assessment was performed (Video 1). Based on the patient’s clinical presentation and interpretation of the video clips, what is the likely source behind the patient’s recurrent PE?
e2
Downloaded From: http://journal.publications.chestnet.org/ by David Kinnison on 10/03/2013
Postgraduate Education Corner
Answer: Tumor invasion into the inferior vena cava with direct extension into the right atrium. This raises suspicion for pulmonary tumor emboli. Discussion The clinical presentation raises concern for submassive PE; therefore, the immediate focus is to evaluate the right ventricle (RV) for signs of failure.1 Video 1 begins with a standard parasternal long-axis view of the heart. This video shows the RV outflow tract and the left ventricle (LV), appearing grossly normal. The next view is the parasternal short axis, which serves to assess global LV function and septal kinetics. When there is pressure or volume overload in the RV, the interventricular septum will flatten during systole or diastole, respectively. This gives the LV a D-shaped appearance (the so-called “D-sign”). In this patient, both LV function and septal kinetics appear normal. In the apical four-chamber view, information on the RV size is provided. A ratio of RV to LV end-diastolic diameter . 1 is evidence for RV enlargement.2 This patient did not have an enlarged RV; however, this view did reveal an echogenic mass that appeared within the right atrium (RA). This is also seen on the subcostal view but is somewhat obscure. The next view shown is the inferior vena cava (IVC) in long axis. A soft tissue-like mass is seen obstructing the IVC and appears to have the same consistency as the liver. Given this finding, a parasternal short-axis view at the base of the heart was obtained (shown in Video 2). This is not a standard view; however, it can be easily obtained by the intensivist. Starting off with a basic parasternal short-axis view, slight angulation of the probe superiorly at the aortic valve level will result in a parasternal short-axis view of the base of the heart, which includes the RA, tricuspid valve, RV outflow tract, pulmonic valve, and pulmonary artery. In this image, a large RA mass is seen, with a mobile component extending into the RV. In addition, the RA mass seems contiguous with a nonmobile, soft tissue-like structure that obstructs the IVC. Following this, a bedside compression ultrasonography of the proximal lower extremity veins was done and was negative for thrombus (image not shown). Given the patient’s history of therapeutic INR values and the bedside ultrasonographic findings, tumor embolism was suspected rather than the common thromboembolic phenomenon. The patient underwent an ultrasound-guided percutaneous biopsy of the hepatic mass, confirming a diagnosis of hepatocellular carcinoma (HCC). In contrast with those who present with overt shock due to acute PE, the benefit of thrombolytic therapy in the setting of submassive PE is less clear, and treatment should be individualized.1 Even among hemodynamically stable patients who present with acute PE,
findings of RV hypokinesis and dilation have been shown to be independent predictors of 30-day mortality.3 Therefore, in the management of submassive PE, the clinician is faced with a theoretical equipoise and is in urgent need to identify the two factors to determine whether the patient is more likely to benefit from fibrinolysis: (1) evidence of present or developing circulatory or respiratory insufficiency; or (2) evidence of moderate to severe RV injury.4 In this setting, bedside echocardiography often plays a central role in making this determination and is most helpful if done early in the management algorithm. Findings of a large residual venous thrombus in the lower extremity veins, thrombus in transit (thrombus seen in the IVC, the RA, or the RV), and signs of RV strain are ultrasonographic findings of high-mortality risk of PE. With basic training in critical care ultrasonography, the intensivist can become knowledgeable in identifying signs of RV failure and assist in decision-making, regardless of the time of day.5 In our case, the availability of bedside ultrasonography played a dual role: evaluating the RV for signs of failure and raising suspicion of potential tumor invasion of the IVC and tumor emboli. This was further supported by the normal compression of the proximal lower extremity veins in ruling out deep vein thrombosis. This bedside ultrasound technique in evaluating the deep veins for thrombosis can be performed by the intensivist with good diagnostic accuracy, even after a short period of training.6 The rapid assessment of the ultrasonographic findings directed the management away from thrombolytic therapy and led the team to a diagnosis, avoiding further intervention and potential harm. Cancer is a known risk factor for VTE, a syndrome that encompasses thrombus formation in the deep veins of the legs and can propagate to the lungs.7 However, cancer can induce not only VTE but also PE composed of tumor cells and may not necessarily originate from the lower extremities.8 The clinical management of the latter condition is somewhat unclear, and primary tumor embolism (PTE) findings are based largely on autopsy data. PTE is estimated to be in the range of 2.4% to 26% in patients with solid malignant tumors and varies based on size and type of tumor.8 HCC is the most commonly reported cause of PTE, and the risk seems to increase in the presence of largevein tumor invasion.8 Furthermore, the frequency of intracardiac mass lesions in HCC is exceedingly rare, and when observed it tends to extend directly from the tumor via the IVC into the RA.9 The prognosis of patients with intracavitary cardiac involvement from HCC is grim, with a mean survival ranging from 1 to 4 months, roughly 25% eventually dying from cardiovascular collapse.9 The patient was not a candidate for surgical resection because of large tumor size associated with large
journal.publications.chestnet.org
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vein and intracardiac invasion. Given his imminent risk of recurrent tumor emboli and resultant RV failure, mechanical thrombectomy was attempted. The procedure was only partially successful because adherence of the tumor was to the IVC wall. Histopathologic examination of the resected tissue confirmed a sample to be formed entirely by tumor cells and no thrombus. The patient wished to enroll in hospice service and died 2 months later. This case illustrates how bedside echocardiography allowed the clinician to make a rapid and accurate assessment of the patient’s RV dysfunction and assist in decision-making regarding thrombolytic therapy. Additional benefit from bedside ultrasonography was achieved when an intracardiac abnormality was found. This allowed the intensivist, who had full control of transducer operation, to move swiftly from cardiac examination to further characterize the discovered mass and its contiguity with the liver, ultimately leading to the source of the emboli. These findings led to avoidance of potentially harmful interventions and earlier focus on supportive and palliative measures. Reverberations 1. In the setting of acute submassive PE, bedside echocardiography can identify signs of RV pressure overload to guide therapeutic decisions, such as thrombolysis or cardiovascular or interventional radiology consultation. 2. Hyperechoic intraluminal filling defect within the IVC may represent venous thrombosis or tumor mass. Given this patient’s therapeutic INR and hepatic lesion, recurrent tumor embolus was suspected. Acknowledgments Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any
companies/organizations whose products or services may be discussed in this article. Other contributions: We thank Aleksandr Rovner, MD, for providing several of the videos used. CHEST worked with the authors to ensure that the Journal policies on patient consent to report information were met. Additional information: To analyze this case with the videos, see the online article.
References 1. Piazza G, Goldhaber SZ. Management of submassive pulmonary embolism. Circulation. 2010;122(11):1124-1129. 2. Matthews JC, McLaughlin V. Acute right ventricular failure in the setting of acute pulmonary embolism or chronic pulmonary hypertension: a detailed review of the pathophysiology, diagnosis, and management. Curr Cardiol Rev. 2008;4(1):49-59. 3. Agnelli G, Becattini C. Acute pulmonary embolism. N Engl J Med. 2010;363(3):266-274. 4. Jaff MR, McMurtry MS, 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. Circulation. 2011;123(16): 1788-1830. 5. Mayo PH, Beaulieu Y, Doelken P, et al. American College of Chest Physicians/La Société de Réanimation de Langue Française statement on competence in critical care ultrasonography. Chest. 2009;135(4):1050-1060. 6. Kory PD, Pellecchia CM, Shiloh AL, Mayo PH, DiBello C, Koenig S. Accuracy of ultrasonography performed by critical care physicians for the diagnosis of DVT. Chest. 2011;139(3): 538-542. 7. Tapson VF. Acute pulmonary embolism. N Engl J Med. 2008; 358(10):1037-1052. 8. Sakuma M, Fukui S, Nakamura M, et al. Cancer and pulmonary embolism: thrombotic embolism, tumor embolism, and tumor invasion into a large vein. Circ J. 2006;70(6):744-749. 9. Sung AD, Cheng S, Moslehi J, Scully EP, Prior JM, Loscalzo J. Hepatocellular carcinoma with intracavitary cardiac involvement: a case report and review of the literature. Am J Cardiol. 2008;102(5):643-645.
e4
Downloaded From: http://journal.publications.chestnet.org/ by David Kinnison on 10/03/2013
Postgraduate Education Corner
Postgraduate Education Corner ULTRASOUND CORNER
A 44-Year-Old Man With Progressive Shortness of Breath and Left-Sided Pleuritic Chest Pain Sandeep Khosa, MD; Grace Dosanjh, MD; Vidya Krishnan, MD; and Ziad Shaman, MD, FCCP
CHEST 2013; 144(4):e1–e4
man presented to our ED with proA44-year-old gressive shortness of breath and left-sided pleuritic
chest pain. His history was remarkable for alcohol and tobacco abuse. On examination, his vital signs were stable except for sinus tachycardia (119 beats/min). Laboratory values for cardiac markers were within normal limits, and chest roentgenogram was notable for a wedge-shaped infiltrate (Fig 1). Acute pulmonary embolism (PE) was suspected, and CT pulmonary angiography (CTPA) was performed. The CTPA showed multiple PEs in segmental branches and wedge-shaped infarcts in the bilateral lower lobes (Fig 2). In addition, a mass was noted near the periphery of the right hepatic lobe, suspicious for a malignancy (Fig 3). The patient was treated for acute PE with heparin and transitioned to warfarin. In addition, investigations were undertaken to further characterize the liver mass. Biopsy of the liver mass was deferred because of the immediate need for anticoagulation and was scheduled to be obtained as an outpatient. The patient was discharged with improvement in his symptoms. Three weeks later, the patient returned to the ED because of sudden onset of chest pain and shortness of breath. The patient had been compliant with his anticoagulation, and records indicated international norManuscript received April 21, 2013; revision accepted August 20, 2013. Affiliations: From the Division of Pulmonary, Critical Care, and Sleep Medicine (Drs Khosa, Krishnan, and Shaman), MetroHealth Medical Center, Case Western Reserve University, Cleveland, OH; and the Department of Gastroenterology and Hepatology (Dr Dosanjh), Mayo Clinic, Rochester, MN. Correspondence to: Sandeep Khosa, MD, Division of Pulmonary, Critical Care, and Sleep Medicine, Bell-Greve Third Floor, MetroHealth Medical Center, Case Western Reserve University, Cleveland, OH; e-mail: [email protected] © 2013 American College of Chest Physicians. Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details. DOI: 10.1378/chest.13-0803
Figure 1. Chest roentgenogram showing a left lower lobe opacity, suspicious for pulmonary infarct. A, Posteroanterior. B, Lateral.
malized ratios in the therapeutic range. His BP was 134/83 mm Hg, heart rate was 115 beats/min, respiratory rate was 24 breaths/min, temperature was 36.6°C, and pulse oximetry was 90% on room air. ECG showed sinus tachycardia with T-wave inversions in the anterior leads, and his troponin I level was elevated at 0.39 ng/mL (normal , 0.21 ng/mL). A repeat CTPA was performed, showing an interval increase of PE at the segmental and subsegmental pulmonary arterial branches bilaterally. Given the concern for impending hemodynamic instability, the patient was admitted
Figure 2. CT pulmonary angiography. A, The axial image shows filling defects in the segmental pulmonary arteries. B, There is also evidence of pulmonary infarction in the left lower lobe on the sagittal view, corresponding to the opacity seen in Figure 1.
journal.publications.chestnet.org
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CHEST / 144 / 4 / OCTOBER 2013
e1
Figure 3. Upper abdominal cross-sectional slices of the CT pulmonary angiography showing a heterogeneous mass at the periphery of the right hepatic lobe, suspicious for malignancy.
to our medical ICU, and a bedside, goal-directed ultrasound assessment was performed (Video 1). Based on the patient’s clinical presentation and interpretation of the video clips, what is the likely source behind the patient’s recurrent PE?
e2
Downloaded From: http://journal.publications.chestnet.org/ by David Kinnison on 10/03/2013
Postgraduate Education Corner
Answer: Tumor invasion into the inferior vena cava with direct extension into the right atrium. This raises suspicion for pulmonary tumor emboli. Discussion The clinical presentation raises concern for submassive PE; therefore, the immediate focus is to evaluate the right ventricle (RV) for signs of failure.1 Video 1 begins with a standard parasternal long-axis view of the heart. This video shows the RV outflow tract and the left ventricle (LV), appearing grossly normal. The next view is the parasternal short axis, which serves to assess global LV function and septal kinetics. When there is pressure or volume overload in the RV, the interventricular septum will flatten during systole or diastole, respectively. This gives the LV a D-shaped appearance (the so-called “D-sign”). In this patient, both LV function and septal kinetics appear normal. In the apical four-chamber view, information on the RV size is provided. A ratio of RV to LV end-diastolic diameter . 1 is evidence for RV enlargement.2 This patient did not have an enlarged RV; however, this view did reveal an echogenic mass that appeared within the right atrium (RA). This is also seen on the subcostal view but is somewhat obscure. The next view shown is the inferior vena cava (IVC) in long axis. A soft tissue-like mass is seen obstructing the IVC and appears to have the same consistency as the liver. Given this finding, a parasternal short-axis view at the base of the heart was obtained (shown in Video 2). This is not a standard view; however, it can be easily obtained by the intensivist. Starting off with a basic parasternal short-axis view, slight angulation of the probe superiorly at the aortic valve level will result in a parasternal short-axis view of the base of the heart, which includes the RA, tricuspid valve, RV outflow tract, pulmonic valve, and pulmonary artery. In this image, a large RA mass is seen, with a mobile component extending into the RV. In addition, the RA mass seems contiguous with a nonmobile, soft tissue-like structure that obstructs the IVC. Following this, a bedside compression ultrasonography of the proximal lower extremity veins was done and was negative for thrombus (image not shown). Given the patient’s history of therapeutic INR values and the bedside ultrasonographic findings, tumor embolism was suspected rather than the common thromboembolic phenomenon. The patient underwent an ultrasound-guided percutaneous biopsy of the hepatic mass, confirming a diagnosis of hepatocellular carcinoma (HCC). In contrast with those who present with overt shock due to acute PE, the benefit of thrombolytic therapy in the setting of submassive PE is less clear, and treatment should be individualized.1 Even among hemodynamically stable patients who present with acute PE,
findings of RV hypokinesis and dilation have been shown to be independent predictors of 30-day mortality.3 Therefore, in the management of submassive PE, the clinician is faced with a theoretical equipoise and is in urgent need to identify the two factors to determine whether the patient is more likely to benefit from fibrinolysis: (1) evidence of present or developing circulatory or respiratory insufficiency; or (2) evidence of moderate to severe RV injury.4 In this setting, bedside echocardiography often plays a central role in making this determination and is most helpful if done early in the management algorithm. Findings of a large residual venous thrombus in the lower extremity veins, thrombus in transit (thrombus seen in the IVC, the RA, or the RV), and signs of RV strain are ultrasonographic findings of high-mortality risk of PE. With basic training in critical care ultrasonography, the intensivist can become knowledgeable in identifying signs of RV failure and assist in decision-making, regardless of the time of day.5 In our case, the availability of bedside ultrasonography played a dual role: evaluating the RV for signs of failure and raising suspicion of potential tumor invasion of the IVC and tumor emboli. This was further supported by the normal compression of the proximal lower extremity veins in ruling out deep vein thrombosis. This bedside ultrasound technique in evaluating the deep veins for thrombosis can be performed by the intensivist with good diagnostic accuracy, even after a short period of training.6 The rapid assessment of the ultrasonographic findings directed the management away from thrombolytic therapy and led the team to a diagnosis, avoiding further intervention and potential harm. Cancer is a known risk factor for VTE, a syndrome that encompasses thrombus formation in the deep veins of the legs and can propagate to the lungs.7 However, cancer can induce not only VTE but also PE composed of tumor cells and may not necessarily originate from the lower extremities.8 The clinical management of the latter condition is somewhat unclear, and primary tumor embolism (PTE) findings are based largely on autopsy data. PTE is estimated to be in the range of 2.4% to 26% in patients with solid malignant tumors and varies based on size and type of tumor.8 HCC is the most commonly reported cause of PTE, and the risk seems to increase in the presence of largevein tumor invasion.8 Furthermore, the frequency of intracardiac mass lesions in HCC is exceedingly rare, and when observed it tends to extend directly from the tumor via the IVC into the RA.9 The prognosis of patients with intracavitary cardiac involvement from HCC is grim, with a mean survival ranging from 1 to 4 months, roughly 25% eventually dying from cardiovascular collapse.9 The patient was not a candidate for surgical resection because of large tumor size associated with large
journal.publications.chestnet.org
Downloaded From: http://journal.publications.chestnet.org/ by David Kinnison on 10/03/2013
CHEST / 144 / 4 / OCTOBER 2013
e3
vein and intracardiac invasion. Given his imminent risk of recurrent tumor emboli and resultant RV failure, mechanical thrombectomy was attempted. The procedure was only partially successful because adherence of the tumor was to the IVC wall. Histopathologic examination of the resected tissue confirmed a sample to be formed entirely by tumor cells and no thrombus. The patient wished to enroll in hospice service and died 2 months later. This case illustrates how bedside echocardiography allowed the clinician to make a rapid and accurate assessment of the patient’s RV dysfunction and assist in decision-making regarding thrombolytic therapy. Additional benefit from bedside ultrasonography was achieved when an intracardiac abnormality was found. This allowed the intensivist, who had full control of transducer operation, to move swiftly from cardiac examination to further characterize the discovered mass and its contiguity with the liver, ultimately leading to the source of the emboli. These findings led to avoidance of potentially harmful interventions and earlier focus on supportive and palliative measures. Reverberations 1. In the setting of acute submassive PE, bedside echocardiography can identify signs of RV pressure overload to guide therapeutic decisions, such as thrombolysis or cardiovascular or interventional radiology consultation. 2. Hyperechoic intraluminal filling defect within the IVC may represent venous thrombosis or tumor mass. Given this patient’s therapeutic INR and hepatic lesion, recurrent tumor embolus was suspected. Acknowledgments Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any
companies/organizations whose products or services may be discussed in this article. Other contributions: We thank Aleksandr Rovner, MD, for providing several of the videos used. CHEST worked with the authors to ensure that the Journal policies on patient consent to report information were met. Additional information: To analyze this case with the videos, see the online article.
References 1. Piazza G, Goldhaber SZ. Management of submassive pulmonary embolism. Circulation. 2010;122(11):1124-1129. 2. Matthews JC, McLaughlin V. Acute right ventricular failure in the setting of acute pulmonary embolism or chronic pulmonary hypertension: a detailed review of the pathophysiology, diagnosis, and management. Curr Cardiol Rev. 2008;4(1):49-59. 3. Agnelli G, Becattini C. Acute pulmonary embolism. N Engl J Med. 2010;363(3):266-274. 4. Jaff MR, McMurtry MS, 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. Circulation. 2011;123(16): 1788-1830. 5. Mayo PH, Beaulieu Y, Doelken P, et al. American College of Chest Physicians/La Société de Réanimation de Langue Française statement on competence in critical care ultrasonography. Chest. 2009;135(4):1050-1060. 6. Kory PD, Pellecchia CM, Shiloh AL, Mayo PH, DiBello C, Koenig S. Accuracy of ultrasonography performed by critical care physicians for the diagnosis of DVT. Chest. 2011;139(3): 538-542. 7. Tapson VF. Acute pulmonary embolism. N Engl J Med. 2008; 358(10):1037-1052. 8. Sakuma M, Fukui S, Nakamura M, et al. Cancer and pulmonary embolism: thrombotic embolism, tumor embolism, and tumor invasion into a large vein. Circ J. 2006;70(6):744-749. 9. Sung AD, Cheng S, Moslehi J, Scully EP, Prior JM, Loscalzo J. Hepatocellular carcinoma with intracavitary cardiac involvement: a case report and review of the literature. Am J Cardiol. 2008;102(5):643-645.
e4
Downloaded From: http://journal.publications.chestnet.org/ by David Kinnison on 10/03/2013
Postgraduate Education Corner