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• W2040901388 abstract "Platypnea-orthodeoxia syndrome is a rare dyspnea with arterial hypoxemia. Symptoms occur when the patient is in an upright position and are relieved when the patient is supine. The syndrome is caused by anatomical defects or functional deformity in the atrial septum (1Seward J.B. Hayes D.L. Smith H.C. et al.Platypnea-orthodeoxia clinical profile, diagnostic workup, management, and report of seven cases.Mayo Clin Proc. 1984; 59: 221-231Abstract Full Text Full Text PDF PubMed Scopus (192) Google Scholar, 2Cheng T.O. Platypnea-orthodeoxia syndrome Etiology, differential diagnosis, and management.Catheter Cardiovasc Interv. 1999; 47: 64-66Crossref PubMed Google Scholar, 3Cheng T.O. Mechanisms of platypnea-orthodeoxia what causes water to flow uphill?.Circulation. 2002; 105: 47Crossref Google Scholar). We report a young, healthy man who presented respiratory distress with platypnea-orthodeoxia syndrome after blunt chest trauma.A 34-year-old man had a motorcycle accident with blunt trauma to the anterior part of his chest and abdomen. He was immediately sent to the local hospital. Computed tomographic (CT) scan of his abdomen showed mild spleen laceration. He was treated conservatively. Three days later, he developed chest tightness and dyspnea on exertion and presented to the emergency department. His blood pressure was 80/50 mmHg, with a pulse of 110 beats per minute, and a respiratory rate of 26 breaths per minute. A grade II/VI systolic murmur was heard over the left lower sternal border, and a mildly engorged jugular vein and peripheral cyanosis was noted.The chest radiograph showed normal heart size. Electrocardiography showed right ventricular hypertrophy with sinus tachycardia and incomplete right bundle branch block. Creatinine kinase and troponin I levels were within the normal range. Arterial blood gas analysis on 100% oxygen showed a pH level of 7.45, a Po2 level of 48 mm Hg, a Pco2 level of 23 mmHg, and a Hco3 level of 16 mmol/L. Oxygen saturation was 90% while the patient was supine, and 80% while he was sitting. An emergent CT scan of the chest revealed no evidence of pulmonary embolism. Transthoracic echocardiogram showed normal left ventricular size and function, minimal pericardial effusion, and a moderately enlarged right atrium with severe acute tricuspid regurgitation and highly mobile atrial septum. The premature opening of the pulmonary valve was also observed using a pulsed Doppler recording (Figure, A). Transesophageal echocardiography clearly demonstrated the transaction of the anterior papillary muscle head of the anterior tricuspid valve resulting in severe tricuspid regurgitation (Figure, B and C). Doppler color mapping also showed the tricuspid regurgitant flow directed to the left atrium through a patent foramen ovale, which created a right-to-left atrial shunt (Figure, D).The patient underwent emergent surgical repair because of severe hypoxemia and unstable hemodynamic status. During surgery, the two papillary muscle heads of the anterior and posterior tricuspid valves were torn; they were repositioned and the patent foramen ovale was closed. After the operation, the patient’s hypoxemia was relieved immediately, and no dynamic hypoxemia during position change was observed.Platypnea-orthodeoxia is caused by atrial septal defect, constrictive pericarditis, parenchymal lung disease, pulmonary embolism, obstructive lung disease, pulmonary vascular shunts, and aortic aneurysm or elongation (1Seward J.B. Hayes D.L. Smith H.C. et al.Platypnea-orthodeoxia clinical profile, diagnostic workup, management, and report of seven cases.Mayo Clin Proc. 1984; 59: 221-231Abstract Full Text Full Text PDF PubMed Scopus (192) Google Scholar, 2Cheng T.O. Platypnea-orthodeoxia syndrome Etiology, differential diagnosis, and management.Catheter Cardiovasc Interv. 1999; 47: 64-66Crossref PubMed Google Scholar). Two mechanisms of right-to-left interatrial shunting in the presence of normal pulmonary arterial pressure have been proposed. One involves phasic changes in right atrial pressure from tricuspid insufficiency, and the other is the streaming of blood from the inferior vena cava into the left atrium across a patent foramen ovale (3Cheng T.O. Mechanisms of platypnea-orthodeoxia what causes water to flow uphill?.Circulation. 2002; 105: 47Crossref Google Scholar, 4Chiu W.C. Shindler D.M. Scholz P.M. Boyarsky A.H. Traumatic tricuspid regurgitation with cyanosis diagnosis by transesophageal echocardiography.Ann Thorac Surg. 1996; 61: 992-993Abstract Full Text PDF PubMed Scopus (18) Google Scholar).Somers et al reported a case of platypnea-orthodeoxia syndrome after a blunt chest trauma due to direct mechanical distortion and opening of the foramen ovale while the patient was supine, causing interatrial right-to-left shunt (5Somers C. Slabbynck H. Paelinck B.P. Echocardiographic diagnosis of playtpnoea-orthdexoia syndrome after blunt chest trauma.Acta Cardiol. 2000; 55: 199-201Crossref PubMed Scopus (12) Google Scholar). However, the current patient’s syndrome is attributed to tricuspid valve papillary muscle rupture after blunt chest trauma, which caused severe acute tricuspid valve regurgitation. The pulsed Doppler tracing showed premature opening of the pulmonary valve, which indicated elevated right ventricular end-diastolic pressure. The severity of tricuspid regurgitation increased when the patient was upright. In contrast, the forward blood flow crossing the tricuspid and pulmonic valve increased when he was supine, due to higher right atrial pressure. The shunt flow across the patent foramen ovale decreased when he was in his supine position.Platypnea-orthodeoxia syndrome is extremely rare, especially after blunt chest trauma. The usual cardiac injuries after such a trauma include myocardial contusion, valvular disruption, and chamber rupture (6Hirata K. Kyushima M. Asato H. et al.Tricuspid regurgitation due to blunt chest trauma.Jpn Heart J. 1993; 34: 361-375Crossref PubMed Scopus (11) Google Scholar). We present this case to alert physicians that an intracardiac shunt should be considered if a patient presents with persistent, refractory hypoxemia related to position changes. Early recognition of the causes and hemodynamic consequences after blunt chest trauma and institution of appropriate surgical intervention is vital for saving the patient’s life. Echocardiography is also useful in the diagnosis of this unusual respiratory manifestation. Platypnea-orthodeoxia syndrome is a rare dyspnea with arterial hypoxemia. Symptoms occur when the patient is in an upright position and are relieved when the patient is supine. The syndrome is caused by anatomical defects or functional deformity in the atrial septum (1Seward J.B. Hayes D.L. Smith H.C. et al.Platypnea-orthodeoxia clinical profile, diagnostic workup, management, and report of seven cases.Mayo Clin Proc. 1984; 59: 221-231Abstract Full Text Full Text PDF PubMed Scopus (192) Google Scholar, 2Cheng T.O. Platypnea-orthodeoxia syndrome Etiology, differential diagnosis, and management.Catheter Cardiovasc Interv. 1999; 47: 64-66Crossref PubMed Google Scholar, 3Cheng T.O. Mechanisms of platypnea-orthodeoxia what causes water to flow uphill?.Circulation. 2002; 105: 47Crossref Google Scholar). We report a young, healthy man who presented respiratory distress with platypnea-orthodeoxia syndrome after blunt chest trauma. A 34-year-old man had a motorcycle accident with blunt trauma to the anterior part of his chest and abdomen. He was immediately sent to the local hospital. Computed tomographic (CT) scan of his abdomen showed mild spleen laceration. He was treated conservatively. Three days later, he developed chest tightness and dyspnea on exertion and presented to the emergency department. His blood pressure was 80/50 mmHg, with a pulse of 110 beats per minute, and a respiratory rate of 26 breaths per minute. A grade II/VI systolic murmur was heard over the left lower sternal border, and a mildly engorged jugular vein and peripheral cyanosis was noted. The chest radiograph showed normal heart size. Electrocardiography showed right ventricular hypertrophy with sinus tachycardia and incomplete right bundle branch block. Creatinine kinase and troponin I levels were within the normal range. Arterial blood gas analysis on 100% oxygen showed a pH level of 7.45, a Po2 level of 48 mm Hg, a Pco2 level of 23 mmHg, and a Hco3 level of 16 mmol/L. Oxygen saturation was 90% while the patient was supine, and 80% while he was sitting. An emergent CT scan of the chest revealed no evidence of pulmonary embolism. Transthoracic echocardiogram showed normal left ventricular size and function, minimal pericardial effusion, and a moderately enlarged right atrium with severe acute tricuspid regurgitation and highly mobile atrial septum. The premature opening of the pulmonary valve was also observed using a pulsed Doppler recording (Figure, A). Transesophageal echocardiography clearly demonstrated the transaction of the anterior papillary muscle head of the anterior tricuspid valve resulting in severe tricuspid regurgitation (Figure, B and C). Doppler color mapping also showed the tricuspid regurgitant flow directed to the left atrium through a patent foramen ovale, which created a right-to-left atrial shunt (Figure, D). The patient underwent emergent surgical repair because of severe hypoxemia and unstable hemodynamic status. During surgery, the two papillary muscle heads of the anterior and posterior tricuspid valves were torn; they were repositioned and the patent foramen ovale was closed. After the operation, the patient’s hypoxemia was relieved immediately, and no dynamic hypoxemia during position change was observed. Platypnea-orthodeoxia is caused by atrial septal defect, constrictive pericarditis, parenchymal lung disease, pulmonary embolism, obstructive lung disease, pulmonary vascular shunts, and aortic aneurysm or elongation (1Seward J.B. Hayes D.L. Smith H.C. et al.Platypnea-orthodeoxia clinical profile, diagnostic workup, management, and report of seven cases.Mayo Clin Proc. 1984; 59: 221-231Abstract Full Text Full Text PDF PubMed Scopus (192) Google Scholar, 2Cheng T.O. Platypnea-orthodeoxia syndrome Etiology, differential diagnosis, and management.Catheter Cardiovasc Interv. 1999; 47: 64-66Crossref PubMed Google Scholar). Two mechanisms of right-to-left interatrial shunting in the presence of normal pulmonary arterial pressure have been proposed. One involves phasic changes in right atrial pressure from tricuspid insufficiency, and the other is the streaming of blood from the inferior vena cava into the left atrium across a patent foramen ovale (3Cheng T.O. Mechanisms of platypnea-orthodeoxia what causes water to flow uphill?.Circulation. 2002; 105: 47Crossref Google Scholar, 4Chiu W.C. Shindler D.M. Scholz P.M. Boyarsky A.H. Traumatic tricuspid regurgitation with cyanosis diagnosis by transesophageal echocardiography.Ann Thorac Surg. 1996; 61: 992-993Abstract Full Text PDF PubMed Scopus (18) Google Scholar). Somers et al reported a case of platypnea-orthodeoxia syndrome after a blunt chest trauma due to direct mechanical distortion and opening of the foramen ovale while the patient was supine, causing interatrial right-to-left shunt (5Somers C. Slabbynck H. Paelinck B.P. Echocardiographic diagnosis of playtpnoea-orthdexoia syndrome after blunt chest trauma.Acta Cardiol. 2000; 55: 199-201Crossref PubMed Scopus (12) Google Scholar). However, the current patient’s syndrome is attributed to tricuspid valve papillary muscle rupture after blunt chest trauma, which caused severe acute tricuspid valve regurgitation. The pulsed Doppler tracing showed premature opening of the pulmonary valve, which indicated elevated right ventricular end-diastolic pressure. The severity of tricuspid regurgitation increased when the patient was upright. In contrast, the forward blood flow crossing the tricuspid and pulmonic valve increased when he was supine, due to higher right atrial pressure. The shunt flow across the patent foramen ovale decreased when he was in his supine position. Platypnea-orthodeoxia syndrome is extremely rare, especially after blunt chest trauma. The usual cardiac injuries after such a trauma include myocardial contusion, valvular disruption, and chamber rupture (6Hirata K. Kyushima M. Asato H. et al.Tricuspid regurgitation due to blunt chest trauma.Jpn Heart J. 1993; 34: 361-375Crossref PubMed Scopus (11) Google Scholar). We present this case to alert physicians that an intracardiac shunt should be considered if a patient presents with persistent, refractory hypoxemia related to position changes. Early recognition of the causes and hemodynamic consequences after blunt chest trauma and institution of appropriate surgical intervention is vital for saving the patient’s life. Echocardiography is also useful in the diagnosis of this unusual respiratory manifestation." @default.
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• W2040901388 title "Platypnea-orthodeoxia syndrome occurring after a blunt chest trauma with acute tricuspid regurgitation" @default.
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