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Late Cardiac Strangulation due to an Iatrogenic Pericardial Defect
2 Lotz Sp' Engel AG, Nishino H, Stevens JC, Litchy WJ. Inclusion body myositis: observation in 40 patients. Brain 1989; 112:727-47 3 Dalakas M. Polymyositis, dennatomyositis and inclusion body myositis. N Eng! J Med 1991; 21:1487-98 4 Carpenter S, Karpati G, Heller I, Eisen A. Inclusion body myositis: a distinct variety of idiopath ic in8ammatory myopathy. Neurology 1978; 28:8-17 5 Purvis J, Fam AG, Lewis A. Clinically unsuspected inclusion body myositis. J Rheumatoll991; 18:289-92
I
II Late Cardiac Strangulation due to an Iatrogenic P~ricardial pefect* fllroshl Ohahima, M.D. ; Hiroaki Takeuchi, M.D .; Tetau Yamaguchi, M.D .; Riichlrou Takapashl , M.D .; and Kouichl Tsunoda, M.D .
A 14-year-old boy developed broad posterolateral myocardial infarction, During cardiac surgery at age five, a small pericardial window had been made. Autopsy revealed an extensive left-sided pericardial defect and necrosis of the left ventricular free wall, which had herniated and strangulated through the enlarged pericardial defect . (Cheat 1993; 104:977-78)
III
aVR
~
T
he presence of the pericardium is not generally considered necessary to preserve life, but it does provide protection for the heart. In this article, we present the case of a 14-year-old boy who died of cardiac strangulation due to herniation of the left ventricle through an acquired pericardial defect which had been made 9 years before . CASE REpORT A five-year-old Japanese boy underwent an operation for patent ductus arteriosus. To prevent cardiac tamponade, a pericardial window, 10 x 15 mm In size, was made over the left ventricle. At 14 years old, however, he suddenly developed chest pain. Acute heart failure occurred. The ECG showed marked ST elevation in leads 1, 2, aVL, and V,-V. and ST depression in leads 3, aVF, and V,-V3 (FiK I), which later changed to a poor R wave in leads 1, aVL, and V,-V. and a high R wave in leads V, and V" The chest xray /lIm demonstrated pulmonary congestion and a bulge of the left cardiac border, which disappeared later. The white blood cell count was markedly elevated with the peak value of 18,8OOImm 3 as well as serum creatine kinase level of 5,760 UIL, but viral titers were unremarkable . Echocardiography revealed severe dilatation (LVDdI: 51 mm/m l ) and akinesia of the left ventricular free wall. Thallium 201 myocardial perfusion scintigraphy showed a large defect in the posterolateral wall of the left ventricle. A diagnosis was made of acute posterolateral myocardial infarction ; the patient died of intractable heart failure . Autopsy revealed an extensive left-sided pericardial defect and myocardial uecrosis of the left ventricular free wall (Fig 2). Postmortem coronary angiography and pathologic examination showed no siK"i/lcant coronary stenosis. There was no in8ammatory cell in/lltration. *From the Center for Cardiovascular Disease (Drs. Ohshima, Takeuchi, and Yamaguchi) and Department of Pathology (Dr. 'Iakanashi), Mitsui Memorial Hospital, Tokyo, Japan; and Chiba Emergency Medical Center (Dr. Tsunoda), Chiba, Japan . Reprint requests: Dr. Ohahima , New lbkyo Hospital, 473-1 Nemoto, Mataudo , japan
aVL~ Vs
aVF~
Vs
FIGURE 1. An ECG at 2 h after the onset presented the changes of acute posterolateral myocardial infarction . DISCUSSION
This patient suffered from acute myocardial infarction as confirmed by the clinical and autopsy findings. However, the infarct zone was not explained by the coronary distribution but instead corresponded to a large pericardial defect . The extensive myocardial necrosis was not caused by either coronary occlusion or myocarditis. We concluded that cardiac herniation through the pericardial defect had produced myocardial infarction. . There are some patients with congenital pericardial defect who are discovered by chance and usually remain asymptomatte.' It is quite common to resect a part ofthe pericardium and to leave it open during cardiac surgery. However, there have been seven cases of sudden death due to cardiac strangulation caused by herniation through a congenital pericardial partial defect. 2.3 Moreover, intrapericardial CHEST I 104 I 3 I SEPTEMBER, 1993
9T7
Acute Ventilatory Failure From Massive Subcutaneous Emphysema* Rick Conetta, M.D .. F.e .c.p; A. Addison Bannan. M .D .. FC .C.P.; Chris lako(J()fI . M .n .; and Raul]. Marokayan. M .D .
A 66-year-old woman developed massive subcutaneous emphysema following intubation. Acute thoracic restriction developed resulting in life-threatening respiratory acidosis. The patient could not be ventilated with conventional means. A tracheostomy was performed to decompress the chest and mediastinum with rapid resolution following. Although ventilatory failure from subcutaneous emphysema is very unusual, decompression with tracheostomy can be life saving. (Chest 1993; 104:978·80)
S
ubcutaneous emphysema is a well-known complication of positive pressure ventilation. Usually it is only a cosmetic problem and does not pose a serious threat to the patient. We have observed one case in which extra-alveolar gas accumulated under pressure resulting in ventilatory failure while the patient was on a mechanical ventilator. CASE REPOHT
Fll;l'IIE 2 . Autopsy reveale-d an extensive left -sidt'd pertcardiul defect, left posterolateral view of the re secte-d heart .
pneumonectomy occasionally brought acute cardiac strangulation. which appeared to occur regardless of the defect size or duration from tilt' operation . I ,S It is difficult to assume that a pericardia] window produced surgically 9 years prior to this incident enlarged with growth . In this cast', it is supposed that the heart had eventually herniated at or near tilt' site of surgery with enlargement of the pericardia] window and strangulated the heart 9 years later, This is tilt' first report oflate cardiac strangulation due to an iatrogenic pericardial defect. This case suggests unnecessary pericardiectomy should he avoided and the pericardial defects should he dosed to prevent possible cardiac herniation and strangulation. REFEHENCES
Bernal JM . Lapiedra JO. Conzalez I . Saez A. Pastor E. Miralles PJ. Au~io(:ardio~raphic demonstration of a partial defect of the pericardium with herniation of the left atrium and ventricle. J Cardiovasc Surg rsss, 27:344-46 2 Saito R, Hotta F. Conge-nital pericardia] dt·ft·et associated with cardiac mcarceranou. Am Heart J 19I1O; 100:H66-70 3 Jones J\\: McMauus 8M . Fatal ca rd iae strangulation hy congenital partial pericardial defect. Am Heart J 19114: 107:1113-&'5 4 Gat es GF. Sette RS. Cop« JA. Acute cardiac herniat ion with incarceration followin~ pneumonectomy; Radiology 1970: 94:56162 5 Castillo M . Oldham S. Cardiac volvulus: plain film recognition of an o/ien fatal mnditioll . AJR H1Il5: 145:271-72
978
A 66-year-old woman with a history of seizure disorder was brought to the emergency department after an episode of tonicclonic seizures at horne . At the scene , the emergency medical service found her in a grand mal seizure that responded to 5 mg of intravenous diazepam . She was intubated orally hy the ambulance team with an Il-mm endotracheal tuhe without difficulty. Within I h of arrival at the hospital , she became alert and re spo nsive with a hlond pressure of 152/108 mm Hg . Bilateral rhonchi were noted on chest auscultation. The initial chest radiograph showed the endotracheal tube to he in proper position and was otherwise unremarkable. She was then sent from the emergency department for computed tomography of the head. When she returned. she was found to he restless and thrashing in the stretcher. The nurse noted subcutaneous emphysema on the left side of her neck. face. and tnmk. No breath sounds were auscultated on the left side of the chest , A presumptive diagnosis of pneumothorax was made . A che st tube was then inserted into th e left hemithorax by a surgical resident . A large air leak was noted . Over the ensuing 3 h. the subcutaneous emphyse-ma continued to progress producing swelling of the face, eyelids. and entire torso down to the thighs and calves. The mechanical ventilator began to exceed its set pressure lim it on each breath . Although the inspired tidal volume had heen set at 650 ml, the exhaled volumes wert' varying between 150 and 250 ml per breath . Bilateral breath sounds were audible and proper endotracheal tube position was again confirmed by chest radiography. The blood pressure dropped to 91/69 mm Hg. Because of the rising airway pressures with no other obvious explanation. it was suspected that the subcutaneous emphysema had produced an acute thoracic restrietion . In addition . it was believed that high intrapleural pressures may have been impeding venous return causing the fall in blood pressure . Ten sion pneumomediastinum or pneumopericardium , although not radiographically evident , were other considerations .
* From
the Departments of Medicine and Smgt'ry. Flushing Hospital Medical Center. Flushing, NY. Reprint requests: Dr. Ctmetta, Flushing. Hospital Medical Center.
Flushing, NY 11.3.5.5
Ventilatory Failure from Massive Subcutaneous Emphysema (Conetta
at at)
I
II Late Cardiac Strangulation due to an Iatrogenic P~ricardial pefect* fllroshl Ohahima, M.D. ; Hiroaki Takeuchi, M.D .; Tetau Yamaguchi, M.D .; Riichlrou Takapashl , M.D .; and Kouichl Tsunoda, M.D .
A 14-year-old boy developed broad posterolateral myocardial infarction, During cardiac surgery at age five, a small pericardial window had been made. Autopsy revealed an extensive left-sided pericardial defect and necrosis of the left ventricular free wall, which had herniated and strangulated through the enlarged pericardial defect . (Cheat 1993; 104:977-78)
III
aVR
~
T
he presence of the pericardium is not generally considered necessary to preserve life, but it does provide protection for the heart. In this article, we present the case of a 14-year-old boy who died of cardiac strangulation due to herniation of the left ventricle through an acquired pericardial defect which had been made 9 years before . CASE REpORT A five-year-old Japanese boy underwent an operation for patent ductus arteriosus. To prevent cardiac tamponade, a pericardial window, 10 x 15 mm In size, was made over the left ventricle. At 14 years old, however, he suddenly developed chest pain. Acute heart failure occurred. The ECG showed marked ST elevation in leads 1, 2, aVL, and V,-V. and ST depression in leads 3, aVF, and V,-V3 (FiK I), which later changed to a poor R wave in leads 1, aVL, and V,-V. and a high R wave in leads V, and V" The chest xray /lIm demonstrated pulmonary congestion and a bulge of the left cardiac border, which disappeared later. The white blood cell count was markedly elevated with the peak value of 18,8OOImm 3 as well as serum creatine kinase level of 5,760 UIL, but viral titers were unremarkable . Echocardiography revealed severe dilatation (LVDdI: 51 mm/m l ) and akinesia of the left ventricular free wall. Thallium 201 myocardial perfusion scintigraphy showed a large defect in the posterolateral wall of the left ventricle. A diagnosis was made of acute posterolateral myocardial infarction ; the patient died of intractable heart failure . Autopsy revealed an extensive left-sided pericardial defect and myocardial uecrosis of the left ventricular free wall (Fig 2). Postmortem coronary angiography and pathologic examination showed no siK"i/lcant coronary stenosis. There was no in8ammatory cell in/lltration. *From the Center for Cardiovascular Disease (Drs. Ohshima, Takeuchi, and Yamaguchi) and Department of Pathology (Dr. 'Iakanashi), Mitsui Memorial Hospital, Tokyo, Japan; and Chiba Emergency Medical Center (Dr. Tsunoda), Chiba, Japan . Reprint requests: Dr. Ohahima , New lbkyo Hospital, 473-1 Nemoto, Mataudo , japan
aVL~ Vs
aVF~
Vs
FIGURE 1. An ECG at 2 h after the onset presented the changes of acute posterolateral myocardial infarction . DISCUSSION
This patient suffered from acute myocardial infarction as confirmed by the clinical and autopsy findings. However, the infarct zone was not explained by the coronary distribution but instead corresponded to a large pericardial defect . The extensive myocardial necrosis was not caused by either coronary occlusion or myocarditis. We concluded that cardiac herniation through the pericardial defect had produced myocardial infarction. . There are some patients with congenital pericardial defect who are discovered by chance and usually remain asymptomatte.' It is quite common to resect a part ofthe pericardium and to leave it open during cardiac surgery. However, there have been seven cases of sudden death due to cardiac strangulation caused by herniation through a congenital pericardial partial defect. 2.3 Moreover, intrapericardial CHEST I 104 I 3 I SEPTEMBER, 1993
9T7
Acute Ventilatory Failure From Massive Subcutaneous Emphysema* Rick Conetta, M.D .. F.e .c.p; A. Addison Bannan. M .D .. FC .C.P.; Chris lako(J()fI . M .n .; and Raul]. Marokayan. M .D .
A 66-year-old woman developed massive subcutaneous emphysema following intubation. Acute thoracic restriction developed resulting in life-threatening respiratory acidosis. The patient could not be ventilated with conventional means. A tracheostomy was performed to decompress the chest and mediastinum with rapid resolution following. Although ventilatory failure from subcutaneous emphysema is very unusual, decompression with tracheostomy can be life saving. (Chest 1993; 104:978·80)
S
ubcutaneous emphysema is a well-known complication of positive pressure ventilation. Usually it is only a cosmetic problem and does not pose a serious threat to the patient. We have observed one case in which extra-alveolar gas accumulated under pressure resulting in ventilatory failure while the patient was on a mechanical ventilator. CASE REPOHT
Fll;l'IIE 2 . Autopsy reveale-d an extensive left -sidt'd pertcardiul defect, left posterolateral view of the re secte-d heart .
pneumonectomy occasionally brought acute cardiac strangulation. which appeared to occur regardless of the defect size or duration from tilt' operation . I ,S It is difficult to assume that a pericardia] window produced surgically 9 years prior to this incident enlarged with growth . In this cast', it is supposed that the heart had eventually herniated at or near tilt' site of surgery with enlargement of the pericardia] window and strangulated the heart 9 years later, This is tilt' first report oflate cardiac strangulation due to an iatrogenic pericardial defect. This case suggests unnecessary pericardiectomy should he avoided and the pericardial defects should he dosed to prevent possible cardiac herniation and strangulation. REFEHENCES
Bernal JM . Lapiedra JO. Conzalez I . Saez A. Pastor E. Miralles PJ. Au~io(:ardio~raphic demonstration of a partial defect of the pericardium with herniation of the left atrium and ventricle. J Cardiovasc Surg rsss, 27:344-46 2 Saito R, Hotta F. Conge-nital pericardia] dt·ft·et associated with cardiac mcarceranou. Am Heart J 19I1O; 100:H66-70 3 Jones J\\: McMauus 8M . Fatal ca rd iae strangulation hy congenital partial pericardial defect. Am Heart J 19114: 107:1113-&'5 4 Gat es GF. Sette RS. Cop« JA. Acute cardiac herniat ion with incarceration followin~ pneumonectomy; Radiology 1970: 94:56162 5 Castillo M . Oldham S. Cardiac volvulus: plain film recognition of an o/ien fatal mnditioll . AJR H1Il5: 145:271-72
978
A 66-year-old woman with a history of seizure disorder was brought to the emergency department after an episode of tonicclonic seizures at horne . At the scene , the emergency medical service found her in a grand mal seizure that responded to 5 mg of intravenous diazepam . She was intubated orally hy the ambulance team with an Il-mm endotracheal tuhe without difficulty. Within I h of arrival at the hospital , she became alert and re spo nsive with a hlond pressure of 152/108 mm Hg . Bilateral rhonchi were noted on chest auscultation. The initial chest radiograph showed the endotracheal tube to he in proper position and was otherwise unremarkable. She was then sent from the emergency department for computed tomography of the head. When she returned. she was found to he restless and thrashing in the stretcher. The nurse noted subcutaneous emphysema on the left side of her neck. face. and tnmk. No breath sounds were auscultated on the left side of the chest , A presumptive diagnosis of pneumothorax was made . A che st tube was then inserted into th e left hemithorax by a surgical resident . A large air leak was noted . Over the ensuing 3 h. the subcutaneous emphyse-ma continued to progress producing swelling of the face, eyelids. and entire torso down to the thighs and calves. The mechanical ventilator began to exceed its set pressure lim it on each breath . Although the inspired tidal volume had heen set at 650 ml, the exhaled volumes wert' varying between 150 and 250 ml per breath . Bilateral breath sounds were audible and proper endotracheal tube position was again confirmed by chest radiography. The blood pressure dropped to 91/69 mm Hg. Because of the rising airway pressures with no other obvious explanation. it was suspected that the subcutaneous emphysema had produced an acute thoracic restrietion . In addition . it was believed that high intrapleural pressures may have been impeding venous return causing the fall in blood pressure . Ten sion pneumomediastinum or pneumopericardium , although not radiographically evident , were other considerations .
* From
the Departments of Medicine and Smgt'ry. Flushing Hospital Medical Center. Flushing, NY. Reprint requests: Dr. Ctmetta, Flushing. Hospital Medical Center.
Flushing, NY 11.3.5.5
Ventilatory Failure from Massive Subcutaneous Emphysema (Conetta
at at)