Cardiac tamponade without pericardial effusion after blunt chest trauma

198

January 1996 American Heart Journal

Levin et al.

though first described more than 40 years ago, controversy continues to exist over the clinical significance of myocardial bridging. A large angiographic study 4and two necropsy studies 2, 5 have found little or no atherosclerotic plaque formation at the site of the bridge. Therefore it is believed that the myocardial bridge may protect the coronary artery from significant atherosclerosis by limiting its exposure to the forces of the systolic pulse wave and potentially rainimizing endothelial trauma. However, several reports 69 have disputed this finding, and recent evidence now questions the protective effect afforded by a myocardial bridge. To our knowledge only three case reports 79 have described significant coronary artery stenosis at the site of a myocardial bridge documented by angiography. Two cases 7, 8 similar to our patient were found after angioplasty of the coronary artery stenosis was performed. One case involved the left anterior descending coronary artery 7 and the other the right coronary artery, s The third patient 9 underwent coronary artery bypass graft surgery because of multivessel disease after a myocardial bridge was discovered in the left anterior descending coronary artery. In the case described previously the culprit stenosis was at the proximal portion of a myocardial bridge in the left anterior descending coronary artery, and the patient had a similar clinical presentation with chest pain and ST segment elevation on the ECG. Myocardial bridging of the coronary segment was not discovered in our case, as in two previous cases, until angioplasty was performed, possibly because of the fixed underlying atherosclerotic stenosis limiting coronary inflow and masking systolic compression. Once angioplasty was performed, the characteristic "milking effect" consistent with myocardial bridging was noted. Transient coronary occlusion caused by plaque rupture and thrombotic occlusion or vasospasm may have been responsible for this patients' event. Fortunately a significant myocardial infarction was aborted, and subsequent angina was relieved with conventional angioplasty. Currently the patient has no symptoms. Myocardial bridging has been associated with angina, myocardial infarction, and sudden death. 3 These clinical events have been attributed to transient coronary occlusion (thrombotic or vasospastic) at the site of the myocardial bridge when myocardial bridging is the only coronary abnormality present on angiography. Noninvasive clinical studies have shown mixed results ranging from normal exercise treadmill testing to fLxed or reversible defects found on thallium-201 scintigraphy. 3 One invasive report 8 has described coronary vasospasm induced by intracoronary acetylcholine at the site of the myocardial bridge, indicating endothelial dysfunction. Apparently "kinking" of the entrapped vessel during systole may cause intimal trauma, endothelial damage, or both. Recently Ge et al. 1° reported the presence of atherosclerosis in the coronary segment proximal to the myocardial bridge by intravascular ultrasound and reduced coronary flow reserve by Doppler flow wire. In all reported cases of atherosclerotic narrowing at the site of a myocardial bridge including our own, the initial result was a success; however, optimal therapy of this con-

dition is not known. Until further data are available, treatment should be aimed at relief of symptoms, and clinical decisions regarding patients with symptoms and critical stenoses should be made in the standard fashion. Therapeutic decisions in patients with noncritical stenoses may be aided by the use of intravascular ultrasound and intracoronary Doppler flow wire, although this has yet to be proven. In conclusion, we report a rare case of coronary artery stenosis at the site of a myocardial bridge that was apparent only after angioplasty. It is evident from this report and others that the presence of myocardial bridging does not necessarily offer protection from significant coronary artery disease. REFERENCES

1. Stolte M, Weis P, Prestele H. Muscle bridges over the left anterior descending coronary artery: their influence on arterial disease. Virchows Arch Pathol Anat 1977;375:23-36. 2. Lee SS, Wu TL. The role of mural coronary artery in prevention ofcoronary atherosclerosis. Arch Pathol 1972;93:32-5. 3. Angelini P, Trivellato M, Donis J, Leachman RD. Myocardial bridges: a review. Prog Cardiovasc Dis 1983;26:75-88. 4. Channer KS, Bukis E, Hartnell G, Rees JR. Myocardial bridging of the coronary arteries. Clin Radiol 1989;40:355-9. 5. Ishii T, Asuwa N, Masuda S, Ishikawa Y, Kiguchi H, Shimada K. Atherosclerosis suppression in the lei~ anterior descending coronary artery by the presence of a myocardial bridge: an ultrastructural study. Mod Pathol 1991;4:424-31. 6. Edwards JC, Burnsides CN, Swarm RL, Lansing AI. Arteriosclerosis in the intramural and extramural portions of coronary arteries in the human heart. Circulation 1956;13:235-42. 7. Laifer LI, Weiner BH. Percutaneous transtuminal coronary angloplasty of a coronary stenosis at the site of myocardial bridging. Cardiology 1991;79:245-8. 8. Munakata K, Sato N, Sasaki Y, Yasutake M, Kusama Y, Takayama M, Kishida H, Hayakawa H. Two cases of variant form angina pectoris associated with myocardial bridge: a possible relationship among coronary vasospasm, atherosclerosis and myocardial bridge. Jpn Circ J 1992;56:1248-52. 9. Parashara DK, Ledley GS, Kotler MN,,Yazdanfar S. The combined presence of myocardial bridging and fixed coronary artery stenosis. AM HEARTJ 1993;125:1170-2. 10. Ge J, Erbel R, Rupprecht H J, Koch L, Kearney P, George G, Haude M, Meyer J. Comparison of intravascular ultrasound and angiography in the assessment of myocardial bridging. Circulation 1994;89:1725-32.

Cardiac tamponade without pericardial effusion after blunt chest trauma Steven Levin, MD, Ivan Maldonado, MD, Christina Rehm, MD, Steven Ross, MD, and Richard L. Weiss, MD Camden, N.J. Tension pneumopericardium is an unusual complication in the patient undergoing critical care and may carry a high From the Department of Surgery and Medicine, Cooper Hospital/University Medical Center; the University of Medicine and Dentistry of New Jersey; and the Robert Wood Johnson Medical School at Camden. Reprint requests: Richard L. Weiss, MD, One Cooper Plaza, Camden, NJ 08103. AM HEARTJ 1996;131:198-200. Copyright © 1996 by Mosby-Year Book, Inc. 0002-8703/96/$5.00 + 0 4J4J68069

Volume 131, Number 1

L e v i n et al.

American Heart Journal

199

Fig. 1. Portable chest x-ray film obtained in t r a u m a admitting area.

Fig. 2. Biplane transesophageal M-mode echocardiogram of right ventricular (RV) outflow tract. S o l i d a r r o w indicates collapse of RV wall in diastole. Note: no pericardial effusion on images. C l e a r a r r o w (in RV outflow tract) demonstrates normal wall thickening in systole, thereby excluding RV tardokinesia as cause of abnormality.

Fig. 3. Computed tomography scan of chest revealing large retrosternal air compressing the heart.

mortality rate. Typically the patient has hemodynamic instability with adequate intravascular volume and stable airway pressure. The chest x-ray film (Fig. 1) shows a small heart classically surrounded by air. 1 We present a case with normal x-ray film, hemodynamic instability, and a transesophageal echocardiogram suggesting tamponade. However, no pericardial effusion was seen. The patient was a 57-year-old unrestrained automobile

driver with chronic obstructive pulmonary disease, after undergoing a head-on collision. She had hypotension (systolic blood pressure = 70), bradycardia, tachypneia, and peripheral cyanosis. Her neck veins were not assessable, and she did not have a pulsus paradoxus. She underwent intubation and fluid resuscitation, and her blood pressure was stabilized. An initial chest x-ray film was normal (Fig. 1). Transesophageal echocardiography revealed a normal

200

January 1996 American Heart Journal

Grigsby et al.

aorta, no pericardial effusion, b u t severe diastolic collapse of the right ventricular outflow t r a c t consistent with tamponade (Fig. 2). To assess h e r injuries further, a computed tomography scan was obtained a n d revealed a left pneumothorax p n e u m o p e r i c a r d i u m (Fig. 3). While the comp u t e d tomography scan was being done, ventilation became difficult to perform, and the p a t i e n t h a d hypotension a n d bradycardia. An e m e r g e n t needle was passed through the t h i r d intercostal space left p a r a s t e r n a l decompression. This procedure restored hemodynamic stability. The patient was t a k e n to the operating room for i m m e d i a t e exploration and definite d r a i n a g e of the pericardium. Bil a t e r a l chest tubes were placed, and a subxiphoid pericardial window was performed. A significant r u s h of air was released from the pericardial sac on opening the pericardium. Abdominal exploration revealed a r u p t u r e d spleen, which was removed, b u t no hollow viscous injury. H e r postoperative course was complicated by prolonged respir a t o r y insufficiency and ventilator dependence. However, she did not have a n y cardiac sequelae and eventually was discharged to a rehabilitation facility. Cardiac t a m p o n a d e as a result of pneumopericardium has been shown to be a serious problem associated with a high m o r t a l i t y r a t e (56%). 2 Tension pneumopericardium occurs only r a r e l y after b l u n t chest t r a u m a . Most cases occur in association with p r e m a t u r e infants on positive pressure ventilation. Other causes include positive pressure ventilation in patients with a s t h m a , 3 penet r a t i n g chest t r a u m a , and fistulous tracts between infected or cancerous organs contiguous with the pericardial sac. Macklin 4 provided histelogic evidence of how air from r u p t u r e d alveoli travels along peribronchial and perivascular sheathes to the lung h i l u m and from t h e r e gains access to the pericardial sac. Pericardial collagenous tissue is not continuous a t the reflection of p a r i e t a l onto visceral p e r i c a r d i u m n e a r the ostia of the p u l m o n a r y veins, which m a k e s dissection of air into the pericardial sac even easier. 5 Air in the pericardial sac has been shown to cause hemodynamic compromise once the p r e s s u r e within the sac exceeds 145 m m H20 as d e m o n s t r a t e d by Adcock et al.6 The results of the t r a n s e s o p h a g e a l echocardiography were initially confusing because of the presence of p r o m i n e n t diastolic collapse of the right ventricle consistent with a tense pericardial effusion, but no effusion was present. Usually pericardial air does not allow a d e q u a t e imaging of the heart, b u t in this case excellent images were obtained. Subsequent computed t o m o g r a p h y resolved the causes of h e r instability, revealing p n e u m o p e r i c a r d i u m and pneumothorax (Fig. 2). The air was p r e s e n t r e t r o s t e r n a l l y a n d thus did not compromise the image quality, because air did not dissect between the esophagus and heart, which m a y also account for the normal a p p e a r a n c e of the chest x-ray film. In s u m m a r y , p n e u m o p e r i c a r d i u m carries a high m o r t a l i t y rate, so early diagnosis is important. It m a y be p r e s e n t with a n o r m a l chest x-ray film on presentation. This diagnosis should be considered if classic findings of t a m p o n a d e a r e seen on echocardiography a n d no pericardial effusion is identified.

REFERENCES

1. Mirvis SE, Indeck M, Shour RM. Posttraumatic tension pneumopericardium: the "small heart" sign. Radiology1986;158:663-9. 2. Cummings RG, Wesley RLR, Adams DH, Lowe JE. Pneumopericardium resulting in cardiac tamponade. Ann Thorac Surg 1989;37:511-8. 3. Toledo TM, Moore WL, Nash DA, North RL. Spontaneous pneumopericardium in acute asthma. Chest 1972i62:118-20. 4. Macklin CC. Transport of air along sheathes of pulmonary bloodyessels fromalveolito mediastinum:clinicalapplications.Arch Intern Med 1939;64:913-21. 5. MansfieldPB, Graham CB, BeckwithJB, Hall DG, Sauvage LR. Pneumopericardium and pneumomediastinum in infants and children. J Pediatr Surg 1973;8:691-8. 6. AdcockJD, Lyons RH, Barnwell JB. The circulatory effects produced in a patient with pneumopericardinmby artificiallyvarying the intrapericardial pressure. AMHEARTJ 1940;19:283-91.

Pseudocoarctation of the aorta complicated by saccular aneurysm: Treatment by aortic arch replacement J. Lee Grigsby, MD, Timothy Galbraith, MD, Scott S h u r m u r , MD, and U b e y d u l l a h Deligonul, MD

Omaha, Neb. Pseudocoarctation of t h e a o r t a is a r a r e condition described as a n elongation of the aortic arch with "kinking" at the level of the l i g a m e n t u m arteriosum. In this article we p r e s e n t a p a t i e n t who h a d a large a n e u r y s m as a complication of pseudocoarctation. The p a t i e n t was a 49-year-old m a n with recent occurrence of light-headedness after exertion. He denied dyspn e a on exertion, syncope, chest pressure, or fatigue. No history of r h e u m a t i c fever or chest t r a u m a was reported. The physical examination was significant for a grade 3/6 h a r s h systolic m u r m u r of the left sternal border t h a t radiated to the carotids and apex of the heart; $4 was noted. The carotid upstroke was delayed. The pulses were equal throughout without bruits. An echocardiographic examination indicated the aortic valve a r e a to be 1.1 cm 2 with a m e a n g r a d i e n t of 22 m m Hg. The cardiac catheterization was performed percutaneously with the right femoral approach. Some difficulty was encountered in t r a v e r s i n g the aortic arch, which required over-the-wire catheter exchanges. A n aortic injection d e m o n s t r a t e d a large saccular a n e u r y s m of the aortic arch (Fig. 1). The arch itself was noted to be elongated and tortuous with kinking. A n 11 m m Hg p e a k pressure g r a d i e n t was seen across the a r e a of pseudocoarctation. Moderate a o r t i c stenosis was demons t r a t e d as shown in Table I. Retrospective review of the medical records noted a routine chest x-ray evaluation 4 years previously t h a t was suspicious for a superior mediFrom the Section of Cardiology, Department of Internal Medicine, University of Nebraska Medical Center, Omaha. Reprint requests: U. Deligonu], MD, Cardiology Section, UNMC, 600 S. 42nd St., Omaha, NE 68198-2265. AM I-IEARTJ 1996;131:200-2. Copyright © 1996 by Mosby-Year Book, Inc. 0002-8703/96/$5.00 + 0 4]4]68063