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Pneumopericardium following closed chest injury: a report of two cases
injury,
4, 221-224
221
Pneumopericardium following closed chest injury: a report of two cases A. O’R. Cargill Registrar, Accident Service, Radcliffe Infirmary
C. S. B. Galasko First Assistant, Accident Service, Radcliffe infirmary
A. J. Gunning Consultant
Thoracic Surgeon, Radcliffe Infirmary
Summary
Two cases of pneumopericardium complicating closed chest injury are reported. The first of these was complicated by aortic rupture and made a good recovery. We have been unable to find this combination of injuries previously documented in the literature. The second case was discovered at post-mortem examination.
Four hours after admission, laparotomy was performed because of an increase in abdominal tenderness and girth. A very large extraperitoneal and a large right perinephric haematoma were found, though there was no significant intraperitoneal damage. Therefore, after washing out the peritoneal cavity, the abdomen was closed. At the end of the operation the patient was bronchoscoped. The carina and right main bronchus were normal as was the
INTRODUCTION PNEUMOPERICARDIUM following closed chest injury is rare. We have recently treated a patient who sustained this injury as well as a rupture of his thoracic aorta, and in a second patient pneumopericardium was found at post-mortem examination.
CASE REPORTS Case 7 On 12 Nov.,
1971, a 22-year-old male motor-cyclist who had been involved in a collision with a lorry was admitted to the Radcliffe Infirmary. He was found to be mildly shocked with a blood-pressure of lOO/SO and a pulse-rate of 130 per minute. There were no signs of increased venous pressure. The only external signs of thoracic injury were some minor abrasions over the right rib cage. On auscultation of the heart a loud splashing sound was audible, maximal at the base of the heart. This was associated with some mullling of the heart-sounds. Radiography showed a slight widening of the upper mediastinal shadow which was thought at the time not to be due to aortic rupture, as well as a pneumopericardium, the sharp pericardial outline being separated from the cardiac outline by an area of uniform translucency (Fig. 1). There were no signs of air in the pleural cavities or mediastinum.
Fig. 1.-Case 1. Postero-anterior radiograph showing widening of the upper mediastinal outline and the sharp outline of the pericardial sac [marked by arrows) which contains the pneumopericardium.
222
posterior wall of the left main bronchus. The anterior wall of the left main bronchus was reddened and contused about 2 cm. distal to the carina, but no definite tear was seen. The postoperative radiograph showed that a right pneumothorax had developed. This was treated by intercostal drainage. A chest radiograph 8 hours after admission showed that the pneumopericardium had resolved. The patient initially made a satisfactory recovery, but on the seventh postoperative day he developed severe central chest pain, tachypnoea, and tachycardia. His blood-pressure did not change and no definite pulse differential between the upper and lower limbs could be demonstrated. It was thought that these symptoms could be due to aortic dissection and retrograde aortography was performed. This revealed a well-defined false aneurysm, approximately 4 cm. in diameter, bulging anteromedially from the descending aorta just distal to the origin of the left subclavian artery (Fig. 2).
injury: the British Journal of Accident
Surgery Vol. ~/NO. 3
and incised transversely through its centre. The incision opened into a false aneurysm containing organized blood-clot. The aorta had a transverse tear extending approximately three-quarters of the way around its circumference, and an intramural aortic dissection was found to extend for 33 cm. distal to this tear. There was no evidence of fresh leakage from the rupture. The tear was completed and the resulting two ends were connected by a 2+ cm. dacron graft. Following re-establishment of full circulation to the lower aorta, the patient had a cardiac arrest. Internal massage for a period of approximately 20 minutes, transfusion of 23 litres of blood and intraventricular injections of adrenaline were required before a good cardiac beat was restored. The patient made a good recovery, although 4 weeks passed before the pulse-rate returned to normal. Case 2 A 25year-old male driver of a car was involved in a road traffic accident. He was trapped in the car and it took 20 minutes before he could be extricated by the Fire Brigade. On arrival at hospital he was shocked, with a blood-pressure of 20/O, and despite efforts at resuscitation, he died approximately 20 minutes after arrival. At autopsy, multiple rib fractures and marked interstitial emphysema were found. The latter had tracked to the mediastinum and a large pneumopericardium was present. In addition there was an extensive laceration of the liver and splenic rupture with profuse intraperitoneal haemorrhage.
DISCUSSION
Fig. 2.-C&e 1. Traumatic aortic aneurysm shown by retrograde aortography. The aneurysm arises from the medial wall of the descending aorta, just distal to the origin of the left subclavian artery. A left thoracotomy was performed through the bed of the fourth rib. The aorta was bruised and oedematous in the region of the ductus, the mediastinal pleura appeared to be intact, and there was no fresh blood in the pleural cavities. The aorta proximal and distal to this bruised area appeared normal. The bruised area of the aorta was isolated, left ventriculo-aortic by-pass was established using a one-piece disposable plastic cannula (Gunning, 1972), and the bruised aorta was cautiously dissected away from the mediastinal tissues
Pneumopericardium is an uncommon condition, less than a hundred cases having been reported. The first documented case report of pneumopericardium was by Brichteau in 1844. Shackleford (1931), reviewing this condition, quoted 75 cases and reported a further 1. He provided the first working classification of the aetiology of the condition. He described four groups :1. Those patients in whom there was no demonstrable opening in the pericardium. This group includes the only 3 cases attributable to blunt chest injury; 2 in patients who had fallen from a height and 1 patient who had suffered a blow over the sternum. In the other 5 patients in this group the pneumopericardium was secondary to involvement of the pericardium in the inflammatory process of a neighbouring viscus. 2. Those cases in which the pericardium was perforated from without. This group included a large number of penetrating injuries, either through the chest wall or through the oesophagus.
Cargill et al.
: Pneumopericardium
after Closed Chest Injury
This was the largest group, comprising 58 of Shackleford’s 76 cases. 3. Those patients in whom the pathological process began in an intact pericardium and ruptured outward into some air-containing organ. This group contained 2 cases secondary to purulent pericarditis. 4. Those cases in which it was not known whether there was a perforation of the pericardium. This group consisted of 7 cases where recovery precluded an accurate pathological diagnosis. The loud splashing sound which was described by Brichteau (1844) as ‘ bruit de moulin ’ is so characteristic, that of the 76 cases reviewed by Shackleford, in only 8 was the diagnosis not made before death despite the fact that the condition was being seen for the first time by the individual clinicians. The most dramatic signs arose from the presence of an air/fluid mixture within the pericardial cavity. The noise may be very loud, and in one case described by Brichteau (1844) the noise prevented the patient from sleeping and could be heard five feet away from the patient. Other quoted signs included a tympanitic percussion note over the precordium and occasionally a loss of definition of heart-sounds which returned when the patient sat up. The presence of air in the pericardium, provided that it is not under tension, seems to have no deleterious effect on the circulation. In the past it was fashionable to treat purulent pericarditis by injection of large volumes of air or nitrogen into the pericardial cavity, following pericardiocentesis (Wenkebach, 1910). The aims of this treatment were to prevent the formation of adhesions by keeping the inflamed pericardial surfaces apart and to aid the circulation by substituting air for a highly viscous exudate within a closed sac. Oppenheimer (1924) believed that the rate of reformation of the exudate was slower following therapeutic pneumopericardium, and he insufflated as much as 500 ml. of air following pericardiocentesis. Cimmino (1967), in a critical review of the radiological features, suggested that pneumopericardium was overdiagnosed, and that it had been mistaken on occasions for pneumomediastinum and pneumothorax. Pneumopericardium could be differentiated on the radiographs by the pericardial shadow which outlined the air and which extended to the lower part of the aortic arch, the site of the pericardial reflexion. In many cases secondary to inflammatory causes, the pericardial line was thickened. The radiological findings in our first patient fell within his
223
definition of pneumopericardium. We believe that in our first patient the air entered the pericardial cavity from a small rupture of the anterior wall of the left main bronchus. At bronchoscopy a contusion was seen where the bronchus lay in close anatomical contact with the transverse sinus of the pericardium. An alternative mechanism has been described by Rosen, Vaudagna, and Jamplis (1963). They suggested that alveoli could rupture following a sudden rise in expiratory pressure. The air thus released passed through the interstitial tissues of the lung and was guided along the sheaths of the pulmonary vascular system to the mediastinum, the neck, the retroperitoneal spaces, and rarely to the pericardial sac itself. Rosen and his colleagues have demonstrated this continuous pathway by anatomical dissection. Traumatic aortic rupture has been very well documented as an entity related to the increasing incidence of high velocity road traffic accidents. Strassman (1947) found 72 cases of traumatic aortic rupture in a consecutive series of 7000 autopsies, an incidence of 1 per cent, yet no mention is made of coexisting pneumopericardium in this series. Seventy per cent of these occurred in patients killed in road traffic accidents. The injury is classically described as being a deceleration phenomenon, occurring at the junction of the relatively fixed aortic arch and the mobile descending thoracic aorta, just below the root of the left subclavian artery. In 55 per cent of Strassman’s (1947) series, rupture occurred at this point. To develop the extremely high intraluminal pressure of 1000-3000 mm. Hg which is necessary to rupture the aorta, a deceleration from 120 to 0 m.p.h. in 0.1-0.2 sec. is required experimentally. It is possible that twisting and shearing forces are of importance, and as a result much lower pressures may cause aortic rupture. In complete aortic rupture, death is instantaneous, but Parmley, Mattingley, Mannion, and Jahnke (1958) stated that lo-20 per cent of patients survived to reach hospital. This percentage represents those patients with incomplete tears, usually sparing the adventitial layer of the aorta. Delayed death is also well documented by Parmley and others (1958), who described 8 patients with complete transection who survived for at least 5 days. Steinberg quoted a patient where delayed fatal rupture occurred 20 years after the original injury (Steinberg, 1957). Our first case emphasizes the need for constant alertness for the presence of traumatic aortic rupture. Aortography should be performed in all cases in which the diagnosis is suspect,irrespective
Injury:
224 of the apparently stable clinical condition of the patient. Blake, Inmon, and Spencer (1960) recommended the use of an intravenous method or a right heart catheter technique and suggested that retrograde aortography might precipitate aortic rupture. In our patient, the only sign of aortic rupture when he first presented was a slight widening of the mediastinum. His peripheral pulses were normal. Aortography was carried out because of the development of symptoms which, in retrospect, were probably not due to any extension of the rupture. Slaney, Ashton, and Abrams (1966) stressed that cardiac damage may be present in 40 per cent of patients and that operation should not be performed, if possible, until a normal blood-pressure and normal electrocardiograph have been obtained. Our patient developed cardiac arrest which necessitated prolonged internal cardiac massage before normal rhythm could be restored. This was probably due to myocardial damage and reinforces their warning.
Acknowledgements We would like to thank Mr. J. C. Scott, under whose care these two patients were admitted, for his help. We would also like to thank the Department of Medical Illustrations, Radcliffe Infirmary, for the photographs, and Miss Jane Wrixon for typing the manuscript. Requests
for reprints
should be addressed to:-A.
Cargill,
Esq.,
the British Journal of Accident Surgery Vol. ~/NO. 3
REFERENCES BLAKE, H. A., INMON, T. W., and SPENCER,F. C. (1960), ‘ Emergency use of antegrade aortography in diagnosis of acute aortic rupture ‘, Ann. Surg., 152, 954. BRICHTEAU,J. (1844), Arch g&. M&d., series 4, 4, 334. CIMMINO, V. (1967), ‘ Some radio-diagnostic notes on pneumomediastinum, pneumothorax, and pneumopericardium ‘, Vu med. Mon., 94,205. GUNNING, A. J. (1972), ‘ A disposable one-piece left ventriculo-aortic bypass cannula ‘, Thorax, 27, 371. OPPENHEIMER, C. (I 924), ‘ Therapeutic pneumopericardium in pericarditis with effusion ‘, J. Am. med. Ass., 82, 1685. PARMLEY, L. F., MATTINGLEY, T. W., MANNION, W. C.. and JAHNKE,E. J. (1958). ‘ Nonpenetratina traumatic injury of the aorta”: Circ&rion, 17; 1086. ROSEN, A., VAUDAGNA, J., and JAMPLIS, R. (1963), ‘ Spontaneous pneumopericardium ‘, Am. Rev. resp. Dis., 87, 764. SHACKLEFORD, R. T. (I 93 l), ‘ Hydropneumopericardium ‘, J. Am. med. Ass., 96, 187. SLANEY, G., ASHTON, F., and ABRAMS, L. D. (1966), ‘ Traumatic rupture of the aorta ‘, Br. J. Surg., 53, 361. STEINBERG,I. (1957), ‘ Chronic traumatic aneurysm of the thoracic aorta ‘, New Engl. J. Med., 257, 913. STRASSMAN, N. G. (1947), ‘ Traumatic rupture of aorta ‘, Am. Heart J., 33, 508. WENKEBACH,A. (1910), Z. klin. Med., 71, 402.
F.R.C.S.(Edin.),
Radcliffe
Infirmary,
Oxford
OX2
6HE
4, 221-224
221
Pneumopericardium following closed chest injury: a report of two cases A. O’R. Cargill Registrar, Accident Service, Radcliffe Infirmary
C. S. B. Galasko First Assistant, Accident Service, Radcliffe infirmary
A. J. Gunning Consultant
Thoracic Surgeon, Radcliffe Infirmary
Summary
Two cases of pneumopericardium complicating closed chest injury are reported. The first of these was complicated by aortic rupture and made a good recovery. We have been unable to find this combination of injuries previously documented in the literature. The second case was discovered at post-mortem examination.
Four hours after admission, laparotomy was performed because of an increase in abdominal tenderness and girth. A very large extraperitoneal and a large right perinephric haematoma were found, though there was no significant intraperitoneal damage. Therefore, after washing out the peritoneal cavity, the abdomen was closed. At the end of the operation the patient was bronchoscoped. The carina and right main bronchus were normal as was the
INTRODUCTION PNEUMOPERICARDIUM following closed chest injury is rare. We have recently treated a patient who sustained this injury as well as a rupture of his thoracic aorta, and in a second patient pneumopericardium was found at post-mortem examination.
CASE REPORTS Case 7 On 12 Nov.,
1971, a 22-year-old male motor-cyclist who had been involved in a collision with a lorry was admitted to the Radcliffe Infirmary. He was found to be mildly shocked with a blood-pressure of lOO/SO and a pulse-rate of 130 per minute. There were no signs of increased venous pressure. The only external signs of thoracic injury were some minor abrasions over the right rib cage. On auscultation of the heart a loud splashing sound was audible, maximal at the base of the heart. This was associated with some mullling of the heart-sounds. Radiography showed a slight widening of the upper mediastinal shadow which was thought at the time not to be due to aortic rupture, as well as a pneumopericardium, the sharp pericardial outline being separated from the cardiac outline by an area of uniform translucency (Fig. 1). There were no signs of air in the pleural cavities or mediastinum.
Fig. 1.-Case 1. Postero-anterior radiograph showing widening of the upper mediastinal outline and the sharp outline of the pericardial sac [marked by arrows) which contains the pneumopericardium.
222
posterior wall of the left main bronchus. The anterior wall of the left main bronchus was reddened and contused about 2 cm. distal to the carina, but no definite tear was seen. The postoperative radiograph showed that a right pneumothorax had developed. This was treated by intercostal drainage. A chest radiograph 8 hours after admission showed that the pneumopericardium had resolved. The patient initially made a satisfactory recovery, but on the seventh postoperative day he developed severe central chest pain, tachypnoea, and tachycardia. His blood-pressure did not change and no definite pulse differential between the upper and lower limbs could be demonstrated. It was thought that these symptoms could be due to aortic dissection and retrograde aortography was performed. This revealed a well-defined false aneurysm, approximately 4 cm. in diameter, bulging anteromedially from the descending aorta just distal to the origin of the left subclavian artery (Fig. 2).
injury: the British Journal of Accident
Surgery Vol. ~/NO. 3
and incised transversely through its centre. The incision opened into a false aneurysm containing organized blood-clot. The aorta had a transverse tear extending approximately three-quarters of the way around its circumference, and an intramural aortic dissection was found to extend for 33 cm. distal to this tear. There was no evidence of fresh leakage from the rupture. The tear was completed and the resulting two ends were connected by a 2+ cm. dacron graft. Following re-establishment of full circulation to the lower aorta, the patient had a cardiac arrest. Internal massage for a period of approximately 20 minutes, transfusion of 23 litres of blood and intraventricular injections of adrenaline were required before a good cardiac beat was restored. The patient made a good recovery, although 4 weeks passed before the pulse-rate returned to normal. Case 2 A 25year-old male driver of a car was involved in a road traffic accident. He was trapped in the car and it took 20 minutes before he could be extricated by the Fire Brigade. On arrival at hospital he was shocked, with a blood-pressure of 20/O, and despite efforts at resuscitation, he died approximately 20 minutes after arrival. At autopsy, multiple rib fractures and marked interstitial emphysema were found. The latter had tracked to the mediastinum and a large pneumopericardium was present. In addition there was an extensive laceration of the liver and splenic rupture with profuse intraperitoneal haemorrhage.
DISCUSSION
Fig. 2.-C&e 1. Traumatic aortic aneurysm shown by retrograde aortography. The aneurysm arises from the medial wall of the descending aorta, just distal to the origin of the left subclavian artery. A left thoracotomy was performed through the bed of the fourth rib. The aorta was bruised and oedematous in the region of the ductus, the mediastinal pleura appeared to be intact, and there was no fresh blood in the pleural cavities. The aorta proximal and distal to this bruised area appeared normal. The bruised area of the aorta was isolated, left ventriculo-aortic by-pass was established using a one-piece disposable plastic cannula (Gunning, 1972), and the bruised aorta was cautiously dissected away from the mediastinal tissues
Pneumopericardium is an uncommon condition, less than a hundred cases having been reported. The first documented case report of pneumopericardium was by Brichteau in 1844. Shackleford (1931), reviewing this condition, quoted 75 cases and reported a further 1. He provided the first working classification of the aetiology of the condition. He described four groups :1. Those patients in whom there was no demonstrable opening in the pericardium. This group includes the only 3 cases attributable to blunt chest injury; 2 in patients who had fallen from a height and 1 patient who had suffered a blow over the sternum. In the other 5 patients in this group the pneumopericardium was secondary to involvement of the pericardium in the inflammatory process of a neighbouring viscus. 2. Those cases in which the pericardium was perforated from without. This group included a large number of penetrating injuries, either through the chest wall or through the oesophagus.
Cargill et al.
: Pneumopericardium
after Closed Chest Injury
This was the largest group, comprising 58 of Shackleford’s 76 cases. 3. Those patients in whom the pathological process began in an intact pericardium and ruptured outward into some air-containing organ. This group contained 2 cases secondary to purulent pericarditis. 4. Those cases in which it was not known whether there was a perforation of the pericardium. This group consisted of 7 cases where recovery precluded an accurate pathological diagnosis. The loud splashing sound which was described by Brichteau (1844) as ‘ bruit de moulin ’ is so characteristic, that of the 76 cases reviewed by Shackleford, in only 8 was the diagnosis not made before death despite the fact that the condition was being seen for the first time by the individual clinicians. The most dramatic signs arose from the presence of an air/fluid mixture within the pericardial cavity. The noise may be very loud, and in one case described by Brichteau (1844) the noise prevented the patient from sleeping and could be heard five feet away from the patient. Other quoted signs included a tympanitic percussion note over the precordium and occasionally a loss of definition of heart-sounds which returned when the patient sat up. The presence of air in the pericardium, provided that it is not under tension, seems to have no deleterious effect on the circulation. In the past it was fashionable to treat purulent pericarditis by injection of large volumes of air or nitrogen into the pericardial cavity, following pericardiocentesis (Wenkebach, 1910). The aims of this treatment were to prevent the formation of adhesions by keeping the inflamed pericardial surfaces apart and to aid the circulation by substituting air for a highly viscous exudate within a closed sac. Oppenheimer (1924) believed that the rate of reformation of the exudate was slower following therapeutic pneumopericardium, and he insufflated as much as 500 ml. of air following pericardiocentesis. Cimmino (1967), in a critical review of the radiological features, suggested that pneumopericardium was overdiagnosed, and that it had been mistaken on occasions for pneumomediastinum and pneumothorax. Pneumopericardium could be differentiated on the radiographs by the pericardial shadow which outlined the air and which extended to the lower part of the aortic arch, the site of the pericardial reflexion. In many cases secondary to inflammatory causes, the pericardial line was thickened. The radiological findings in our first patient fell within his
223
definition of pneumopericardium. We believe that in our first patient the air entered the pericardial cavity from a small rupture of the anterior wall of the left main bronchus. At bronchoscopy a contusion was seen where the bronchus lay in close anatomical contact with the transverse sinus of the pericardium. An alternative mechanism has been described by Rosen, Vaudagna, and Jamplis (1963). They suggested that alveoli could rupture following a sudden rise in expiratory pressure. The air thus released passed through the interstitial tissues of the lung and was guided along the sheaths of the pulmonary vascular system to the mediastinum, the neck, the retroperitoneal spaces, and rarely to the pericardial sac itself. Rosen and his colleagues have demonstrated this continuous pathway by anatomical dissection. Traumatic aortic rupture has been very well documented as an entity related to the increasing incidence of high velocity road traffic accidents. Strassman (1947) found 72 cases of traumatic aortic rupture in a consecutive series of 7000 autopsies, an incidence of 1 per cent, yet no mention is made of coexisting pneumopericardium in this series. Seventy per cent of these occurred in patients killed in road traffic accidents. The injury is classically described as being a deceleration phenomenon, occurring at the junction of the relatively fixed aortic arch and the mobile descending thoracic aorta, just below the root of the left subclavian artery. In 55 per cent of Strassman’s (1947) series, rupture occurred at this point. To develop the extremely high intraluminal pressure of 1000-3000 mm. Hg which is necessary to rupture the aorta, a deceleration from 120 to 0 m.p.h. in 0.1-0.2 sec. is required experimentally. It is possible that twisting and shearing forces are of importance, and as a result much lower pressures may cause aortic rupture. In complete aortic rupture, death is instantaneous, but Parmley, Mattingley, Mannion, and Jahnke (1958) stated that lo-20 per cent of patients survived to reach hospital. This percentage represents those patients with incomplete tears, usually sparing the adventitial layer of the aorta. Delayed death is also well documented by Parmley and others (1958), who described 8 patients with complete transection who survived for at least 5 days. Steinberg quoted a patient where delayed fatal rupture occurred 20 years after the original injury (Steinberg, 1957). Our first case emphasizes the need for constant alertness for the presence of traumatic aortic rupture. Aortography should be performed in all cases in which the diagnosis is suspect,irrespective
Injury:
224 of the apparently stable clinical condition of the patient. Blake, Inmon, and Spencer (1960) recommended the use of an intravenous method or a right heart catheter technique and suggested that retrograde aortography might precipitate aortic rupture. In our patient, the only sign of aortic rupture when he first presented was a slight widening of the mediastinum. His peripheral pulses were normal. Aortography was carried out because of the development of symptoms which, in retrospect, were probably not due to any extension of the rupture. Slaney, Ashton, and Abrams (1966) stressed that cardiac damage may be present in 40 per cent of patients and that operation should not be performed, if possible, until a normal blood-pressure and normal electrocardiograph have been obtained. Our patient developed cardiac arrest which necessitated prolonged internal cardiac massage before normal rhythm could be restored. This was probably due to myocardial damage and reinforces their warning.
Acknowledgements We would like to thank Mr. J. C. Scott, under whose care these two patients were admitted, for his help. We would also like to thank the Department of Medical Illustrations, Radcliffe Infirmary, for the photographs, and Miss Jane Wrixon for typing the manuscript. Requests
for reprints
should be addressed to:-A.
Cargill,
Esq.,
the British Journal of Accident Surgery Vol. ~/NO. 3
REFERENCES BLAKE, H. A., INMON, T. W., and SPENCER,F. C. (1960), ‘ Emergency use of antegrade aortography in diagnosis of acute aortic rupture ‘, Ann. Surg., 152, 954. BRICHTEAU,J. (1844), Arch g&. M&d., series 4, 4, 334. CIMMINO, V. (1967), ‘ Some radio-diagnostic notes on pneumomediastinum, pneumothorax, and pneumopericardium ‘, Vu med. Mon., 94,205. GUNNING, A. J. (1972), ‘ A disposable one-piece left ventriculo-aortic bypass cannula ‘, Thorax, 27, 371. OPPENHEIMER, C. (I 924), ‘ Therapeutic pneumopericardium in pericarditis with effusion ‘, J. Am. med. Ass., 82, 1685. PARMLEY, L. F., MATTINGLEY, T. W., MANNION, W. C.. and JAHNKE,E. J. (1958). ‘ Nonpenetratina traumatic injury of the aorta”: Circ&rion, 17; 1086. ROSEN, A., VAUDAGNA, J., and JAMPLIS, R. (1963), ‘ Spontaneous pneumopericardium ‘, Am. Rev. resp. Dis., 87, 764. SHACKLEFORD, R. T. (I 93 l), ‘ Hydropneumopericardium ‘, J. Am. med. Ass., 96, 187. SLANEY, G., ASHTON, F., and ABRAMS, L. D. (1966), ‘ Traumatic rupture of the aorta ‘, Br. J. Surg., 53, 361. STEINBERG,I. (1957), ‘ Chronic traumatic aneurysm of the thoracic aorta ‘, New Engl. J. Med., 257, 913. STRASSMAN, N. G. (1947), ‘ Traumatic rupture of aorta ‘, Am. Heart J., 33, 508. WENKEBACH,A. (1910), Z. klin. Med., 71, 402.
F.R.C.S.(Edin.),
Radcliffe
Infirmary,
Oxford
OX2
6HE