Paraplegia 17
(1979-80) 294-297
PARAPLEGIA FOLLOWING CARDIOVASCULAR SURGERY By NORVAL WATSON
Spinal Injuries Unit, Lodge Moor Hospital, Sheffield, England Key words: Paraplegia; Aortic surgery; Anterior horn damage.
PARAPLEGIA is an uncommon but very serious complication of surgery of the heart and aorta. In 1910 Carrell reported the occurrence of paraplegia after the aorta was clamped for more than 15 minutes during experimental surgery. In 1948 Bing reported a case of human paraplegia following resection of a coarctation of the aorta. In 1951 Lam and Aram reported a reversible paraplegia after resection of In 1952 Crafoord reported paraplegia an aneurysm of the descending aorta. after clamping of the aorta for the repair of a patent ductus arteriosus. In 1969 Borst and Lembcke published a comprehensive article on the subject of spinal cord damage following surgery on the descending aorta and it is from their paper that most of my information has come.
Incidence There is a definite relationship between the occurrence of paraplegia and the underlying pathology. In coarctation of the aorta the risk of paraplegia was 'reported' at between I and 5 per cent. The higher figure was reported following an operation which is no longer performed, an anastomosis between the left subclavian artery and the distal aorta. In non-stenotic disease of the descending aorta the incidence of spinal 'cord' damage was higher at 5-80 per cent. In resection of an aneurysm under normal temperatures and without other measures, clamping of the aorta will cause para plegia in a majority of cases. If preventive measures were taken during resection of the aneurysm, the danger of paraplegia could be reduced almost to zero. In cases of dissecting aneurysm, especially in acute cases, there was a risk of paraplegia of 5-10 per cent, even when hypothermia or bypass were used. In patent ductus arteriosus when the aorta was clamped for 18-45 minutes, 15 per cent of cases developed paraplegia.
Pathology Borst reported the pathological changes in a case of coarctation who developed paraplegia after surgery and subsequently died. The spinal cord was normal down to the 12th dorsal segment. In the 1st lumbar segment and below, the anterior horn cells showed complete degeneration. The posterior horns and the white matter were unaffected. The changes were most marked in the middle of the lumbar and sacral segments. This is surprising in view of the anatomy of the blood supply to the spinal
294
PAPERS READ AT THE ANNUAL SCIENTIFIC MEETING 1978
295
cord. We all know that the upper dorsal area of the cord appears to be the water shed in the blood supply to the cord and is only supplied with blood from above and below in the last instance. We might expect that any spinal cord infarction would be maximal in the upper dorsal area but the clinical picture does not sup port this assumption. In paraplegia following aortic surgery, the level of the lesion is usually in the lumbar and sacral segments and this will be confirmed by my own clinical cases.
Patho -physiology According to Borst, paraplegia can occur in two ways. I. The blood supply to a segmental end-artery can be cut off by the fact that the area of aorta resected includes the feeding branches. 2. The blood supply to the spinal arteries distal to the clamping can be diminished by that clamping. Experiments in dogs have shown that the first way is the less common cause of spinal cord damage. In the second way clamping of the aorta causes a rise of blood pressure proximally, and a severe drop of blood pressure distally, to the clamped area. This low pressure drops further the more distally the aorta is clamped. The risk of paraplegia is increased when other factors, e.g. blood loss, anaesthesia, further lower the aortic pressures. In dogs clamping of the aorta just above the diaphragm almost always causes paraplegia. Two pathways exist for the development of a collateral circulation to the lumbar and sacral cord in aortic surgery: (a) from the subclavian arteries, via the cervical and thoracic arteries to the intercostal arteries distal to the clamping and then to the distal part of the aorta, and (b) anastomosis via the spinal arteries. Experiments in dogs have shown that the first pathway is much more satis factory than the second pathway. In coarctation paraplegia is common when the left subclavian artery is clamped. The occlusion of a pair of intercostal arteries by the resection of a coarctation at that level commonly does not result in paraplegia. There is a higher risk in a minimal stenotic coarctation as the collateral circulation is less well developed. The existence of a patent ductus arteriosus in addition to a coarctation increases the risk of paraplegia. In non-stenotic lesions when the aorta is clamped, paraplegia can be expected but it can be diminished by the use of one or other preventive measures, e.g. bypass. The satisfactory results from the use of bypass in maintaining blood supply to the distal aorta indicates the importance of the Adamkiewicz artery. Besides surgical techniques, other factors are important in the development of neurological damage: I. duration of clamping, 2. blood pressure and 3. body temperature. Paraplegia is liable to occur if clamping lasts more than 20 minutes. Longer periods of clamping can occur without the development of paraplegia and this is considered to be due to a resting circulation in the distal part of the body. This resting circulation depends, however, on the degree of hypotension from blood loss or anaesthesia. Hypothermia reduces the incidence of neurological damage. Clinical measures to prevent paraplegia therefore include: (a) duration of clamping as short as possible, and (b) prevention of hypotension by reducing blood loss and giving transfusion. Any essential period of hypotension should be kept to a minimum. In coarctation the minimal stenotic type is the most dangerous as far as
296
PARAPLEGIA
paraplegia is concerned due to the poorly developed collateral circulation. If the distal aortic pressure is less than 60 nun Hg, bypass is indicated. In aneurysm as there is no collateral circulation, bypass is indicated. The danger is less in the fusiform chronic aneurysm than in the acute dissecting aneurysm. I now present details of four cases of paraplegia following surgical procedures on the aorta, admitted to Lodge Moor in the last 2 years. Case A was a young man at college who was found to have high blood pressure and a cardiac murmur at routine medical examination. He had suffered from headache and epistaxis previously but played games normally. Investigations revealed a coarctation of the aorta. At operation the coarctation was unusual and great technical difficulty was experienced in the repair by graft, and bleeding was troublesome and difficult to control. Postoperatively he was found to have a paraplegia which was virtually complete below DI2 as far as the motor function was concerned, except for a flicker of the right quads but he had good posterior column sensory sparing to touch and posture. One year later he still had weak movement in the right quads only and the same sparing of touch and postural sensation with a good straining type of bladder. He was very mobile in calipers and crutches, did not use a chair in college but still required treatment for persistent hypertension. Bypass was not used in this operation as the pressures were measured throughout and appeared adequate. Case B was a very fit man of 40 years who was found to have an aneurysm on routine chest X-ray examination. Fifteen years previously he had had a chest injury in a motor cycle accident and it was thought that he had developed a traumatic aneurysm. He had a resection of his aneurysm and a Dacron graft replacement, using a Gott aortic shunt. On recovery from the operation he was found to have a partial paraplegia below D8 level with power grade 1-2 in the legs in most groups but with a complete paralysis of the adductors, hamstrings and dorsiflexors of the feet. He had loss of appreciation of pain and temperature over the lower dorsal and lumbar segments with normal sacral sensa tion and no reflexes. Six months later the power in those muscles which were weak had improved to power 3 but there was no recovery at all in those groups which were paralysed post operatively. He was able to ambulate with long calipers and crutches and regained an almost normal bladder action. Case Cwas a young girl of lOYears who underwent operation for a Fallot's Tetralogy. Bypass was used intermittently during the operation as the pressures indicated. Para plegia was noted after the operation and when she was transferred to Lodge Moor a month later she had a complete flaccid motor paralysis below D8 with loss of pain and temperature below that level but with good sparing of touch and posture appreciation at all levels. One year later she had regained weak power grade 2 in both hip flexors and left foot only but was otherwise still completely paralysed. Sensation to pain and temperature had improved on the legs. She could walk slowly in calipers and crutches and had regained a good straining type of bladder action. Case D was a young girl of 12 years with a coarctation of the aorta who had an operation to correct the anomaly. Bypass was not used as there appeared to be good collateral circulation in the internal mammary arteries and the pressures appeared satis factory. There was, however, some postoperative bleeding and the chest had to be re opened the same evening. Paraplegia was noted the next day and worsened on the following day, but then some recovery occurred and the residual deficit consisted of paralysis of the adductors, quads and hamstrings but with good power otherwise in the hips, feet and buttocks with almost normal sensation and good bladder action.
Our four cases demonstrate that the maximum damage occurred to the anterior horn cells of the lumbar segments of the cord and less often to the sacral
PAPERS READ AT THE ANNUAL SCIENTIFIC MEETING, 1978
297
segments. The spino-thalamic tracts carrying pain and temperature were damaged occasionally and to a varying degree. The posterior column sensory functions of touch and postural appreciation were never affected and always spared. Satis factory bladder function was usually regained. All cases were able to ambulate well in calipers and crutches, even those with very minimal motor recovery, in dicating the importance of the preservation of posterior column functions in ambulation. The highest level of recorded deficit was D8 but this was a partial sensory impairment only which later recovered and there was no residual neuro logical deficit above DI2. Our small group of cases therefore supports and confirms the findings of Borst and Lembcke that neurological damage after operations on the aorta are confined to the anterior parts of the lumbar and sacral segments of the cord, particularly the anterior horn cells of the lumbar segments. Three of these cases, the two coarctations and the aneurysm occurred in the last 2 years, one coming from each of the three major cardio-thoracic surgical centres in the area serving a population of over five million people, so that the incidence of neurological damage following aortic surgery is very low indeed. Acknowledgement. I am indebted to Dr C. Spreuwers of Leuven, Belgium, at present working in this Unit, for assistance with translations.
SUMMARY A study of recent cases of spinal cord damage following aortic surgery con firmed previous reports that damage was confined to the anterior horn cells of the lumbar and sacral segments of the cord, with preservation of posterior column function and satisfactory bladder control.
RESUME L'etude de nos cas recentes de paraplegie apres chirurgie de l'aorte thoracique con firme les publications precedentes. La lesion pathologique est localisee surtout dans les cornes anterieures de Ie moelle lumbaire et sacrale. Les colonnes posterieures sont pre servees et Ie controle de la fonction vesicale est satisfaissant.
ZUSAMMENFASSUNG Die klinischen Beobachtungen in unseren Flillen von Riickenmarksschaden als Folge operativer Eingriffe an der thorakalen Aorta descendens, bestatigt die Erfahrung anderen Autoren. Die Riickenmarkschadigung betrifft stets die lumbosakrale Zone und beson derns die Ganglienzellen der Vorderhorner. Die Hinterstrange bleiben weitgehend intakt und es besteht eine gute Kontrolle der Blasenfunktion.
REFERENCES BING et al.
(1948).
The surgical treatment and physiopathology of coarctation of aorta.
Ann. Surg., 128, 803. BORST and LEMBCKE (1969). Spinal cord damage. Aerzttl Forsch., 23, 285-299. CARRELL, A. (1910). Report on the experimental surgery of the thoracic aorta and heart. Ann. Surg., 52, 83. LAM and ARAM (1951). Resection of descending thoracic aorta for aneurysm. Ann. Surg.,
134, 243·
17/3-C
(1979-80) 294-297
PARAPLEGIA FOLLOWING CARDIOVASCULAR SURGERY By NORVAL WATSON
Spinal Injuries Unit, Lodge Moor Hospital, Sheffield, England Key words: Paraplegia; Aortic surgery; Anterior horn damage.
PARAPLEGIA is an uncommon but very serious complication of surgery of the heart and aorta. In 1910 Carrell reported the occurrence of paraplegia after the aorta was clamped for more than 15 minutes during experimental surgery. In 1948 Bing reported a case of human paraplegia following resection of a coarctation of the aorta. In 1951 Lam and Aram reported a reversible paraplegia after resection of In 1952 Crafoord reported paraplegia an aneurysm of the descending aorta. after clamping of the aorta for the repair of a patent ductus arteriosus. In 1969 Borst and Lembcke published a comprehensive article on the subject of spinal cord damage following surgery on the descending aorta and it is from their paper that most of my information has come.
Incidence There is a definite relationship between the occurrence of paraplegia and the underlying pathology. In coarctation of the aorta the risk of paraplegia was 'reported' at between I and 5 per cent. The higher figure was reported following an operation which is no longer performed, an anastomosis between the left subclavian artery and the distal aorta. In non-stenotic disease of the descending aorta the incidence of spinal 'cord' damage was higher at 5-80 per cent. In resection of an aneurysm under normal temperatures and without other measures, clamping of the aorta will cause para plegia in a majority of cases. If preventive measures were taken during resection of the aneurysm, the danger of paraplegia could be reduced almost to zero. In cases of dissecting aneurysm, especially in acute cases, there was a risk of paraplegia of 5-10 per cent, even when hypothermia or bypass were used. In patent ductus arteriosus when the aorta was clamped for 18-45 minutes, 15 per cent of cases developed paraplegia.
Pathology Borst reported the pathological changes in a case of coarctation who developed paraplegia after surgery and subsequently died. The spinal cord was normal down to the 12th dorsal segment. In the 1st lumbar segment and below, the anterior horn cells showed complete degeneration. The posterior horns and the white matter were unaffected. The changes were most marked in the middle of the lumbar and sacral segments. This is surprising in view of the anatomy of the blood supply to the spinal
294
PAPERS READ AT THE ANNUAL SCIENTIFIC MEETING 1978
295
cord. We all know that the upper dorsal area of the cord appears to be the water shed in the blood supply to the cord and is only supplied with blood from above and below in the last instance. We might expect that any spinal cord infarction would be maximal in the upper dorsal area but the clinical picture does not sup port this assumption. In paraplegia following aortic surgery, the level of the lesion is usually in the lumbar and sacral segments and this will be confirmed by my own clinical cases.
Patho -physiology According to Borst, paraplegia can occur in two ways. I. The blood supply to a segmental end-artery can be cut off by the fact that the area of aorta resected includes the feeding branches. 2. The blood supply to the spinal arteries distal to the clamping can be diminished by that clamping. Experiments in dogs have shown that the first way is the less common cause of spinal cord damage. In the second way clamping of the aorta causes a rise of blood pressure proximally, and a severe drop of blood pressure distally, to the clamped area. This low pressure drops further the more distally the aorta is clamped. The risk of paraplegia is increased when other factors, e.g. blood loss, anaesthesia, further lower the aortic pressures. In dogs clamping of the aorta just above the diaphragm almost always causes paraplegia. Two pathways exist for the development of a collateral circulation to the lumbar and sacral cord in aortic surgery: (a) from the subclavian arteries, via the cervical and thoracic arteries to the intercostal arteries distal to the clamping and then to the distal part of the aorta, and (b) anastomosis via the spinal arteries. Experiments in dogs have shown that the first pathway is much more satis factory than the second pathway. In coarctation paraplegia is common when the left subclavian artery is clamped. The occlusion of a pair of intercostal arteries by the resection of a coarctation at that level commonly does not result in paraplegia. There is a higher risk in a minimal stenotic coarctation as the collateral circulation is less well developed. The existence of a patent ductus arteriosus in addition to a coarctation increases the risk of paraplegia. In non-stenotic lesions when the aorta is clamped, paraplegia can be expected but it can be diminished by the use of one or other preventive measures, e.g. bypass. The satisfactory results from the use of bypass in maintaining blood supply to the distal aorta indicates the importance of the Adamkiewicz artery. Besides surgical techniques, other factors are important in the development of neurological damage: I. duration of clamping, 2. blood pressure and 3. body temperature. Paraplegia is liable to occur if clamping lasts more than 20 minutes. Longer periods of clamping can occur without the development of paraplegia and this is considered to be due to a resting circulation in the distal part of the body. This resting circulation depends, however, on the degree of hypotension from blood loss or anaesthesia. Hypothermia reduces the incidence of neurological damage. Clinical measures to prevent paraplegia therefore include: (a) duration of clamping as short as possible, and (b) prevention of hypotension by reducing blood loss and giving transfusion. Any essential period of hypotension should be kept to a minimum. In coarctation the minimal stenotic type is the most dangerous as far as
296
PARAPLEGIA
paraplegia is concerned due to the poorly developed collateral circulation. If the distal aortic pressure is less than 60 nun Hg, bypass is indicated. In aneurysm as there is no collateral circulation, bypass is indicated. The danger is less in the fusiform chronic aneurysm than in the acute dissecting aneurysm. I now present details of four cases of paraplegia following surgical procedures on the aorta, admitted to Lodge Moor in the last 2 years. Case A was a young man at college who was found to have high blood pressure and a cardiac murmur at routine medical examination. He had suffered from headache and epistaxis previously but played games normally. Investigations revealed a coarctation of the aorta. At operation the coarctation was unusual and great technical difficulty was experienced in the repair by graft, and bleeding was troublesome and difficult to control. Postoperatively he was found to have a paraplegia which was virtually complete below DI2 as far as the motor function was concerned, except for a flicker of the right quads but he had good posterior column sensory sparing to touch and posture. One year later he still had weak movement in the right quads only and the same sparing of touch and postural sensation with a good straining type of bladder. He was very mobile in calipers and crutches, did not use a chair in college but still required treatment for persistent hypertension. Bypass was not used in this operation as the pressures were measured throughout and appeared adequate. Case B was a very fit man of 40 years who was found to have an aneurysm on routine chest X-ray examination. Fifteen years previously he had had a chest injury in a motor cycle accident and it was thought that he had developed a traumatic aneurysm. He had a resection of his aneurysm and a Dacron graft replacement, using a Gott aortic shunt. On recovery from the operation he was found to have a partial paraplegia below D8 level with power grade 1-2 in the legs in most groups but with a complete paralysis of the adductors, hamstrings and dorsiflexors of the feet. He had loss of appreciation of pain and temperature over the lower dorsal and lumbar segments with normal sacral sensa tion and no reflexes. Six months later the power in those muscles which were weak had improved to power 3 but there was no recovery at all in those groups which were paralysed post operatively. He was able to ambulate with long calipers and crutches and regained an almost normal bladder action. Case Cwas a young girl of lOYears who underwent operation for a Fallot's Tetralogy. Bypass was used intermittently during the operation as the pressures indicated. Para plegia was noted after the operation and when she was transferred to Lodge Moor a month later she had a complete flaccid motor paralysis below D8 with loss of pain and temperature below that level but with good sparing of touch and posture appreciation at all levels. One year later she had regained weak power grade 2 in both hip flexors and left foot only but was otherwise still completely paralysed. Sensation to pain and temperature had improved on the legs. She could walk slowly in calipers and crutches and had regained a good straining type of bladder action. Case D was a young girl of 12 years with a coarctation of the aorta who had an operation to correct the anomaly. Bypass was not used as there appeared to be good collateral circulation in the internal mammary arteries and the pressures appeared satis factory. There was, however, some postoperative bleeding and the chest had to be re opened the same evening. Paraplegia was noted the next day and worsened on the following day, but then some recovery occurred and the residual deficit consisted of paralysis of the adductors, quads and hamstrings but with good power otherwise in the hips, feet and buttocks with almost normal sensation and good bladder action.
Our four cases demonstrate that the maximum damage occurred to the anterior horn cells of the lumbar segments of the cord and less often to the sacral
PAPERS READ AT THE ANNUAL SCIENTIFIC MEETING, 1978
297
segments. The spino-thalamic tracts carrying pain and temperature were damaged occasionally and to a varying degree. The posterior column sensory functions of touch and postural appreciation were never affected and always spared. Satis factory bladder function was usually regained. All cases were able to ambulate well in calipers and crutches, even those with very minimal motor recovery, in dicating the importance of the preservation of posterior column functions in ambulation. The highest level of recorded deficit was D8 but this was a partial sensory impairment only which later recovered and there was no residual neuro logical deficit above DI2. Our small group of cases therefore supports and confirms the findings of Borst and Lembcke that neurological damage after operations on the aorta are confined to the anterior parts of the lumbar and sacral segments of the cord, particularly the anterior horn cells of the lumbar segments. Three of these cases, the two coarctations and the aneurysm occurred in the last 2 years, one coming from each of the three major cardio-thoracic surgical centres in the area serving a population of over five million people, so that the incidence of neurological damage following aortic surgery is very low indeed. Acknowledgement. I am indebted to Dr C. Spreuwers of Leuven, Belgium, at present working in this Unit, for assistance with translations.
SUMMARY A study of recent cases of spinal cord damage following aortic surgery con firmed previous reports that damage was confined to the anterior horn cells of the lumbar and sacral segments of the cord, with preservation of posterior column function and satisfactory bladder control.
RESUME L'etude de nos cas recentes de paraplegie apres chirurgie de l'aorte thoracique con firme les publications precedentes. La lesion pathologique est localisee surtout dans les cornes anterieures de Ie moelle lumbaire et sacrale. Les colonnes posterieures sont pre servees et Ie controle de la fonction vesicale est satisfaissant.
ZUSAMMENFASSUNG Die klinischen Beobachtungen in unseren Flillen von Riickenmarksschaden als Folge operativer Eingriffe an der thorakalen Aorta descendens, bestatigt die Erfahrung anderen Autoren. Die Riickenmarkschadigung betrifft stets die lumbosakrale Zone und beson derns die Ganglienzellen der Vorderhorner. Die Hinterstrange bleiben weitgehend intakt und es besteht eine gute Kontrolle der Blasenfunktion.
REFERENCES BING et al.
(1948).
The surgical treatment and physiopathology of coarctation of aorta.
Ann. Surg., 128, 803. BORST and LEMBCKE (1969). Spinal cord damage. Aerzttl Forsch., 23, 285-299. CARRELL, A. (1910). Report on the experimental surgery of the thoracic aorta and heart. Ann. Surg., 52, 83. LAM and ARAM (1951). Resection of descending thoracic aorta for aneurysm. Ann. Surg.,
134, 243·
17/3-C
