Subdural Hematoma Following Open-Heart Operations Henry F. Krous, M.D., Lore Tenckhoff, B.M., B.Ch., Nevenka S. Gould, M.D., and Stanley J. Stamm, M.D. ABSTRACT Six patients who died following open-heart operations were found at postmortem examination to have acute subdural hematomas. On the basis of the clinical and postmortem findings, two factors in the pathogenesisof the hemorrhage are postulated. In the presence of intraoperative heparin administration, significant hematoma formation may result from damage to the bridging dural veins from minor, inadvertent head trauma or alterations in cerebral volume from fluid shifts. Manipulation of the head in patients who have been given heparin should be undertaken with extreme care, particularly in infants. In any patient with neurological dysfunction who has also had an open-heart operation, the possibility of an expanding subdural hematoma must be considered.
A
variety of neurological complications may occur following an openheart operation, especially when extracorporeal circulation is utilized. A number of factors have been implicated, including embolic phenomena [5,6, 17,20-221, hypoperfusion [151, hypotension [151, and carotid artery hyperperfusion [ 193. The present report suggests that subdural hematomas may also occur during operation or in the immediate postoperative period, and that such hematomas may be an additional cause for immediate or subsequent neurological complications. Six patients who died following open-heart operations were found at postmortem examination to have acute subdural hematomas. On the basis of the clinical and postmortem findings it seems likely that two factors render these patients particularly vulnerable to subdural hemorrhage. Minor and inadvertent head trauma or alterations in cerebral volume from fluid shifts may cause tearing of the dural bridging veins. In the presence of intraoperative heparin administration, even small tears may result in significant hematoma formation. Although such hematomas may be small, as in 4 of our 6 patients, the formation of a chronic subdural membrane might result in fluid absorption and expansion of the hematoma, thus leading to the late onset of neurological symptoms.
Case Reports Pertinent data on the 6 patients are shown in the Table, and some additional information on individual patients is summarized below. Preexisting neurological dysfunction was present in 1 individual (Patient 1). From the Departments of Pathology and Cardiology, Children’s Orthopedic Hospital and Medical Center, Seattle, Wash. Accepted for publication July 29, 1974. Address reprint requests to Dr. Tenckhoff, Children’s Orthopedic Hospital and Medical Center, 4800 Sand Point Way N.E., Seattle, Wash. 98105. VOL. 19, NO. 3, MARCH, 1975
269
3. Boy; 3 yr 10 mo
2. Boy; 7 yr
1. Boy; 2 yr 5 mo
Age
sex, &
Patient, Pump Time
Transposition Mustard 4 hr of great baffle; arteries; imbricasubpulmonic tion of stenosis; ventricuaneurysm of lar septal membranous aneurysm; ventricular resection of left septum ventricu(preop. lar outflow hematocrit tract 65%) Tetralogy of Pericar3 hr Fallot dial patch 19 min closure of (preop. hematocrit, VSD; resection 43%) of right ventricular outflow tract Pulmonary Tetralogy of 2 hr valve comFallot 50 min missurotomy; (Pl-eOP. hematocrit, right ventricular 43%) outflow tract resection; pericardial patch closure of VSD; return to bypass for pericardial patch widening of outflow tract
Cardiac Defect
Operative Procedure
None preop. or postop.
None preop. or postop.
None preop.; immediate postop. coagulopathy corrected by multiple transfusions
Coagulopathy
No
Yes
Yes
Protamine Reversal
CASE REPORTS
IntraOP. death
4 days
2 days
Survival
Subgaleal Hematoma
No
No
Bilateral occipital, 50 ml total
Bilateral cerebral, total 60 ml; posterior fossa, 25 ml
?
?
Left parietal, 15ml
Other Findings
Moderate cerebral edema; petechiae of gastrointestinal mucosa
Superior cerebellar subarachnoid hemorrhage; mild edema
Bilateral cystic cerebral infarctions
Postmortem Findings Subdural Hematoma
Hemiplegia, Left generalized parietal, seizures 1OX 1Ocm controlled with medication
Preop. Neurological Dysfunction
6. Girl; 5 yr 2 mo
5. Boy; 5 yr 3 mo
4. Boy; 10 mo
Resection of left ventricular outflow tract
10 min
1 hr
Atrial septal Direct defect, secun- dosure; dumtype reopera(preop. tive hematocrit, closure 30%) with pencardial patch grafts
1 hr
endocardial fibroelastosis, extensive (preop. hematocrit, 30%) Ventricular Pericardial 2 hr septal defect; patch do20 min previous pulsure of VSD; monary artery removal of banding (at age pulmonary 6 mo) artery band; (PWOP. insertion of hematocrit, pulmonary 30%) artery graft
Sis;
Valvular & subvalvular aortic steno-
None preop. or postop.
None preop. or postop.
None preop. or postop.
Yes
Yes
No
1 hr
3 days
IntraOP. death
No
No
No
Bilateral, 10 ml each
Right frontal,
3X4cm
Left parietooccipital, 6 ml
Right parasagittal, 10 ml
?
?
pulmonary hemorrhage
Diffuse
Left parietooccipital submchnoid hemorrhage; microscopic encephalomalacia in cerebrum and e r e bellum; seroSal8c intestinal mucd petechiae; mild bilateral adrenal hemorrhage
Mild edema
KROUS ET AL. Cardiopulmonary bypass was used in all 6 patients; for 4 of the 6 (Patients 1, 3, 4, and 5 ) hypothermia was employed as well. All patients were screened for coagulopathies and had normal values preoperatively. Heparin was routinely given intraoperatively to all 6 patients, with protamine reversal being carried out in all except the 2 patients who died intraoperatively (Patients 3 and 4).Massive postoperative bleeding occurred in 1 patient (Patient 1). Intraoperative serum electrolyte monitoring reflected a stable electrolyte status. PATIENT 1
A 29-month-old boy with transposition of the great arteries and an intact ventricular septum required a balloon atrial septostomy at 2 days of age. He then did well until the age of 13 months, at which time he developed a left hemiplegia and seizures, probably on the basis of a cerebral thrombosis. With anticonvulsant therapy the seizureswere reduced to one a day. By the age of 29 months there was evidence of progressive subpulmonic stenosis; at operation this was found to be due to two abnormalities, a displacement of the anterior papillary muscle into the left ventricular outflow tract and an aneurysmal bulging of the membranous septum into the outflow area. These obstructions were relieved through operation, and a Mustard atrial baffle was inserted. A severe hemorrhagic diathesis developed immediately after the operation, followed by ventricular arrhythmia, a falling cardiac output, and uremia (requiring peritoneal dialysis). The patient died two days postoperatively. PATIENT 2
An Indian boy with tetralogy of Fallot was sufficiently handicapped by the age of 7 years to require operative correction. The surgical procedure was prolonged both by a large coronary artery crossing the right ventricular outflow tract, which limited the ventriculotomy and impaired visualization of the ventricular septa1defect, and by a highly vascular infundibular myocardium that necessitated careful hemostasis during resection. The postoperative course was complicated by low cardiac output with pulmonary edema and a pseudomonas tracheobronchitis. The latter was unresponsive to antibiotic therapy, and the patient died on the fourth postoperative day. PATIENT 3
An open-heart operation was undertaken in a boy 3 years 10 months of age who had tetralogy of Fallot because of increasingly frequent cyanotic spells and a rising hematocrit. At operation right ventricular pressure could be reduced only after extensive widening of the outflow tract. At the end of the operation the left ventricle was unable to maintain an adequate cardiac output and the patient died. PATIENT 4
Valvular and subvalvular aortic stenosis were demonstrated to be present and thought to be responsible for the cardiac failure already evident at 4 months of age in this white male infant. Only with difficulty was the child managed on a medical regimen, including propranolol and diuretics, over the next six months. Re-
272
THE ANNALS OF THORACIC SURGERY
Subdural Hematoma
catheterization prior to operation at 10 months of age again demonstrated valvular and subvalvular aortic stenosis. The left ventricle, although thick-walled, contracted well, yielding no clue to the presence of the extensive inner mantle of endocardial fibroelastosis found at operation and confirmed at postmortem examination. The endocardial fibroelastosis undoubtedly was the major factor responsible for the left ventricle failure leading to death immediately after operation. PATIENT 5
A white boy 5 years 3 months old with ventricular septal defect had undergone pulmonary artery banding at 6 months of age because of chronic cardiac failure. Shunt reversal was noted at 4 years. At operation the ventricular septal defect involved the membranous septum but extended unusually far posteriorly. In addition the pulmonary artery band was firmly adherent, necessitating resection and insertion of a graft. Immediately after operation his course was satisfactory. Subsequently he developed cardiac arrhythmia, a low cardiac output, and oliguria, the last requiring peritoneal dialysis. The patient died three days postoperatively. PATIENT 6
This patient was known on clinical grounds to have a secundum type of atrial defect. Cardiac catheterization at the age of 5 years 2 months demonstrated a four-to-one left-to-right shunt at the atrial level without pulmonary hypertension. At operation the atrial septal defect was first closed by direct suturing since the size of the left atrium seemed adequate. However, immediately following operation, progressive pulmonary edema and hypoxia with rapid clinical deterioration necessitated reoperation; at this time the left atrium was seen and felt to be tense. The atrial septal defect was reopened and then repaired with a pericardial patch. Although cardiac output was good immediately after operation, the pulmonary edema and hypoxia did not resolve, leading to cardiac arrhythmia and multiple cardiac arrests. Death occurred one hour postoperatively.
Comment The data on the 6 patients discussed here indicate that subdural hematomas may occur during or immediately after open-heart operations and should be considered in the differential diagnosis of both early and late neurological dysfunction. Classically, subdural hematomas result from tearing of the bridging veins between the dura and cerebral hemispheres, usually as a result of trauma 1 1,181. Subdural hematomas have been described in hypernatremic dehydration with brain shrinkage [12, 131, in patients being given heparin after a myocardial infarction [30], in elderly persons with cerebral atrophy and minor trauma [23], in hemophiliacs [25], and as a complication of hemodialysis from the administration of heparin and sudden fluid shifts [9, 271. In many of these, trivial, forgotten trauma has been implicated. On the basis of the clinical and postmortem findings two interacting factors are thought to be responsible for these subdural hematomas. Intraoperative
VOL. 19, NO. 3, MARCH, 1975
273
KROUS ET AL. administration of heparin renders these patients susceptible to abnormally extensive hemorrhage in the event of blood vessel damage. Such damage could result either from minor and inadvertent trauma or from fluctuations in cerebral volume as a result of fluid shifts. All 6 of our patients were given heparin intraoperatively. (All but the 2 who died intraoperatively had protamine reversal postoperatively.)In 2 children there was documented evidence of head trauma in the form of subgaleal hematomas. The postmortem examination reports for the remaining 4 made no mention of the presence or absence of subgaleal hematomas, but since their significance often is not recognized, they may have been overlooked. Further support for the contention that trauma and hypocoagulability may have acted synergistically in at least 1 instance is evidenced in Patient 6. In this patient a large secundum atrial septa1 defect was first closed by direct suture. Rapidly progressive pulmonary edema led to reoperation, at which time the surgeon noted a tense left atrium, suggesting that the chamber was too small to accommodate pulmonary venous return. The lungs may well have sustained the “trauma” of pulmonary venous hypertension which, in the presence of heparin, resulted in the diffuse, severe hemorrhage of the lungs found at postmortem examination. A subgaleal hematoma had likewise occurred in this patient, indicating head trauma. That the subgaleal, subdural, and pulmonary hemorrhages were not a reflection of widespread vascular damage or uncontrolled hemorrhage was confirmed by the absence of hemorrhage elsewhere in the body. Rapid fluid shifts with fluctuations in cerebral volume may lead to tearing of the dural bridging veins [9]. Patients developing subdural hematomas on this basis would be expected to show no evidence of head trauma such as subgaleal hematoma. It is unlikely that this mechanism played a major role in our patients’ problems, as electrolyte monitoring during open-heart operations showed no deviation from the normal other than mild hyponatremia. Two patients had peritoneal dialysis, which, in contrast to hemodialysis, has not been reported in association with subdural hematomas. Additional evidence that tearing of the bridging veins following heparin therapy can result in subdural hemorrhage comes from experimental studies [161. Seven dogs had silk suture placed around one dural bridging vein and carried to the outside. Two dogs were given heparin. On the third postoperative day the sutures were pulled out, tearing the bridging dural vein. The 2 dogs previously given heparin died of massive subdural and subarachnoid hemorrhages. Of the 5 animals not given heparin only 1 died of acute subdural hemorrhage; the rest remained well and active. Although the number of experimental animals is small, these findings do show that tearing of one dural bridging vein can be well tolerated under normal conditions but that in the presence of a hypocoagulable state massive hemorrhage does result. It is well documented that cerebral disorders may occur following open-heart operations as a result of either hypotension or cerebral embolism [5, 6, 15, 17, 20-221. In reviewing studies which correlate neuropathological changes and cerebral disorders [ l , 2, 4, 10, 15, 26, 28, 291, it was found that subdural hematomas were documented in only one series [31; 274
T H E ANNALS OF THORACIC SURGERY
Subdural Hematoma however, most of these reports were concerned primarily with microscopical changes within the brain substance. It seems likely that the true incidence of subdural hematomas following open-heart operations utilizing bypass has been underestimated. Of our 6 patients, 4 had small hematomas which presumably could be reabsorbed with no further neurological symptoms. However, small hematomas may at times persist, expand, and reach sufficient size to cause late neurological abnormalities, including seizures [7]. A subdural hematoma might cause noticeable constriction of a rapidly developing infant brain [24],which approximately doubles its size in the first five months of life and redoubles in the next three and one-half years [8]. The infant brain is more vulnerable to subdural hemorrhage than that of the older individual in other ways. Minimal trauma can more readily lead to tearing of the parasagittal bridging dural veins, since the supporting protective arachnoid granulations are not fully developed [ 141. Further, the soft, less myelinated infant brain is more readily subject to cerebral distortion from trauma, further contributing to damage of the dural veins through stretching. These factors assume increasing importance with the current emphasis on corrective cardiac operations in infancy which employ a combination of hypothermia and pump oxygenation and therefore, in most instances, the administration of heparin intraoperatively. They further underline the extreme care with which manipulation of the head should be carried out following heparin therapy, both during and immediately after open-heart operations, with particular care being exercised in the highly vulnerable infant age group. Finally, in any patient with a past history of open-heart operation who manifests neurological problems, the possibility of an expanding subdural hematoma must be kept in mind.
References 1 . Aguilar, M. J., Gerbode, F., and Hill, J. D. Neuropathologic complications of cardiac surgery. J Thorac Cardiouusc Surg 6 1 :676, 197 1 . 2. Bjork, V. O., and Hultquist, G. Brain damage in children after deep hypothermia for open-heart surgery. Thorax 15:284, 1960. 3. Brierley, J. B. Neuropathological findings in patients dying after open-heart surgery. Thorax 18:291, 1963. 4. Brierley, J. B. Brain damage complicating open-heart surgery: A neuropathological study of 46 patients. Proc R SOCMed 60:858, 1967. 5. Callaghan, J. C., Despres, J. P., and Benvenuto, R. Study of causes of 60 deaths following total cardiopulmonary bypass. J Thorac Cardiouusc Surg 42:489, 1961. 6. Clowes, G. H. A., Jr., Neville, W. E., Hopkins, A., Anjoice, J., and Simeone, F. A. Factors contributing to success or failure in use of pump oxygenator for complete bypass of heart and lung, experimental and clinical. Surgery 36:557, 1954. 7. Cole, M., and Spatz, E. Seizures in chronic subdural hematoma. N Engl J Med 265:628, 196 1 . 8. Coppelletta,J. M., and Wolbach, S. B. Body length and organ weights of infants and children. Am J Pathol 9:55, 1933. 9. del Greco, F., and Krumlousky, F. Subdural hematoma in the course of hemodialysis. Lancet 2: 1009, 1969. 10. Ehrenhaft, J. L., Claman, M. A., Layton, J. M., and Zimmerman, G. R. Cerebral complications of open-heart surgery: Further observations. J Thorac Cardiovusc Surg 41:503, 1961.
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KROUS ET AL. 11. Elvidge, A. R., and Jackson, R. J. Subdural hematoma and effusion in infants: Review of 55 cases. Am J Dis Child 78:635, 1949. 12. Fineberg, L. Pathogenesis of lesions in the nervous system in hypernatremic states: I. Clinical observations in infants. Pediatrics 23:40, 1959. 13. Fineberg, L. Hypernatremic dehydration. Adv Pediutr 16:325, 1969. 14. Ford, F. R. Diseases of the Neroous System in Infuncy, Childhood and Adolescence (3d ed). Springfield, Ill.: Thomas, 1952. Pp 994-999. 15. Gilman, S. Cerebral disorders after open heart operations. N Engl J Med 272:489, 1965. 16. Goodell, C. L., and Mealey, J., Jr. Pathogenesis of chronic subdural hematoma. Neurology 8:99, 1963. 17. Hill, J. D., Aguilar, M. J . ? Baranco, A., delanerolle, P., and Gerbode, F. Neuropathological manifestations of cardiac surgery. Ann Thoruc Surg 7:409, 1969. 18. Inglis, K. Subdural hemorrhages, cysts, and false membranes. Bruin 69:157, 1946. 19. Krous, H. F., Mansfield, P. B., and Sauvage, L. R. Carotid artery hyperfusion during open heart surgery. J Thoruc Curdiouasc Surg 66: 118, 1973. 20. Lindberg, D. A. B., Lucas, F. U., Sheagren, J., and Malm, J. R. Silicone embolization during clinical and experimental heart surgery employing bubble oxygenator. Am J Pathol 39:129, 1961. 2 1. Nichols, H. T., Morse, D. P., and Hirose, T. Coronary and other air embolism during open cardiac surgery: Prevention by use of gaseous carbon dioxide. Surgery 43:236, 1958. 22. Patrick. R. T., Kirklin, 1. W., and Theye. R. A. Effects of Extracorporeal Circulation on Brain. In J. A. Ga'rrott (Ed), Extracorporeal Circulation. Springfikld, Ill.: Thomas, 1958. P 518. 23. Perlmutter, F. Subdural hematoma in older patients. JAMA 176:212, 1961. 24. Rabe, E. F., Flynn, R. E., and Dodge, P. R. Subdural collectionsof fluid in infants and children. Neurology 18:559, 1968. 25. Silverstein, A. Intracranial bleeding in hemophilia. Arch Neurol 3: 141, 1960. 26. Stephens, J. W. Neurologic sequelae of congenital heart surgery. Arch Neurol7:450, 1962. 27. Talalla, A., Halbrook, H., Barbour, B. H., and Kurze, T. Subdural hematoma associated with long-term hemodialysis for chronic renal disease. JAMA 2 12:1847, 1970. 28. Terplan, K. L. Patterns of brain damage in infants and children with congenital heart disease. Am J DZS Child 125:175, 1973. 29. Tufo, H. M., Ostfeld, A. M., and Shekelle, R. Central nervous system dysfunction following open heart surgery. JAMA 212: 1333, 1970. 30. Wiener, L. M., and Nathanson, M. The relationship of subdural hematoma to anticoagulant therapy. Arch Neurol 6:282, 1962.
276
THE ANNALS OF THORACIC SURGERY
A
variety of neurological complications may occur following an openheart operation, especially when extracorporeal circulation is utilized. A number of factors have been implicated, including embolic phenomena [5,6, 17,20-221, hypoperfusion [151, hypotension [151, and carotid artery hyperperfusion [ 193. The present report suggests that subdural hematomas may also occur during operation or in the immediate postoperative period, and that such hematomas may be an additional cause for immediate or subsequent neurological complications. Six patients who died following open-heart operations were found at postmortem examination to have acute subdural hematomas. On the basis of the clinical and postmortem findings it seems likely that two factors render these patients particularly vulnerable to subdural hemorrhage. Minor and inadvertent head trauma or alterations in cerebral volume from fluid shifts may cause tearing of the dural bridging veins. In the presence of intraoperative heparin administration, even small tears may result in significant hematoma formation. Although such hematomas may be small, as in 4 of our 6 patients, the formation of a chronic subdural membrane might result in fluid absorption and expansion of the hematoma, thus leading to the late onset of neurological symptoms.
Case Reports Pertinent data on the 6 patients are shown in the Table, and some additional information on individual patients is summarized below. Preexisting neurological dysfunction was present in 1 individual (Patient 1). From the Departments of Pathology and Cardiology, Children’s Orthopedic Hospital and Medical Center, Seattle, Wash. Accepted for publication July 29, 1974. Address reprint requests to Dr. Tenckhoff, Children’s Orthopedic Hospital and Medical Center, 4800 Sand Point Way N.E., Seattle, Wash. 98105. VOL. 19, NO. 3, MARCH, 1975
269
3. Boy; 3 yr 10 mo
2. Boy; 7 yr
1. Boy; 2 yr 5 mo
Age
sex, &
Patient, Pump Time
Transposition Mustard 4 hr of great baffle; arteries; imbricasubpulmonic tion of stenosis; ventricuaneurysm of lar septal membranous aneurysm; ventricular resection of left septum ventricu(preop. lar outflow hematocrit tract 65%) Tetralogy of Pericar3 hr Fallot dial patch 19 min closure of (preop. hematocrit, VSD; resection 43%) of right ventricular outflow tract Pulmonary Tetralogy of 2 hr valve comFallot 50 min missurotomy; (Pl-eOP. hematocrit, right ventricular 43%) outflow tract resection; pericardial patch closure of VSD; return to bypass for pericardial patch widening of outflow tract
Cardiac Defect
Operative Procedure
None preop. or postop.
None preop. or postop.
None preop.; immediate postop. coagulopathy corrected by multiple transfusions
Coagulopathy
No
Yes
Yes
Protamine Reversal
CASE REPORTS
IntraOP. death
4 days
2 days
Survival
Subgaleal Hematoma
No
No
Bilateral occipital, 50 ml total
Bilateral cerebral, total 60 ml; posterior fossa, 25 ml
?
?
Left parietal, 15ml
Other Findings
Moderate cerebral edema; petechiae of gastrointestinal mucosa
Superior cerebellar subarachnoid hemorrhage; mild edema
Bilateral cystic cerebral infarctions
Postmortem Findings Subdural Hematoma
Hemiplegia, Left generalized parietal, seizures 1OX 1Ocm controlled with medication
Preop. Neurological Dysfunction
6. Girl; 5 yr 2 mo
5. Boy; 5 yr 3 mo
4. Boy; 10 mo
Resection of left ventricular outflow tract
10 min
1 hr
Atrial septal Direct defect, secun- dosure; dumtype reopera(preop. tive hematocrit, closure 30%) with pencardial patch grafts
1 hr
endocardial fibroelastosis, extensive (preop. hematocrit, 30%) Ventricular Pericardial 2 hr septal defect; patch do20 min previous pulsure of VSD; monary artery removal of banding (at age pulmonary 6 mo) artery band; (PWOP. insertion of hematocrit, pulmonary 30%) artery graft
Sis;
Valvular & subvalvular aortic steno-
None preop. or postop.
None preop. or postop.
None preop. or postop.
Yes
Yes
No
1 hr
3 days
IntraOP. death
No
No
No
Bilateral, 10 ml each
Right frontal,
3X4cm
Left parietooccipital, 6 ml
Right parasagittal, 10 ml
?
?
pulmonary hemorrhage
Diffuse
Left parietooccipital submchnoid hemorrhage; microscopic encephalomalacia in cerebrum and e r e bellum; seroSal8c intestinal mucd petechiae; mild bilateral adrenal hemorrhage
Mild edema
KROUS ET AL. Cardiopulmonary bypass was used in all 6 patients; for 4 of the 6 (Patients 1, 3, 4, and 5 ) hypothermia was employed as well. All patients were screened for coagulopathies and had normal values preoperatively. Heparin was routinely given intraoperatively to all 6 patients, with protamine reversal being carried out in all except the 2 patients who died intraoperatively (Patients 3 and 4).Massive postoperative bleeding occurred in 1 patient (Patient 1). Intraoperative serum electrolyte monitoring reflected a stable electrolyte status. PATIENT 1
A 29-month-old boy with transposition of the great arteries and an intact ventricular septum required a balloon atrial septostomy at 2 days of age. He then did well until the age of 13 months, at which time he developed a left hemiplegia and seizures, probably on the basis of a cerebral thrombosis. With anticonvulsant therapy the seizureswere reduced to one a day. By the age of 29 months there was evidence of progressive subpulmonic stenosis; at operation this was found to be due to two abnormalities, a displacement of the anterior papillary muscle into the left ventricular outflow tract and an aneurysmal bulging of the membranous septum into the outflow area. These obstructions were relieved through operation, and a Mustard atrial baffle was inserted. A severe hemorrhagic diathesis developed immediately after the operation, followed by ventricular arrhythmia, a falling cardiac output, and uremia (requiring peritoneal dialysis). The patient died two days postoperatively. PATIENT 2
An Indian boy with tetralogy of Fallot was sufficiently handicapped by the age of 7 years to require operative correction. The surgical procedure was prolonged both by a large coronary artery crossing the right ventricular outflow tract, which limited the ventriculotomy and impaired visualization of the ventricular septa1defect, and by a highly vascular infundibular myocardium that necessitated careful hemostasis during resection. The postoperative course was complicated by low cardiac output with pulmonary edema and a pseudomonas tracheobronchitis. The latter was unresponsive to antibiotic therapy, and the patient died on the fourth postoperative day. PATIENT 3
An open-heart operation was undertaken in a boy 3 years 10 months of age who had tetralogy of Fallot because of increasingly frequent cyanotic spells and a rising hematocrit. At operation right ventricular pressure could be reduced only after extensive widening of the outflow tract. At the end of the operation the left ventricle was unable to maintain an adequate cardiac output and the patient died. PATIENT 4
Valvular and subvalvular aortic stenosis were demonstrated to be present and thought to be responsible for the cardiac failure already evident at 4 months of age in this white male infant. Only with difficulty was the child managed on a medical regimen, including propranolol and diuretics, over the next six months. Re-
272
THE ANNALS OF THORACIC SURGERY
Subdural Hematoma
catheterization prior to operation at 10 months of age again demonstrated valvular and subvalvular aortic stenosis. The left ventricle, although thick-walled, contracted well, yielding no clue to the presence of the extensive inner mantle of endocardial fibroelastosis found at operation and confirmed at postmortem examination. The endocardial fibroelastosis undoubtedly was the major factor responsible for the left ventricle failure leading to death immediately after operation. PATIENT 5
A white boy 5 years 3 months old with ventricular septal defect had undergone pulmonary artery banding at 6 months of age because of chronic cardiac failure. Shunt reversal was noted at 4 years. At operation the ventricular septal defect involved the membranous septum but extended unusually far posteriorly. In addition the pulmonary artery band was firmly adherent, necessitating resection and insertion of a graft. Immediately after operation his course was satisfactory. Subsequently he developed cardiac arrhythmia, a low cardiac output, and oliguria, the last requiring peritoneal dialysis. The patient died three days postoperatively. PATIENT 6
This patient was known on clinical grounds to have a secundum type of atrial defect. Cardiac catheterization at the age of 5 years 2 months demonstrated a four-to-one left-to-right shunt at the atrial level without pulmonary hypertension. At operation the atrial septal defect was first closed by direct suturing since the size of the left atrium seemed adequate. However, immediately following operation, progressive pulmonary edema and hypoxia with rapid clinical deterioration necessitated reoperation; at this time the left atrium was seen and felt to be tense. The atrial septal defect was reopened and then repaired with a pericardial patch. Although cardiac output was good immediately after operation, the pulmonary edema and hypoxia did not resolve, leading to cardiac arrhythmia and multiple cardiac arrests. Death occurred one hour postoperatively.
Comment The data on the 6 patients discussed here indicate that subdural hematomas may occur during or immediately after open-heart operations and should be considered in the differential diagnosis of both early and late neurological dysfunction. Classically, subdural hematomas result from tearing of the bridging veins between the dura and cerebral hemispheres, usually as a result of trauma 1 1,181. Subdural hematomas have been described in hypernatremic dehydration with brain shrinkage [12, 131, in patients being given heparin after a myocardial infarction [30], in elderly persons with cerebral atrophy and minor trauma [23], in hemophiliacs [25], and as a complication of hemodialysis from the administration of heparin and sudden fluid shifts [9, 271. In many of these, trivial, forgotten trauma has been implicated. On the basis of the clinical and postmortem findings two interacting factors are thought to be responsible for these subdural hematomas. Intraoperative
VOL. 19, NO. 3, MARCH, 1975
273
KROUS ET AL. administration of heparin renders these patients susceptible to abnormally extensive hemorrhage in the event of blood vessel damage. Such damage could result either from minor and inadvertent trauma or from fluctuations in cerebral volume as a result of fluid shifts. All 6 of our patients were given heparin intraoperatively. (All but the 2 who died intraoperatively had protamine reversal postoperatively.)In 2 children there was documented evidence of head trauma in the form of subgaleal hematomas. The postmortem examination reports for the remaining 4 made no mention of the presence or absence of subgaleal hematomas, but since their significance often is not recognized, they may have been overlooked. Further support for the contention that trauma and hypocoagulability may have acted synergistically in at least 1 instance is evidenced in Patient 6. In this patient a large secundum atrial septa1 defect was first closed by direct suture. Rapidly progressive pulmonary edema led to reoperation, at which time the surgeon noted a tense left atrium, suggesting that the chamber was too small to accommodate pulmonary venous return. The lungs may well have sustained the “trauma” of pulmonary venous hypertension which, in the presence of heparin, resulted in the diffuse, severe hemorrhage of the lungs found at postmortem examination. A subgaleal hematoma had likewise occurred in this patient, indicating head trauma. That the subgaleal, subdural, and pulmonary hemorrhages were not a reflection of widespread vascular damage or uncontrolled hemorrhage was confirmed by the absence of hemorrhage elsewhere in the body. Rapid fluid shifts with fluctuations in cerebral volume may lead to tearing of the dural bridging veins [9]. Patients developing subdural hematomas on this basis would be expected to show no evidence of head trauma such as subgaleal hematoma. It is unlikely that this mechanism played a major role in our patients’ problems, as electrolyte monitoring during open-heart operations showed no deviation from the normal other than mild hyponatremia. Two patients had peritoneal dialysis, which, in contrast to hemodialysis, has not been reported in association with subdural hematomas. Additional evidence that tearing of the bridging veins following heparin therapy can result in subdural hemorrhage comes from experimental studies [161. Seven dogs had silk suture placed around one dural bridging vein and carried to the outside. Two dogs were given heparin. On the third postoperative day the sutures were pulled out, tearing the bridging dural vein. The 2 dogs previously given heparin died of massive subdural and subarachnoid hemorrhages. Of the 5 animals not given heparin only 1 died of acute subdural hemorrhage; the rest remained well and active. Although the number of experimental animals is small, these findings do show that tearing of one dural bridging vein can be well tolerated under normal conditions but that in the presence of a hypocoagulable state massive hemorrhage does result. It is well documented that cerebral disorders may occur following open-heart operations as a result of either hypotension or cerebral embolism [5, 6, 15, 17, 20-221. In reviewing studies which correlate neuropathological changes and cerebral disorders [ l , 2, 4, 10, 15, 26, 28, 291, it was found that subdural hematomas were documented in only one series [31; 274
T H E ANNALS OF THORACIC SURGERY
Subdural Hematoma however, most of these reports were concerned primarily with microscopical changes within the brain substance. It seems likely that the true incidence of subdural hematomas following open-heart operations utilizing bypass has been underestimated. Of our 6 patients, 4 had small hematomas which presumably could be reabsorbed with no further neurological symptoms. However, small hematomas may at times persist, expand, and reach sufficient size to cause late neurological abnormalities, including seizures [7]. A subdural hematoma might cause noticeable constriction of a rapidly developing infant brain [24],which approximately doubles its size in the first five months of life and redoubles in the next three and one-half years [8]. The infant brain is more vulnerable to subdural hemorrhage than that of the older individual in other ways. Minimal trauma can more readily lead to tearing of the parasagittal bridging dural veins, since the supporting protective arachnoid granulations are not fully developed [ 141. Further, the soft, less myelinated infant brain is more readily subject to cerebral distortion from trauma, further contributing to damage of the dural veins through stretching. These factors assume increasing importance with the current emphasis on corrective cardiac operations in infancy which employ a combination of hypothermia and pump oxygenation and therefore, in most instances, the administration of heparin intraoperatively. They further underline the extreme care with which manipulation of the head should be carried out following heparin therapy, both during and immediately after open-heart operations, with particular care being exercised in the highly vulnerable infant age group. Finally, in any patient with a past history of open-heart operation who manifests neurological problems, the possibility of an expanding subdural hematoma must be kept in mind.
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