The role of craniectomy in the treatment of chronic subdural hematomas

1980 ◽  
Vol 52 (6) ◽  
pp. 776-781 ◽  
Author(s):  
George Tyson ◽  
W. Ellis Strachan ◽  
Peter Newman ◽  
H. Richard Winn ◽  
Albert Butler ◽  
...  

✓ A consecutive series of 48 adult patients with a chronic subdural hematoma is reported. These patients were treated according to a protocol consisting of a sequence of conventional surgical procedures ranging from simple burr-hole drainage to craniotomy and subdural membranectomy. Seven patients (15%) continued to demonstrate severe neurological dysfunction, or suffered acute neurological deterioration after completion of this protocol. However, after undergoing excision of the cranial vault overlying the hematoma site, six of these seven patients demonstrated a significant clinical improvement. Based on analysis of these seven cases, the authors suggest that craniectomy be considered in those patients who suffer a symptomatic reaccumulation of subdural fluid following craniotomy and membranectomy, or who demonstrate further neurological deterioration as a result of cerebral swelling subjacent to the hematoma site. However, this procedure probably has no efficacy once extensive cerebral infarction has occurred.

1982 ◽  
Vol 57 (2) ◽  
pp. 254-257 ◽  
Author(s):  
Henry A. Shenkin

✓ In a consecutive series of 39 cases of acute subdural hematoma (SDH), encountered since computerized tomography diagnosis became available, 61.5% were found to be the result of bleeding from a small cortical artery, 25.6% were of venous origin, 7.7% resulted from cerebral contusions, and 5% were acute bleeds into chronic subdural hematomas. Craniotomy was performed promptly on admission, but there was no difference in survival (overall 51.3%) between patients with arterial and venous bleeds. The only apparent factor affecting survival in this series was the preoperative neurological status: 67% of patients who were decerebrate and had fixed pupils prior to operation died. Of patients with less severe neurological dysfunction, only 20% failed to survive.


1986 ◽  
Vol 64 (1) ◽  
pp. 29-34 ◽  
Author(s):  
Robert A. Solomon ◽  
Christopher M. Loftus ◽  
Donald O. Quest ◽  
James W. Correll

✓ In a consecutive series of 1930 carotid endarterectomies there were eight cases of postoperative intracerebral hemorrhage. One of these patients was operated on 2 weeks following cerebral infarction and had severe uncontrollable hypertension after surgery. A second patient had an intraoperative embolus and bled while fully heparinized on the 3rd postoperative day. Only one patient in the series bled into an area of documented cerebral infarction. The remainder of the cases represented hemorrhage into essentially normal brain. Seven of the eight patients with intracerebral hemorrhage had high-grade internal carotid artery stenosis preoperatively. Although several factors have contributed to the brain hemorrhages in this series of patients, postoperative cerebral hyperperfusion which often follows endarterectomy may have played an important role. Defective cerebrovascular autoregulation in chronically ischemic brain regions may predispose patients to intracerebral hemorrhage after removal of a high-grade stenosis of the internal carotid artery.


1981 ◽  
Vol 55 (3) ◽  
pp. 390-396 ◽  
Author(s):  
Thomas-Marc Markwalder ◽  
Klaus F. Steinsiepe ◽  
Matthias Rohner ◽  
Walter Reichenbach ◽  
Hans Markwalder

✓ A consecutive series of 32 adult patients with chronic subdural hematoma was studied in respect to postoperative cerebral reexpansion (reduction in diameter of the subdural space) after burr-hole craniostomy and closed-system drainage. Patients with high subdural pressure showed the most rapid brain expansion and clinical improvement during the first 2 days. Nevertheless, a computerized tomography (CT) scan performed on the 10th day after surgery demonstrated persisting subdural fluid in 78% of cases. After 40 days, the CT scan was normal in 27 of the 32 patients. There was no mortality and no significant morbidity. Our study suggests that well developed subdural neomembranes are the crucial factors for cerebral reexpansion, a phenomenon that takes at least 10 to 20 days. However, blood vessel dysfunction and impairment of cerebral blood flow may participate in delay of brain reexpansion. It may be argued that additional surgical procedures, such as repeated tapping of the subdural fluid, craniotomy, and membranectomy or even craniectomy, should not be evaluated earlier than 20 days after the initial surgical procedure unless the patient has deteriorated markedly.


1984 ◽  
Vol 60 (1) ◽  
pp. 14-22 ◽  
Author(s):  
Alfred J. Luessenhop ◽  
Louis Rosa

✓ To address the problems of surgical risk versus natural risk associated with cerebral arteriovenous malformations (AVM's), and the role of the intravascular operative approach, the authors have assessed a 20-year experience with 450 patients. Results of direct surgery in 90 patients indicate that for the smaller AVM's (Grades I and II), mortality and morbidity rates are lower than a reasonably projected natural risk. Hence, these patients are candidates for surgery in most instances. However, for more extensive AVM's (Grades III and IV), consideration of anticipated future years of exposure to natural risk and the location of the AVM in the brain are necessary for determining operability. In general, neither seizures nor incipient focal neurological dysfunction alone are indications for surgery, and the risks of disability or death from hemorrhage after the fifth decade of life are probably less than the surgical risks by present operative techniques. Considering the usual age of patients at the time of diagnosis, it is estimated that surgical risk is currently less than the natural risk for about 65% to 70% of all AVM patients. The categories of AVM's in which the angiographic effectiveness of the intravascular approach is the greatest correspond to the same categories of AVM's that can be surgically removed with low risk. The intravascular approach is most useful for management of large AVM's causing progressive neurological dysfunction or as a preliminary step to surgery in selected cases in which access to major feeding arteries is difficult. The authors believe that the future of the intravascular approach should be directed toward transforming large inoperable AVM's into operable ones, but that the overall capability for this with acceptable risk is uncertain at present.


1977 ◽  
Vol 46 (2) ◽  
pp. 248-251 ◽  
Author(s):  
J. Parker Mickle ◽  
James E. McLennan ◽  
Je G. Chi ◽  
Craig W. Lidden

✓ A patient with Wegener's granulomatosis is reported in whom a life-threatening cortical vein thrombosis was identified as the process causing acute neurological deterioration. The literature dealing with the neurological and neuropathological manifestations in Wegener's granulomatosis is reviewed.


1976 ◽  
Vol 45 (1) ◽  
pp. 26-31 ◽  
Author(s):  
Haruhide Ito ◽  
Shinjiro Yamamoto ◽  
Toshio Komai ◽  
Hidetaka Mizukoshi

✓ The authors describe studies performed on material aspirated from chronic subdural hematomas. Patients were given 51Cr-labeled red cells prior to aspiration, and it was possible to demonstrate that the mean daily hemorrhage into the hematoma space amounted to 10.2% of its volume. Immunoelectrophoresis of the aspirated hematoma fluid by monospecific anti-human fibrinogen revealed the presence of fibrin and fibrinogen degradation products that, measured by hemagglutination-inhibition immunoassay techniques, varied between 5.0 and 10,500 µg/ml with an average of 2604 µg/ml in 18 cases. The tissue activator was demonstrated by Todd's histological localization in the outer membrane of the chronic subdural hematoma in 11 cases, but not in the inner membrane. These results indicate that if a clot in the subdural space causes the formation of neomembrane, and excessive fibrinolysis occurs, the subdural clot would not only liquefy, but also enlarge by continuous hemorrhage from the neomembrane. Therefore, local hyperfibrinolysis and continuous bleeding are important in the etiology of the chronic subdural hematoma.


2000 ◽  
Vol 93 (supplement_3) ◽  
pp. 113-119 ◽  
Author(s):  
D. Hung-Chi Pan ◽  
Wan-Yuo Guo ◽  
Wen-Yuh Chung ◽  
Cheng-Ying Shiau ◽  
Yue-Cune Chang ◽  
...  

Object. A consecutive series of 240 patients with arteriovenous malformations (AVMs) treated by gamma knife radiosurgery (GKS) between March 1993 and March 1999 was evaluated to assess the efficacy and safety of radiosurgery for cerebral AVMs larger than 10 cm3 in volume. Methods. Seventy-six patients (32%) had AVM nidus volumes of more than 10 cm3. During radiosurgery, targeting and delineation of AVM nidi were based on integrated stereotactic magnetic resonance (MR) imaging and x-ray angiography. The radiation treatment was performed using multiple small isocenters to improve conformity of the treatment volume. The mean dose inside the nidus was kept between 20 Gy and 24 Gy. The margin dose ranged between 15 to 18 Gy placed at the 55 to 60% isodose centers. Follow up ranged from 12 to 73 months. There was complete obliteration in 24 patients with an AVM volume of more than 10 cm3 and in 91 patients with an AVM volume of less than 10 cm3. The latency for complete obliteration in larger-volume AVMs was significantly longer. In Kaplan—Meier analysis, the complete obliteration rate in 40 months was 77% in AVMs with volumes between 10 to 15 cm3, as compared with 25% for AVMs with a volume of more than 15 cm3. In the latter, the obliteration rate had increased to 58% at 50 months. The follow-up MR images revealed that large-volume AVMs had higher incidences of postradiosurgical edema, petechiae, and hemorrhage. The bleeding rate before cure was 9.2% (seven of 76) for AVMs with a volume exceeding 10 cm3, and 1.8% (three of 164) for AVMs with a volume less than 10 cm3. Although focal edema was more frequently found in large AVMs, most of the cases were reversible. Permanent neurological complications were found in 3.9% (three of 76) of the patients with an AVM volume of more than 10 cm3, 3.8% (three of 80) of those with AVM volume of 3 to 10 cm3, and 2.4% (two of 84) of those with an AVM volume less than 3 cm3. These differences in complications rate were not significant. Conclusions. Recent improvement of radiosurgery in conjunction with stereotactic MR targeting and multiplanar dose planning has permitted the treatment of larger AVMs. It is suggested that gamma knife radiosurgery is effective for treating AVMs as large as 30 cm3 in volume with an acceptable risk.


1995 ◽  
Vol 82 (2) ◽  
pp. 296-299 ◽  
Author(s):  
Michael K. Morgan ◽  
Maurice J. Day ◽  
Nicholas Little ◽  
Verity Grinnell ◽  
William Sorby

✓ The authors report two cases of treatment by intraarterial papaverine of cerebral vasospasm complicating the resection of an arteriovenous malformation (AVM). Both cases had successful reversal of vasospasm documented on angiography. In the first case sustained neurological improvement occurred, resulting in a normal outcome by the time of discharge. In the second case, neurological deterioration occurred with the development of cerebral edema. This complication was thought to be due to normal perfusion pressure breakthrough, on the basis of angiographic arterial vasodilation and increased cerebral blood flow. These two cases illustrate an unusual complication of surgery for AVMs and demonstrate that vasospasm (along with intracranial hemorrhage, venous occlusion, and normal perfusion pressure breakthrough) should be considered in the differential diagnosis of delayed neurological deterioration following resection of these lesions. Although intraarterial papaverine may be successful in dilating spastic arteries, it may also result in pathologically high flows following AVM resection. However, this complication has not been seen in our experience of treating aneurysmal subarachnoid hemorrhage by this technique.


2000 ◽  
Vol 92 (6) ◽  
pp. 1040-1044 ◽  
Author(s):  
Gregory W. Hornig

✓ This report documents clinical features in five children who developed transient reddening of the skin (epidermal flushing) in association with acute elevations in intracranial pressure (ICP). Four boys and one girl (ages 9–15 years) deteriorated acutely secondary to intracranial hypertension ranging from 30 to 80 mm Hg in the four documented cases. Two patients suffered from ventriculoperitoneal shunt malfunctions, one had diffuse cerebral edema secondary to traumatic brain injury, one was found to have pneumococcal meningitis and hydrocephalus, and one suffered an intraventricular hemorrhage and hydrocephalus intraoperatively. All patients were noted to have developed epidermal flushing involving either the upper chest, face, or arms during their period of neurological deterioration. The response was transient, typically lasting 5 to 15 minutes, and dissipated quickly. The flushing reaction is postulated to be a centrally mediated response to sudden elevations in ICP. Several potential mechanisms are discussed. Flushing has clinical importance because it may indicate significant elevations in ICP when it is associated with neurological deterioration. Because of its transient nature, the importance of epidermal flushing is often unrecognized; its presence confirms the need for urgent treatment.


1992 ◽  
Vol 76 (4) ◽  
pp. 635-639 ◽  
Author(s):  
Shigeru Nishizawa ◽  
Nobukazu Nezu ◽  
Kenichi Uemura

✓ Vascular contraction is induced by the activation of intracellular contractile proteins mediated through signal transduction from the outside to the inside of cells. Protein kinase C plays a crucial role in this signal transduction. It is hypothesized that protein kinase C plays a causative part in the development of vasospasm after subarachnoid hemorrhage (SAH). To verify this directly, the authors measured protein kinase C activity in canine basilar arteries in an SAH model with (γ-32P)adenosine triphosphate and the data were compared to those in a control group. Protein kinase C is translocated to the membrane from the cytosol when it is activated, and the translocation is an index of the activation; thus, protein kinase C activity was measured both in the cytosol and in the membrane fractions. Protein kinase C activity in the membrane in the SAH model was remarkably enhanced compared to that in the control group. The percentage of membrane activity to the total was also significantly greater in the SAH vessels than in the control group, and the percentage of cytosol activity in the SAH group was decreased compared to that in the control arteries. The results indicate that protein kinase C in the vascular smooth muscle was translocated to the membrane from the cytosol and was activated when SAH occurred. It is concluded that this is direct evidence for a key role of protein kinase C in the development of vasospasm.


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