Immunohistochemical localization of tissue-type plasminogen activator in the lining wall of chronic subdural hematoma

Fujisawa, Hironori; Ito, Hiroki; Saitô, Kenichi; Ikeda, Keisuke; Nitta, Hisashi; Yamashita, Junkoh

doi:10.1016/0090-3019(91)90177-b

Cited by 71 publications

(35 citation statements)

References 19 publications

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“…2,[25][26][27] Bleeding then occurs repeatedly from capillaries with degenerating endothelium, and is accompanied by local hyperfibrinolysis, which is one of the causes of the growth of effusions into CSDH. 8,13,14) Several experimental studies of CSDH have shown that contact of cerebrospinal fluid (CSF) and/or fibrin in the blood with the dura mater is an essential precursor to outer membrane formation. 1,42) Some of our clinical data also suggest factors in the etiology of CSDH.…”

Section: Discussionmentioning

confidence: 99%

Surgical Treatment of Chronic Subdural Hematoma in 500 Consecutive Cases: Clinical Characteristics, Surgical Outcome, Complications, and Recurrence Rate.

Mori

Maëda

2001

Neurol. Med. Chir.(Tokyo)

457

335

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Chronic subdural hematoma (CSDH) is one of the most common clinical entities in daily neurosurgical practice. The diagnosis and treatment are well established, but recurrence, complications, and factors related to these problems, especially in the elderly, are not completely understood. This study evaluated the clinical features, radiological findings, and surgical results in a large series of the patients treated at the same institution. 500 consecutive patients (359 men and 141 women) with CSDH were treated by burr hole craniostomy with closed system drainage from January 1987 through February 1999. Causes, clinical and computed tomographic findings, surgical results, re-expansion of brain after surgery, and hematoma recurrence were statistically analyzed to elucidate the potential risks of CSDH. Most patients (89.4%) had good recovery, 8.4% showed no change, and 2.2% worsened. Six patients (1.2%) died, three due to disseminated intravascular coagulation. Recurrence of hematoma was recognized in 49 patients (9.8%), at 1 to 8 weeks (3.5 ± 1.9 weeks) after the first operation. The brain reexpansion rate at one week after operation was 45.0 ± 21.4% in patients with hematoma recurrence and significantly lower than 55.3 ± 19.1% in patients without recurrence (p º 0.001). Old age, preexisting cerebral infarction, and persistence of subdural air after surgery were significantly correlated with poor brain re-expansion (p º 0.001). Twenty-seven patients (5.4%) suffered postoperative complications, of which 13 cases were acute subdural hematoma caused by incomplete hemostasis of the scalp wound and four cases were tension pneumocephalus. Careful hemostasis and complete replacement of subdural hematoma by normal saline to prevent influx of air into the subdural space will further improve the surgical outcome for patients with CSDH.

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Section: Discussionmentioning

confidence: 99%

Surgical Treatment of Chronic Subdural Hematoma in 500 Consecutive Cases: Clinical Characteristics, Surgical Outcome, Complications, and Recurrence Rate.

Mori

Maëda

2001

Neurol. Med. Chir.(Tokyo)

457

335

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“…Santarius et al performed a randomized controlled trial comparing draining subdural hematomas relieved by burr hole drilling versus drilling the holes without chronically draining the internal fluid through a catheter. Drainage was theorized to reduce the recurrence of bleeding from a treated hematoma by the removal of fibrinolytic elements in the accumulated fluid 22,56,57 . The presence of a drain was so strongly associated with a reduction in recurrence (9% to 24%) in addition to less stark improvements in long term mortality and post-surgical Rankin scores that the study was stopped and all participants were placed on drainage 58 .…”

Section: Treatments For Csdhmentioning

confidence: 99%

“…Wilfred Trotter originally hypothesized in 1914 that this proliferation of dural border cells results in production of a neomembrane, and subsequent growth of new vessels directly within the subdural space 21 . Subsequent studies show that chronic SDH can result from bleeding from these vessels by repeated microhaemorrhage from the neomembrane 22 .…”

Section: Introductionmentioning

confidence: 99%

Evolving management of symptomatic chronic subdural hematoma: experience of a single institution and review of the literature

Balser

Rodgers

Johnson

et al. 2013

Neurological Research

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Objective-Chronic subdural hematoma has an increasing incidence and results in high morbidity and mortality. We review here the ten-year experience of a single institution and the literature regarding the treatment and major associations of chronic subdural hematoma (cSDH).Methods-We retrospectively reviewed all cSDHs surgically treated from 2000 to 2010 at our institution to evaluate duration from admission to treatment, type of treatment, length of stay in critical care, length of stay in the hospital and recurrence. The literature was reviewed with regards to incidence, associations and treatment of cSDH. [2000][2001][2002][2003][2004][2005][2006][2007][2008]44 patients were treated with burr holes. From 2008 to 2010, 29 patients were treated with twist drill evacuation (SEPS). 4 patients from each group were readmitted for reoperation (9% vs. 14%; p=.53). The average time to intervention for SEPS (11.2±15.3 hrs) was faster than for burr holes (40.3±69.1 hrs) (p=.02). The total hospital LOS was shorter for SEPS (9.3±6.8 days) versus burr holes (13.4±10.2 days) (p=.04); both were significantly longer than for a brain tumor patient undergoing craniotomy (7.0±0.5 days, n=94, P<. 01). Results-FromConclusion-Despite decreasing lengths of stay over time as treatment for cSDH evolved from burr holes to SEPS, the length of stay for a cSDH is still greater than that of a patient undergoing craniotomy for brain tumor. We noted 11% recurrence in our series of patients, which included individuals who recurred as late as 3 years after initial diagnosis.

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“…This similarity raises the possibility that growth of CAs could be similar to that proposed for CSDHs, namely, repeated hemorrhage and re-endothelialization of the clot cavity, neovasculariza tion and granulation, then further hemorrhage [12], This mechanism of CSDH growth is supported, in part, by the finding of local fibrinolytic activity in CSDH membranes [13,14], This activity has been correlated with tissue plas minogen activator (TPA) localized to the CSDH fluid [ 15] and to the endothelial lining of the CSDH membrane neovascular channels [12], Given the similarities in histopathology noted between CAs and CSDHs, we investi gated the presence of TPA in CA in an effort to link the mechanisms of hemorrhage that might be common be tween these two entities.…”

Section: Introductionmentioning

confidence: 54%

Immunohistochemically Identifiable Tissue Plasminogen Activator in Cavernous Angioma: Mechanism for Re-Hemorrhage and Lesion Growth

Frim

Zee²,

Golden³

et al. 1996

Pediatr Neurosurg

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The mechanisms governing growth of cavernous angiomas of the brain and their propensity to hemorrhage remain unknown. Repetitive hemorrhage with neovascularization during clot organization and maturation of new vessels into a larger cavernous angioma has been hypothesized as one mechanism. This hypothesis is largely based on the histopathological similarity between the organizing clot surrounding cavernous malformations and the organizing phase of the membranes surrounding chronic subdural hematoma. The presence of tissue plasminogen activator (TPA) in the vascular endothelium of vessels contained within chronic subdural membranes has been used to argue that an intrinsic thrombolytic process is responsible, in part, for rebleeding within chronic subdural cavities. By analogy, we sought to identify whether TPA is located in tissues in and around cavernous angiomas. Cavernous malformations, surgically removed and pathologically confirmed by standard staining techniques, were immunohistochemically stained for TPA. Eleven of thirteen lesions (85%) studied contained vascular endothelial cells which stained for TPA. Of the 2 lesions which did not contain TPA, 1 was non-hemorrhagic and calcified; 7 of 11 (64%) lesions which contained TPA presented clinically with hemorrhage. These data support the hypothesis that a local thrombolytic process may be responsible for the frequent hemorrhagic nature of cavernous angiomas. Alternatively, since local elaboration of TPA is common to both chronic subdural membranes and cavernous angiomas, this finding may represent a more global characteristic of fibrinolytic homeostasis in cerebral tissues.

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Immunohistochemical localization of tissue-type plasminogen activator in the lining wall of chronic subdural hematoma

Cited by 71 publications

References 19 publications

Surgical Treatment of Chronic Subdural Hematoma in 500 Consecutive Cases: Clinical Characteristics, Surgical Outcome, Complications, and Recurrence Rate.

Surgical Treatment of Chronic Subdural Hematoma in 500 Consecutive Cases: Clinical Characteristics, Surgical Outcome, Complications, and Recurrence Rate.

Evolving management of symptomatic chronic subdural hematoma: experience of a single institution and review of the literature

Immunohistochemically Identifiable Tissue Plasminogen Activator in Cavernous Angioma: Mechanism for Re-Hemorrhage and Lesion Growth

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