Why do chronic subdural hematomas continue to grow slowly and not coagulate? Role of thrombomodulin in the mechanism

Hideki Murakami, Yuichi Hirose, Masachika Sagoh, Kazuhiro Shimizu, Masaru Kojima, Kazuhiro Gotoh, Yutaka Mine, Takuro Hayashi, Takeshi Kawase

Research output: Contribution to journalArticle

66 Citations (Scopus)

Abstract

Object. Thrombomodulin is a thrombin receptor on vascular endothelial cells that is highly expressed when these cells are injured, and it has anticoagulating activity. The authors investigated thrombomodulin expression to clarify why chronic subdural hematomas (CSDHs) continue to grow slowly, like a tumor, and are liquefied. Methods. Burr hole craniotomy and drainage were performed in all 35 patients with CSDH who were included in the study. The plasma-soluble thrombomodulin and blood clotting factor values were determined in the hematoma and in peripheral blood. In the seven most recent cases, the plasma-soluble thrombomodulin values were determined in the residual hematoma collected from the drainage tube the day after surgery. The outer membranes of the CSDH that were obtained as specimens at operation were stained with monoclonal antibody against thrombomodulin for immunohistochemical studies. The plasma-soluble thrombomodulin values were higher (p < 0.0001), and conversely the values for factors V and VIII were lower in the hematoma than in peripheral blood (p < 0.0001). The plasma-soluble thrombomodulin values were lower in the residual hematomas than in the same lesions at operation (p= 0.018). The endothelial cells on the sinusoidal vessels exhibited immunoreactivity with thrombomodulin antibody in 28 (93%) of 30 cases. Conclusions. The thrombomodulin is expressed on the sinusoidal vessels, and the blood coagulation system is inhibited in the hematoma. These findings indicate that these vessels are continuously injured and fail to heal. As a result, the bleeding from the sinusoidal vessels may persist, and the hematoma may grow slowly and fail to coagulate. It is suspected that transmitted pulsation variations in the hematoma cavity generate sinusoidal vessel injury.

Original languageEnglish
Pages (from-to)877-884
Number of pages8
JournalJournal of Neurosurgery
Volume96
Issue number5
DOIs
Publication statusPublished - 01-01-2002

Fingerprint

Hematoma, Subdural, Chronic
Thrombomodulin
Hematoma
Blood Coagulation
Drainage
Endothelial Cells
Thrombin Receptors
Blood Coagulation Factors
Factor V
Craniotomy
Factor VIII
Ambulatory Surgical Procedures
Monoclonal Antibodies
Hemorrhage

All Science Journal Classification (ASJC) codes

  • Surgery
  • Clinical Neurology

Cite this

Murakami, Hideki ; Hirose, Yuichi ; Sagoh, Masachika ; Shimizu, Kazuhiro ; Kojima, Masaru ; Gotoh, Kazuhiro ; Mine, Yutaka ; Hayashi, Takuro ; Kawase, Takeshi. / Why do chronic subdural hematomas continue to grow slowly and not coagulate? Role of thrombomodulin in the mechanism. In: Journal of Neurosurgery. 2002 ; Vol. 96, No. 5. pp. 877-884.
@article{46227f1cd18746c4808d206b47f6ae52,
title = "Why do chronic subdural hematomas continue to grow slowly and not coagulate? Role of thrombomodulin in the mechanism",
abstract = "Object. Thrombomodulin is a thrombin receptor on vascular endothelial cells that is highly expressed when these cells are injured, and it has anticoagulating activity. The authors investigated thrombomodulin expression to clarify why chronic subdural hematomas (CSDHs) continue to grow slowly, like a tumor, and are liquefied. Methods. Burr hole craniotomy and drainage were performed in all 35 patients with CSDH who were included in the study. The plasma-soluble thrombomodulin and blood clotting factor values were determined in the hematoma and in peripheral blood. In the seven most recent cases, the plasma-soluble thrombomodulin values were determined in the residual hematoma collected from the drainage tube the day after surgery. The outer membranes of the CSDH that were obtained as specimens at operation were stained with monoclonal antibody against thrombomodulin for immunohistochemical studies. The plasma-soluble thrombomodulin values were higher (p < 0.0001), and conversely the values for factors V and VIII were lower in the hematoma than in peripheral blood (p < 0.0001). The plasma-soluble thrombomodulin values were lower in the residual hematomas than in the same lesions at operation (p= 0.018). The endothelial cells on the sinusoidal vessels exhibited immunoreactivity with thrombomodulin antibody in 28 (93{\%}) of 30 cases. Conclusions. The thrombomodulin is expressed on the sinusoidal vessels, and the blood coagulation system is inhibited in the hematoma. These findings indicate that these vessels are continuously injured and fail to heal. As a result, the bleeding from the sinusoidal vessels may persist, and the hematoma may grow slowly and fail to coagulate. It is suspected that transmitted pulsation variations in the hematoma cavity generate sinusoidal vessel injury.",
author = "Hideki Murakami and Yuichi Hirose and Masachika Sagoh and Kazuhiro Shimizu and Masaru Kojima and Kazuhiro Gotoh and Yutaka Mine and Takuro Hayashi and Takeshi Kawase",
year = "2002",
month = "1",
day = "1",
doi = "10.3171/jns.2002.96.5.0877",
language = "English",
volume = "96",
pages = "877--884",
journal = "Journal of Neurosurgery",
issn = "0022-3085",
publisher = "American Association of Neurological Surgeons",
number = "5",

}

Murakami, H, Hirose, Y, Sagoh, M, Shimizu, K, Kojima, M, Gotoh, K, Mine, Y, Hayashi, T & Kawase, T 2002, 'Why do chronic subdural hematomas continue to grow slowly and not coagulate? Role of thrombomodulin in the mechanism', Journal of Neurosurgery, vol. 96, no. 5, pp. 877-884. https://doi.org/10.3171/jns.2002.96.5.0877

Why do chronic subdural hematomas continue to grow slowly and not coagulate? Role of thrombomodulin in the mechanism. / Murakami, Hideki; Hirose, Yuichi; Sagoh, Masachika; Shimizu, Kazuhiro; Kojima, Masaru; Gotoh, Kazuhiro; Mine, Yutaka; Hayashi, Takuro; Kawase, Takeshi.

In: Journal of Neurosurgery, Vol. 96, No. 5, 01.01.2002, p. 877-884.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Why do chronic subdural hematomas continue to grow slowly and not coagulate? Role of thrombomodulin in the mechanism

AU - Murakami, Hideki

AU - Hirose, Yuichi

AU - Sagoh, Masachika

AU - Shimizu, Kazuhiro

AU - Kojima, Masaru

AU - Gotoh, Kazuhiro

AU - Mine, Yutaka

AU - Hayashi, Takuro

AU - Kawase, Takeshi

PY - 2002/1/1

Y1 - 2002/1/1

N2 - Object. Thrombomodulin is a thrombin receptor on vascular endothelial cells that is highly expressed when these cells are injured, and it has anticoagulating activity. The authors investigated thrombomodulin expression to clarify why chronic subdural hematomas (CSDHs) continue to grow slowly, like a tumor, and are liquefied. Methods. Burr hole craniotomy and drainage were performed in all 35 patients with CSDH who were included in the study. The plasma-soluble thrombomodulin and blood clotting factor values were determined in the hematoma and in peripheral blood. In the seven most recent cases, the plasma-soluble thrombomodulin values were determined in the residual hematoma collected from the drainage tube the day after surgery. The outer membranes of the CSDH that were obtained as specimens at operation were stained with monoclonal antibody against thrombomodulin for immunohistochemical studies. The plasma-soluble thrombomodulin values were higher (p < 0.0001), and conversely the values for factors V and VIII were lower in the hematoma than in peripheral blood (p < 0.0001). The plasma-soluble thrombomodulin values were lower in the residual hematomas than in the same lesions at operation (p= 0.018). The endothelial cells on the sinusoidal vessels exhibited immunoreactivity with thrombomodulin antibody in 28 (93%) of 30 cases. Conclusions. The thrombomodulin is expressed on the sinusoidal vessels, and the blood coagulation system is inhibited in the hematoma. These findings indicate that these vessels are continuously injured and fail to heal. As a result, the bleeding from the sinusoidal vessels may persist, and the hematoma may grow slowly and fail to coagulate. It is suspected that transmitted pulsation variations in the hematoma cavity generate sinusoidal vessel injury.

AB - Object. Thrombomodulin is a thrombin receptor on vascular endothelial cells that is highly expressed when these cells are injured, and it has anticoagulating activity. The authors investigated thrombomodulin expression to clarify why chronic subdural hematomas (CSDHs) continue to grow slowly, like a tumor, and are liquefied. Methods. Burr hole craniotomy and drainage were performed in all 35 patients with CSDH who were included in the study. The plasma-soluble thrombomodulin and blood clotting factor values were determined in the hematoma and in peripheral blood. In the seven most recent cases, the plasma-soluble thrombomodulin values were determined in the residual hematoma collected from the drainage tube the day after surgery. The outer membranes of the CSDH that were obtained as specimens at operation were stained with monoclonal antibody against thrombomodulin for immunohistochemical studies. The plasma-soluble thrombomodulin values were higher (p < 0.0001), and conversely the values for factors V and VIII were lower in the hematoma than in peripheral blood (p < 0.0001). The plasma-soluble thrombomodulin values were lower in the residual hematomas than in the same lesions at operation (p= 0.018). The endothelial cells on the sinusoidal vessels exhibited immunoreactivity with thrombomodulin antibody in 28 (93%) of 30 cases. Conclusions. The thrombomodulin is expressed on the sinusoidal vessels, and the blood coagulation system is inhibited in the hematoma. These findings indicate that these vessels are continuously injured and fail to heal. As a result, the bleeding from the sinusoidal vessels may persist, and the hematoma may grow slowly and fail to coagulate. It is suspected that transmitted pulsation variations in the hematoma cavity generate sinusoidal vessel injury.

UR - http://www.scopus.com/inward/record.url?scp=0036236396&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0036236396&partnerID=8YFLogxK

U2 - 10.3171/jns.2002.96.5.0877

DO - 10.3171/jns.2002.96.5.0877

M3 - Article

VL - 96

SP - 877

EP - 884

JO - Journal of Neurosurgery

JF - Journal of Neurosurgery

SN - 0022-3085

IS - 5

ER -