Subdural hematoma associated with disseminated intravascular coagulation in patients with advanced cancer

1983 ◽  
Vol 58 (3) ◽  
pp. 398-401 ◽  
Author(s):  
Tomoo Furui ◽  
Kaoru Ichihara ◽  
Akira Ikeda ◽  
Suguru Inao ◽  
Nagatoshi Hirai ◽  
...  
Keyword(s):  
Cancer Patients ◽  
Advanced Cancer ◽  
Disseminated Intravascular Coagulation ◽  
Subdural Hematoma ◽  
Content Type ◽  
Intravascular Coagulation ◽  
Fine Print

✓ Nontraumatic subdural hematoma following disseminated intravascular coagulation (DIC) due to advanced cancer was encountered in four patients. It is suggested that DIC plays an important role in the formation of subdural hematoma in cancer patients.

Disseminated intravascular coagulation following cranial trauma

1980 ◽  
Vol 52 (2) ◽  
pp. 266-269 ◽  
Author(s):  
Jerrold A. Clark ◽  
Robert E. Finelli ◽  
Martin G. Netsky
Keyword(s):  
Brain Tissue ◽  
Disseminated Intravascular Coagulation ◽  
Spinal Trauma ◽  
Clotting System ◽  
Content Type ◽  
Intravascular Coagulation ◽  
Cranial Trauma ◽  
Venous Sinuses ◽  
Fine Print ◽  
Dural Venous Sinuses

✓ Cranial and spinal trauma resulted in disseminated intravascular coagulation (DIC) in a 78-year-oldman, causing widespread bleeding and incoagulable blood. Traumatized brain tissue was found in the lumina of dural venous sinuses. The mechanisms of DIC are reviewed. It is suggested that intravascular release ofpotent cerebral thromboplastin contributed to the severity of DIC in this patient, by causing activation of the extrinsic clotting system. Intrasinus brain tissue in cases of human trauma has not previously been reported.

Disseminated intravascular coagulation associated with massive brain injury

1973 ◽  
Vol 39 (2) ◽  
pp. 178-180 ◽  
Author(s):  
Rudolph M. Keimowitz ◽  
Byron L. Annis
Keyword(s):  
Brain Injury ◽  
Disseminated Intravascular Coagulation ◽  
Brain Trauma ◽  
Content Type ◽  
Intravascular Coagulation ◽  
Diagnostic Studies ◽  
Fine Print

✓ The authors report a case of disseminated intravascular coagulation in a patient with massive brain trauma. It is suggested that the condition was caused by the liberation of thromboplastin. The detailed diagnostic studies and related theories are discussed.

Successful Evacuation of Subdural Hematoma in the Presence of Severe Coagulopathy

Neurosurgery ◽  
1982 ◽  
Vol 11 (2) ◽  
pp. 277-279 ◽  
Author(s):  
Ken Winston ◽  
Scott Conner
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Satisfactory Result ◽  
Subdural Hematoma ◽  
Acute Subdural Hematoma ◽  
Intravascular Coagulation ◽  
Severe Coagulopathy

Abstract An acute subdural hematoma was evacuated in the presence of a severe coagulopathy that was probably due to disseminated intravascular coagulation. A satisfactory result was achieved.

The contrast-enhanced CT scan in the diagnosis of isodense subdural hematoma

1979 ◽  
Vol 50 (1) ◽  
pp. 64-69 ◽  
Author(s):  
Fong Y. Tsai ◽  
James E. Huprich ◽  
Hervey D. Segall ◽  
James S. Teal
Keyword(s):  
Cerebral Cortex ◽  
Ct Scan ◽  
Subdural Hematoma ◽  
Correct Diagnosis ◽  
Content Type ◽  
Subdural Hematomas ◽  
Contrast Enhanced Ct ◽  
Contrast Enhanced ◽  
Enhanced Ct ◽  
Fine Print

✓ The authors review 29 cases of surgically-proven isodense subdural hematomas examined by non-contrast and contrast-enhanced computerized tomography scans. Three types of isodense collections were noted: homogeneous isodense collections, mixed-density collections, and gravitational layering within subdural collections. Contrast enhancement within the cerebral cortex, cortical vessels, and subdural membranes led to the correct diagnosis in each case. Contrast-enhanced scans are essential for the evaluation of isodense subdural hematomas.

Acute subdural hematoma

1982 ◽  
Vol 57 (2) ◽  
pp. 254-257 ◽  
Author(s):  
Henry A. Shenkin
Keyword(s):  
Computerized Tomography ◽  
Subdural Hematoma ◽  
Neurological Status ◽  
Neurological Dysfunction ◽  
Acute Subdural Hematoma ◽  
Consecutive Series ◽  
Content Type ◽  
Subdural Hematomas ◽  
Fine Print

✓ 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.

Middle meningeal artery embolization for refractory chronic subdural hematoma

2000 ◽  
Vol 93 (4) ◽  
pp. 686-688 ◽  
Author(s):  
Shinya Mandai ◽  
Masaru Sakurai ◽  
Yuzo Matsumoto
Keyword(s):  
Liver Cirrhosis ◽  
Subdural Hematoma ◽  
Therapeutic Approach ◽  
Chronic Subdural Hematoma ◽  
Middle Meningeal Artery ◽  
Artery Embolization ◽  
Content Type ◽  
Meningeal Artery ◽  
Fine Print

✓ The authors present a case of refractory chronic subdural hematoma (CSH) in a 59-year-old man with coagulopathy due to liver cirrhosis. The patient was successfully treated by embolization of the middle meningeal artery after several drainage procedures. This new therapeutic approach to recurrent CSH is discussed.

Angiographic extravasation of contrast medium in acute traumatic subdural hematoma from arterial rupture

1972 ◽  
Vol 37 (2) ◽  
pp. 226-228 ◽  
Author(s):  
Jusuke Ito ◽  
Komei Ueki ◽  
Hisayuki Ishikawa
Keyword(s):  
Contrast Medium ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Subdural Hematoma ◽  
Carotid Angiography ◽  
Content Type ◽  
Arterial Rupture ◽  
Visual Evidence ◽  
Subpial Hemorrhage ◽  
Fine Print

✓ Carotid angiography of a patient with suspected subdural hematoma showed extravasation of the contrast medium from an ascending branch of the middle cerebral artery. The leak was verified at operation. There was no visual evidence of an aneurysm, angioma, subarachnoid or subpial hemorrhage.

Chronic subdural hematoma simulating transient cerebral ischemic attacks

1975 ◽  
Vol 42 (1) ◽  
pp. 101-103 ◽  
Author(s):  
Eldad Melamed ◽  
Slvan Law ◽  
Avinoam Reches ◽  
Abraham Sahar
Keyword(s):  
Subdural Hematoma ◽  
Clinical Picture ◽  
Chronic Subdural Hematoma ◽  
Sensory Deficit ◽  
Transient Ischemic Attacks ◽  
Neurological Manifestations ◽  
Content Type ◽  
Pathophysiological Mechanisms ◽  
Cerebral Ischemic ◽  
Fine Print

✓ A patient is presented in whom chronic subdural hematoma simulated transient ischemic attacks. The neurological manifestations were those of recurrent, transient episodes of expressive dysphasia preceded by focal sensory deficit. Various pathophysiological mechanisms which could have caused the unusual clinical picture are briefly considered.

Chronic subdural hematoma in infancy

1990 ◽  
Vol 73 (2) ◽  
pp. 201-205 ◽  
Author(s):  
Nobuhiko Aoki
Keyword(s):  
Computerized Tomography ◽  
Subdural Hematoma ◽  
Treatment Protocol ◽  
Chronic Subdural Hematoma ◽  
Neurological Deficits ◽  
Acute Subdural Hematoma ◽  
Hemorrhagic Diathesis ◽  
Content Type ◽  
Fine Print ◽  
Subdural Tapping

✓ The cases of 30 infants with chronic subdural hematoma treated surgically between 1978 and 1987 (after the introduction of computerized tomography) were reviewed. This series was limited to infants presenting with increased intracranial pressure, neurological deficits, or developmental retardation. Nineteen patients were male and 11 were female, ranging in age from 1 to 14 months (average 6.1 months). The surgical treatment was initiated with percutaneous subdural tapping which was repeated periodically, if indicated, for 2 weeks. If the patients failed to respond to subdural tapping, subdural-peritoneal shunting was installed. The follow-up periods were from 3 months to 9 years 8 months (average 4 years 10 months). Computerized tomography at that time disclosed disappearance or minimal collection of subdural fluid in 28 cases (93%) and a significant collection (> 5 mm) in two (7%). Neurological examination revealed that the patients were “normal” in 17 cases (57%), “mildly or moderately disabled” in nine (30%), and “severely disabled” in four (13%). The majority of disabled patients had lesions secondary to infantile acute subdural hematoma, child abuse, or hemorrhagic diathesis. These results indicate that the treatment protocol in the present series is acceptable for the elimination of subdural hematoma. Together, early diagnosis and treatment of the etiological conditions causing the lesion are indispensable for obtaining a satisfactory neurological outcome.

Acute brain edema in fatal head injury: analysis by dynamic CT scanning

1985 ◽  
Vol 63 (6) ◽  
pp. 830-839 ◽  
Author(s):  
Eiji Yoshino ◽  
Tarumi Yamaki ◽  
Toshihiro Higuchi ◽  
Yoshiharu Horikawa ◽  
Kimiyoshi Hirakawa
Keyword(s):  
Head Injury ◽  
Brain Edema ◽  
Subdural Hematoma ◽  
Ct Scans ◽  
Acute Subdural Hematoma ◽  
Dynamic Ct ◽  
Content Type ◽  
Injured Patients ◽  
Fine Print ◽  
Diffuse Brain

✓ Dynamic computerized tomography (CT) was performed on 42 patients with acute head injury to evaluate the hemodynamics and to elucidate the nature of fatal diffuse brain bulk enlargement. Patients were divided into two groups according to the outcome: Group A included 17 nonfatally injured patients, eight with acute epidural hematomas and nine with acute subdural hematomas; Group B included 25 fatally injured patients, 16 with acute subdural hematomas and nine with bilateral brain bulk enlargement. Remarkable brain bulk enlargement could be seen in all fatally injured patients with acute subdural hematoma. In 29 (69%) of 42 patients, dynamic CT was performed within 2 hours after the impact. In the nonfatally injured patients with brain bulk enlargement, dynamic CT scans suggested a hyperemic state. On the other hand, in 17 (68%) of the 25 fatally injured patients, dynamic CT scans revealed a severely ischemic state. In the fatally injured patients with acute subdural hematoma, CT Hounsfield numbers in the enlarged hemisphere (hematoma side) were significantly lower than those of the opposite side (p < 0.001). Severe diffuse brain damage confirmed by follow-up CT scans and uncontrollable high intracranial pressure were noted in the fatally injured patients. Brain bulk enlargement following head injury originates from acute brain edema and an increase of cerebral blood volume. In cases of fatal head injury, acute brain edema is the more common cause of brain bulk enlargement and occurs more rapidly than is usually thought.

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