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At least 19 recordsLinked to original sources
PubMed1993

The osteogenic potential of fracture hematoma and its mechanism on bone formation--through fracture hematoma culture and transplantation of freeze-dried hematoma.

This study was conducted to provide further evidence of the inherent osteogenic potential of the fracture hematoma. The fracture hematoma was separated into its cellular and extracellular elements. The hematoma cells were cultured to study bone formation by the cellular elements alone. Bone formation acceleration factor was added to the cultured fracture hematoma cells. The cell responded to this stimulation by differentiation into chondrocytes. Fracture hematoma was freeze-dried to study the presence of osteoinduction by the extracellular factors in the fracture hematoma. The freeze-dried fracture hematoma was packaged in methylmethacrylate pellets and within capsules of hydroxyapatite. These pellets and capsules in response to extracellular humoral factors from the freeze-dried fracture hematoma. The results of experimental implantation of the cultured fracture hematoma cells revealed that these cells had the potential to differentiate into chondroblasts or osteoblasts when bone induction factors and bone acceleration factor was added to their media. These extracellular humoral factors are known to be present in the fracture hematoma.

Animals↗
PubMed1976

Physiopathogenesis of subdural hematomas. Part 1: Histological and biochemical comparisons of subcutaneous hematoma in rats with subdural hematoma in man.

The dorsal subcutaneous injection in rats of 12 ml or more of autologous hemolyzed whole blood clotted in situ induced the formation of sterile, hemispheric lesions, 47% of which showed an initial decrease in volume followed by a progressive enlargement. The behavior, histology, and biochemical characteristics of the liquid contents of these lesions were found to be remarkably similar to those of subdural hematomas in man. To evaluate the role of the various blood components that may have influenced the formation and growth of these lesions, more than 150 clots composed of human platelet-free plasma, autologous hemolyzed blood, or autologous whole blood were implanted subcutaneously in rats by either surgical or injection techniques. The in vitro behavior of the different clots used was also assessed. This systematic approach led to the following conclusions: 1) the composition and volumes of the clots are critical variables; 2) plasma-fibrin provides the matrix shape of the lesions; 3) the breakdown products derived from erythrocytes, hemoglobin, leukocytes, and other solid blood elements induce neomembrane formation and contribute to the lesion's subsequent growth; and 4) inflammation mechanisms appear to be essential, while cerebrospinal fluid plays no discernable role in this process.

Animals↗
PubMed1988

[Growing factors of chronic subdural hematoma--significance of CK activity in hematoma contents and neomembrane].

The growing mechanism of the chronic subdural hematoma has not fully understood yet, in spite of numerous studies about hematoma neomembranes. However, it is well known that the majority of the chronic subdural hematomas are well healed by a simple irrigation of hematoma. These facts suggested that the hematoma contents could have important growing factors of the chronic subdural hematoma. Thus, LDH and CK activities were estimated in 52 cases of hematoma contents and 15 cases of hematoma neomembranes in order to search growing factors, biochemically. Hematocrit and hemoglobin values in hematoma contents were also examined simultaneously. As a result, hematocrit and hemoglobin values in hematoma contents were gradually increased, these facts might be due to the concentration of hematoma contents. LDH and CK activities in hematoma contents were high around 60 days after the hematoma inducing head trauma, and these enzyme activities were not correlated with hematocrit value. In isozyme analysis of LDH and CK activities, LDH-1,2 and CK-MM showed high values but CK-BB, MB could not be recognized. These findings suggested that LDH activity in the hematoma contents were caused by hemolysis which had been reported to be a main cause, and CK activity might originate from muscular tissues. Therefore, author hypothesized that the CK activity in hematoma contents had originated from the neomembrane, since there was a good correlation between the mature stage of neomembrane and the high level of CK-MM, and the myofibroblast was found in neomembrane recently. CK-MM could be released from the myofibroblast in neomembrane. However, CK activity in hematoma neomembrane could not be recognized, biochemically nor immunohistochemically.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Intraoperative development of contralateral epidural hematoma during evacuation of traumatic extraaxial hematoma.

Intraoperative development of an epidural hematoma contralateral to a craniotomy for acute traumatic extraaxial hematoma has been previously reported. This entity, however, has never been distinctly defined and differentiated from either the delayed or the bilateral acute epidural hematoma. We present 3 new cases of intraoperative contralateral acute epidural hematoma and review the 14 previously reported cases. The typical clinical presentation is a severe head injury with an acute extraaxial hematoma and severe ipsilateral brain displacement during craniotomy. If brain displacement is not noted at craniotomy, then the contralateral hematoma is manifested by immediate postoperative neurological deterioration or intractable elevated intracranial pressure. The presence of any of these signs makes an immediate postoperative CT scan or burr holes contralateral to the original craniotomy mandatory for early diagnosis. In addition to defining "intraoperative contralateral epidural hematoma," stricter definitions of the terms "delayed epidural hematoma" (no hematoma present on the initial CT scan but one present on a later scan) and "bilateral epidural hematomas" (present on the initial scan) are proposed.

Adolescent↗
PubMed1989

[Clinical aspects of traumatic intracerebral hematomas. Pathogenesis of delayed traumatic intracerebral hematomas].

Eighty three cases of traumatic intracerebral hematomas (maximum diameter of at least 3 cm) were classified into the following two groups. Group-1 consisted of 34 cases in which intracerebral hematomas were confirmed in the initial CT scans on admission. Group-2 consisted of 49 cases in which intracerebral hematomas were found not in the initial CT scans on admission, but in the second or later CT scans. This is the so-called CT-diagnosed delayed traumatic intracerebral hematomas which have been widely reported in recent years with the increasing use of CT scans. These two groups were studied clinically and the following results were obtained. 1) Traumatic intracerebral hematomas were apt to occur in middle-aged or elderly patients, and more delayed cases increased in patients of 60 or older. 2) The times when the formation of traumatic intracerebral hematomas were judged as completed showed two peaks: within 6 hours after the trauma and 12 to 24 hours after the trauma. 3) Excluding traumatic hemorrhages in the basal ganglia, there were many hematomas in the frontal lobes in the cases of coup injuries by anteroposterior force or contre-coup injuries by posteroanterior force and in the temporal lobes in the cases of contre-coup injuries by lateral force. Traumatic hemorrhages in the basal ganglia were seen in 10 cases, six of which were in Group-1. In all six of these cases, the intracerebral hematoma was confirmed within 6 hours after the trauma and the direction of the external force was unclear. Except for the findings described in 1) to 3), there were no differences in the basic pathogenesis and characteristics between the two groups. These results indicate that there is no essential difference in pathogenesis between CT-diagnosed delayed traumatic intracerebral hematomas and other intracerebral hematomas, as far as the present clinical studies are concerned.

Adolescent↗
PubMed1992

[Acute epidural hematoma following evacuation of chronic subdural hematoma with continuous closed system drainage].

The authors report a case of acute epidural hematoma occurring after evacuation of chronic subdural hematoma with continuous closed system drainage. Laboratory data of the patient including bleeding time were within normal limits. The cause of the postoperative intracranial hematoma was the rapid surgical decompression of the initial lesion, and we considered that it could be prevented if chronic subdural hematoma was treated using closed system drainage and slow decompression. But acute epidural hematoma occurred after this operative procedure and it was accelerated by evacuation of the chronic subdural hematoma through the drain. An emergent craniotomy and removal of the hematoma was performed, so the patient was discharged from hospital with satisfactory neurological recovery. A careful check of the evacuated hematoma volume is very important, and CT scanning should be immediately performed if postoperative hematoma is suspected.

Acute Disease↗
PubMed1994

Analysis of plasma and hematoma lipids related to choline glycerophospholipid in patients with chronic subdural hematoma.

The levels of platelet-activating factor (PAF) and lipid metabolites related to choline glycerophospholipid were measured in the plasma and hematoma samples obtained from patients with chronic subdural hematoma. The ratio of lyso-choline glycerophospholipids (lysoPC) to choline glycerophospholipids (PC) in hematoma correlated with the interval between the onset of symptoms and surgery. PC and lysoPC fatty acyl moieties in plasma and hematoma were essentially similar. These results suggest that the lysoPC to PC ratio in hematoma can determine the age of the chronic subdural hematoma, and that the origin of hematoma may be circulating blood. The levels of PAF in the plasma of chronic subdural hematoma patients were significantly greater than in healthy volunteers. PAF may be involved in the enlargement of chronic subdural hematoma.

Aged↗
PubMed1993

[Bilateral chronic subdural hematoma with communication between the hematoma cavities: report of an adult case].

The authors present a case of bilateral chronic subdural hematoma with communication between the hematoma cavities. This 24-year-old male had hit his forehead while playing football and visited our hospital. An initial plain CT scan revealed extracerebral low density areas in the bifrontal region, which were considered to be post-traumatic subdural hygromas. The lesion was followed up with repeat CT scans. On plain CT scan performed seven weeks after the injury, the lesion had evolved into bilateral chronic subdural hematoma and the patient was admitted to our ward. He underwent burr hole drainage on the left side, because the hematoma volume on the left side was considerably larger than that on the right side. A plain CT scan on the day following the operation revealed complete resolution of the hematomas on both sides. A favorable re-expansion of the brain was confirmed on consecutive CT scan performed two months after the operation. In general bilateral chronic subdural hematomas in adults are considered to have no communication between the hematoma cavities and therefore they should be evacuated on both sides simultaneously. In our case, on the contrary, the operation revealed a communication between the hematoma cavities. The falx cerebri is narrow in front and this narrow anterior part is frequently perforated by one or more apertures. We attributed the communication to this anatomical feature of the falx cerebri. On preoperative CT scan, in addition, the inner surface of the bifrontal hematoma cavity demonstrated a smooth concave figure indicating retrospectively that the cavity on the left side was continuous with that on the right side.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

[Acute hematoma between the dura and the external membrane of hematoma capsule of after the removal of bilateral chronic subdural hematomas by trepanation. Case report].

A case of reported of complication following surgical treatment of bilateral subdural haematomas in an elderly man. Acute haematoma developed after the operation between the dura and the external surface of the capsule of the haematoma which had been removed several hours earlier through a trepanation hole. Attention is called to the atypical localization of the complication with bleeding externally to the capsule and not into the space left after haematoma evacuation which is usually observed in case of haematoma recurrence. The problem is discussed, whether such bleeding during chronic persistence of haematoma can lead to the development of multilayer and multilocular haematomas. In the presented case quick recognition of the complication followed by reoperation with removal of haematoma and bleeding capsule through craniotomy with rehabilitation treatment after the operation has led to very good therapeutic effect.

Acute Disease↗
PubMed2003

Significance of consecutive bilateral surgeries for patients with acute subdural hematoma who develop contralateral acute epi- or subdural hematoma.

BACKGROUND: Although rare, patients with acute subdural hematoma (ASDH) because of severe head injury can develop contralateral acute epi- or subdural hematoma, requiring consecutive surgical procedures. The choice of treatment strategies for such patients is clinically important. METHODS: Among 88 patients with ASDH who were surgically treated over 13 years, we encountered and studied 5 patients who developed contralateral acute epi- or subdural hematoma (5.7%). RESULTS: All 5 patients were male, ranging in age from 17 to 40. According to the Glasgow Coma Scale on admission, 1 patient was rated 3, 1 was 4, 1 was 5, and 2 were 6. All patients underwent consecutive surgical procedures for ASDH and contralateral ASDH and/or acute epidural hematoma, and were given postoperative supportive therapy with barbiturates and mild hypothermia. Patients' outcomes according to the Glasgow Outcome Scale were as follows: 1 patient, good recovery (20.0%); 1, mild disability (20.0%); 2, severe disability (40.0%), and 1, persistent vegetative state (20.0%). No patients died. Although decompressive craniectomy and evacuation of hematoma may lead to contralateral acute epi- or subdural hematoma in patients with ASDH, this therapy is justified because hematoma irrigation with trephination therapy has a poor outcome for comatose patients. CONCLUSION: Awareness of intraoperative brain swelling is important, as it suggests the development of contralateral hematoma. Immediate computed tomography and a rapid return to the operating room are therefore critical.

Adolescent↗
PubMed2003

[Relationship of survival rate, hematoma thickness and midline shift in patients with acute subdural hematomas].

OBJECTIVE: To estimate outcomes of patients with acute subdural hematomas by analysing the hematoma thickness, midline shift and the differences between them. METHODS: Ninety-five patients with acute subdural hematoma were retrospectively studied by calculating hematoma thickness, midline shift and their difference with a statistical analysis of Kaplan-Meier, Wilcoxon-Mann-Whitney U test. RESULTS: The hematoma thickness ranged from 5.0 to 40.0 mm and midline shift was from 0 to 35.0 mm. Among these patients, 51% died and 49% survived after surgery. 18 patients (19%) showed good or satisfactory results. Kaplan-Meier analysis proved that the survival for patients with hematoma thickness approximately equal to l7 mm and a midline shift 15 mm or whose midline shift exceeded hematoma thickness by 2.2 mm, the survival rate was 50%. Glasgow outcome scale scores were correlated significantly with these parameters. CONCLUSION: The hematoma thickness, midline shift and their difference provided a database from which criteria could be derived, that is crucial for prognosis estimation.

Adolescent↗
PubMed1995

Carbon-11-methionine PET evaluation of intracerebral hematoma: distinguishing neoplastic from non-neoplastic hematoma.

UNLABELLED: We evaluated whether PET with L-methyl-11C-methionine (11C-methionine) was clinically useful in distinguishing neoplastic from non-neoplastic intracerebral hematoma. METHODS: We examined eight patients with neoplastic (n = 4) or non-neoplastic (n = 4) intracerebral hematomas between 5 and 68 days after the bleeding episode using PET with 11C-methionine (Met-PET). RESULTS: Carbon-11-methionine accumulated in the area surrounding the hematoma in both groups, except in one patient with an acute hypertensive hematoma. Between 22 and 45 days after the ictus, non-neoplastic hematomas showed increased 11C-methionine accumulation largely in accordance with the contrast-enhanced areas on CT or MR images; whereas between 14 and 68 days after bleeding, neoplastic hematomas showed increased 11C-methionine accumulation that extended beyond the contrast-enhanced areas on CT or MR images. The intensity of 11C-methionine accumulation in tumor tissue was greater than that in non-neoplastic hematomas. CONCLUSION: Preliminary results suggest that Met-PET can distinguish neoplastic from non-neoplastic hematomas on the basis of differences in lesion extent compared with CT or MR findings.

Adult↗
PubMed1998

[A study of acute subdural hematoma developing into hematoma with capsule formation].

There are some cases in which conservatively treated acute subdural hematoma (ASDH) does not disappear naturally and progresses to chronic subdural hematoma-like hematoma (CSDH) (hematoma with capsule formation). The objective of the present study was to identify factors which can be used to predict this unfavorable course during the early phase after the onset of the lesion. During the past 13 years, 10 of 96 cases of mild, conservatively treated ASDH (excluding suckling infants) progressed to CSDH, and those 10 patients showed the following background characteristics. There were 7 males and 3 females, and the mean age was 63.1 years. Five of the patients had a history of alcohol consumption, and one case each had a history of cerebral infarction, cerebral hemorrhage and a VP shunt. Acute-phase computerized tomography (CT) at the time of ASDH showed, in all 10 cases, an expansive-type lesion with a low density area in the hematoma, with expansion of the hematoma into the interhemispheric fissure. The hematoma was observed to undergo transient natural shrinkage in the acute phase. The period for progression to CSDH was indicated to be a mean of 20.5 days after the onset of the lesion, and its cure was possible with trepanation. In consideration of these results, it was surmised that ASDH patients with the following characteristics have a high risk of progression to CSDH during the subacute and chronic phases when conservative therapy is administered during the acute phase of the lesion: (1) old age, (2) a history indicative of brain atrophy, (3) an expansive-type image of ASDH on acute-phase CT, and (4) acute-phase CT indicative of cerebrospinal fluid mixing in the hematoma.

Acute Disease↗
PubMed1991

Spinal epidural hematoma following epidural anesthesia versus spontaneous spinal subdural hematoma. Two case reports.

Two cases of lumbar hemorrhage with subsequent persistent neurologic sequelae are presented and their possible causes are discussed in the context of a literature review: one patient with spontaneous spinal subdural hematoma with no trauma or lumbar puncture and one with spinal epidural hematoma associated with preceding epidural catheterization for postoperative pain relief. The subdural hematoma was associated with a thrombocytopenia of about 90,000/microliters due to intraoperative blood loss. This might have been contributory to the formation or expansion of the hematoma, but it is not convincing since a platelet count of this amount should not lead to spontaneous bleeding. Both patients received low-dose heparin, but since coagulation tests were normal, prolonged bleeding does not appear to be a likely cause, although it cannot be excluded. In conclusion, the reasons for both hematoma remain unclear. With regard to the epidural hematoma and low-dose heparinization, the possible coincidence of spontaneous lumbar hematoma and lumbar regional block should be taken into consideration.

Anesthesia, Epidural↗
PubMed1989

[Studies on the operative factors affecting the reduction of chronic subdural hematoma, with special reference to the residual air in the hematoma cavity].

The authors previously reported the effect of preoperative factors affecting the reduction of chronic subdural hematoma. In this report, we evaluated some operative factors, including operative methods, duration of drainage, and residual air volume, with newly developed CT volumetry technique. As described before, the hematoma volume reduces exponentially. An exponential curve was fitted to the reduction curve using the least square method, and its half reduction days (HRD) was calculated. This HRD represents a mathematical indicator of the reduction rate of CSDH. Using this technique, the relationship between this HRD and operative method, the duration of drainage and the volume of the postoperative residual air were examined in 61 patients. Operative method (burr hole or small craniotomy) has no correlation with HRD. The duration of drainage also has no correlation. However, the volume of the residual air was highly correlated with the reduction rate of hematoma (r = 0.430; p less than 0.01). These results suggest that the residual air in the hematoma cavity may delay the reduction rate of the hematoma. Based on these results, the authors pay attention to the following points; 1) Less invasive burr hole method should be selected. 2) Patient's head position should be controlled to make the burr hole at the highest level in the operative field. 3) Hematoma cavity should be filled with saline as much as possible. 4) The inner membrane should never be injured, as it may cause tension pneumocephalus. Moreover, the drainage of cerebrospinal fluid may reduce the counter pressure and it leads to the delay of the hematoma reduction.

Adult↗
PubMed1997

[A case of infected subdural hematoma complicating chronic subdural hematoma in a healthy adult man].

The authors report a case of so-called "infected subdural hematoma" as a complication of chronic subdural hematoma. The patient was a 55-year-old man who had sustained a small laceration of the forehead in a traffic accident on March 29, 1995. No fractures were detected on skull roentgenograms, and general and neurological examinations failed to reveal any abnormal findings. In early August 1995, the patient began to experience headaches, and on August 5 he developed a fever of 38 degrees C. On August 8 he suffered a left motor seizure and was admitted to our hospital. Laboratory studies revealed a peripheral leukocyte count of 10,800/mm3 and a C-reactive protein level of 18.1 mg/dl. Computed tomography scans showed a thick right fronto-parietal subdural low density mass and a thin left frontal subdural low density mass. An emergency operation was performed via a single right fronto-parietal burr hole. A chronic subdural hematoma containing slightly yellowish, bloody, purulent fluid was found beneath an outer membrane. The hematoma was irrigated with physiological saline containing antibiotics, and a drain was inserted into the subdural space. A subdural membrane was also present on the left but it contained no pus. Aggressive antibiotic therapy was performed, and the patient was discharged without any neurological deficit. Histologically the membrane was determined to be the outer membrane of a typical chronic subdural hematoma. Enterococcus faecalis, which has rarely been reported to cause infection of the central nervous system, was detected in a bacterial culture of the pus. Systemic investigation showed no evidence of otorhinologic or other focal infection. The above clinical findings suggested that hematogenous seeding of a chronic subdural hematoma had occurred in this patient. Subdural empyema arising from hematogenous seeding to a pre-existing subdural hematoma by an infection is very rare, but this type of complication must be kept in mind not only in the elderly, infants, and compromised hosts, but in patients without complications as well.

Chronic Disease↗