Serial changes in acute extradural hematoma size and associated changes in level of consciousness and intracranial pressure

The authors report the cases of 37 patients encountered during the past 4 years who exhibited acute extradural hematoma but were initially treated conservatively because no or only small hematomas were observed on admission. The frequency of hematoma enlargement, hematoma size, and changes in the level of consciousness and intracranial pressure (ICP) were examined in these patients. The hematomas enlarged in 24 (64.9%) of the 37 patients, and attained a maximum thickness of 25 mm or greater in 19 patients (51.3%). The level of consciousness could be closely observed during enlargement of the hematomas in 13 patients: the level remained unchanged in eight, deteriorated in two, and improved in three, indicating relative stability in the state of consciousness despite the marked changes in hematoma size. The patients whose hematoma enlarged after the initial examination included three who underwent initial CT examination 5 hours after the injury. In five patients enlargement of extradural hematomas was observed unexpectedly during conservative treatment under ICP monitoring. The ICP also remained stable in three patients until the follow-up examination, but showed a rapid increase in two after a period of stability. However, there was no difference in the final size of the hematomas between the patients showing an increase in ICP and those who did not. These findings suggest that extradural hematomas enlarge progressively at rates varying with the condition of the source of hemorrhage. Moreover, a period of stability in the level of consciousness, such as the lucid interval seen in patients with extradural hematoma, is considered to be a period during which compensatory mechanisms can maintain the stability of the intracranial condition during progressive enlargement of the hematoma.     

Clinical significance of intracranial hemorrhage caused by cerebral arteriovenous malformations: with special reference to intraventricular hemorrhage

Forty-two cases with intracranial hemorrhage caused by cerebral arteriovenous malformation (AVM), which was diagnosed by CT scan, were reviewed with regard to the clinical significance of intracranial hemorrhage, especially intraventricular hemorrhage (IVH). Twenty-one patients were defined as poor risk cases whose level of consciousness at admission was 100 to 300 according to the Japan Coma Scale, whereas the remaining 21 patients were defined as good risk cases. Surgical excision of AVM was undertaken in 35 out of the 42 cases. Urgent surgical removal of intracerebral hematoma and AVM within 24 hours following onset was undertaken in 11 cases. In 14 patients, urgent continuous ventricular drainage was carried out. The effects of the following factors on the level of consciousness at admission, and on the result of AVM treatment were investigated to clarify the clinical significance of intracranial hemorrhage; 1) cast formation of 3rd and/or 4th ventricle, 2) volume of intraventricular hematoma, 3) accompanying intracerebral hematoma and 4) acute hydrocephalus. It was confirmed that all these factors significantly contributed to the development of serious disturbance of consciousness in the acute stage following intracranial hemorrhage. For good risk cases, the rate of patients who showed a good recovery or only moderate disability according to the Glasgow Outcome Scale reached 91%, whereas for poor risk cases, it was only 43%. The presence of large intracerebral hematomas of more than 4 cm in diameter accompanied with IVH was significantly correlated with the result of AVM treatment. The presence or absence of cast formation of 3rd and/or 4th ventricle, volume of intraventricular hematoma and acute hydrocephalus were not significantly related to the result of AVM treatment.(ABSTRACT TRUNCATED AT 250 WORDS)     

Predictors of hematoma enlargement in patients with intracerebral hemorrhage treated with rapid administration of antifibrinolytic agents and strict blood pressure control

OBJECT: Hematoma enlargement is a major cause of poor outcome in patients with intracerebral hemorrhage (ICH). A combination of rapid administration of antifibrinolytics and strict blood pressure (BP) control for prevention of hematoma enlargement has been recently reported. The authors examined the incidence and predictors of hematoma enlargement in patients with ICH who were treated with this therapy. METHODS: Rapid administration of antifibrinolytic agents consisted of intravenous administration of 2 g tranexamic acid over 10 minutes. Systolic BP was strictly maintained below 150 mm Hg using intravenous nicardipine. Immediately after diagnosis of ICH on computed tomography (CT), 188 patients who were admitted within 24 hours of symptom onset were treated with a combination of rapid administration of antifibrinolytic agents and BP control. Hematoma enlargement was determined on the basis of a second CT scan performed the day after admission. Several factors, including those that have been reported to affect hematoma enlargement, were compared between patients with and without hematoma enlargement. Hematoma enlargement (> or =20% volume increase) was observed in eight (4.3%) of 188 patients. Previous use of antiplatelet agents was significantly more frequent in patients with hematoma enlargement (p < 0.05). No significant between-group difference was found for any other factors Conclusions. Previous use of antiplatelet agents was a predictor of hematoma enlargement in patients with ICH treated with rapid administration of antifibrinolytic agents and BP control.     

Involvement of fluctuating high blood pressure in the enlargement of spontaneous intracerebral hematoma.

The correlations between changes in blood pressure after admission and hematoma expansion were investigated in 118 patients with spontaneous intracerebral hematoma admitted within 24 hours of onset who underwent serial computed tomography. Multiple logistic regression was performed to assess correlations between hematoma enlargement and clinical characteristics on admission. Hematoma enlargement was predominantly correlated with time of onset (p = 0.01567), and not well correlated with blood pressure at admission (p = 0.07908). Serial changes in blood pressure were investigated in 57 patients admitted within 6 hours of ictus whose blood pressures were monitored every hour from admission. Wilcoxon signed-rank analysis was used to determine the relationships between hematoma enlargement and blood pressure. Patients with hematoma enlargement was significantly correlated with increased blood pressure (p = 0.0004). Increases in blood pressure after admission may be a factor in hematoma enlargement.     

Unusual postoperative hemorrhage in a patient with ruptured aneurysm and hemophilia B

A case of ruptured cerebral aneurysm with hemophilia B is reported, and discussion is made concerning the management of mild type hemophilia in surgical operations. A 41-year-old male came to our hospital with complaints of severe headache, vomiting, and transient consciousness disturbance. His dentist said the patient had a mild bleeding tendency when he was 30 years old, however no postoperative hemorrhage was repeated in appendectomy in his childhood. He also had had no episodes of spontaneous bleeding. CT scan on admission showed subarachnoid hemorrhage, and angiography revealed a ruptured aneurysm at the trifurcation of the left middle cerebral artery. His coagulation screening tests (bleeding time, clotting time, prothrombin time, and activated partial thromboplastin time) were normal. An aneurysmal neck clipping was carried out, and operators did not detect any bleeding tendency during the surgery. CT scan on the next day showed no remarkable finding. On the third postoperative day, right hemiparesis occurred. Left putaminal hemorrhage took place. His coagulation tests and FDP were also normal. The hematoma was partially evacuated. After the second operation his condition was good, and rehabilitation program started. On the 15th hospital day his consciousness deteriorated suddenly, and CT scan showed a massive epidural hematoma on the left. His prothrombin time elongated mildly, but other tests were normal. Coagulation factors VIII and IX were examined and the factor IX was 22.5% of control. He was thought to be a patient with mild type hemophilia B. Despite a third operation for hematoma removal he died on the 20th hospital day. Mild type hemophilia B does not bleed spontaneously.(ABSTRACT TRUNCATED AT 250 WORDS)     

Physiopathology of chronic subdural hematoma

Coagulation, fibrinolysis and kinin-kallicrein system disorders could explain chronic subdural hematoma pathophysiology. The marked decrease in antithrombin III in the hematoma suggest that the decreased levels of clotting factors were caused by excessive coagulation resulting in clotting factors consumption. The decrease in alpha 2-antiplasmin with the increase of fibrin degradation products suggest that hyperfibrinolytic activity of the subdural hematoma. Coagulation and fibrinolysis disorders could explain repetitive hemorrhages from the outer membrane, which cause progressive enlargement of the hematoma. Kinin-kallicrein system disorders raise the hemorrhage by its action on the outer membrane. Nowadays, the earliest osmotic theory should reasonably be abandoned.     

Stereotactic evacuation of hypertensive cerebellar hemorrhage using plasminogen activator

Treatment for hypertensive cerebellar hemorrhage still remains controversial as to whether direct surgical procedure is indicated or not. This is so even after the introduction of CT scan which easily demonstrates the location and size of the hematoma and the presence of hydrocephalus. In this paper, we present our experience of 20 patients with cerebellar hemorrhage treated by stereotactic evacuation using Komai's CT-stereotactic apparatus. All the patients had vertigo, cerebellar symptoms, dysfunction of brain stem or consciousness disturbance. The hematomas on CT scan were more than 28 mm in diameter. Acute obstructive hydrocephalus occurred in 90% of the patients with hematoma 40 mm or larger in size. The patients with consciousness disturbance were immediately operated on after the attack, and a drainage tube was placed in the hematoma cavity to drain cerebrospinal fluid and liquefied hematoma for one to eight days. On the other hand, when patients with hematoma around 30 mm in diameter complained vertigo for about two weeks, they also were operated on stereotactically. After the operation, their symptoms improved rapidly. The stereotactic operation could aspirate about 85% of the estimated hematoma volume and improved the hydrocephalus, except in one case in which the patient rapidly deteriorated to coma level with a large cerebellar hemorrhage and brain stem damage. This stereotactic evacuation of cerebellar hematoma using a plasminogen activator is effective for not only the removal of hematoma, but also for the treatment of secondary hydrocephalus following obstruction of the fourth ventricle by cerebellar hemorrhage.(ABSTRACT TRUNCATED AT 250 WORDS)     

Coagulation and fibrinolysis in chronic subdural hematoma

In 19 patients with chronic subdural hematoma, coagulation and fibrinolysis in venous blood taken at the time of surgery and in the hematoma contents aspirated from chronic subdural hematoma were studied. Compared with coagulation results for venous blood, the hematoma contents demonstrated marked prolongation of the recalcification time, prothrombin time, and activated partial thromboplastin time, and marked reduction of clotting factor V, the hepaplastin test, prothrombin, and fibrinogen. Antithrombin III was also decreased, and fibrinopeptide A was increased in the hematomas. Fibrinolytic results demonstrated that both plasminogen and alpha 2-plasmin inhibitor were decreased, and both fibrinopeptide B beta 15-42 and fibrin and fibrinogen degradation products were increased in the hematomas. These findings indicate excessive activation of the clotting system, thrombin generation, and increased fibrinolytic activity occurring in the hematomas. From these results, excessive activation of both the clotting and fibrinolytic systems is emphasized to be the possible etiological factor for the origin and development of chronic subdural hematoma.     

Paramedian suboccipital mini-craniectomy for evacuation of spontaneous cerebellar hemorrhage

Patients with spontaneous cerebellar hemorrhage are usually treated by large suboccipital craniectomy for hematoma evacuation or by computed tomography-guided stereotactic aspiration of the hematoma. The present study evaluated the outcome and complications in 25 patients with spontaneous cerebellar hemorrhage treated by paramedian suboccipital mini-craniectomy and 21 patients treated by large suboccipital craniectomy. There were no significant differences between the two groups with respect to age, clinical grade, hematoma volume, hematoma location, hydrocephalus, and mean interval from admission to operation. There was also no significant difference in postoperative outcome between the two groups. However, patients treated by paramedian suboccipital mini-craniectomy were less likely to require blood transfusion, had a shorter operating time, and had less postoperative liquorrhea compared with those undergoing extensive suboccipital craniectomy. Paramedian suboccipital mini-craniectomy is a simple and effective method for hematoma evacuation that causes fewer complications.     

Grading and operative indication for hypertensive cerebellar hemorrhage

Fifty six patients with hypertensive cerebellar hemorrhage diagnosed by CT scan were hospitalized from November 1976 up to June 1984. The 35 male and 21 female patients ranged in age from 24 to 84 years, and 39 of them were operated on. The important factors related to prognosis of cerebellar hemorrhage were level of consciousness, size of hematoma on CT scan, and massive ventricular hemorrhage resulting in obstruction of the ventricular system. We classified the patient with cerebellar hemorrhage into 5 grades, according to the severity of these factors. Grade I indicates cerebellar signs without disturbance of consciousness and size of hematoma less than 25 mm measured by CT scan. Grade II indicates disturbance of consciousness (stupor), or progressive neurological deficits, and size of hematoma less than 50 mm without acute hydrocephalus. Grade III reveals disturbance of consciousness (stupor-semicoma), and size of hematoma less than 50 mm with acute hydrocephalus. Grade IV reveals severe disturbance of consciousness (semicoma), and size of hematoma less than 50 mm with massive ventricular hemorrhage. Grade V exhibits deep coma, and more than 50 mm diameter of hematoma. The prognosis of all of 9 patients in Grade I was good, Eleven out of 13 patients (85%) in Grade II and all of 9 patients in Grade III were alive. Fourteen out of 19 patients (74%) in Grade IV and all of 6 patients in Grade V expired in spite of operation. The patients of Grade I should be treated by conservative therapy. The patients of Grade II, Grade III, and Grade IV should be managed surgically. Surgical treatment for Grade V is not advisable.     

The relationship between delayed traumatic intracerebral hematoma and coagulopathy in patients diagnosed with a traumatic subarachnoid hemorrhage

It has long been recognized that a traumatic insult to brain tissue may result in substantive coagulation abnormalities. The present study was carried out in an attempt to find out the association of coagulopathy and the development of delayed traumatic intracerebral hematoma (DTICH) in patients diagnosed with a traumatic subarachnoid hemorrhage (TSAH). Sixty-three patients were diagnosed as having TSAH from the initial CT scans obtained within 2 hours after trauma. On admission, peripheral blood samples for coagulation studies were taken within 6 hours after injury. All patients had subsequent CT scans performed within 24 hours of admission. Thirty (47.6%) of 63 patients exhibited radiological evidence of DTICH on their subsequent CT scans. There was a significant correlation between the increased value of serum fibrinogen degradation product (FDP > 40 micrograms/ml) and the development of DTICH. We observed that the origin of the hematoma might be caused by those radiographically unidentifiable parenchymal lesions often found with TSAH on the initial CT scan. We conclude that a clotting study at the time of admission is of value in predicting the occurrence of DTICH associated with TSAH.     

Prognostic factors in acute subdural hematoma and the significance of serum FDP measurement

Sixty-two cases of acute subdural hematoma were clinically analyzed with special reference to such prognostic factors as age, Glasgow Coma Scale (GCS) score on admission, pupillary signs, decerebration, and initial computed tomography (CT) findings. Intraparenchymal lesions demonstrated by CT were evaluated according to Yamaura's classification. In 19 cases, serum fibrin and fibrinogen degradation products (FDP) were measured at the time of admission. Emergency surgery was performed in 46 cases, and the remaining 16 patients were treated conservatively. The final outcome was judged according to the Glasgow Outcome Scale, and patients were divided into a "good outcome" group (good recovery or moderate disability) and a "poor outcome" group (severe disability, vegetative state, or death). In general, the outcomes proved to be unsatisfactory. Forty-four patients (71%) had a poor outcome, with 32/62 (52%) mortality, and only 18 (29%) had a good outcome. The clinical factors associated with a poor outcome were age over 64 years, a GCS score on admission of less than 7, decerebration, and absence of pupillary reaction to light. Initial CT scans showed brain damage in 46 patients (74%), 39 (85%) of whom had a poor outcome. This indicates that the outcome was significantly related to brain injury complicating the acute subdural hematoma. A high serum FDP level was similarly related to a poor outcome, which suggests that the serum FDP level reflects the degree of both primary and secondary brain injury. Thus, measurement of serum FDP may be valuable both in assessing clinical status and in evaluating the extent of brain injury in acute subdural hematoma.     

Prediction of death in patients with primary intracerebral hemorrhage: a prospective study of a defined population

OBJECT: Predictors of early (30-day) and long-term (1-year) mortality rates after primary intracerebral hemorrhage (ICH) were studied in a large population in southern Sweden. METHODS: All cases of primary ICH, verified using computerized tomography (CT) scanning or autopsy study, were prospectively registered at the 12 hospitals covering a defined population of 1.14 million during the calendar year 1996. Mortality was analyzed in relation to CT findings (hematoma location and volume and ventricular extension) and clinical parameters (patient age and sex, level of consciousness on admission, and history of preictal risk factors) by using univariate and multivariate statistical methods. Three hundred forty-one cases of primary ICH were detected. The overall mortality rate was 36% at the 30-day and 47% at the 1-year follow up. Multivariate analysis revealed that initial level of consciousness, hematoma volume, and a history of heart disease were independent predictors of death at 30 days postictus. One year after bleeding, independent predictors of mortality were the initial level of consciousness, patient age, and hematoma location. CONCLUSIONS: Primary ICH remains a stroke subtype associated with a high mortality rate and for which the level of consciousness on admission is the strongest predictor of fatal outcome both at 30 days and during the 1st year after bleeding. A preictal history of heart disease increased the 30-day mortality rate.     

Immediate surgery reduces mortality in deeply comatose patients with spontaneous cerebellar hemorrhage

Cerebellar hemorrhage is regarded as a neurosurgical emergency. However, patients with deteriorating consciousness are very likely to die irrespective of the choice of therapy, and it is not clear if surgical intervention can benefit patients in a deeply comatose state. We reviewed 20 patients with a Glasgow Coma Scale score of 3 at admission to ascertain the salvage rate and determine the prognostic factors. Four patients who were managed conservatively died within 2 days. Sixteen patients underwent decompressive suboccipital craniectomy and hematoma evacuation. At discharge, three patients were moderately disabled, three were severely disabled, four were persistently vegetative, and six had died. The overall mortality was 50%. The mean interval between the onset of symptoms and the operation was 1.67 +/- 0.29 hours in patients with favorable outcome, and significantly longer at 2.42 +/- 0.49 hours in patients with an unfavorable outcome (p = 0.025). Immediate evacuation of the hematoma reduces morbidity and mortality even in deeply comatose patients, especially if the time interval between the onset and surgery is within 2 hours.     

Relationship between abnormalities of coagulation and fibrinolysis and postoperative intracranial hemorrhage in head injury

Abnormalities of coagulation and fibrinolysis in 12 head-injured patients were studied in early (within 24 hours of onset) and late (10th to 17th day after onset) stages. alpha 2 Plasmin inhibitor (alpha 2PI), antithrombin III (ATIII), and fibrinopeptide A (FPA) and B beta 15-42 (FPB beta) were measured in particular, in addition to the usual tests (platelet count (PLT), prothrombin time (PT), partial thromboplastin time, fibrinogen, and fibrin/fibrinogen degradation products (FDP)). alpha 2PI was abnormally lower, and FPA and FPB beta were much higher; fibrinogen and ATIII were moderately lower in the early stage than in the late stage in 6 head-injured patients with postoperative intracranial hemorrhage. alpha 2PI, ATIII, and fibrinogen were moderately lower and FPA was moderately higher in the early stage than in the late stage in 6 head-injured patients without postoperative intracranial hemorrhage. PLT and fibrinogen were lower, alpha 2PI was much lower, and FPA was much higher in the 6 patients with postoperative intracranial hemorrhage than in the 6 patients without postoperative intracranial hemorrhage. One patient with acute epidural and subdural hematomas had recurrent postoperative intracerebral hematoma twice. This recurrent hemorrhage was due to disseminated intravascular coagulation (DIC) caused by primary brain damage and was associated with extremely high FPA and FPB beta levels and abnormally low alpha 2PI and PLT. Fresh-frozen plasma and intravenous low-dose heparin were administered after the two recurrent hemorrhages, after which FPA and FPB beta normalized immediately, although other screening tests showed only gradual improvement.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ruptured dissecting aneurysm of the vertebral artery concurrent with contralateral intracerebellar hemorrhage

A case of a dissecting vertebral aneurysm concurrent with contralateral cerebellar hemorrhage is reported. A 69-year-old man was referred to our hospital for treatment of subarachnoid hemorrhage (SAH). On admission, CT scanning showed SAH and left cerebellar hematoma. Angiography was performed and it revealed a dissecting aneurysm of the right vertebral artery. Proximal clipping of the right vertebral dissecting artery was performed through right suboccipital craniotomy. During the operation, the cerebellar hemisphere gradually became firm, but the operation was finished without any complications. After the operation, the patient's consciousness level decreased from somnolence to semicomatose for a period of 2 hours 30 min. CT scanning showed the left cerebellar hematoma expanding. The cerebellar hematoma was evacuated immediately by midline suboccipital craniectomy, and the patient's consciousness level improved. In such a case, care must be taken to discover the cause of the expansion and to prevent concurrent hematoma during the operation. Through this case, discussion was held concerning the pitfalls of treatment of aneurysmal subarachnoid hemorrhage concurrent with intracerebral hematoma in the remote region.     

Preventive effect of aggressive blood pressure lowering on hematoma enlargement in patients with ultra-acute intracerebral hemorrhage

The preventive effect of aggressive blood pressure lowering on hematoma enlargement was investigated in patients with ultra-acute spontaneous intracerebral hemorrhage (ICH). Retrospective review of 248 patients (145 males, 103 females) with spontaneous ICH treated in our hospital between 2005 and 2008 identified patients with ultra-acute ICH who were directly taken to our institute by ambulance within 3 hours after onset. Patients who could not be assessed twice by computed tomography (CT) within 24 hours after arrival were excluded. Systolic blood pressure (SBP) was aggressively controlled in all patients using intravenous nicardipine to below 140 mmHg as soon as possible after diagnosis of ICH with CT. Hematoma enlargement was defined as increase in volume of more than 33% or more than 12.5 ml in the first 24 hours. Hematoma enlargement was observed in 11 of the 73 patients (15.0%). The time course of SBP change was not significantly different in patients with and without hematoma enlargement. The incidence of hematoma enlargement in patients with ultra-acute ICH in this study was 15.0%, which was lower than that in other series in which blood pressure was not reduced aggressively. This finding suggests that aggressive SBP lowering to below 140 mmHg has a preventive effect on hematoma enlargement in patients with ultra-acute ICH.     

Head injury and coagulation disorders

Coagulation studies (plasma fibrinogen, ethanol gelation test, and fibrin/fibrinogen degradation product concentration) were done in 150 patients who were admitted after blunt head injury. Results were abnormal in 60 patients and were found to be correlated with the level of consciousness and with the presence of neurological signs. Many of these patients had fractures, but findings in a control group of 26 patients with major fractures without head injury indicate that fractures were not of paramount importance in causing clotting changes. Conclusive evidence of disseminated intravascular coagulation was found in 12 patients. Cases with a fatal clinical course were mostly associated with very high fibrin/fibrinogen degradation product concentrations. Some case histories are reported, confirming the hypothesized correlation between coagulation results and brain tissue destruction rather than brain compression. It was concluded that some degree of disseminated intravascular coagulation in patients with blunt head injury occurs more often than expected and that coagulation studies might have both diagnostic and prognostic value.     

Three cases of cryptic arteriovenous malformation in basal ganglia manifested by putaminal hemorrhage

Three cases of histologically proven cryptic arteriovenous (AV) malformation of the basal ganglia are reported. Seventeen cases of patients showing putaminal hemorrhage in the CT scan underwent craniotomy for evacuation of a hematoma between January 1986 and December 1988. The preoperative diagnosis was hypertensive putaminal hemorrhage. In all three cases a network of abnormal vessels around the internal capsule was detected at surgery. Case 1: A 62-year-old male was admitted to our hospital with consciousness disturbance (JCS 20), total aphasia and right hemiparesis. The CT scan showed left putaminal hemorrhage. The volume of the hematoma was 45 ml by CT criteria. Left carotid angiography did not demonstrate any abnormal findings. Case 2: 69-year-old male was admitted with consciousness disturbance (JCS 10) and right hemiparesis. Left putaminal hemorrhage (volume 25 ml) was recognized on the CT scan. Two hours after admission, the consciousness level suddenly deteriorated (JCS 100). At that moment, the volume of the putaminal hematoma had increased to 100 ml. AV malformation was not detected by left carotid angiography. Case 3: A 50-year-old male was admitted with consciousness disturbance (JCS 20), total aphasia and right hemiparesis. The CT scan showed left putaminal hemorrhage of 73 ml. Pathohistological examination proved AV malformation in each case. The three cases described here suggest the following; 1) The incidence of the basal ganglia cryptic AV malformation has been considered low, but meticulous examination shows that among the cases diagnosed as hypertensive hemorrhage, AV malformation is not infrequently the hidden cause.(ABSTRACT TRUNCATED AT 250 WORDS)     

Superior Outcome of Nafamostat Mesilate as an Anticoagulant in Patients Undergoing Maintenance Hemodialysis with Intracerebral Hemorrhage

Aims. The incidence of complications associated with cerebrovascular diseases in patients who receive hemodialysis for a long-term period is higher than that of other complications. It is known that mortality due to cerebral hemorrhage is two times higher compared to non-dialysis patients. Anti-coagulants used for hemodialysis are essential. Accordingly, in cases in which the cerebral hemorrhage occurred, the selection of anti-coagulants for the prevention of further bleeding poses a great challenge to physicians. The change of hematoma and patient prognosis has a direct relationship. Many ongoing studies are conducted to examine the causative factors causing the increased hematoma and their related prognostic factors. In the current study, we examined the effect of nafamostat mesylate (a serine protease inhibitor) on the change of hematoma compared to heparin in hemodialysis patients.?Methods. The current study was conducted in 17 hemodialysis patients who developed a cerebral hemorrhage. These patients were assigned to two groups based on the type of anti-coagulants that they used (i.e., nafamostat mesylate and heparin). Then, the factors affecting the change of hematoma following the onset of cerebral hemorrhage were examined. The prognosis of hematoma was assessed based on brain CT scans, which were performed two weeks after the onset of cerebral hemorrhage in four groups. Following this, groups 1 (the decreased hematoma) and 2 (the decreased delay) were merged to group A (resolving group), and groups 3 (the increased hematoma) and 4 (the death following the aggravation) were merged to group B (the expansion group) for further analysis. Results. There were no significant differences in baseline characteristics between the nafamostat group and the heparin group. A comparison between the resolving group and the expansion group also showed that there were no significant differences in baseline characteristics. In the anti-coagulants and the change of hematoma, however, there were significant differences between the two groups (p = 0.024). A comparison of the change of hematoma between the four groups was also made. This showed that platelet counts and BUN level were significant factors (Platelet; p = 0.042, BUN; p = 0.043 ANOVA with resolving group). Conclusions. Nafamostat mesylate has a similar profile of anti-coagulative activity to heparin. It is assumed, however, that nafamostat has an affirmative effect on the recovery of damaged sites following the onset of cerebral hemorrhage. It is an anti-coagulant that can be safely used for hemodialysis following the onset of cerebral hemorrhage.