Relationship of postoperative residual air and recurrence in chronic subdural hematoma

The possibility exists that residual air after surgery is one cause of recurrence of chronic subdural hematoma. We have devised a new simple method which decreases postoperative residual air, using external drainage and an endoscope. First, we make endoscopic observations of the inner aspect of the hematoma cavity. Then, we insert external drainage apparatus into the most frontal area of the hematoma cavity, we regard this location as the most appropriate place to ensure most effective drainage. The present study included 37 chronic subdural hematomas in 32 patients who had been treated between January and December, 1999. Their ages ranged from 48 to 86 years old, with an average of 72 years. Insertion of external drainage in the most frontal area of the hematoma cavity was successfully achieved in 27 (73%, Group I) out of 37 cases and resulted in no recurrence. In the remaining 10 hematomas (27%, Group II), external drainage was not able to be inserted in the most frontal area, and four hematomas (40%) had recurrence (p < 0.01 vs Group I). Insertion in the most frontal area of the hematoma cavity decreases residual air after surgery, and may be effective for the prevention of recurrence of chronic subdural hematoma.     

Orbital subperiotal hematoma associated with extradural hematoma: one case report

Subperiotal hematoma of the orbit associated with extradural hematoma has been rarely reported in the literature. We report a case of an 8-year-old girl who presented after traumatism, a subperiotal hematoma of the orbit with two extradural hematomas. During the first clinical examination realized while the patient was unconscious, left exophthalmia was found, but after conscious improvement, we discovered ophtalmoplegia and a grade I papilla edema. The CT scan showed two extradural hematomas and a left intraorbital hematoma. The intraorbital hematoma was drained by surgical way but the extradural hematomas were not surgical. The outcome has been marked by the neurological improvement and the oculomotricity recovering.     

Endoscopic findings in chronic subdural hematoma

On the genesis of chronic subdural hematoma (CSH), it is one of the possible explanations that a head injury triggers uncertain cause off for the formation of the hematoma membrane, where the bleeding occurs to form and enlarge the hematoma. Although some reports on the staging classification based on computed tomography (CT) findings are available the natural course or history of the hematoma formation is not yet known. As previously reported, we have been using an endoscopically guided method in which a drainage tube is placed in the most frontal area of the cavity so as to evacuate the residual air efficiently. In this study, we analyzed the endoscopic findings in hematoma cavities and compared them with the clinical data, focusing on the post-trauma interval and recurrence of the hematoma. Between January 1999 and October 2000, we had an opportunity to observe the inner aspect of 60 hematomas in 48 patients. A trabecular structure was found in 39 hematoma cavities (65%), whereas apparent clot formation was observed in 18 cavities (30%). Septum formation leading to a multi-loculated hematoma was observed in 10 cavities (17%). Twenty-six patients with 32 hematomas with the obvious history of head injury were classified into 4 groups according to the post-traumatic interval to the surgery, which are stage I; less than 30 days, stage II; 31 to 60 days, stage III; 61 to 90 days and stage IV; more than 91 days. Clot formation and a trabecular structure were frequently seen in stages II and III. Clot formation was statistically and significantly seen in the recurrent group. The results suggest that CSHs increase in size in stages II and III, when clot formation and a trabecular structure are frequently observed. Endoscopic observation of hematomas may assist to know hematomas, and clot formation may be a warning of hematoma recurrence.     

Simultaneous multiple hypertensive intracerebral hematoma

Hypertensive intracerebral hemorrhage (HIH) occurring simultaneously in different locations is rare. We encountered 11 such cases between January 1990 and November 2002. The diagnosis of all 11 cases was established by computed tomography, and the location of the hematomas was: cerebellum and basal ganglia in 5 cases, pons and basal ganglia in 4, and subcortex and basal ganglia in 2. Our patients were analyzed with respect to clinical characteristics, pathogenesis of multiple hematomas, and indication of operation. These patients represented 1% of all 1,069 patients we encountered with HIH. As past history, there were no characteristic disorders except hypertension. There were no characteristic initial symptoms suggesting that hemorrhage had occurred simultaneously. Both supra- and infra-tentorial hematomas were observed in 80% of the patients, and the size of the multiple hematomas was proportional in principle. Cerebellar hematomas were often mild, and pontine hematomas were often severe. The outcome in those patients whose neurological grading was 1 to 3 was good with conservative therapy or surgical treatment. The severity, treatment methods, and outcomes in these patients were similar to those in patients with single HIH, which suggests only a slight influence of multiple lesions on outcome. As for the possible mechanism of simultaneous multiple hemorrhages, we speculated that bleeding occurred simultaneously in the different regions, or that the initial bleeding was followed after a short time by secondary bleeding due to high intracranial pressure and circulatory disturbance. In patients with cerebellar hematoma, initial symptoms suggested the development of secondary hemorrhage after primary hemorrhage. The surgical treatment for multiple hematomas should be determined by the location and maximum axis of the hematoma. We proposed that cerebellar hematomas should be removed if the supra-tentorial hematoma is small.     

Mortality in retroperitoneal hematoma

Eighty-one patients sustained retroperitoneal hematoma (RH) from blunt (70%) and penetrating (30%) trauma. Retroperitoneal hematomas were classified into 10 centro-medial Zone I, 25 lateral Zone II, and 46 pelvic Zone III hematomas. The mean injury Severity Score (ISS) for the entire series was 26.4 +/- 14. The mean ISS of nonsurvivors was 37.6 +/- 12. Overall mortality was 20%; if head injury deaths are excluded (six), mortality was 13%. Retroperitoneal hematoma associated with pelvic fracture had a mortality of 19%. Incidence of respiratory failure for entire series, excluding head trauma, was 29%. Respiratory failure occurred in 37% of patients with Zone III injuries. A requirement for ventilatory support greater than 48 hours was associated with a mortality of 35%. PaO2/FIO2 at 48 hours in intubated patients was significantly decreased in nonsurvivors compared to survivors, whereas the mean ISS of this subset of patients did not differentiate between survivors and nonsurvivors.     

Multilocular encapsulated intracerebral hematoma

Encapsulated intracerebral hematoma is so rarely seen that only two cases have been reported, by Hirsh et al. Recently, we experienced a case of multilocular encapsulated intracerebral hematoma containing 9 to 10 capsules of different sizes. The capsules of the hematoma were easily dissected from the surrounding brain tissues and found to be grayish white in color, tough in hardness and 1 to 3 mm in thickness. The capsular contents ranged from very old to relatively new, which contents were hard on soft solid hematomas, liquid hematomas or xanthochromic fluid. These findings indicated the development of intracerebral hematomas with different chronic courses at different times. It is very interesting that the frequency of the convulsive seizure was almost consistent with the number of capsules. For etiology of multilocular intracerebral hematoma, either occult vascular malformation or bleeding from the sinusoidal channel layer of the capsules like that of chronic subdural hematoma is considered.     

Subperiosteal hematoma of the orbit associated with subfrontal extradural hematoma

Subperosteal hematoma is rarely associated with extradural hematoma and orbital roof fracture. We report a case observed in a 16-year-old boy who developed exophthalmos, diplopia and visual loss after blunt head trauma. Computed tomography demonstrated the subperiosteal hematoma associated with a thin extradural hematoma and an orbital roof fracture. The hematomas were removed during the same procedure via fronto-orbito craniotomy. Surgery led to complete recovery without functional sequelae. We stress the importance of early diagnosis and treatment of post-traumatic exophthalmos.     

Diffusion-weighted imaging of traumatic subdural hematoma in the subacute stage

Five cases of traumatic subdural hematomas in the subacute stage (from 7 to 20 days after head injury) were treated in one male and four females, aged from 63 to 82 years, with evacuation via craniotomy in three and aspiration via burr hole surgery in two. All hematomas were evaluated by T1-, T2-, and diffusion-weighted magnetic resonance imaging, and measurement of the apparent diffusion coefficient (ADC). Diffusion-weighted imaging showed the hematoma as a crescent high intensity area with a low intensity rim close to the brain surface (two-layered structure) in four cases and as high intensity with low intensity components in one case. The high intensity areas under the dura mater on diffusion-weighted imaging appeared as homogeneous high intensity on T1- and T2-weighted imaging in four cases, and inhomogeneous high intensity on T1- and isointensity on T2-weighted imaging in one case. The mean ADC value of the high intensity areas was 0.58 +/- 0.23 (mean +/- standard deviation) x 10(-3) mm2/sec. The operative findings revealed the high intensity areas as solid clots. The low intensity areas on diffusion-weighted imaging appeared as homogeneous high intensity in four cases and inhomogeneous isointensity with high intensity components in one case on T1- and T2-weighted imaging. The mean ADC value of the low intensity areas was 2.03 +/- 0.27 x 10(-3) mm2/sec. The operative findings revealed the low intensity areas as mixtures of resolved clot and cerebrospinal fluid. Diffusion-weighted imaging showed the characteristic two-layered structure in traumatic subdural hematomas in the subacute stage, and analysis of the ADC values was useful for differentiating solid from liquid hematoma and for selection of the surgical procedure.     

Subperiosteal orbital hematoma: visual recovery following delayed drainage

Subperiosteal orbital hematomas are rare sequelae of blunt periorbital trauma. Visual loss in such cases is very infrequent, but reportedly irreversible, unless treated with early decompression. A 17-year-old boy developed marked visual loss secondary to an acutely developing traumatic subperiosteal orbital hematoma. Despite delayed referral surgical evacuation of the hematoma remarkably restored his vision. Postoperative clinical examination, fluorescein angiography, and electrophysiologic testing confirmed that a compressive optic neuropathy had caused the visual dysfunction. Although immediate surgical decompression remains the treatment of choice for subperiosteal hematomas producing visual loss, this case demonstrates that the optic nerve may recover dramatically even after a prolonged period of dysfunction from compression.     

Posterior fossa subdural hematoma

One case of traumatic posterior fossa subdural hematoma (PFSH) is described. This location represent 1% of the subdural hematomas. Computerized Tomography (CT) was used in the diagnosis and follow-up of the hematoma. The etiology and physiopathology of this process are discussed.     

猫脑内立体定向注射胶原酶建立脑内血肿模型

目的　采用立体定向注射胶原酶于猫脑尾状核,建立一种新的脑内血肿模型。方法　在实验中采用立体定向技术,将一定量的胶原酶（加或不加肝素）用微量注射泵精确地注入猫脑尾状核［ 坐标（Ａ１．０ ,Ｌ５．０ ,Ｈ１４．０）］。术后２４ 小时处死动物,取全脑固定于福马林溶液,观察大体及镜下改变,测量血肿大小。结果　注射胶原酶（ 加或不加肝素）可以形成局灶性出血,且出血量大小与胶原酶用量有关,加用肝素后血肿扩大。结论　注射胶原酶（２ Ｕ／２０μｌ） 于猫脑尾状核,血肿大小适中,动物术后有短时间昏迷及固定的对侧偏瘫。     

Subdural hyperintense band on diffusion-weighted imaging of chronic subdural hematoma indicates bleeding from the outer membrane

The diffusion-weighted magnetic resonance (MR) imaging characteristics of chronic subdural hematoma and the correlation between hematoma liquidity and apparent diffusion coefficient (ADC) were investigated in 26 consecutive patients, 16 males and 10 females aged 42 to 92 years (mean +/- SD 73.3 +/- 13.1 years), with 31 chronic subdural hematomas. The chronic subdural hematomas were divided into homogeneous, separate, and trabecular types based on diffusion-weighted MR imaging findings. Almost all hematomas were low intensity on diffusion-weighted imaging, and the mean ADC value was 1.81 +/- 0.79 x 10(-3) mm2/sec. The high intensity areas in the subdural hematomas consisted of several types: high intensity line along the dura mater (subdural hyperintense band), high intensity along the intrahematoma septum, and laminar shape along the inner membrane. The subdural hyperintense bands accounted for almost all high intensity areas in the subdural hematomas. The mean ADC value of the high intensity areas was 0.76 +/- 0.24 x 10(-3) mm2/sec, close to that of the normal brain. The subdural hyperintense bands were considered to be intracellular and/or extracellular methemoglobin based on the T1- and T2-weighted imaging and intraoperative findings. The subdural hyperintense band is an important finding indicating relatively fresh bleeding from the outer membrane. Diffusion-weighted imaging shows liquid subdural hematoma as low intensity, and measurement of the ADC values can differentiate between liquid and solid components of the chronic subdural hematoma.     

Two-level ligamentum flavum hematoma in the lumbar spine. Case report

Ligamentum flavum hematoma is a rare cause of spinal root or cord compression that usually occurs at a single level. No case of multiple-level ligamentum flavum hematoma has previously been reported. We report an extremely rare case of double, contiguous ligamentum flavum hematomas in the lumbar spine. A 71-year-old man with hypertension and degenerative lumbar scoliosis presented with pain and muscle weakness in the left lower extremity after physical exertion. Magnetic resonance imaging of the lumbar spine showed severe spinal stenosis caused by two-level ligamentum flavum hematoma (L3-L4 and L4-L5). Both hematomas were completely removed and the diagnosis was histologically confirmed. Symptoms completely resolved after surgery. Despite being extremely rare, ligamentum flavum hematoma with involvement of multiple levels may be observed.     

Contralateral development of chronic subdural hematoma after evacuation of chronic subdural hematoma. A case report

Contralateral acute complications such as acute epi/subdural hematomas can be encountered after evacuation of a chronic subdural hematoma, though they are rare. We found only one case of chronic subdural hematoma following the surgery for contralateral chronic subdural hematoma, have been published in English language literature. A 73-year-old male admitted to our hospital with a right-sided subdural hematoma. The subdural hematoma was evacuated through a burr-hole. A left-sided subdural higroma appeared after operation and turned into classical subdural hematoma in the course of time. After evacuation of contralateral chronic subdural hematoma, the patient recovered completely. All stages of the development of contralateral chronic subdural hematomas were shown by serial computed tomograms. It was suggested that traumatic chronic subdural hematomas develop from mostly subdural higromas. If contralateral subdural higroma is seen after surgical evacuation of a chronic subdural hematoma, the possibility of development of contralateral chronic subdural hematoma must be kept on mind.     

Spontaneous hematoma of the cerebellum

Forty spontaneous cerebellar hematomas have been observed in 39 patients whose age ranged from 13 to 82 years, 26 being older than 60. Arterial hypertension is the most frequent aetiological factor. Amongst the other causes, vascular malformations, which may also be present in older people, anticoagulant therapy, metastatic tumor, sepsis were found; one case remained unsolved. Diagnosis is no longer a challenge since the introduction of C.T. scan, whilst M.R.I. may give most valuable informations concerning aetiology, especially when a vascular malformation is present. In this study, the influence of the hematoma size and of hydrocephalus on consciousness was demonstrated; development of hydrocephalus is favoured by the size and by a rather median location of the hematoma. In the future, M.R.I. should give better precisions concerning an eventual extension of the hemorrhage to the brainstem. The purpose of surgical treatment is twofold: alleviating brainstem compression and correcting hydrocephalus; yet, divergent opinions have been put forward in retrospective studies, concerning evacuation of the hematoma and drainage of hydrocephalus. In this series, direct attack doesn't seem to be indicated in hematomas less than 3.5 cm diameter, unless a causal lesion has to be removed. The ideal moment for hematoma evacuation is, finally, dictated by the clinical status and its evolution; however, the authors prefer, if possible, to delay it for at least 48 hours. Amongst the 39 patients, 14 deceased; of the 25 survivors, 19 were autonomous, 7 being nearly asymptomatic, 6 patients remained handicapped. Consciousness is a main prognostic factor, whilst coma in the first hours has a clearly unfavourable significance.     

Acute spinal subdural hematoma. A case report and review of literature

A case of acute spinal subdural hematoma is reported in a 24-year-old woman. Presentation occurred in the postpartum period, 4 days following epidural anesthesia. Emergency decompressive laminectomy attained partial recovery. Subsequent pathology demonstrated evidence of a low-grade ependymoma. Reported cases of spinal subdural hematomas are reviewed and compared with the characteristics of this unique case.     

The significance of thrombocytopenia in the development of postoperative intracranial hematoma

A group of 35 patients undergoing intracranial surgery who exhibited perioperative thrombocytopenia (platelet count less than 150,000/microliters) was studied retrospectively. Of the 35 patients, 14 (40%) developed postoperative intracranial hematomas requiring reoperation and seven (20%) died within 2 weeks after the operation. Analysis revealed that a perioperative platelet count below 100,000/microliters in a patient who failed to respond to platelet transfusions was associated with a higher risk of postoperative hematoma formation. All six patients with this profile developed postoperative hematomas. If the platelet count rose promptly from below 100,000/microliters to a normal level after platelet transfusions, the incidence of hematoma formation decreased dramatically. None of the three patients with this response developed postoperative hematoma. In patients in whom an acute drop in platelet count from the normal range to between 100,000 and 124,000/microliters occurred in the immediate perioperative period, there was a significantly higher change of hematoma formation; this finding has not hitherto been described. Of the 14 patients with this clinical course, eight developed postoperative hematoma after craniotomy for tumors and vascular lesions. This latter observation was substantiated by the fact that thrombocytopenic patients with postoperative hematomas had a greater reduction in platelet count than thrombocytopenic patients with no postoperative hematomas (p = 0.0004).     

Delayed epidural hematoma. Apropos of a series of 8 cases

The authors report 8 patients who developed an epidural hematoma after having been submitted to 1 or 2 computed tomographies (CT) which did not yet show the hematoma. The initial CT was done 1 to 6 hours after the accident. The delayed hematoma was diagnosed 3 and a half hours to 7 days after the accident. Secondary clinical deterioration occurred in 6 patients and was dramatic in 4 of them. Delayed epidural hematoma seems to be a frequent event; our 8 cases represent 10 % of all epidural hematomas operated during the period under consideration. This has to be taken into account when taking care of head injured patients after negative CT. The authors propose a list of indications for repeating CT. The current views on mechanisms of formation of epidural hematomas are discussed in the light of the increasing number of reported cases of delayed epidural hematoma.     

Acute brain swelling during evacuation of subdural hematoma caused by delayed contralateral extradural hematoma: report of two cases

Two patients experienced severe brain swelling during the evacuation of acute subdural hematomas. Postoperative computed tomographic (CT) scans revealed delayed extradural hematomas on the sides opposite the subdural hematomas. Extradural bleeding occurred in the area of the fractured skull. One patient improved neurologically after evacuation of the extradural hematoma, and the other was not operated because he was moribund. Drilling exploratory burr holes in the fractured area may have been a better strategy than awaiting a postoperative CT scan. The reduction of intracranial pressure after the removal of subdural hematoma was postulated to be the most important factor contributing to the formation of the extradural hematoma.     

High intraoperative blood loss may be a risk factor for postoperative hematoma

The authors studied the incidence of postoperative intracranial hematoma to improve care after intracranial surgery. Five years (1995-1999) of surgical records were analyzed retrospectively. Patients were included if evacuation of an intracranial postoperative hematoma was reported. A control group was randomly selected. Forty-nine patients (0.8%) had postoperative hematomas requiring evacuation. The amount of intraoperative blood loss was significantly larger in the hematoma group (762 +/-735 mL [median 500 mL]) than in the control group (415 +/-403 mL; median 300 mL) (P = 0.004). Clinical deterioration occurred within the first 24 hours in 80%, within 6 hours in 51%, and within 1 hour in 12% of the patients. Those who deteriorated within 24 hours had a faster and more life-threatening deterioration than those who had a hematoma after 24 hours. A decreased level of consciousness was found in 61% and increased focal neurologic signs were found in 33% of the patients. An elevated intracranial pressure was seen significantly more often in the hematoma group (9/10 patients, 90%) than in the control group (1/8 patients, 12.5%) (P = 0.001). In this study, a large amount of intraoperative blood loss and elevated intracranial pressure were warning signs of postoperative hematoma and should alert the clinician to the increased risk. Most hematomas occurred within 24 hours after surgery, and in this time period the deterioration was more severe compared with the hematomas that occurred later.