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A case of a 14-year-old girl who developed a spinal subdural hematoma after placement of a ventriculoperitoneal shunt is presented. Such a complication has not been previously reported. We believe that this represented an extension of intracranial subdural hematoma fluid into the spinal subdural space.
The combined spinal-epidural technique is widely used in obstetric anaesthetic practice. Epidural catheter migration through a dural hole is a theoretical but rarely described complication. We report a case of acute and life-threatening respiratory depression following administration of diamorphine through an epidural catheter after a single space combined spinal-epidural technique for caesarean section. We believe this complication occurred as a result of catheter migration through a dural hole into the subdural space and rupture of the thin arachnoid layer causing massive subarachnoid blockade.
The concentrations of ethanol in peripheral blood, subdural hematomas and various regions of the brain were determined 1, 2, 4, and 6 h after the induction of a hemorrhage into a subdural space in the right temple of rabbits. The concentrations were compared to cases of intravenous administration of ethanol-free i.v. fluid. Concentrations of ethanol in the subdural hematomas gradually decreased to correspond to those in the peripheral blood. The influence of an intravenous infusion of ethanol-free i.v. fluid was not observed. Concentrations in the brain of the right temporal, parietal and frontal lobes were high and those in the right temporal lobe were maintained during the 6 h of our experiment. Therefore, to determine if a human victim was under the influence of ethanol at the time of injury, we recommend that brain concentrations of ethanol be determined. This is apparently the first study to confirm that the estimation of ethanol in the brain provides a more accurate determination of how much ethanol had been ingested.
The first case of Pasteurella Multocida subdural empyema is reported. This was secondary to hematogenous spread from the pharynx to a chronic subdural hematoma. Positive cultures were obtained from the primary source, the blood and the subdural space. The patient was discharged with no neurological deficit following surgical drainage and parenteral antibiotics. The incidence, predisposing factors, clinical features, bacteriology, diagnostic procedures, treatment and mortality of subdural empyema are briefly discussed.
The authors reported a case of subdural effusion secondary to dural metastasis of prostatic cancer. A 61-year-old man was referred for headache, vomiting and gait disturbance. He had undergone hormonal therapy for prostatic cancer. He showed a mild left hemiparesis and anemia without bleeding. CT-scan disclosed a multilobular crescent shaped low density area in the right hemisphere. Under the diagnosis of chronic subdural hematoma, burr hole irrigation therapy was performed. Xanthochromic fluid was evacuated from the subdural space, in which no tumor cells were shown to exist. CT-scan on the 21st day disclosed a low density area, which was diagnosed as recurrent chronic subdural effusion. Therefore, craniotomy was performed to evacuate the subdural fluid and to explore the dura mater. Removal of the red hemorrhagic tumor at the dura mater and the fluid was performed. The patient died of heart failure in the 16th month despite complete recovery after the second operation. Histopathological examination of the tumor revealed adenocarcinoma at the outer part of the dura mater and the adjacent skull bone, where capillaries were embolized with tumor cells. However, no tumor cells were found in the subdural fluid. The authors could find in the literature 30 cases of subdural hematoma or effusion secondary to dural metastasis of carcinoma. The pathogenesis of the subdural hematoma in this case might be due to circulatory disturbance at the dura mater brought about by the invasion of the tumor or tumor cells emboli in the capillaries.
The incidence of acute subdural hematoma (SDH) due to a ruptured intracranial aneurysm varies from 0.5% to 7.9% of all intracranial aneurysms. Pure acute SDH without subarachnoid hemorrhage (SAH) is rare. According to the literature, only 18 cases (including our case) of pure acute SDH identified by CT scan have been reported. Here we report a case of an internal carotid-posterior communicating artery (IC-PC) aneurysm presenting pure acute SDH identified by CT. We summarize the 18 reported cases. A 55-year-old female experienced severe headache on October 9, 1999, which did not improve after medication. Four days later, left ptosis began. She was admitted to the department of ophthalmology to treat oculomotor nerve paresis. A computed tomography (CT) scan obtained on admission, revealed no obvious abnormality. She was treated by hormonal therapy, but her symptoms continued. Ten days later, she suddenly lost consciousness and was transferred to our hospital. Although the CT scan revealed a thick left SDH with marked midline shift, SAH was absent. Her neurological state was Hunt & Kosnik grade IV. A left carotid angiogram revealed an IC-PC aneurysm with active extravasation. The patient was taken to the operating room for emergency removal of the SDH and aneurysmal neck clipping. During the operation, adhesion between the aneurysmal dome and the arachnoid was observed, but subarachnoid hemorrhage was not identified at all. The aneurysm was successfully clipped. Postoperatively, her consciousness improved immediately. In this case, the pure acute SDH identified by CT was responsible for causing the direct hemorrhage into the subdural space via an adhesive lesion.
The authors report clinical and morphological analysis of 31 autopsied cases of subdural haematomas unrecognized during life. The most frequent erroneous clinical diagnosis was cerebrovascular brain disease, psychiatric syndrome or brain tumour. The greatest diagnostic difficulties were encountered in cases of subdural haematoma developing in elderly subjects (in this material 24 patients were aged above 60 years). Brain atrophy delayed in them the appearance of intracranial raised pressure syndrome, coexistence of vascular changes masked the signs of subdural haematoma and frequent memory disturbances made history taking difficult. Brain atrophy in elderly subjects may be also a factor contributing to development of subdural haematoma. Widening of subdural space causes greater tension of bridging veins and their easier rupture when the brain is displaced during trauma. Absence of inflammatory changes in the neuropathological findings in cases of subdural haemorrhage suggests that the term "chronic subdural haematoma" is better than the older term "pachymeningitis haemorrhagic interna".
Eighty three chronic subdural hematomas, obtained by surgery or by necropsy, were examinated. The patient age distribution curve of the non-complicated operative cases showed the highest incidence in the first year of life and also a moderate increase in the elderly group. Recurrent hemorrhage in the walls and in the cavity, was observed in twenty of the seventy three non-complicated cases of chronic subdural hematoma. In five cases the membranes and the subdural sac were invaded by leucemic cells and in the five remaining ones the hematoma was transformed in a subdural empyema. All these complicated subdural hematomas showed evidence of recurrent bleeding, suggesting that the leucemic cells or the infectious agent had spread to the subdural space by this way.
A clinical computed tomographic (CT) study of six patients, two with tension and four with benign postoperative subdural pneumocephalus, was done coupled with a data analysis of the literature. The mass effect of a tension subdural pneumatoma was demonstrable as shift in the midline structures when the air was unilateral, whereas an asymptomatic pneumocephalus showed no actual mass effect. Inspection of the digital lateral scout view studies usually provides a rough estimate of the magnitude of a pneumatoma; the volume of the air could be computed on the axial transverse CT scans. In a preliminary in vivo volume estimation, the subdural air measured more than 65 cm3 for the two symptomatic patients and less than 20 cm3 for the asymptomatic ones. Of 21 reported cases of postsurgical tension pneumocephalus, 18 (86%) had the pneumatoma in the subdural space. The predisposing neurosurgical conditions to tension pneumatoma included: (a) a preexisting open cerebrospinal fluid drainage device; (b) surgery on the posterior fossa in the sitting position; and (c) chronic subdural hematoma.
The ability of a competitive N-methyl-D-aspartate (NMDA) receptor antagonist (D-CPP-ene) to reduce irreversible brain damage has been examined in a rodent model of acute subdural hematoma. Acute subdural hematoma was produced by the slow injection of 400 microliters homologous blood into the subdural space overlying the parietal cortex in halothane-anesthetized rats. Brain damage was assessed histologically in sections at multiple coronal planes in animals sacrificed 4 hours after induction of the subdural hematoma. Pretreatment with D-CPP-ene (15 mg/kg) significantly reduced the volume of ischemic brain damage produced by the subdural hematoma from 62 +/- 8 cu mm (mean +/- standard error of the mean) in vehicle-treated control rats to 29 +/- 7 cu mm in drug-treated animals. These data demonstrate the anti-ischemic efficacy of NMDA antagonists in an animal model of intracranial hemorrhage in which intracranial pressure is elevated, and suggest that excitotoxic mechanisms (which are susceptible to antagonism by D-CPP-ene) may play a role in the ischemic brain damage which is observed in patients who die after acute subdural hematoma.
The authors study 26 children with macrocranium and pericerebral effusion as diagnosed by C.T. Three groups are described: 10 with the classical C.T. features of subdural effusion, 12 with features of external hydrocephalus and 4 with massive pericerebral effusion. C.T. performed after lumbar subarachnoid injection of contrast medium, shows that all the effusions are subdural. In only one case, opacification of the subdural space occurred. The authors conclude that plain C.T. alone is unable to demonstrate the precise localization of pericerebral effusion in children and that all these effusions are, in their experience, subdural in localization.
Nine patients with intracranial hemorrhage associated with long-term anticoagulation therapy were evaluated at the Wadsworth Veterans Administration Hospital over a 30-month period. The relationships of the hemorrhage to other variables, both in this series and in the review of the literature, are analyzed. The most common site of the intracranial hemorrhage was the subdural space. No direct correlation between the presence of arterial hypertension or prothrombin activity and intracranial hemorrhage existed. The outcome was favorable in six of the patients, four of whom had a subdural hematoma.
OBJECT: The authors undertook a retrospective study to evaluate the effectiveness of diverting intracranial fluid into the subgaleal space for temporary absorption by the membranes of the scalp. METHODS: Eighty-one patients were treated over a 20-year period. There were 22 cases of hypertensive hydrocephalus, 52 cases of acute head trauma, and seven cases of chronic subdural hematoma. The simple surgical technique is described. Subgaleal shunting provided effective short-term treatment of hydrocephalus and increased intracranial pressure, which was monitored directly in 22 cases of cerebral contusion and edema. CONCLUSIONS: The closed method for drainage of cerebrospinal fluid avoids the complications of open ventriculostomy or open drainage of the subdural space.
OBJECTIVE: To investigate the mechanism of the adverse effect of midline shift after severe traumatic brain injury. METHODS: This study compared averaged cerebral metabolic parameters of patients with midline shift > 5 mm (S) on initial computerized tomography scan to those of patients with shift < or = 5 mm (NS). The effect of an acute subdural hematoma (SDH) was determined by separating patients into those with and those without SDH and then re-examining the effect of shift in these subgroups. RESULTS: Four hundred fifty-four patients were studied. Cerebral metabolic rate of oxygen (CMRO2, in mL/100 g per min) was always lower with shift: 1.74 for SDH-S versus 2.21 for SDH-NS (p < 0.001), and 1.80 for non-SDH-S versus 2.24 for non-SDH-NS (p < 0.001). No other major effects of shift were seen in SDH patients. Among non-SDH patients, shift was associated with higher intracranial pressure (ICP): 23.1 mm Hg versus 16.3 mm Hg (p < 0.001). Other differences between shift and nonshift patients in the non-SDH group were due at least in part to interventions to treat the elevated ICP. CONCLUSION: Midline shift after severe traumatic brain injury is associated with reduced CMRo2, regardless of whether or not SDH is present. The deleterious effects of subdural blood may be related more to the mass effect of large SDHs than to the biochemical abnormalities caused by small amounts of blood in the subdural space.
A ruptured giant aneurysm of the azygos anterior cerebral artery (ACA) associated with an acute subdural hematoma (SDH) occurred in a 67-year-old male with two episodes of sudden severe headache and transient loss of consciousness. Neurologically, he had mild weakness of the left lower extremity. Computed tomography showed an elliptical heterogeneous hyperdense mass in the interhemispheric fissure in front of the corpus callosum and an acute SDH on the right. Angiography disclosed a giant aneurysm (2.8 x 2.0 cm) at the distal end of the azygos ACA. Removal of the SDH and aneurysmal neck clipping achieved a good outcome. Successive small bleedings may allow the aneurysmal dome to develop adhesions to the arachnoid membrane, and the final rupture will occur into the subdural space, resulting in a SDH.
Arachnoid cysts (AC) are usually asymptomatic. However, very rarely they can become symptomatic due to cyst enlargement or haemorrhage, often after head trauma. In such cases bleeding is often confined to the subdural space, but intracystic haemorrhage has rarely been observed. We report a case of a child who had intracranial hypertension syndrome due to a right middle cranial fossa AC with intracystic bleeding and subdural haematoma.
An AIDS patient with a subdural empyema as a complication of candida sinusitis is presented. Clinical features resembled those of invasive aspergillosis or phycomycosis. Microbiological diagnosis was established by blood cultures, sinus cultures, and histopathological examination. An aggressive surgical approach first to the sinuses and then to the subdural space, together with fluconazole produced a satisfactory result.
Two cases of acute idiopathic subdural hematoma with delayed intracranial hypertension were presented. The first case was a 68-year-old man admitted for vomiting following headache for eight days. There was no history of head trauma. A CT scan revealed a high-density mass that had a concave inner margin in the left temporo-parietal region with a slight midline shift. No vascular lesion was noted on the angiogram. The consciousness of the patient deteriorated suddenly on the 12th day. An operation was performed because of a marked midline shift on the CT. At operation, a subdural clot was removed. The postoperative recovery was good. The patient was discharged 7 days later without any neurological deficit. The second case was a 69-year-old man who was admitted with sudden onset of headache. There was no history of head trauma. A CT scan showed a high density mass in the right temporoparietal subdural space with a slight midline shift. The consciousness of the patient deteriorated suddenly on the 15th day. An operation was performed because of a marked midline shift on the CT. At operation, a subdural hematoma was removed. Two days later, suddenly his consciousness deteriorated. A CT scan showed his severe brain edema with a marked midline shift without increased hematoma. External decompression was performed immediately. The postoperative recovery was very good and 40 days after the second operation, the patient was discharged with no neurological deficit. The delayed intracranial hypertension appeared in these two cases about 10 days after the initial symptom. Two kinds of mechanisms are suspected: 1) swelling of the hematoma because of the adsorption of cerebrospinal fluid, 2) the occurrence of secondary brain edema. From our experience, a repeated CT scan is necessary for 2 to 3 weeks.(ABSTRACT TRUNCATED AT 250 WORDS)