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[Rapid spontaneous resolution of acute subdural hematoma].

Acute subdural hematomas are usually neurosurgical emergencies, although a conservative therapy is indicated in selected cases. In some of these patients a progressive resolution is appreciated. However, rapid spontaneous resolution of an acute suddural hematoma is seldom reported. A patient with antecedent of chronic alcoholism and spontaneous resolution of acute subdural hematoma in less than 18 hours after the head injury is described. The possible mechanisms of this rapid resolution are discussed. A tear in the arachnoid with spilling of CSF into the subdural space and the effect of intracranial antihypertensive measures together with cerebral atrophy, are factors that possibly contribute to dilution and redistribution of blood with hematoma disappearing in CT scan.

Atrophy↗

Biomechanics of acute subdural hematoma.

Acute subdural hematoma (ASDH) due to ruptured bridging veins occurs under acceleration conditions associated with rates of acceleration onset. That this is due to the strain-rate sensitivity of these veins was confirmed in an experimental model of ASDH. The results of this model were consistent with the clinical causes of ASDH, where 72% are due to high-strain falls and assaults and 24% are due to lower strain-rate vehicular injuries. A mathematical model embodying the known mechanical properties of subdural veins was used to develop tolerance criteria for the occurrence of ASDH. This tolerance curve was consistent with the clinical and experimental data but differed from tolerances previously proposed for head injury.

Acceleration↗

Surgical management of acute subdural hematomas.

Acute subdural hematoma, local cerebral laceration and severe brain edema must be diagnosed at the earliest possible stage preferably by angiography and must be treated promptly by craniectomy of an adequate size in order to cope with all the blood clot, the lacerated brain tissue and the swollen brain.

Acute Disease↗

Subdural hematomas. I. Acute subdural hematoma: progress in definition, clinical pathology, and therapy.

A series of 206 patients with clotted subdural hematomas operated within 3 days of closed head injury is presented. Sixty-two percent (128) were operated within 24 hours of trauma (acute subdural hematoma) carrying a high incidence of sterotypic motor posturing, impaired oculomotor reflexes, and unilateral dilated fixed pupil. A functional recovery occurred in 27% and a vegetative state or death resulted in 62%. The remaining 38% were operated after 24 but within 72 hours from injury (early subacute subdural hematoma) and generally had less severe neurologic dysfunction. A functional recovery occurred in 54% and vegetative state or death in 34%. The 128 acute cases are presented in detail to establish a logical basis for time differential. The cases requiring operation within 12 hours of injury were the most challenging. Improved outcome is felt to result from prompt referral and large craniotomy in the earliest hours after injury, combined with careful postoperative monitoring. Clinical, operative and autopsy findings are presented and discussed in relation to pathogenesis.

Acute Disease↗

Acute subdural hematoma in infancy.

BACKGROUND: Acute subdural hematoma in infants is distinct from that occurring in older children or adults because of differences in mechanism, injury thresholds, and the frequency with which the question of nonaccidental injury is encountered. The purpose of this study is to analyze the clinical characteristics of acute subdural hematoma in infancy, to discover the common patterns of this trauma, and to outline the management principles within this group. METHODS: Medical records and films of 21 cases of infantile acute subdural hematoma were reviewed retrospectively. Diagnosis was made by computed tomography or magnetic resonance imaging. Medical records were reviewed for comparison of age, gender, cause of injury, clinical presentation, surgical management, and outcome. RESULTS: Twenty-one infants (9 girls and 12 boys) were identified with acute subdural hematoma, with ages ranging from 6 days to 12 months. The most common cause of injury was shaken baby syndrome. The most common clinical presentations were seizure, retinal hemorrhage, and consciousness disturbance. Eight patients with large subdural hematomas underwent craniotomy and evacuation of the blood clot. None of these patients developed chronic subdural hematoma. Thirteen patients with smaller subdural hematomas were treated conservatively. Among these patients, 11 developed chronic subdural hematomas 15 to 80 days (mean = 28 days) after the acute subdural hematomas. All patients with chronic subdural hematomas underwent burr hole and external drainage of the subdural hematoma. At follow-up, 13 (62%) had good recovery, 4 (19%) had moderate disability, 3 (14%) had severe disability, and 1 (5%) died. Based on GCS on admission, one (5%) had mild (GCS 13-15), 12 (57%) had moderate (GCS 9-12), and 8 (38%) had severe (GCS 8 or under) head injury. Good recovery was found in 100% (1/1), 75% (8/12), and 50% (4/8) of the patients with mild, moderate, and severe head injury, respectively. Sixty-three percent (5/8) of those patients undergoing operation for acute subdural hematomas and 62% (8/13) of those patients treated conservatively had good outcomes. CONCLUSIONS: Infantile acute subdural hematoma if treated conservatively or neglected, is an important cause of infantile chronic subdural hematoma. Early recognition and suitable treatment may improve the outcome of this injury. If treatment is delayed or the condition is undiagnosed, acute subdural hematoma may cause severe morbidity or even fatality.

Diagnosis, Differential↗

[Spontaneous resolution of an acute subdural hematoma].

Acute postraumatic subdural hematoma is known to have bad prognosis. Traditionally, its treatment consisted in urgent surgical evacuation. Rapid spontaneous resolution of the hematoma has been infrequently observed. We report a case of a patient with an acute traumatic subdural hematoma which disappeared without surgery. CT-scan showed a left-sided subdural hematoma with marked mass effect. A low density layer, which implied involvement of CSF in the subdural space, was observed between the hematoma and the inner wall of the skull. We think that the spontaneous resolution of the hematoma was due to the dilution and washing-out by the CSF through an arachnoid tear. Another suggested mechanism in the literature is blood redistribution in the subdural space. Selected patients with an acute subdural hematoma can be managed with conservative treatment.

Aged↗

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↗

Spontaneous acute subdural hematoma following contralateral calcified chronic subdural hematoma surgery: an unusual case.

Calcified chronic subdural hematoma (CCSDH) is a well-known disease to many neurosurgeons but only few cases have been reported regarding its surgical complications. We report a spontaneous acute subdural hematoma following contralateral CCSDH surgery in a 16-year-old boy and discuss its possible mechanisms. The first few days of the postoperative period, especially for the cerebral atrophy cases, should be monitored carefully and a control computerized tomography scan should be performed early for possible complications. To our knowledge, spontaneous acute subdural hematoma following contralateral CCSDH surgery has not been reported previously.

Adolescent↗

Effects of hypothermia on intracranial pressure and brain edema formation: studies in a rat acute subdural hematoma model.

Acute subdural hematoma (SDH) is the most common mass lesion in severe head injury, and brain ischemia is the leading pathophysiological mechanism in the development of secondary brain damage following SDH. Hypothermia has been employed as an effective neuroprotective procedure in clinical and laboratory studies on cerebral ischemic and contusional injuries. In the present study, we used a rat acute SDH model to assess the effect of hypothermia on the intracranial pressure (ICP) and also on the brain edema formation at 4 h after hematoma induction. Mild (34 degrees C) and moderate (32 degrees C) hypothermia did not significantly affect the ICP or cerebral perfusion pressure, but they were associated with a significant lower cortical brain edema formation beneath the hematoma (81.09 +/- 0.49%, p<0.05; and 80.88 +/- 0.17%, p<0.01) when compared with the normothermic control group (81.65 +/- 0.52%). This reduction in brain edema formation was comparable to the results of MK-801 treatment (80.95 +/- 0.35%, p<0.01). The present findings indicate that hypothermia represents a potent neuroprotective strategy. The possible protective mechanisms of hypothermic protection afforded in this rat acute SDH model are discussed.

Animals↗

Pupillary sparing oculomotor palsy from acute subdural hematoma.

An acute subdural hematoma presented as a partial third nerve palsy with complete pupillary sparing. The patient was alert and oriented, and except for a subtle hemisensory hypalgesia, there were no other neurologic signs. Preoperative diagnosis was made by CT scan and cerebral angiography. The patient underwent successful craniotomy and within six weeks after surgery, her third nerve palsy had completely resolved.

Adult↗

Spontaneous acute subdural hematomas. A clinical comparison with traumatic acute subdural hematomas.

A comparison was made between factors influencing survival in patients operated on for acute spontaneous subdural hematomas (ASSH) and other groups of patients operated for acute, post-traumatic, subdural hematoma reported in the literature. The data of 17 patients operated on for ASSH were collected. Four variables: early surgical treatment, high Glasgow Coma Scale score on admission, pupillary reactivity and age were statistically analyzed. The most significant factors for good outcome, in order of importance, were early surgical treatment, a high Glasgow Come Scale score on admission, good pupillary reactivity and younger age. The prognostic factors in non-traumatic and traumatic acute subdural hematomas were found to be identical.

Acute Disease↗

Bilateral acute epidural hematoma after evacuation of acute subdural hematoma: brain shift and the dynamics of extraaxial collections.

Acute epidural hematoma following supratentorial decompressive craniectomy is a very seldom described but serious complication. The occurrence of intraoperative brain swelling may suggest the development of a contralateral hematoma. A unique case of bilateral acute epidural following decompressive craniectomy and evacuation of acute subdural hematoma is presented. Awareness of unexplained elevation of intracranial pressure is of paramount importance when routine immediate postoperative computed tomography is not performed. This case provides insight into the well-known but poorly understood dynamic process of brain shift and extraaxial collections.

Aged↗

[A case of internal carotid-posterior communicating artery aneurysm presenting pure acute subdural hematoma].

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.

Aneurysm, Ruptured↗

Role of dural fenestrations in acute subdural hematoma.

OBJECT: Patients with acute subdural hematomas (ASDHs) have higher mortality and lower functional recovery rates compared with those of other head-injured patients. Early surgical decompression and active intensive care treatment represent, so far, the best way to assist these patients. Paradoxically, one of the factors contributing to poor outcomes in cases of ASDHs could be rapid surgical decompression, owing to the severe extrusion of the brain through the craniotomy defect in response to acute brain swelling. To avoid the deleterious consequences of abrupt decompression of the subdural space with disruption of brain tissue, the authors have adopted a new surgical technique for evacuation of ASDHs. This procedure consists of creating multiple fenestrations of the dura (MFD) in a meshlike fashion and removing clots through the small dural openings that are left open, avoiding the creation of a wide dural opening and the disruption of and additional damage to brain tissue. METHODS: Thirty-one patients (26 male and five female patients with a mean age of 32.5 years) harboring ASDHs were treated using this method. On admission there were 16 patients (51.5%) with Glasgow Coma Scale (GCS) scores of 3 to 5, 11 patients (35.5%) with GCS scores of 6 to 8, and four patients (12.9%) with GCS scores of 9 to 12. Postoperative computerized tomography scans of the brain revealed evacuation of more than 80% of the hematoma in 29 of 31 patients. The overall mortality rate in this group was 51.6%. CONCLUSIONS: This preliminary report of a new surgical approach for patients who have sustained ASDHs should be considered to avoid abrupt disruption of the brain and to allow the gradual and gentle release of subdural clots. This is especially important in cases in which there are severe midline shifts and a tight brain. Further clinical studies should be conducted in a more selected series to estimate the impact of this new procedure on morbidity and mortality rates.

Adolescent↗

[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↗

Coexistence of rapidly resolving acute subdural hematoma and delayed traumatic intracerebral hemorrhage.

Rapid resolution of acute subdural hematoma is rare. Delayed traumatic intracerebral hematomas following medical or surgical treatment of increased intracranial pressure have also been reported. Coexistence of a quickly resolving acute subdural hematoma and a delayed traumatic intracerebral hemorrhage has not been reported before. A 13-month-old boy was admitted to our emergency department after a car accident. On CT, a thin acute subdural hematoma on the right frontotemporal region and a small epidural hematoma on the left frontal region could be seen. On 24-hour follow-up CT, the right subdural hematoma was found to be less dense but larger than it had been before. At 36 h after hospitalization, CT showed that the right acute subdural hematoma had completely disappeared; however, a delayed traumatic intracerebral hematoma on the left occipital region was identified. We think that the mechanism involved in the development of a delayed intracerebral hematoma in our case was similar to the one causing delayed traumatic intracerebral hematoma after treatment for increased intracranial pressure.

Accidents, Traffic↗