RESUMEN
BACKGROUND: Derangement of cerebral metabolism occurs after various insults such as ischemia, traumatic brain injury, and subarachnoid hemorrhage (SAH). OBJECTIVE: To investigate the course of cerebral blood flow and metabolic parameters in the first hours after experimental SAH. METHODS: Sixteen Sprague-Dawley rats were subjected to SAH using the endovascular filament model or served as controls (8 rats in each group). Local cerebral blood flow and intracranial pressure were measured continuously. Microdialysis samples were acquired in 30-minute intervals for 6 hours after SAH. Concentrations of glucose, lactate, pyruvate, and glutamate were determined. RESULTS: After induction of SAH, cerebral perfusion pressure and local cerebral blood flow sharply decreased. The decrease in local cerebral blood flow exceeded the decrease in cerebral perfusion pressure throughout the observation period. Glutamate concentrations in microdialysis samples increased sixfold and recovered to baseline levels. Lactate concentrations immediately increased after SAH, recovered incompletely, and remained above the levels of control animals until the end of the sampling period. Pyruvate concentrations showed a delayed increase starting 2 hours after SAH. CONCLUSION: The course of cerebral blood flow after SAH resembles global ischemia followed by a continuous low-flow state caused by a sudden decrease in cerebral perfusion pressure and acute vasoconstriction. The courses of lactate and pyruvate concentrations indicate a persistently deranged aerobic metabolism.
Asunto(s)
Encéfalo/metabolismo , Encéfalo/fisiopatología , Circulación Cerebrovascular/fisiología , Hemorragia Subaracnoidea/metabolismo , Hemorragia Subaracnoidea/fisiopatología , Animales , Encéfalo/irrigación sanguínea , Química Encefálica/fisiología , Microdiálisis , Ratas , Ratas Sprague-Dawley , TiempoRESUMEN
OBJECTIVE: To examine whether the maintenance of elevated magnesium serum concentrations by intravenous administration of magnesium sulfate can reduce the occurrence of cerebral ischemic events after aneurysmal subarachnoid hemorrhage. DESIGN: Prospective, randomized, placebo-controlled study. SETTING: Neurosurgical intensive care unit of a University hospital. INTERVENTIONS: One hundred ten patients were randomized to receive intravenous magnesium sulfate or to serve as controls. Magnesium treatment was started with a bolus of 16 mmol, followed by continuous infusion of 8 mmol/hr. Serum concentrations were measured every 8 hrs, and infusion rates were adjusted to maintain target levels of 2.0-2.5 mmol/L. Intravenous administration was continued for 10 days or until signs of vasospasm had resolved. Thereafter, magnesium was administered orally and tapered over 12 days. MEASUREMENTS AND MAIN RESULTS: Delayed ischemic infarction (primary end point) was assessed by analyzing serial computed tomography scans. Transcranial Doppler sonography and digital subtraction angiography were used to detect vasospasm. Delayed ischemic neurologic deficit was determined by continuous detailed neurologic examinations; clinical outcome after 6 months was assessed using the Glasgow outcome scale. Good outcome was defined as Glasgow outcome scale score 4 and 5.The incidence of delayed ischemic infarction was significantly lower in magnesium-treated patients (22% vs. 51%; p = .002); 34 of 54 magnesium patients and 27 of 53 control patients reached good outcome (p = .209). Delayed ischemic neurologic deficit was nonsignificantly reduced (9 of 54 vs. 15 of 53 patients; p = .149) and transcranial Doppler-detected/angiographic vasospasm was significantly reduced in the magnesium group (36 of 54 vs. 45 of 53 patients; p = .028). Fewer patients with signs of vasospasm had delayed cerebral infarction. CONCLUSION: These data indicate that high-dose intravenous magnesium can reduce cerebral ischemic events after aneurysmal subarachnoid hemorrhage by attenuating vasospasm and increasing the ischemic tolerance during critical hypoperfusion.
Asunto(s)
Bloqueadores de los Canales de Calcio/uso terapéutico , Aneurisma Intracraneal/complicaciones , Sulfato de Magnesio/uso terapéutico , Hemorragia Subaracnoidea/tratamiento farmacológico , Vasoespasmo Intracraneal/prevención & control , Adulto , Anciano , Bloqueadores de los Canales de Calcio/administración & dosificación , Femenino , Hospitales Universitarios , Humanos , Hipoxia-Isquemia Encefálica/etiología , Hipoxia-Isquemia Encefálica/prevención & control , Infusiones Intravenosas , Unidades de Cuidados Intensivos , Sulfato de Magnesio/administración & dosificación , Masculino , Persona de Mediana Edad , Estudios Prospectivos , Hemorragia Subaracnoidea/etiología , Vasoespasmo Intracraneal/etiologíaRESUMEN
Present knowledge about hemodynamic and metabolic changes after subarachnoid hemorrhage (SAH) originates from neuromonitoring usually starting with aneurysm surgery and animal studies that have been focusing on the first 1 to 3 h after SAH. Most patients, however, are referred to treatment several hours after the insult. We examined the course of hemodynamic parameters, cerebral blood flow, and tissue oxygenation (ptiO2) in the first 6 h after experimental SAH. Sixteen Sprague-Dawley rats were subjected to SAH using the endovascular filament model or served as controls (n=8). Bilateral local cortical blood flow, intracranial pressure, cerebral perfusion pressure, and ptiO2 were followed for 6 h after SAH. After induction of SAH, local cortical blood flow rapidly declined to 22% of baseline and returned to 80% after 6 h. The decline of local cortical blood flow markedly exceeded the decline of cerebral perfusion pressure. ptiO2 declined to 57%, recovered after 2 h, and reached > or =140% of baseline after 6 h. Acute vasoconstriction after SAH is indicated by the marked discrepancy of cerebral perfusion pressure and local cortical blood flow. The excess tissue oxygenation several hours after SAH suggests disturbed oxygen utilization and cerebral metabolic depression. Aside from the sudden increase of intracranial pressure at the time of hemorrhage and delayed cerebral vasospasm, the occurrence of acute vasoconstriction and disturbed oxygen utilization may be additional factors contributing to secondary brain damage after SAH.
Asunto(s)
Circulación Cerebrovascular , Oxígeno/metabolismo , Hemorragia Subaracnoidea/fisiopatología , Animales , Presión Sanguínea , Corteza Cerebral/irrigación sanguínea , Hemodinámica , Ratas , Ratas Sprague-Dawley , Factores de Tiempo , Vasoconstricción , Vasoespasmo IntracranealRESUMEN
OBJECT: Immediate vasoconstriction after subarachnoid hemorrhage (SAH) has been observed in a number of experimental studies. However, it has not yet been examined which pattern this acute-type vascular reaction follows and whether it correlates with the intensity of SAH. It was the purpose of the present study to vary the extent of SAH using the endovascular filament model of SAH with increasing filament sizes and to compare the course of intracranial pressure (ICP), cerebral perfusion pressure (CPP), and regional cerebral blood flow (rCBF). METHODS: Male Sprague-Dawley rats were subjected to SAH using the endovascular filament model. Subarachnoid hemorrhage was induced using a 3-0, 4-0, or 5-0 Prolene monofilament (8 rats in each group). Eight animals served as controls. Bilateral rCBF (laser Doppler flowmetry), mean arterial blood pressure, and ICP were continuously monitored. Thereafter, the rats were allowed to wake up. Twenty-four hours later, the animals were killed, their brains were removed, and the extent of SAH was determined. RESULTS: After induction of SAH, ICP steeply increased while CPP and rCBF rapidly declined in all groups. With increasing size of the filament, the increase of ICP and the decrease of CPP were more pronounced. However, the decline of rCBF exceeded the decline of CPP in all SAH groups. In a number of animals with minor SAH, an oscillating pattern of rCBF was observed during induction of SAH and during early recovery. CONCLUSIONS: The disparity between the decline and recovery of CPP and rCBF suggests that acute vasoconstriction occurs even in SAH of a minor extent. Acute vasoconstriction may contribute significantly to a perfusion deficit in the acute stage after SAH. The oscillating pattern of rCBF in the period of early recovery after SAH resembles the pattern of synchronized vasomotion, which has been thoroughly examined for other vascular territories and may yield therapeutic potential.
Asunto(s)
Circulación Cerebrovascular/fisiología , Hemorragia Subaracnoidea/fisiopatología , Vasoconstricción/fisiología , Animales , Presión Sanguínea/fisiología , Presión Intracraneal/fisiología , Flujometría por Láser-Doppler , Masculino , Ratas , Ratas Sprague-Dawley , Flujo Sanguíneo RegionalRESUMEN
OBJECTIVE: Spontaneous acute subdural hematoma (aSDH) may be caused by aneurysm rupture. Patients can present in very poor clinical condition with anisocoria or even bilaterally dilated pupils, absent brainstem reflexes, and cardiac insufficiency. For the clinician, the question is how should these patients be treated? Large series on this subject do not exist because aSDH is a rare event. This report focuses on the prognosis and adverse prognostic factors of these patients. CLINICAL PRESENTATION: We present eight cases of aSDH and subarachnoid hemorrhage attributable to aneurysm rupture. All patients were World Federation of Neurosurgical Societies Grade 5. Four presented with anisocoria, three presented with bilaterally fixed and dilated pupils, and one developed anisocoria in the course of treatment. TREATMENT: As a result of prolonged hypoxia before admission, one patient was not treated and died. In one patient, surgical decompression could not be performed in the acute phase as a result of significant comorbidity. All other patients received decompressive surgery, obliteration of the aneurysm, and medical therapy as well as extensive rehabilitation measures. After 6 months, four had no or only minor neurological deficits; one patient was independent despite hemiparesis. Two patients whose surgical decompression had to be delayed as a result of severe cardiac instability recovered poorly, showed severe neurological deficits, and required permanent care. However, none of the patients survived in a persistent vegetative state. CONCLUSION: Within the spectrum of aneurysmatic hemorrhage, patients with aSDH represent a distinct subgroup. Despite a very poor clinical condition on admission, recovery with only minor deficits or even without neurological deficit is possible. Mass effect and herniation induce a poor clinical condition, which is not directly related to the underlying subarachnoid hemorrhage. Hence, clinical grading systems such as the Hunt and Hess scale or World Federation of Neurosurgical Societies grading are not applicable. We suggest that whenever the medical condition allows, rapid surgical decompression should be performed even in patients who present in very poor neurological condition.
Asunto(s)
Cuidados Críticos/métodos , Hematoma Subdural Agudo/diagnóstico , Hematoma Subdural Agudo/terapia , Adulto , Enfermedad Crítica , Diagnóstico Diferencial , Femenino , Humanos , Persona de Mediana Edad , Pronóstico , Resultado del TratamientoRESUMEN
The size of a cerebral contusion is not finite at the moment of trauma, but liable to secondary increase during the following hours and days. In the present study we investigated whether this phenomenon may be related to changes in cortical blood flow (cCBF). In rats a cortical lesion grew to 140% of its initial volume during the first 24 h after injury. During the time of most rapid lesion expansion (<6 h after the insult) marked hypoperfusion (approximately 30% of baseline) was found in the ipsilateral hemisphere by laser Doppler scanning fluxmetry. In the peri-contusional area cCBF slowly recovered to approximately 80% of baseline, while in the distant brain not affected by delayed cell death, significant hyperperfusion (approximately 160% of baseline) was observed. Thus, early hypoperfusion might be an important mechanism for secondary lesion expansion.
Asunto(s)
Corteza Cerebral/irrigación sanguínea , Animales , Corteza Cerebral/lesiones , Corteza Cerebral/patología , Frío/efectos adversos , Flujometría por Láser-Doppler/instrumentación , Flujometría por Láser-Doppler/métodos , Masculino , Necrosis , Ratas , Ratas Sprague-Dawley , Flujo Sanguíneo Regional , Factores de Tiempo , Trepanación/métodosRESUMEN
A cortical tissue necrosis from focal trauma expands between 30% and 300% from its initial size within 24 h, depending on the species studied. To shed light on the pathophysiological processes in the penumbra 1 zone after a focal cortical lesion, the release of excitatory amino acids into the traumatic penumbra zone 1 was measured throughout the entire period of necrosis expansion. A microdialysis probe was inserted at an oblique angle into the cortex of Sprague-Dawley rats 2 mm below the brain surface. One day later, a highly standardized cortical freezing lesion was induced at the brain cortex above the microdialysis probe. Dialysate was continuously collected prior to, during, and up to 24 h after trauma and analyzed for primary amino acids. In each animal, it was confirmed histologically that the tip of the microdialysis probe was localized in the gray matter in close proximity to the primary lesion. Following induction of the trauma, a statistically significant sharp increase of the dialysate level of aspartate, glutamate, glycine, and serine was observed. Thereafter, the dialysate levels of these amino acids returned to baseline levels without any further increase throughout the remaining observation period. This process ranged in time from a few minutes to a few hours. The level of alanine in the dialysate was essentially not altered throughout the experiment. Although the early post-traumatic increase of the excitatory neurotransmitters aspartate and glutamate may well contribute to the secondary lesion growth of a cortical necrosis after trauma, glutamate receptor targeted therapeutic intervention may be in view of these findings of limited use when initiated post trauma.