Control perioperatorio del tratamiento anticoagulante en pacientes con hemorragia intracraneana / Perioperative management of anticoagulant treatment in patients with intracranial hemorrhage

Se analizó el control perioperatorio del tratamiento anticoagulante y trombolítico de 22 pacientes con una hemorragia intracraneana. La TAC mostró que la hemorragia fue intraparenquimatosa en 12, subdural en 9 y mixta en 1. Se consideraron la suspensión, corrección, mantenimiento y reanudación de la anticoagulación en el pre y postoperatorio. En todos los casos una vez hecho el diagnóstico se suspendió el anticoagulante. En 4 casos no se normalizó la coagulación y fallecieron 3 (1 por resangrado), en 1 no se mantuvo la corrección y falleció por resangrado. Los casos que sobrevivieron a la hemorragia inicial si era necesario fueron reanticoagulante: 1 a las 72 horas y 6 entre el 8§ y 10§ días del postoperatorio sin inconvenientes; 1 a las 24 horas y resangró; 2 no fueron reanticoagulados y sufrieron complicaciones tromboembólicas falleciendo. La mortalidad global fue del 69,2 por ciento (13 casos). Se consideró que en 7 casos el control perioperatorio de la anticoagulación no fue el apropiado.

Control perioperatorio del tratamiento anticoagulante en pacientes con hemorragia intracraneana / Perioperative management of anticoagulant treatment in patients with intracranial hemorrhage

Se analizó el control perioperatorio del tratamiento anticoagulante y trombolítico de 22 pacientes con una hemorragia intracraneana. La TAC mostró que la hemorragia fue intraparenquimatosa en 12, subdural en 9 y mixta en 1. Se consideraron la suspensión, corrección, mantenimiento y reanudación de la anticoagulación en el pre y postoperatorio. En todos los casos una vez hecho el diagnóstico se suspendió el anticoagulante. En 4 casos no se normalizó la coagulación y fallecieron 3 (1 por resangrado), en 1 no se mantuvo la corrección y falleció por resangrado. Los casos que sobrevivieron a la hemorragia inicial si era necesario fueron reanticoagulante: 1 a las 72 horas y 6 entre el 8º y 10º días del postoperatorio sin inconvenientes; 1 a las 24 horas y resangró; 2 no fueron reanticoagulados y sufrieron complicaciones tromboembólicas falleciendo. La mortalidad global fue del 69,2 por ciento (13 casos). Se consideró que en 7 casos el co

Management of 50 spontaneous cerebellar haemorrhages. Importance of obstructive hydrocephalus.

The records of 50 cerebellar haemorrhages were reviewed retrospectively. In this series the most important factor for clinical development, management and mortality was the presence of obstructive hydrocephalus (p < 0.01). Slowly progressive (type 1) and abruptly developing (type 2) deterioration of consciousness was significantly related to high mortality; this holds also true for the combination of hydrocephalus with an haematoma diameter > 3 cm. Larger haematomas had a higher mortality but this relation, analyzed alone, did not reach statistical significance (p > 0.05). In cases with hydrocephalus mortality could significantly be reduced by surgical evacuation of the haematoma (p < 0.01). The treatment of cerebellar haemorrhages must be directed at resolving obstructive hydrocephalus.

Electrophysiological studies of long-term electrical stimulation of the cerebellum in monkeys.

Six rhesus monkeys were stimulated on the paravermal cortex for 205 hours (18 days) with different charge densities in order to determine the electrode performance and neural damage that may result from long-term cerebellar stimulation comparable to that being used in man. The electrode-tissue interface was relatively stable and no neural damage was found when the charge/phase (0.5 muC/ph) or charge density (7.4 muC/sq cm/ph) was very low. At all higher charge levels tested (2.4, 4.8, 10, and 22 muC/ph), changes in the electrode-tissue interface, meningeal encapsulation, and neural damage were directly related to the charge density delivered. Unstimulated electrodes on the opposite paravermal cortex exhibited mild tissue reactivity and cell damage, probably due to mechanical compression of the molecular layer and pial vessels. Motor cortex field potentials could be evoked by charges as low as 0.1 muC/ph delivered to paravermal cortex; for a given charge/phase longer pulses were more effective than short pulses. After neural damage resulting from 205 hours of 4.8 muC pulses at 10 per second (total charge 14.76 C), the threshold for the motor cortex evoked potential increased by a factor of four or more. With the charge held constant to different-sized electrodes placed bilaterally in the same monkey, damage was greater under the smaller electtrode. This finding suggests that the charge density to cerebellar cortex must be controlled to avoid neural damage.

Tissue reactions to long-term electrical stimulation of the cerebellum in monkeys.

Light and electron microscopic analyses were carried out on the stimulated and unstimulated paravermal cortices of six rhesus monkeys that had electrodes implanted on their cerebella for 2 months. The electrodes and the stimulation regime (10 p.p.s.: 8 min on, 8 min off) were similar to those used to stimulate the human cerebellum for treatment of certain neurological disorders. Mere presence of the electrode array in the posterior fossa for 2 months resulted in some meningeal thickening, attenuation of the molecular layer, and loss of Purkinje cells immediately beneath the electrode array. There was no evidence of scarring. After 205 hours of stimulation (7.35 X 10(6) pulses) over 18 days, a charge of 0.5 muC/ph or estimated charge density of 7.4 muC/sq cm/ph resulted in no damage to the cerebellum attributable to electrical stimulation per se. Such a charge/phase is about five times the threshold for evocation of cerebellar efferent activity, and might be considered "safe" for stimulation of human cerebellum. Charge density/phase and charge/phase were directly related to increased cerebellar injury in the six other cerebellar cortices stimulated. Leptomeningeal thickening increased with increased charge density. Injury included severe molecular layer attenuation, ongoing destruction of Purkinje cells, gliosis, ongoing degeneration of myelinated axons, collagen intrusion, and increased levels of local polysaccharides. In all cases, even with damage that destroyed all conducting elements beneath the electrodes, there was no damage further than 1 to 2 mm from the edges of the electrode arrays.