Return to home early days after acute aortic dissection surgery.

AIM: The length of hospital stay after acute aortic dissection surgery tends to be prolonged. The aim of this study is to assess the feasibility of our protocol for early discharge after acute aortic dissection surgery. METHODS: This study enrolled 17 consecutive acute aortic dissection patients who returned to their own home within 2 weeks of surgery. In seven patients total aortic arch replacement was performed and in 7 partial arch replacement. The main aim of the first 24 h after surgery was to achieve early extubation. Patients were encouraged to return to their own home 4 days and later after surgery. The prerequisite criteria for discharge were the following: independent mobility, stable hemodynamics, apyrexia, adequate oral intake, normal bowel function, healthy surgical wound and the patient's agreement for discharge. RESULTS: The mean age of these patients was 59. The postoperative ventilation time, length of intensive care unit stay and postoperative hospital stay were 11 h, 37 h and 6.9 days, respectively. Two (12%), 13 (76%) and 14 (82%) patients returned to their own home by postoperative day 4, 7 and 10, respectively. Three patients were readmitted to a peripheral hospital in the 4 week postoperative period. The reason for all readmissions was lack of family support. Two other patients underwent pericardiocentesis for pericardial effusion at an other hospital as outpatients. There was no complication caused by early discharge. CONCLUSIONS: Early discharge after aortic dissection surgery is safe and recommended to patients who have normal bowel function and adequate family support.

Effects of ebselen on cerebral ischemia and reperfusion evaluated by microdialysis.

Since ebselen is known to have glutathione peroxidase-like activity and inhibitory effects on lipoxygenase and cyclo-oxygenase, we investigated its protective effects against cerebral ischemia in the rat using microdialysis. Ebselen was given through a gastric tube 30 min before occlusion in the experimental groups. Ischemia was induced using 4-vessel occlusion either transiently (20-min occlusion of the arteries followed by reperfusion), or over a prolonged period (120-min occlusion). Extracellular lactate, pyruvate and purine catabolites were sampled using microdialysis and measured by high performance liquid chromatography. During ischemia, the level of lactate, adenosine, inosine and hypoxanthine in the control group increased markedly. The lactate: pyruvate ratio increased during ischemia and decreased after reperfusion. Although the level of lactate and adenosine decreased immediately after reperfusion, those of inosine and hypoxanthine showed delayed decrease. Ebselen reduced the maximum values of lactate and purine catabolites significantly and markedly in transient ischemia. Although it reduced the values significantly in prolonged ischemia, the decrements were less marked than those in transient ischemia. Based on these results we consider ebselen to protect against ischemic metabolic changes and to accelerate the recovery during reperfusion.

Normal perfusion pressure hyperperfusion in cerebral arteriovenous malformation surgery: model study on the hemodynamics and mechanisms.

A simulation study was undertaken using a compartmental flow model of a large high-flow cerebral arteriovenous malformation to investigate the hemodynamic changes during obliteration procedures. Under certain autoregulatory conditions, marked hyperperfusion (92 ml/100 g/min) could be induced in association with increased wall stress of the arterioles. Narrowing of the autoregulatory pressure range and its shift to a low pressure level are suspected to be among the possible causes of normal perfusion pressure breakthrough phenomenon.

[Hemodynamic simulation study of cerebral arteriovenous malformations: changes of wall stress and early detection of NPPB].

Obliteration procedures for large high-flow arteriovenous malformations (AVM) were simulated using a compartmental flow model to investigate the role of altered autoregulatory conditions in the development of hyperperfusion and normal perfusion pressure breakthrough (NPPB). Since the arterioles are primarily responsible for autoregulatory function, the role of these structural changes on the development of hyperperfusion was also studied by evaluating the wall thickness (T), internal radius (Ri) and tangential wall stress (sigma). As the AVM flow was decreased during the obliteration procedures, the perfusion pressure (delta P) of the brain tissue surrounding the AVM increased. When the autoregulatory condition was impaired [AR (-)] and the lower limit of the autoregulatory pressure range (LAR) was shifted from 60 mmHg (LAR60) to 40 mm Hg (LAR40), the flow volume in the surrounding brain (Fb) increased markedly, from 67 ml/100g/min to 92 ml/100g/min, with the progress of the obliteration procedures. In these conditions, T/Ri was supposed to be constant and sigma value increased uniformly. In the presence of the autoregulatory mechanism [AR (+)], T/Ri increased against increasing delta P, which resulted in smaller sigma value than that under AR (-) conditions. When the contracted vascular wall yielded on the process of increasing wall stress, delta P and feeder pressure (Pf) decreased to some degree. Concomitantly increase of the sigma value and marked hyperperfusion developed in the brain. The yield of the contracted vascular wall would result in the decrease of a pressure gradient across the arteriole and the reciprocal increase of pressure load on the walls of the capillary and venula, which might lead to NPPB. Since the decrease of delta P or Pf during the progress of the obliterating procedures is considered specific to the appearance of hyperperfusion or NPPB, monitoring these parameters would be useful for its early detection. If the upper limit of the autoregulatory pressure range was assumed to decrease and become the yield point in the brain surrounding high flow AVMs, hyperfusion or NPPB could be considered to develop in the conditions with the autoregulatory pressure range being narrowed and/or shifted to the lower pressure level. Induced systemic hypotension was found to be effective in reducing the magnitude of Fb, delta P, and Pf when induction was appropriately performed in stepwise fashion. T/Ri and sigma were kept in narrow ranges compared to those before induction of hypotension.

Hemodynamic simulation study of cerebral arteriovenous malformations. Part 2. Effects of impaired autoregulation and induced hypotension.

The hemodynamic changes occurring during obliteration procedures for arteriovenous malformations (AVM) have not been fully elucidated. Therefore, we undertook a simulation study using a compartmental flow model to investigate the role of altered autoregulatory conditions in the development of hyperperfusion during obliteration of large high-flow AVM. Induced hypotension was also simulated to evaluate its usefulness in reducing the incidence and severity of the event. As the AVM flow was decreased during the obliteration procedures, feeder pressure increased and drainer pressure decreased, with a concomitant increase in the perfusion pressure in the brain tissue surrounding the AVM. Cerebral blood flow (CBF) remained constant at 50 ml 100 g-1 min-1 in the presence of autoregulation and increased to 67 ml 100 g-1 min-1 in its absence. When the lower limit of the autoregulatory pressure range (LAR) was shifted from 60 to 50 or 40 mm Hg, the flow volume increased markedly from 67 to 77 ml 100 g-1 min-1 or to 92 ml 100 g-1 min-1 after complete obliteration. Decrease in LAR would be a cause of the hyperperfusion. Induced systemic hypotension was found to be effective in reducing the magnitude of these hemodynamic changes, when induction was appropriately performed in a stepwise fashion. A simulation study is useful in clarifying the various hemodynamic changes that develop during the treatment of AVM.

Dissociated changes of frontal and parietal somatosensory evoked potentials in sleep.

We studied the changes of frontal and parietal somatosensory evoked potentials (SEPs) in the awake state versus different stages of sleep in 10 normal adult subjects. Frontal and parietal SEP components were affected differentially as sleep stages progressed. In general, the amplitudes of frontal components, notably P22, were increased in sleep, whereas the amplitudes of parietal components were decreased in sleep. A sensitive waveform change from the awake state to sleep was present in the frontal response, where a subtle notched negativity, termed "N40," was present only in the awake state and quickly dissipated in all stages of sleep, including stage 1. The amplitude changes from the awake state to stage 3/4 sleep were neither linear nor parallel among SEP components. The most discordant changes occurred in stage 3/4. The amplitudes for the frontal N18-P22-N30 complex and parietal N20-P26-N32 complex increased from stage 2 to stage 3/4, while those for frontal N30-fP40 and parietal N32-pP40 decreased. In contrast to these divergent amplitude changes, the latencies of all components except P14 and frontal N18 showed progressive prolongation from the awake state to slow-wave sleep. The SEP waveforms and latencies in REM sleep approximated those in the awake state, although amplitudes for frontal peaks still remained slightly higher and amplitudes for parietal peaks slightly lower. We postulate that interactions of excitatory and inhibitory phenomena are responsible for the component-dependent and sleep-stage-dependent amplitude enhancement or depression in sleep.

High-rate sequential sampling of auditory brain-stem and somatosensory evoked responses in hypoxia.

We developed a high-rate sequential recording technique that allowed simultaneous measurements of both auditory brain-stem response (ABR) and somatosensory evoked potential (SEP) every 10 sec. Using this method, a transient increase in amplitude of all the ABR and SEP components in response to hypoxia in dogs could be detected. The increase in amplitude preceded the prolongation of latency. Our study showed that there were successive changes of evoked potentials in response to hypoxia. A transient increase in amplitude is the first to occur, followed by a latency prolongation and an amplitude decrease for both ABRs and SEPs.

[EC-IC bypass surgery using saphenous vein graft: technical improvement in our experience].

We managed ten cases of EC-IC bypass using a vein graft; six cases with multiple cerebral arterial occlusion and four cases with aneurysm necessitating therapeutic occlusion of the parent artery (Table). Patency of the graft was confirmed in seven cases on long-term follow-up ranging from 7 months to 5 years. Of the ten cases, two died within 7 days after surgery from causes unrelated to the bypass and one was lost in follow-up surgery. Hemorrhagic infarction was observed in two cases, one of which underwent removal of the hematoma. In five cases with cerebral occlusive disease, there were no additional ischemic events and two cases with giant aneurysms showed improvement of visual acuity and extraocular movement. We improved on several surgical techniques for vein graft. We used small hemoclips to occlude branches of the saphenous vein instead of ligating them, which shortens the harvesting time of the saphenous vein. Vessel cannula with a small-sized elegant tip and one-directional valve (DLP, INC., USA) was also used to inflate or deflate vein grafts with saline. It was easily attached to the graft and minimized air entrapment in the lumen. Small clips for microvascular anastomosis (Mizuho INC., Japan) were used to temporarily occlude branches or perforators from the recipient artery. One of the branches of the graft was dissected long enough, through which intraluminal air or thrombus was washed out at the final stage of the surgery. These procedures are useful for shortening occlusion time of the recipient artery and decreasing the risk of embolism.

Simulation study on therapeutic vertebral artery occlusion for VA-PICA giant aneurysm.

We investigated haemodynamic effects of therapeutic vertebral artery (VA) occlusion on giant aneurysms at the bifurcation of the VA-posterior inferior cerebellar artery (PICA). An hydraulic model of the human vertebro-basilar artery was manufactured from glass and silicone tubes. Glass-spheres 2.5 cm in diameter were placed at the bifurcation as model aneurysms with respective distances of 8.5, 7.5, 6.5 and 5.5 mm between the VA union and aneurysmal neck. A 40% glycerol solution was perfused in this system and the half-life of the dye injected into aneurysms was regarded as an index of intra-aneurysmal stagnation. Flow conditions in aneurysms depended on the presence or absence of the effect of contralateral VA flow as well as the PICA flow. The half-life increased significantly after VA occlusion proximal to the PICA when the aneurysmal neck was more than 7.5 mm away from the VA union and PICA flow volume was less than 12 ml min-1. The half-life in aneurysms located within 6.5 mm from the union changed little after VA occlusion regardless of the PICA flow volumes. The haemodynamic simulation study would be helpful in speculating on the efficacy of this treatment.