Relation of cerebral energy metabolism and extracellular nitrite and nitrate concentrations in patients after aneurysmal subarachnoid hemorrhage.

In a prospective clinical investigation on neurochemical intensive care monitoring, the authors' aim was to elucidate the temporal profile of nitric oxide metabolite concentrations-that is, nitrite and nitrate (NO(x))--and compounds related to energy-metabolism in the cerebral interstitium of patients after aneurysmal subarachnoid hemorrhage (SAH). During aneurysm surgery, microdialysis probes were implanted in cerebral white matter of the vascular territory most likely affected by vasospasm. Temporal profiles of NO(x) were analyzed in a subset of 10 patients (7 female, 3 male, mean age = 47 +/- 14 years). Microdialysis was performed for 152 +/- 63 hours. Extracellular metabolites (glucose, lactate, pyruvate, glutamate) were recovered from the extracellular fluid of the cerebral parenchyma. NO(x) was measured using a fluorometric assay. After early surgery, SAH patients revealed characteristic decreases of NO(x) from initial values of 46.2 +/- 34.8 micromol/L to 23.5 +/- 9.0 micromol/L on day 7 after SAH (P < 0.05). Decreases in NO(x) were seen regardless of development of delayed ischemia (DIND). Overall NO(x) correlated intraindividually with glucose, lactate, and glutamate (r = 0.58, P < 0.05; r = 0.32, P < 0.05; r = 0.28, P < 0.05; respectively). After SAH, cerebral extracellular concentrations of NO metabolites decrease over time and are associated with concomitant alterations in energy-or damage-related compounds. This could be related to reduced NO availability, potentially leading to an imbalance of vasodilatory and vasoconstrictive factors. On the basis of the current findings, however, subsequent development of DIND cannot be explained by a lack of vasodilatory NO alone.     

Acute haemorrhage into a microcystic meningioma leading to cerebral herniation

Low-grade (WHO level I) meningiomas are slow-growing, benign tumours typically presenting with unspecific symptoms (e.g. headache), seizures, cranial nerve compression and neuropsychological symptoms determined by location and size of the lesion. Haemorrhagic onset and sequelae are rare, and have been described infrequently. This is a case of a 50-year-old male presenting with signs of tentorial herniation secondary to hyperacute intratumoural haemorrhage (ITH) into a previously undiagnosed meningioma. Emergency surgical decompression and exstirpation of the lesion helped to achieve a favourable outcome. ITH has been described in all including benign intracranial neoplasms. Factors associated with a higher risk for haemorrhage in meningiomas are discussed. Though haemorrhages associated with meningiomas have been reported, ITH into low-grade meningiomas leading to herniation remains a rarity. Bearers of known lesions and their treating physicians who opt for conservative or delayed treatment should be aware of this remote complication.     

Columnar specificity of microvascular oxygenation and volume responses: implications for functional brain mapping

Cortical neurons with similar properties are grouped in columnar structures and supplied by matching vascular networks. The hemodynamic response to neuronal activation, however, is not well described on a fine spatial scale. We investigated the spatiotemporal characteristics of microvascular responses to neuronal activation in rat barrel cortex using optical intrinsic signal imaging and spectroscopy. Imaging was performed at 570 nm to provide functional maps of cerebral blood volume (CBV) changes and at 610 nm to estimate oxygenation changes. To emphasize parenchymal rather than large vessel contributions to the functional hemodynamic responses, we developed an ANOVA-based statistical analysis technique. Perfusion-based maps were compared with underlying neuroanatomy with cytochrome oxidase staining. Statistically determined CBV responses localized accurately to individually stimulated barrel columns and could resolve neighboring columns with a resolution better than 400 microm. Both CBV and early oxygenation responses extended beyond anatomical boundaries of single columns, but this vascular point spread did not preclude spatial specificity. These results indicate that microvascular flow control structures providing targeted flow increases to metabolically active neuronal columns also produce finely localized changes in CBV. This spatial specificity, along with the high contrast/noise ratio, makes the CBV response an attractive mapping signal. We also found that functional oxygenation changes can achieve submillimeter specificity not only during the transient deoxygenation ("initial dip") but also during the early part of the hyperoxygenation. We, therefore, suggest that to optimize hemodynamic spatial specificity, appropriate response timing (using < or =2-3 sec changes) is more important than etiology (oxygenation or volume).     

1-year performance of a defibrillation lead with a small electrode surface for high impedance pacing: a randomized,controlled study

A small electrode surface reduces pacing current drain and can extend generator longevity. The study evaluated the performance of a tined, quadripolar defibrillation lead (model 6944) that has a small-surfaced, steroid-eluting electrode tip for high impedance pacing. In a prospective, controlled study, 34 patients with conventional ICD indications were randomized one to one to receive the high impedance model 6944 or a tined defibrillation lead with a conventional sized, steroid-eluting electrode tip model 6942. Lead performance was evaluated at implant, prior to hospital discharge, and 1, 3, 6, and 12 months thereafter. Baseline characteristics did not differ significantly between patients implanted with lead model 6942 (n = 16) or model 6944 (n = 17). One patient randomized to receive the model 6942 was excluded from the study and was implanted with an active-fixation lead after stable lead positioning was neither possible with the 6942 nor with the 6944 electrode. No other lead related adverse events were observed. At implant, there were no significant differences between pacing thresholds, sensing performance, defibrillation impedances, and defibrillation thresholds in both groups, but pacing impedance of the model 6944 (988.6 +/- 217.7 omega) was approximately twice as high as high as in the model 6942 (431.7 +/- 83.7 omega; P < 0.0001). This difference remained highly significant throughout the observation period of 12 months, while R wave amplitudes and pacing thresholds remained equal in both lead models. The use of a tined defibrillation lead with a small, steroid-eluting electrode tip appears safe and results in a high pacing impedance without compromising system performance.     

Filters for radiation reduction: a comparison

Aluminum, yttrium, copper, and R-filters were evaluated with respect to effective beam energy, entrance radiation exposure to the skin, x-ray tube loading, and the quality of resultant radiographs. Since all filters yielded acceptable radiographs, a figure of merit was developed to determine which filter delivered the lowest entrance radiation exposure for the lowest increase in x-ray tube loading. The figure of merit indicated that the best results were obtained with the 0.1-mm Cu filter with 2 mm Al at 60-105 kVp and with the 0.2-mm Cu filter with 2 mm Al at 105-120 kVp. Cu filters produced radiographs with quality comparable to that of R- or Y filters. Cu filters are inexpensive alternatives to rare-earth filters and yielded a reduction in radiation exposure with less x-ray tube loading.     

Short- and long-term results following implantation of the new Wiktor stent in acute coronary occlusion following PTCA

Ten patients, two women and eight men, were treated with the new balloon-expandable Wiktor Stent for acute coronary occlusion after PTCA. Two patients presented with an acute myocardial infarction. Stents with a diameter of 3.0 or 3.5 mm were implanted into the right coronary artery (n = 7), the left anterior descending (n = 2) artery, and the left circumflex coronary artery (n = 1). Stent implantation in the target segment was successful in all cases. Afterwards, patients received coumadine for 3 months and 100 mg acetylsalicyclic acid per day. We observed one acute occlusion after 8 h. Late occlusion occurred in two patients after cessation of anticoagulation within 3 weeks. Control angiography after 6 months in seven patients revealed stenosis within the stent in two cases.     

Edema and brain trauma

Brain edema leading to an expansion of brain volume has a crucial impact on morbidity and mortality following traumatic brain injury (TBI) as it increases intracranial pressure, impairs cerebral perfusion and oxygenation, and contributes to additional ischemic injuries. Classically, two major types of traumatic brain edema exist: "vasogenic" due to blood-brain barrier (BBB) disruption resulting in extracellular water accumulation and "cytotoxic/cellular" due to sustained intracellular water collection. A third type, "osmotic" brain edema is caused by osmotic imbalances between blood and tissue. Rarely after TBI do we encounter a "hydrocephalic edema/interstitial" brain edema related to an obstruction of cerebrospinal fluid outflow. Following TBI, various mediators are released which enhance vasogenic and/or cytotoxic brain edema. These include glutamate, lactate, H(+), K(+), Ca(2+), nitric oxide, arachidonic acid and its metabolites, free oxygen radicals, histamine, and kinins. Thus, avoiding cerebral anaerobic metabolism and acidosis is beneficial to control lactate and H(+), but no compound inhibiting mediators/mediator channels showed beneficial results in conducted clinical trials, despite successful experimental studies. Hence, anti-edematous therapy in TBI patients is still symptomatic and rather non-specific (e.g. mannitol infusion, controlled hyperventilation). For many years, vasogenic brain edema was accepted as the prevalent edema type following TBI. The development of mechanical TBI models ("weight drop," "fluid percussion injury," and "controlled cortical impact injury") and the use of magnetic resonance imaging, however, revealed that "cytotoxic" edema is of decisive pathophysiological importance following TBI as it develops early and persists while BBB integrity is gradually restored. These findings suggest that cytotoxic and vasogenic brain edema are two entities which can be targeted simultaneously or according to their temporal prevalence.     

Poor-grade aneurysmal subarachnoid hemorrhage: relationship of cerebral metabolism to outcome

OBJECT: The majority of patients with poor-grade subarachnoid hemorrhage (SAH), that is, World Federation of Neurosurgical Societies (WFNS) Grades IV and V, have high morbidity and mortality rates. The objective of this study was to investigate cerebral metabolism in patients with low- compared with high-grade SAH by using bedside microdialysis and to evaluate whether microdialysis parameters are of prognostic value for outcome in SAH. METHODS: A prospective investigation was conducted in 149 patients with SAH (mean age 50.9 +/- 12.9 years); these patients were studied for 162 +/- 84 hours (mean +/- standard deviation). Lesions were classified as low-grade SAH (WFNS Grades I-III, 89 patients) and high-grade SAH (WFNS Grade IV or V, 60 patients). After approval by the local ethics committee and consent from the patient or next of kin, a microdialysis catheter was inserted into the vascular territory of the aneurysm after clip placement. The microdialysates were analyzed hourly for extracellular glucose, lactate, lactate/pyruvate (L/P) ratio, glutamate, and glycerol. The 6- and 12-month outcomes according to the Glasgow Outcome Scale and functional disability according to the modified Rankin Scale were assessed. In patients with high-grade SAH, cerebral metabolism was severely deranged compared with those who suffered low-grade SAH, with high levels (p < 0.05) of lactate, a high L/P ratio, high levels of glycerol, and, although not significant, of glutamate. Univariate analysis revealed a relationship among hyperglycemia on admission, Fisher grade, and 12-month outcome (p < 0.005). In a multivariate regression analysis performed in 131 patients, the authors identified four independent predictors of poor outcome at 12 months, in the following order of significance: WFNS grade, patient age, L/P ratio, and glutamate (p < 0.03). CONCLUSIONS: Microdialysis parameters reflected the severity of SAH. The L/P ratio was the best metabolic independent prognostic marker of 12-month outcome. A better understanding of the causes of deranged cerebral metabolism may allow the discovery of therapeutic options to improve the prognosis, especially in patients with high-grade SAH, in the future.     

Pulmonary air embolism in severe head injury

Entry of air into the venous system leading to intracardiac air and pulmonary air embolism (PAE) has been reported in various clinical settings such as neurosurgical interventions in the sitting position and in autopsies on patients with head and neck injuries. We report the case of a 29-year-old male who developed severe pulmonary dysfunction after severe head injury in a high-velocity car accident. Chest X-ray showed bilateral diffuse patchy infiltrates. Pneumothorax, haemothorax, pulmonary aspiration, various forms of pulmonary oedema and pulmonary contusion could be excluded. Furthermore, there was an open laceration of the frontal sinus and maxillo-facial fractures. The history of spontaneous respiration in sitting position at the scene, rapid improvement of pulmonary function within 30 h, small amounts of air in the brain parenchyma, and circulatory shock despite elevated central venous pressure in the initial phase led to the diagnosis of PAE as the primary cause of pulmonary dysfunction. The diagnostic approach and basic therapeutical principles in patients with PAE are described. In conclusion, the case presented emphasizes the importance of considering PAE as a possible cause of respiratory failure in patients with severe head injury.