Intensive care practices in brain death diagnosis and organ donation.

We conducted a multicentre study of 1844 patients from 42 Spanish intensive care units, and analysed the clinical characteristics of brain death, the use of ancillary testing, and the clinical decisions taken after the diagnosis of brain death. The main cause of brain death was intracerebral haemorrhage (769/1844, 42%), followed by traumatic brain injury (343/1844, 19%) and subarachnoid haemorrhage (257/1844, 14%). The diagnosis of brain death was made rapidly (50% in the first 24 h). Of those patients who went on to die, the Glasgow Coma Scale on admission was ≤ 8/15 in 1146/1261 (91%) of patients with intracerebral haemorrhage, traumatic brain injury or anoxic encephalopathy; the Hunt and Hess Scale was 4-5 in 207/251 (83%) of patients following subarachnoid haemorrhage; and the National Institutes of Health Stroke Scale was ≥ 15 in 114/129 (89%) of patients with strokes. Brain death was diagnosed exclusively by clinical examination in 92/1844 (5%) of cases. Electroencephalography was the most frequently used ancillary test (1303/1752, 70.7%), followed by transcranial Doppler (652/1752, 37%). Organ donation took place in 70% of patients (1291/1844), with medical unsuitability (267/553, 48%) and family refusal (244/553, 13%) the main reasons for loss of potential donors. All life-sustaining measures were withdrawn in 413/553 of non-donors (75%).

Pressure-controlled ventilation versus controlled mechanical ventilation with decelerating inspiratory flow.

OBJECTIVE: To ascertain whether pressure-controlled ventilation offers any advantage with respect to conventional controlled mechanical ventilation with decelerating flow. DESIGN: Prospective, comparative study. SETTING: Intensive care unit. PATIENTS: Eleven consecutive critically ill adult patients. MEASUREMENTS AND MAIN RESULTS: Study of respiratory mechanics and arterial blood gases after 30 mins of pressure-controlled ventilation. Repetition of the same measurements after 30 mins of controlled mechanical ventilation with decelerating flow waveform, with equal tidal volumes, using a commercially available mechanical ventilator. Student's t-test for paired comparisons. A lesser maximum inspiratory flow rate was required for pressure-controlled ventilation (55.7 +/- 16 L/sec) than for controlled mechanical ventilation (72 +/- 2 L/sec) (p < .001). Nevertheless, the peak pressures measured in the orotracheal tubes of the patients were higher in pressure-controlled ventilation (20.4 +/- 3.5 cm H2O) than in controlled mechanical ventilation (18.4 +/- 4.8 cm H2O) (p < .05). This model measured pressure in the inspiratory line, providing erroneous information regarding the behavior of pressures in the airway. The peak pressure measured by the ventilator was significantly higher in controlled mechanical ventilation than in pressure-controlled ventilation and was, in addition, reached at initiation of inspiration in ten of 11 patients with controlled mechanical ventilation, while peak pressure measured in the orotracheal tube was invariably reached at the end of the inspiration, both in pressure-controlled ventilation and controlled mechanical ventilation. The rest of the parameters analyzed, including end-inspiratory pressure, mean pressure, intrinsic positive end-expiratory pressure, and arterial blood gases, showed no differences. The difference between quasi-static compliances almost reached statistical significance (72 +/- 25.4 mL/cm H2O in pressure-controlled ventilation vs. 68.8 +/- 24.3 mL/cm H2O in controlled mechanical ventilation; p = .052). CONCLUSIONS: Our study failed to demonstrate any important difference between pressure-controlled ventilation and controlled mechanical ventilation with decelerating inspiratory flow waveform. The differences in the airway pressures detected by the ventilator are spurious and are due to the place (inspiratory line) where these pressures were measured. The difference between the peak pressure measured in the orotracheal tube has statistical, but not clinical, value and is lower in controlled mechanical ventilation. Based on the limited number of variables we studied and unless the tendency indicated in the quasi-static compliance is demonstrated in the future, we do not believe that pressure-controlled ventilation contributes any uniqueness to the theory or practice of mechanical ventilation.

Interaction between intrinsic positive end-expiratory pressure and externally applied positive end-expiratory pressure during controlled mechanical ventilation.

OBJECTIVE: To assess the interaction between intrinsic and externally applied positive end-expiratory pressure (intrinsic PEEP and administered PEEP) in mechanically ventilated patients. DESIGN: Prospective study. SETTING: Intensive care unit of a university hospital. PATIENTS: Twelve consecutive critically ill patients. INTERVENTIONS: Application of an external PEEP of the same value as the intrinsic PEEP. MEASUREMENTS AND MAIN RESULTS: We found that when the administered PEEP was increased from 0 to the baseline value of intrinsic PEEP, mean intrinsic PEEP decreased from 6.5 +/- 4.2 (SD) to 1.3 +/- 0.7 cm H2O (p = .001). The mean end-inspiratory pressure was increased from 20.3 +/- 4.6 to 23.1 +/- 6.1 cm H2O (p < .05). The difference between the modification of intrinsic PEEP and the change in the end-inspiratory pressure was not significantly > 0 cm H2O. Thus, the increase in end-inspiratory pressure may be directly attributable to the increase in total PEEP (administered PEEP plus intrinsic PEEP). None of the other measurements of pulmonary mechanics changed (peak pressure, inspiratory resistance, compliance, and trapped-gas volume). CONCLUSIONS: The administration of positive end-expiratory pressure equal to the intrinsic positive end-expiratory pressure causes the almost total disappearance of the intrinsic positive end-expiratory pressure. When the administered positive end-expiratory pressure does not exceed the intrinsic positive end-expiratory pressure, the former is applied almost in its entirety to the patient's external circuit. The administration of positive end-expiratory pressure without prior quantification of the intrinsic positive end-expiratory pressure results in an overestimation of the beneficial effects of the administered positive end-expiratory pressure on the quasi-static compliance.

[Schwannoma of the spinal nerve]. / Schwanoma del nervio espinal.

A years old woman with a spinal nerve schwannoma is reported. Treatment and main clinical and histopathologic features of this very unusual location are discussed.

Calcium channels and basal prolactin secretion in single male rat lactotropes.

Ba2+ currents through voltage-dependent Ca channels and basal prolactin secretion were measured in single, cultured lactotropes by the combined use of whole cell patch-clamp recording and the reverse hemolytic plaque assay. Measurements of plaque area, a cumulative index of the relative amount of prolactin released by a cell per unit time, indicate that lactotropes can be grouped in two main subpopulations that differ in basal secretory activity: small-plaque (SP) cells and large-plaque (LP) cells. Analysis of Ba2+ currents indicates that both SP and LP lactotropes express two types of Ca channels: low-threshold, inactivating, slowly deactivating (SD) channels and high-threshold, noninactivating, fast deactivating (FD) channels. Ba2+ current amplitude is smaller in SP cells than in LP cells. Plaque area, and thus prolactin release, is positively correlated with the density of Ba2+ current through FD channels, but not with that through SD channels. The results suggest that the surface density of functional FD Ca channels in the plasma membrane is a major factor that determines the rate of basal prolactin secretion in single lactotropes.