Szilárd Szatmári

Impaired cerebrovascular reactivity in sepsis-associated encephalopathy studied by acetazolamide test

IntroductionThe pathophysiology of sepsis-associated encephalopathy (SAE) is not entirely clear. One of the possible underlying mechanisms is the alteration of the cerebral microvascular function induced by the systemic inflammation. The aim of the present work was to test whether cerebral vasomotor-reactivity is impaired in patients with SAE.MethodsPatients fulfilling the criteria of clinical sepsis and showing disturbance of consciousness of any severity were included (n = 14). Non-septic persons whithout previous diseases affecting cerebral vasoreactivity served as controls (n = 20). Transcranial Doppler blood flow velocities were measured at rest and at 5, 10, 15 and 20 minutes after intravenous administration of 15 mg/kgBW acetazolamide. The time course of the acetazolamide effect on cerebral blood flow velocity (cerebrovascular reactivity, CVR) and the maximal vasodilatory effect of acetazolemide (cerebrovascular reserve capacity, CRC) were compared among the groups.ResultsAbsolute blood flow velocities after adminsitration of the vasodilator drug were higher among control subjects than in SAE. Assessment of the time-course of the vasomotor reaction showed that patients with SAE reacted slower to the vasodilatory stimulus than control persons. When assessing the maximal vasodilatory ability of the cerebral arterioles to acetazolamide during vasomotor testing, we found that patients with SAE reacted to a lesser extent to the drug than did control subjects (CRC controls:46.2 ± 15.9%, CRC SAE: 31,5 ± 15.8%, P < 0.01).ConclusionsWe conclude that cerebrovascular reactivity is impaired in patients with SAE. The clinical significance of this pathophysiological finding has to be assessed in further studies.

Reversal of neuromuscular blockade with sugammadex at the reappearance of four twitches to train-of-four stimulation.

Background:Doses of sugammadex required to reverse deep, moderate, and shallow rocuronium-induced neuromuscular blockade have been established. However, no adequate doses for the reversal of reappearance of four twitches of train-of-four (TOF) stimulation (threshold TOF-count-four) have been established. Methods:This single-center, randomized, controlled, double-blind, four-groups parallel-arm study included 80 patients undergoing general anesthesia with propofol, sevoflurane, fentanyl, and rocuronium. Neuromuscular monitoring was performed with calibrated acceleromyography. Once rocuronium-induced neuromuscular blockade recovered spontaneously to threshold TOF-count-four, patients randomly received 0.5, 1.0, 2.0 mg/kg of sugammadex or 0.05 mg/kg of neostigmine. The time between study drug injection and reversal of TOF ratios to 1.0 was measured. Rapid reversal (⩽2.0 min average, upper limit of 5.0 min) was the primary endpoint and slower reversal (⩽5.0 min average, upper limit of 10 min) was the secondary endpoint of the study. Results:Sugammadex, in doses of 1.0 and 2.0 mg/kg, reversed threshold TOF-count-four to TOF ratios of 1.0 in 2.1 ± 0.8 min (mean ± SD) and 1.8 ± 0.9 min, respectively. Sugammadex, 0.5 mg/kg, induced a similar degree of reversal in 4.1 ± 1.9 min (P < 0.001 vs. 1.0 and 2.0 mg/kg). Neostigmine, 0.05 mg/kg, reversed TOF ratios to 1.0 in 8.5 ± 3.5 min (P < 0.001 vs. sugammadex groups). Conclusion:Sugammadex, 1.0 mg/kg, rapidly and effectively reverses rocuronium-induced block that has recovered spontaneously to a threshold TOF-count-four. A dose of 0.5 mg/kg was equally effective, but satisfactory antagonism took as long as 8 min to take place.

Cerebral vasoreactivity to acetazolamide is not impaired in patients with severe sepsis

INTRODUCTION The pathophysiology of sepsis-associated encephalopathy (SAE) is not entirely clear, but one of the possible underlying mechanisms is the alteration of the cerebral microvascular function. The aim of the present work was to test whether cerebral vasomotor reactivity is impaired in patients with severe sepsis. METHODS Patients fulfilling the criteria of clinical sepsis and showing at least 2 organ dysfunctions were included (n = 16). Nonseptic healthy persons without previous diseases affecting cerebral vasoreactivity served as controls (n = 16). Transcranial Doppler blood flow velocities were measured at rest and at 5, 10, 15, and 20 minutes after intravenous administration of 15 mg/kg acetazolamide. The time course of the acetazolamide effect on cerebral blood flow velocity (cerebrovascular reactivity [CVR]) and the maximal vasodilatory effect of acetazolemide (cerebrovascular reserve capacity [CRC]) were compared among the groups. RESULTS Absolute blood flow velocities after administration of the vasodilator drug did not differ between control and septic patients. Assessment of the time course of the vasomotor reaction showed that patients with sepsis reacted in a similar fashion to the vasodilatory stimulus than control persons. When assessing the maximal vasodilatory ability of the cerebral arterioles to acetazolamide during vasomotor testing, we found that there was no difference in vasodilatory ability between septic and healthy subjects (CRC controls, 54.8% ± 11.1%; CRC sepsis-associated encephalopathy, 61.1% ± 34.4%; P = .49). CONCLUSIONS We conclude that cerebrovascular reactivity is not impaired in patients with severe sepsis. It is conceivable that cerebral vasoreactivity may be differently involved at different severity stages of the septic process.

One-lung ventilation does not result in cerebral desaturation during application of lung protective strategy if normocapnia is maintained

BACKGROUND Previously a report has suggested that administration of lung protective strategy for one-lung ventilation(OLV) results in oxygen desaturation of the brain parenchyma. The aim of our work was to confirm that the maintenance of normocapnia during protective OLV strategy results in alteration of cerebral blood fl ow and cerebral oxygen saturation as compared to double-lung ventilation. METHODS Data were obtained from 24 patients undergoing thoracic surgery. Cerebral oxygen saturation (rSO2) was continuously monitored by INVOS 5100C Cerebral Oxymeter System along with measurement of cerebral blood fl ow velocity (MCAV) by transcranial Doppler sonography. Arterial blood samples were taken for blood gas analysis in the awake state, in the supine and lateral decubitus position during double-lung ventilation (DLV), and during OLV. RESULTS When ventilation was changed from DLV to OLV, no significant change was observed in rSO2. A significant decrease of rSO2 was found compared to the value observed during DLV in lateral decubitus at the time point 60 minutes after the start of OLV. No clinically significant changes in the MCAV was observed throughout the course of the thoracic surgical procedure. CONCLUSIONS OLV does not result in clinically relevant decreases in cerebral blood fl ow and cerebral oxygen saturation during application of lung protective ventilation if normocapnia is maintained.