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.

Epidemiology of acute kidney injury in Hungarian intensive care units: a multicenter, prospective, observational study.

BACKGROUND: Despite the substantial progress in the quality of critical care, the incidence and mortality of acute kidney injury (AKI) continues to rise during hospital admissions. We conducted a national, multicenter, prospective, epidemiological survey to evaluate the importance of AKI in intensive care units (ICUs) in Hungary. The objectives of this study were to determine the incidence of AKI in ICU patients; to characterize the differences in aetiology, illness severity and clinical practice; and to determine the influencing factors of the development of AKI and the patients' outcomes. METHODS: We analysed the demographic, morbidity, treatment modality and outcome data of patients (n = 459) admitted to ICUs between October 1st, 2009 and November 30th, 2009 using a prospectively filled in electronic survey form in 7 representative ICUs. RESULTS: The major reason for ICU admission was surgical in 64.3% of patients and medical in the remaining 35.7%. One-hundred-twelve patients (24.4%) had AKI. By AKIN criteria 11.5% had Stage 1, 5.4% had Stage 2 and 7.4% had Stage 3. In 44.0% of patients, AKI was associated with septic shock. Vasopressor treatment, SAPS II score, serum creatinine on ICU admission and sepsis were the independent risk factors for development of any stage of AKI. Among the Stage 3 patients (34) 50% received renal replacement therapy. The overall utilization of intermittent renal replacement therapy was high (64.8%). The overall in-hospital mortality rate of AKI was 49% (55/112). The ICU mortality rate was 39.3% (44/112). The independent risk factors for ICU mortality were age, mechanical ventilation, SOFA score and AKI Stage 3. CONCLUSIONS: For the first time we have established the incidence of AKI using the AKIN criteria in Hungarian ICUs. Results of the present study confirm that AKI has a high incidence and is associated with high ICU and in-hospital mortality.

[Sepsis-associated encephalopathy]. / A szepszishez társuló encephalopathia.

Sepsis-associated encephalopathy is a common but neglected clinical symptom of systemic inflammatory reaction in the early phase. The clinical spectrum of diffuse cerebral dysfunction induced by systemic sepsis--sepsis-associated encephalopathy according to the new terms--varies from transient, reversible encephalopathy, to severe irreversible brain damage. The aim of the present publication is to summarize the pathophysiology, frequent symptoms and possible treatments of the disease based on international and Hungarian articles on this topic. We want to emphasize the importance of monitoring the patient's mental status due to the fact that consciousness' disturbance of different severity is an early warning sign of sepsis, so it has high clinical significance.

Carotid intima-media thickness and cerebrovascular reactivity in long-term type 1 diabetes mellitus.

PURPOSE: Diabetes mellitus (DM) is one of the leading risk factors for cerebrovascular diseases. Both macro- and microvascular damage may occur. The aim of the present work was to assess intima-media thickness as well as cerebral vasoreactivity in patients suffering from type 1 diabetes mellitus (IDDM). METHODS: Intima-media thickness and resting middle cerebral artery blood flow velocity was measured in 33 IDDM patients and 31 healthy controls. After baseline investigations, 30 seconds of breath holding (BH) and 60 seconds of voluntary hyperventilation (HV) were performed by the subjects. Transcranial Doppler measurements were performed in each case after vasodilatory (BH) and vasoconstrictor (HV) stimuli. Cerebrovascular reactivity was expressed as the percentage of change of the middle cerebral mean blood flow velocity after BH or HV. RESULTS: IDDM patients showed a significantly larger intima-media thickness (0.1 +/- 0.02 mm) than healthy controls (0.06 +/- 0.006 mm, p < 0.001). Cerebrovascular reactivity after BH was less intensive in diabetic patients (19.3 +/- 16.1%) than that of the control subjects (38.7 +/- 22.8%, p < 0.01). Similarly, HV induced a less-pronounced decrease of cerebral blood flow velocity in diabetic subjects (-30.1 +/- 13.2%) than in nondiabetics (-37.6 +/- 17.0%, p < 0.05). CONCLUSION: Our results refer to early macro- and microangiopathic involvement of the cerebral vessels, which develop in parallel with angiopathies of the other organs, such as nephropathy and retinopathy. Further prospective studies are needed to clarify the role of these macro- and microangiopathic changes in the development of cerebrovascular complications in patients suffering from DM.