S. Hollerbach

Hepatic encephalopathy is a common problem in cirrhosis. The pathogenesis of this complication of advanced liver disease still remains unclear. Magnetic resonance spectroscopy was used to assess prospectively cerebral metabolism in 51 patients with histologically proven cirrhosis (Child–Pugh classes A, B, and C, 18, 18, and 15, respectively) and 36 healthy volunteers. According to the results of psychometric tests, overt hepatic encephalopathy, subclinical encephalopathy, and no encephalopathy were found in 14, 21, and 16 patients, respectively. Myoinositol/creatine ratios in gray (.36 ± .17) and white (.35 ± .22) matter voxel were reduced significantly ( P < .0001) in cirrhotic patients compared with healthy volunteers (gray matter, .51 ± .11; white matter, .64 ± .16). In addition, patients showed a significant reduction ( P = .024) in white matter choline/creatine ratio (.77 ± .27) compared with controls (.92 ± .25), and glutamine/glutamate level was elevated in cirrhotic patients compared with controls (gray matter, P < .0001; white matter, P = .036). Changes in cerebral myoinositol and glutamine/glutamate levels correlated significantly with the severity of hepatic encephalopathy ( P < .0001). However, these metabolic alterations were also detected in patients without hepatic encephalopathy (normal psychometric test results). N –acetyl aspartate/creatine ratios did not differ between patients and controls. Magnetic resonance imaging detected bright basal ganglia in 37 patients, which correlated significantly with portal–systemic shunting and elevation of glutamine/glutamate, but not with the degree of hepatic encephalopathy. In conclusion, magnetic resonance imaging and spectroscopy showed that alterations of cerebral metabolism are common in patients with cirrhosis, even without evidence of clinical or subclinical hepatic encephalopathy.

We studied the role of brain electrical activity mapping (BEAM) in the assessment of neuropsychiatric disturbances in 48 cirrhotic patients without clinical evidence of hepatic encephalopathy (no HE, n = 19), with subclinical HE (grade 0, denoting pathological psychometric tests, n = 13) and mild-to-moderate HE (grade I, n = 6; grade II, n = 10). Results were compared with 23 healthy controls. BEAM variables quantified were: (i) the peak frequency (PF); (ii) the amplitude of PF; and (iii) the topographic localization of the maximum peak amplitude digitized for quantification by using a coordinate system. Mean amplitudes and their topographic localization in the following frequency-bands were analysed: delta (1.0-3.5 Hz), theta (4.0-7.5 Hz), alpha 1 (8.0-9.5 Hz), alpha 2 (10.0-11.5 Hz), beta 1 (12.0-15.5 Hz), beta 2 (16.0-19.5 Hz), and beta 3 (20.0-23.5 Hz). The PF was significantly slower in all HE patients than in healthy controls (8.5 +/- 2.0 Hz v. 10.1 +/- 1.0 Hz, P< 0.001). Even in no HE, the PF was significantly slower than in controls (8.6 +/- 1.5 Hz v. 10.1 +/- 1.0 Hz, P< 0.01). No relevant topographic differences of PF were observed. The mean amplitudes of the following bands differed significantly between controls and patients: theta (increased in HE, P< 0.05), alpha 2 (decreased in HE, P< 0.05), and beta 2 and beta 3 (increased in HE, (P < 0.05). In HE patients, the topographic localization of all beta bands showed a significant shift from parieto-occipital areas to central areas of the cortex. We conclude that BEAM is a sensitive tool for detecting neuropsychiatric disturbances in cirrhotics with no HE and with subclinical HE. The combination of PF in the theta band, increased mean amplitude in the beta 2 band, and the localization of the latter band in the frontocentral area of the cortex is an objective and sensitive tool for identifying neuropsychiatric disturbances in 85% of cirrhotic patients with no HE. Further studies are required to determine the clinical implications of these abnormal findings in the absence of overt clinical symptoms.

OBJECTIVE: This prospective clinical study investigated whether the relatively simple and cost-effective ultrasonography of the inferior vena cava (IVC) represents a valid clinical tool to assess the effectiveness of diuretic therapy in patients with chronic congestive heart failure (CHF). METHODS: Measurement of the resting and inspiratory diameter of the VCI repeatedly during diuretic therapy in 23 consecutive patients (11 women, 70 +/- 10 years) with CHF and comparing the results to the daily measured body weight and serum creatinine in these patients. Results were compared with the IVC diameter obtained in 33 healthy controls (16 women, 42 +/- 15 years). In addition, the IVC collapse index was calculated to assess inspiratory movements of the IVC in patients on day 1 and 10 of therapy. RESULTS: The IVC diameter at rest was 2.4 +/- 0.6 cm and decreased to 2.0 +/- 0.7 cm at inspiration, which was significantly greater than in healthy controls (1.4 +/- 0.4 cm at rest and 1.05 +/- 0.5 cm at inspiration; p = 0.008 and p = 0.01, respectively). The IVC diameter decreased continuously and significantly (p < 0.003) from day 1 to day 10 during diuretic therapy without a concomitant rise in serum creatinine. At beginning of therapy, the collapse-index of the IVC was significantly greater in patients than in controls. However, after 10 days of therapy this index reached similar values to those observed in controls. CONCLUSION: Ultrasonographic measurements of IVC diameter and inspiratory movements are a quantifiable and reliable approach to assess the hypervolemia associated with CHF. Normalization of inspiratory IVC collapse movement correlates with successful diuretic therapy and can be reliably used for bedside assessment and monitoring treatment in CHF patients.

Drug Prescribing for Patients with Chronic Kidney Disease in General Practice: a Cross-Sectional Study