Validation study of Nexfin® continuous non-invasive blood pressure monitoring in critically ill adult patients.

BACKGROUND: Nexfin® (BMEYE, Amsterdam, The Netherlands) is a totally non-invasive blood pressure and cardiac output (CO) monitor based on finger arterial pulse contour analysis. METHODS: We performed an open observational study in a mix of medical-surgical-burns critically ill patients (N.=45) to validate Nexfin obtained blood pressures (MAPnex) against PiCCO (MAPfem) derived blood pressure measurements. MAPnex, MAPfem and corresponding systolic (SBP) and diastolic (DBP) blood pressures were measured continuously and registered with a 2 hour interval during the 8-hour study period. Statistical analysis was performed by Pearson regression, Bland and Altman, Concordance plot and Polar plot analysis. RESULTS: MAPnex shows excellent correlation with MAPfem (R² 0.88, mean bias ± LA -2.3±12.4 mmHg, 14.7% error) and may be used interchangeably with invasive monitoring. The excellent MAPnex -MAPfem correlation was preserved in subgroup analysis for patients with severe hypotension, high systemic vascular resistance, low CO, hypothermia and in patients supported by inotropic/vasopressive agents. MAPnex is able to follow changes in MAPfem during the same time interval (level of concordance 85.5%). Nexfin SBP and DBP show significant correlation with PiCCO but the criteria for interchangeability were not met. Finally, polar plot analysis showed that trending capabilities were excellent when changes in MAPnex (ΔMAPnex) were compared to ΔMAPfem (96.1% of changes were within the level of 10% limits of agreement). CONCLUSION: In this sample of critically ill patients we found a good correlation between MAPnex and invasive blood pressures obtained by PiCCO.

Localised abdominal compartment syndrome: bladder-over-gastric pressure ratio (B/G ratio) as a clue to diagnosis.

INTRODUCTION: Intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS) have been identified as a cause of organ dysfunction and mortality in critically ill patients. The diagnosis of IAH/ACS depends on accurate intra-abdominal pressure (IAP) measurement, which is usually performed via the bladder or the stomach.The aim of this study was to describe cases where intragastric pressure (IGP) and intrabladder pressure (IBP) were measured simultaneously. PATIENTS AND METHODS: After review of medical records, four patients admitted to our ICU department where both IGP and IBP were measured, could be identified. IGP was measured using the Spiegelberg catheter and IBP was measured using the FoleyManometer LV. In all patients, the bladder-over-gastric pressure ratio (B/G ratio) was calculated. RESULTS: In two of four patients, IGP and IBP differed significantly. In one patient the B/G ratio was lower than 1 suggesting a diagnosis of epigastric ACS and in one patient B/G ratio was greater than 1 leading to a diagnosis of pelvic ACS. The latter patient was spared a decompressive laparotomy due to the additional IGP measurement and the subsequent diagnosis of localized ACS. CONCLUSION: The preferred methods for IAP measurement are via the bladder and via the stomach. In some patients, IGP and IBP may differ significantly and this may have clinical implications. Clinicians should be aware of the possibility of localized ACS. In order to identify risk factors and to recommend treatment for localized ACS, further study of simultaneous IGP and IBP measurements are needed.

Global and right ventricular end-diastolic volumes correlate better with preload after correction for ejection fraction.

BACKGROUND: Volumetric monitoring with right ventricular end-diastolic volume indexed (RVEDVi) and global end-diastolic volume indexed (GEDVi) is increasingly being suggested as a superior preload indicator compared with the filling pressures central venous pressure (CVP) or the pulmonary capillary wedge pressure (PCWP). However, static monitoring of these volumetric parameters has not consistently been shown to be able to predict changes in cardiac index (CI). The aim of this study was to evaluate whether a correction of RVEDVi and GEDVi with a measure of the individual contractile reserve, assessed by right ventricular ejection fraction (RVEF) and global ejection fraction, improves the ability of RVEDVi and GEDVi to monitor changes in preload over time in critically ill patients. METHODS: Hemodynamic measurements, both by pulmonary artery and by transcardiopulmonary thermodilution, were performed in 11 mechanically ventilated medical ICU patients. Correction of volumes was achieved by normalization to EF deviation from normal EF values in an exponential fashion. Data before and after fluid administration were obtained in eight patients, while data before and after diuretics were obtained in seven patients. RESULTS: No correlation was found between the change in cardiac filling pressures (DeltaCVP, DeltaPCWP) and DeltaCI (R(2) 0.01 and 0.00, respectively). Further, no correlation was found between DeltaRVEDVi or DeltaGEDVi and DeltaCI (R(2) 0.10 and 0.13, respectively). In contrast, a significant correlation was found between DeltaRVEDVi corrected to RVEF (DeltacRVEDVi) and DeltaCI (R(2) 0.64), as well as between DeltacGEDVi and DeltaCI (R(2) 0.59). An increase in the net fluid balance with +844 + or - 495 ml/m(2) resulted in a significant increase in CI of 0.5 + or - 0.3 l/min/m(2); however, only DeltacRVEDVi (R(2) 0.58) and DeltacGEDVi (R(2) 0.36) correlated significantly with DeltaCI. Administration of diuretics resulting in a net fluid balance of -942 + or - 658 ml/m(2) caused a significant decrease in CI with 0.7 + or - 0.5 l/min/m(2); however, only DeltacRVEDVi (R(2) 0.80) and DeltacGEDVi (R(2) 0.61) correlated significantly with DeltaCI. CONCLUSION: Correction of volumetric preload parameters by measures of ejection fraction improved the ability of these parameters to assess changes in preload over time in this heterogeneous group of critically ill patients.

Duodenogastroesophageal reflux and esophageal mucosal injury in mechanically ventilated patients.

BACKGROUND & AIMS: Esophagitis has been reported to be the most frequent cause of upper gastrointestinal bleeding in intensive care patients. The mechanisms causing esophagitis are unclear. The aim of this study was to measure esophageal acid and bile reflux and to examine the relationship between reflux and mucosal injury in mechanically ventilated patients. METHODS: Twenty-five critically ill, mechanically ventilated patients with nasogastric tubes were prospectively included for 24-hour esophageal pH and duodenogastroesophageal bile reflux studies (Bilitec 2000 system). All patients received acid-suppressive therapy for stress ulcer prophylaxis with ranitidine. On the day before the study, patients underwent esophageal endoscopy to determine the presence or absence of esophagitis. RESULTS: After approximately 5 days of mechanical ventilation, 12 patients (48%) had erosive esophagitis, 2 patients had pathological acid reflux, and 12 patients had pathological bile reflux. The presence of esophagitis was significantly associated with pathological bile reflux (P = 0.017, Fisher exact test). The severity of esophagitis was significantly correlated with the volume of gastric residual volume and with increasing times of bile reflux. The latter was significantly correlated with the number of organ failures. CONCLUSIONS: Despite acid-suppressive therapy, esophagitis is a frequent finding in critically ill patients after less than a week of mechanical ventilation. In these patients, besides mechanical irritation by the nasogastric tube, chemical injury caused by duodenogastroesophageal reflux seems to have a major role in the pathogenesis of esophageal mucosal lesions.

Varicella-zoster virus infection associated with acute liver failure.

Although acute liver failure due to the varicella-zoster virus is rare, it is frequently fatal. Immunologic impairment is a significant predisposing factor. Classic symptoms at presentation are rash, abdominal pain, and fever. After some days patients go on to develop full-blown liver failure. The diagnosis can be confirmed by histological examination and electron microscopy with fluorescent staining, immunohistochemistry, and in situ hybridization of the liver. In cases of high suspicion, acyclovir therapy should not be delayed.