Vito Fontana

No relationship between red blood cell distribution width and microcirculatory alterations in septic patients

BACKGROUND Increased red cell distribution width (RDW), a quantitative measure of erythrocyte size variability, has been associated with increased mortality in critically ill patients. METHODS In this post-hoc analysis of prospectively collected data, we studied 122 septic patients with and without shock who had undergone sublingual microcirculatory assessment using Sidestream Dark Field (SDF) videomicroscopy. Patient demographics, comorbidities, the Acute Physiology and Chronic Health Evaluation (APACHE) II score on admission and the Sequential Organ Failure Assessment (SOFA) score on the day of the microcirculatory assessment were collected. The RDW was retrospectively collected on the day of the microcirculatory evaluation from the routine daily blood count analysis. RESULTS Median patient age was 68[55-77] years, and median APACHE II and SOFA scores were 22[17-28] and 10[8-12], respectively; ICU mortality was 43%. On the day of the microcirculatory analysis, the median RDW was 13.8[12.8-15.5]% and was elevated (>13.4%) in 74 (61%) patients. There was no correlation between RDW and microcirculatory parameters (functional capillary density, r2 = 0.12; proportion of small perfused vessels, r2 = 0.17; mean flow index, r2 = 0.14). RDW was not related to disease severity, the presence of shock or survival. CONCLUSIONS RDW is not associated with microcirculatory alterations or prognosis in septic patients.

The effects of storage of red blood cells on the development of postoperative infections after noncardiac surgery.

Prolonged storage of red blood cells (RBCs) is a potential risk factor for postoperative infections. The objective of this study was to examine the effect of age of RBCs transfused on development of postoperative infection.

Early Effects of Enteral Urea on Intracranial Pressure in Patients With Acute Brain Injury and Hyponatremia

Background: Hyponatremia occurs commonly after acute brain injury and is often due to the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Urea administration is 1 therapeutic option. Methods: In our Department, enteral urea is routinely administered to patients with acute brain injury who develop hyponatremia consistent with SIADH and do not respond to an initial sodium load. We reviewed the records of all patients over a 2-year period, who had acute brain injury, received enteral urea because of hyponatremia, and had intracranial pressure (ICP) monitoring using an intraventricular catheter. We recorded demographic, biological, and clinical data; mean ICP values during the 6 hours before and after the first dose of urea were also recorded. Results: We included 40 patients (23 subarachnoid hemorrhage, 8 traumatic brain injury, 6 intracranial hemorrhage, 2 postbrain tumor surgery, and 1 ischemic stroke); median age was 54 years (IQRs, 44 to 63 y) and median admission APACHE II score was 19 (13 to 19); 6-month survival was 63%. Median baseline sodium was 133 mEq/L (131 to 135 mEq/L). No patients received additional therapy to decrease ICP during the 6 hours following urea initiation. After the first urea dose (15 g), ICP decreased from 14 (13 to 18 mm Hg) to 11 mm Hg (8 to 13 mm Hg) (P<0.001). Changes in ICP were not correlated to changes in sodium (r2=0.02). The reduction in ICP was larger in patients with ICP≥15 mm Hg (n=22) than in the others (−8 mm Hg [−14 to −3 mm Hg] vs. −2 mm Hg [−3 to 0 mm Hg], P=0.001). Conclusions: Enteral urea administration in patients with acute brain injury and hyponatremia is associated with a significant reduction in ICP independent of changes in sodium levels.

Red Cell Distribution Width After Subarachnoid Hemorrhage

Background: High red cell distribution width (RDW) values have been associated with increased hospital mortality in critically ill patients, but few data are available for subarachnoid hemorrhage (SAH). Methods: We analyzed an institutional database of adult (>18 y) patients admitted to the Department of Intensive Care after nontraumatic SAH between January 2011 and May 2016. RDW (normal value, 10.9% to 13.4%) was obtained daily from admission for a maximum of 7 days, from routine blood analysis. We recorded the occurrence of delayed cerebral ischemia (DCI), and neurological outcome (assessed using the Glasgow Outcome Scale [GOS]) at 3 months. Results: A total of 270 patients were included (median age 54 y—121/270 male [45%]), of whom 96 (36%) developed DCI and 109 (40%) had an unfavorable neurological outcome (GOS, 1 to 3). The median RDW on admission was 13.8 [13.3 to 14.5]% and the highest value during the intensive care unit (ICU) stay 14.2 [13.6 to 14.8]%. The RDW was high (>13.4%) in 177 patients (66%) on admission and in 217 (80%) at any time during the ICU stay. Patients with a high RDW on admission were more likely to have an unfavorable neurological outcome. In multivariable regression analysis, older age, a high WFNS grade on admission, presence of DCI or intracranial hypertension, previous neurological disease, vasopressor therapy and a high RDW (OR, 1.1618 [95% CI, 1.213-2.158]; P=0.001) during the ICU stay were independent predictors of unfavorable neurological outcome. Conclusions: High RDW values were more likely to result in an unfavorable outcome after SAH. This information could help in the stratification of SAH patients already on ICU admission.

Greater temperature variability is not associated with a worse neurological outcome after cardiac arrest

AIM Spontaneous alterations in temperature homeostasis after cardiac arrest (CA) are associated with worse outcome. However, it remains unclear the prognostic role of temperature variability (TV) during cooling procedures. We hypothesized that low TV during targeted temperature management (TTM) would be associated with a favourable neurological outcome after CA. METHODS We reviewed data from all comatose patients after in-hospital or out-of-hospital CA admitted to our Department of Intensive Care between December 2006 and January 2014 who underwent TTM (32-34°C) and survived at least 24h. We collected demographic data, CA characteristics, intensive care unit (ICU) survival and neurological outcome at three months (favourable neurological outcome was defined as cerebral performance category 1-2). TV was expressed using the standard deviation (SD) of all temperature measurements during hypothermia; high TV was defined as an SD >1°C. RESULTS Of the 301 patients admitted over the study period, 72 patients were excluded and a total of 229 patients were studied; 88 had a favourable neurological outcome. The median temperature on ICU admission was 35.8 [34.9-36.9]°C and the median time to hypothermia (body temperature <34°C), was 4 [3-7] h. Median TV was 0.9 [0.6-1.0]°C and 57 patients (25%) had high TV. In multivariable logistic regression, witnessed CA, ventricular fibrillation/tachycardia and previous neurological disease were independent risk factors for high TV. Younger age, bystander cardiopulmonary resuscitation, shorter time to return of spontaneous circulation, cardiac origin of arrest, shockable rhythm and longer time to target temperature were independent predictors of favourable neurological outcome, but TV was not. CONCLUSIONS Among comatose survivors treated with TTM after CA, 25% of patients had high TV; however, this was not associated with a worse neurologic outcome.

Red cells distribution width after cardiac arrest

Methods Retrospective analysis of an institutional database including all adult comatose patients admitted to the Intensive Care Unit (ICU) after CA from January 2007 to December 2014. Inclusion criteria were as follows: age ≥18, non-traumatic arrest and survival ≥ 24 hours after admission. We collected demographics and CA related data. We also collected daily routine blood analyses; RDW (normal values: 10.9-13.4%), was obtained from the day of admission to day 3. We recorded ICU mortality and long-term neurological outcome; a CPC score of 3-5 at 3-months was used to define poor neurological outcome (PNO).

Post-mortem findings in critically ill patients treated with continuous renal replacement therapy

Despite the high incidence of acute kidney injury (AKI) in critically ill patients, studies evaluating histopathological renal findings in these patients yielded inconsistent results. No studied specifically evaluated renal histology in intensive care unit (ICU) patients treated by continuos renal replacement therapy for severe AKI.

Determinants of renal recovery and mortality inpatients undergoing continuous renal replacement therapy in the ICU

Continuous Renal Replacement Therapy (CRRT) is commonly used in critically ill patients with acute kidney injury (AKI). However, factors which influence outcome and the optimal way to integrate CRRT into the care of these patients needs to be better defined[1].

Assessment of chloride levels on renal function after cardiac arrest

Chloride may alter renal function by inducing vasoconstriction of renal afferent arterioles, thereby inducing cortical hypoperfusion. Increased chloride delivery to the distal tube may also induce tubular dysfunction. The effects of chloride balance on renal function after cardiac arrest (CA) remain unknown.

Angiotensin converting enzymes in patients with acute respiratory distress syndrome

Angiotensin converting enzymes (ACEs) are important in the control of the cardiovascular function and their inhibition have a primary role in the treatment of hypertension and heart failure. However they have effects beyond the cardiovascular system. Angiotensin 2 production by ACE and stimulation of the angiotensin 1 (AT1) receptor subtype reduces nitric oxide bioavailability, promotes inflammation and fibrosis. The ACE type 2 (ACE2) increases angiotensin 1-7 production and counterbalances ACE effects. Some animal data have shown a beneficial role of the up-regulation of the ACE2 pathway and a detrimental role for the up-regulation of the ACE classic pathway in different ARDS, but there are no data in patients with ARDS.