Introduction: Elevated plasma B-type natriuretic peptide (BNP) levels in patients with critical sepsis (severe sepsis and septic shock) may indicate septic cardiomyopathy. However, multiple heterogeneous conditions may also be involved in increased BNP level. In addition, the prognostic value of BNP in sepsis remains debatable. In this study, we sought to discover potential independent determinants of BNP elevation in critical sepsis. The prognostic value of BNP was also evaluated. Methods: In this observational study, we enrolled mechanically ventilated, critically septic patients requiring hemodynamic monitoring through a pulmonary artery catheter. All clinical, laboratory and survival data were prospectively collected. Plasma BNP concentrations were measured daily for five consecutive days. Septic cardiomyopathy was assessed on day 1 on the basis of left and right ventricular ejection fractions (EF) derived from echocardiography and thermodilution, respectively. Mortality was recorded at day 28. Results: A total of 42 patients with severe sepsis (N = 12) and septic shock (N = 30) were ultimately enrolled. Daily BNP levels were significantly elevated in septic shock patients compared with those with severe sepsis (P ≤0.002). Critical illness severity (assessed by Acute Physiology and Chronic Health Evaluation II and maximum Sequential Organ Failure Assessment scores), and peak noradrenaline dose on day 1 were independent determinants of BNP elevation (P <0.05). Biventricular EFs were inversely correlated with longitudinal BNP measurements (P <0.05), but not independently. Pulmonary capillary wedge pressures (PCWP) and volume expansion showed no correlation with BNP. In septic shock, increased central venous pressure (CVP) and CVP/PCWP ratio were independently associated with early BNP values (P 800 pg/ml (the best cutoff point) fairly predicted mortality, with a sensitivity%, specificity% and area under the curve values of 65, 64 and 0.70, respectively (95% confidence interval = 0.54 to 0.86; P = 0.03). Plasma BNP levels declined faster in survivors than in nonsurvivors in both critical sepsis and septic shock (P ≤0.002). In septic shock, a BNP/CVP ratio >126 pg/mmHg/ml on day 2 and inability to reduce BNP <500 pg/ml implied increased mortality (P ≤0.036). Conclusions: The severity of critical illness, rather than septic cardiomyopathy, is probably the major determinant of BNP elevation in patients with critical sepsis. Daily BNP values are of limited prognostic value in predicting 28-day mortality; however, fast BNP decline over time and a decrease in BNP <500 pg/ml may imply a favorable outcome.

To investigate aortic functional alterations in the acute phase of aneurysmal subarachnoid hemorrhage and to evaluate the relationship between potential cardiovascular alterations and delayed cerebral infarctions or poor Glasgow Outcome Scale score at discharge from critical care unit. Prospective observational study. Critical Care Departments of two tertiary centers. Thirty-seven patients with aneurysmal subarachnoid hemorrhage. Patients were evaluated at two time points: on admission (acute aneurysmal subarachnoid hemorrhage phase) and at least 21 days later (stable aneurysmal subarachnoid hemorrhage state). At baseline, the severity of aneurysmal subarachnoid hemorrhage was assessed clinically (Hunt and Hess scale) and radiologically (brain computed tomography Fisher grading). Aortic elasticity was evaluated by Doppler-derived pulse-wave velocity and left ventricular function by echocardiography. Serum B-type natriuretic peptide and troponin I were also assessed at the same time points. At the acute phase, 23 patients (62%) were found to present supranormal pulse-wave velocity and 14 patients (38%) presented left ventricular systolic dysfunction; there were significant associations between pulse-wave velocity values and left ventricular ejection fraction (p < .001). Left ventricular ejection fraction and pulse-wave velocity were both associated with Hunt and Hess (p ≤ .004) and Fisher grading (p ≤ .03). Left ventricular ejection fraction and pulse-wave velocity were improved between acute aneurysmal subarachnoid hemorrhage and stable state (p ≤ .005); changes (Δ%) were greater in patients who initially had regional wall motion abnormalities compared to patients who had not (28.7% ± 10.2% vs. 2.4% ± 1.8% [p = .002] and −17.9% ± 3.7% vs. −3.5% ± 4.7% [p = .045], respectively). Pulse-wave velocity/left ventricular ejection fraction ratio was the only independent predictor for delayed cerebral infarctions. Left ventricular ejection fraction, B-type natriuretic peptide, pulse-wave velocity, and pulse-wave velocity/left ventricular ejection fraction showed significant diagnostic performance for predicting delayed cerebral infarctions or poor Glasgow Outcome Scale score (1–3). Our findings suggest that significant cardiovascular alterations in left ventricular function and in aortic stiffness occur during the early phase of aneurysmal subarachnoid hemorrhage. These phenomena were associated with adverse outcomes in this study and their role in the pathogenesis of delayed neurologic complications warrants further investigation.

The aim was to investigate whether the use of N-acetylcysteine and ascorbic acid reduce contrast-induced nephropathy incidence in critical care patients. This was a one-center, two-arm, prospective, randomized, open-label, controlled trial in the Intensive Care Unit of the University Hospital of Larissa, Greece. Patients with stable renal function, who underwent non urgent contrast-enhanced computed tomography for diagnostic purposes, were included in the study. Patients in the treatment group (NacA, n = 60) received intravenously N-acetylcysteine (1200 mg) and ascorbic acid (2 g) dissolved separately in 100 ml of normal saline 2 hours before, and at 10 hours and 18 hours following the infusion of contrast agent, while control group patients (CG, n = 64) received only normal saline. All patients received additional hydration. Contrast-induced nephropathy was defined as relative increase by 25% of the baseline values of serum creatinine. Contrast-induced nephropathy in NacA and CG were 18.33% and 15.6%, respectively (p = 0.81). The percentage change median (interquartile range (IR)) of serum cystatin-C (mg/L) from baseline in patients who underwent contrast-induced tomography, were 37.23% (28.53) and 93.20% (46.90) in NacA and in CG, respectively (p = 0.03). The 8-isoprostane serum levels in NacA were significantly lower compared to CG at 2 hours (p = 0.012) and 24 hours (p = 0.006) following radiocontrast infusion. Multivariate analysis revealed that contrast-induced nephropathy was independently associated with a higher baseline ratio of serum urea/creatinine (odds ratio, 1.02; 95 CI%, 1.00–1.05) and with the use of nephrotoxic medications (odds ratio, 0.24; 95 CI%, 0.06–0.94). Intravenous administration of N-acetylcysteine and ascorbic acid failed to reduce contrast-induced nephropathy in critically ill patients who underwent contrast-enhanced computed tomography, despite a significant reduction of 8-isoprostane levels in treated patients. ClinicalTrials.gov, NCT01017796 . Registered on 20 November 2009.

Background: Fulminant (life-threatening) COVID-19 can be associated with acute respiratory failure (ARF), multi-system organ failure and cytokine release syndrome (CRS). We present a rare case of fulminant COVID-19 associated with reverse-takotsubo-cardiomyopathy (RTCC) that improved with therapeutic plasma exchange (TPE). Case presentation: A 40 year old previous healthy male presented in the emergency room with 4 days of dry cough, chest pain, myalgias and fatigue. He progressed to ARF requiring high-flow-nasal-cannula (flow: 60 L/minute, fraction of inspired oxygen: 40%). Real-Time-Polymerase-Chain-Reaction (RT-PCR) assay confirmed COVID-19 and chest X-ray showed interstitial infiltrates. Biochemistry suggested CRS: increased C-reactive protein, lactate dehydrogenase, ferritin and interleukin-6. Renal function was normal but lactate levels were elevated. Electrocardiogram demonstrated non-specific changes and troponin-I levels were slightly elevated. Echocardiography revealed left ventricular (LV) basal and midventricular akinesia with apex sparing (LV ejection fraction: 30%) and depressed cardiac output (2.8 L/min) consistent with a rare variant of stress-related cardiomyopathy: RTCC. His ratio of partial arterial pressure of oxygen to fractional inspired concentration of oxygen was < 120. He was admitted to the intensive care unit (ICU) for mechanical ventilation and vasopressors, plus antivirals (lopinavir/ritonavir), and prophylactic anticoagulation. Infusion of milrinone failed to improve his cardiogenic shock (day-1). Thus, rescue TPE was performed using the Spectra Optia™ Apheresis System equipped with the Depuro D2000 Adsorption Cartridge (Terumo BCT Inc., USA) without protective antibodies. Over 5 days he received daily TPE (each lasting 4 hours). His lactate levels, oxygenation, and LV function normalized and he was weaned off vasopressors. His inflammation markers improved, and he was extubated on day-7. RT-PCR was negative on day-17. He was discharged to home isolation in good condition. Conclusion: Stress-cardiomyopathy may complicate the course of fulminant COVID-19 with associated CRS. If inotropic therapy fails, TPE without protective antibodies may help rescue the critically ill patient.

Background.Aging is associated with renal structural changes and functional decline. The attributable risk for renal dysfunction from radiocontrast agents in critically ill older patients has not been well established.Methods.In this prospective study, we assessed the incidence of contrast-induced nephropathy (CIN) in critically ill patients with stable renal function who underwent computed tomography with intravenous contrast media. Patients were categorized into two age groups: <65 (YG) or ≥65 years old (OG). CIN was defined as 25% or greater increase from baseline of serum creatinine or as an absolute increase by 0.5 mg/dL until the 5th day after the infusion of contrast agent. We also evaluated the alterations in oxidative stress by assessing serum 8-isoprostane.Results.CIN occurred in 5 of 13 OG patients (38.46%) whereas no YG patient presented CIN (P=0.015). Serum creatinine kinetics in older patients demonstrated a rise over five days following contrast infusion time while a decline was observed in the YG (P=0.005).Conclusions.Older critically ill patients are more prone to develop renal dysfunction after the intravenous infusion of contrast agent in relation to their younger counterparts.