Effects of Terlipressin on Management of Hypotensive Brain-Dead Patients Who are Potential Organ Donors: A Retrospective Study

Background: Administration of terlipressin can reverse hypotension in potential organ donors with norepinephrine-resistance. The aim of this study was to determine the effects of terlipressin on the hemodynamics, liver function, and renal function of hypotensive brain-dead patients who were potential organ donors.Methods: A retrospective study was conducted by using the ICU database of one hospital. 18 patients in a total of 294 brain-dead cases were enrolled and administered terlipressin intravenously. All physiological parameters of recruited patients were obtained at baseline, 24 and 72 h after administration, and immediately before organ procurement.Results: Terlipressin induced significant increases in mean arterial pressure (MAP) from 69.56 ± 10.68 mm Hg (baseline) to 101.82 ± 19.27 mm Hg (immediately before organ procurement) and systolic blood pressure (SBP) from 89.78 ± 8.53 mm Hg (baseline) to 133.42 ± 26.11 mm Hg (immediately before organ procurement) in all patients. The increases in MAP were accompanied by significant decreases in heart rate (HR) from 113.56 ± 28.43 bpm (baseline) to 83.89 ± 11.70 bpm (immediately before organ procurement), which resulted in the decrease of norepinephrine dose over time from 0.8 ± 0.2 μg/kg/min (baseline) to 0.09 ± 0.02 μg/kg/min (immediately before organ procurement). There were no changes in central venous pressure, liver function including aspartate aminotransferase (AST), alanine aminotransferase (ALT), and bilirubin. Renal function, assessed by serum creatinine (SCr), urine output (UOP), creatinine clearance rate (CCr), and estimated glomerular filtration rate (eGFR), improved significantly.Conclusion: Our analysis of brain-dead patients with hypotension indicates that administration of terlipressin can significantly increases MAP, SBP, UOP, CCr, and eGFR, while decreases HR and Scr. Terlipressin appears to help maintain hemodynamic stability, reduce vasoactive support, and improve renal function.

Predictors of Lethal Outcomes in Patients with Refractory Septic Shock

Early prediction of disease severity helps clinicians prevent adverse events and/or minimize losses in the event of a life-threatening complication. This provision fully applies to refractory septic shock, in which norepinephrine administration at a dose exceeding 0.5 μg/kg-1/min-1 is needed to maintain mean arterial pressure.The objective: to determine predictors of lethal outcomes in patients with refractory septic shock.Subjects and methods. A retrospective study included 79 patients with refractory septic shock aged from 42 to 74 years (59.7 ± 7.8), with severity of the condition as per SOFA varying from 8 to 16 scores. The predictive value of indicators was assessed using univariate and multivariate analyses.Results. In multivariate analysis, the only significant predictor of an unfavorable outcome was the SOFA score (adj. OR: 1.626 [95% CI: 1.313; 2.014], p < 0.001). Other putative indicators (age, oxygenation index, lactate and procalcitonin concentrations, and norepinephrine dose) had no predictive value.Conclusion: The SOFA score is an independent predictor of lethality in adult patients with refractory septic shock (аdj. OR: 1.26 [95% CI: 1.313; 2.014], p < 0.001). According to the results of the ROC analysis, along with SOFA, norepinephrine dose was also a significant predictor (AUC 0.989 [95% CI 0.934; 1.000], p < 0.001).

Septic Shock: Phenotypes and Outcomes

Our goal was to determine the relevant variables and patient phenotypes to predict sepsis outcomes. We performed an ancillary study concerning 119 patients from three intensive care units (ICUs) in septic shock at ICU admittance (T0). We defined clinical worsening as having an increased Sequential Organ Failure Assessment (SOFA) score ≥ 1 48 hours after admission (ΔSOFA ≥ 1). We performed univariate and multivariate analyses according to 28-day mortality rate and ΔSOFA ≥ 1, and determined three patient phenotypes: safe, intermediate and poor. Persistence of the intermediate and poor phenotypes after T0 were defined as poor outcomes. At T0, the multivariate analysis showed two variables associated with 28-day mortality rate: norepinephrine dose and serum lactate concentration. Regarding ΔSOFA ≥ 1, we identified three variables at T0: norepinephrine dose, serum lactate concentration and venous-to-arterial carbon dioxide partial pressure difference (P(v-a)CO2). At T0, the three phenotypes (safe, intermediate, and poor) were distributed in 28 (24%), 70 (59%) and 21 (18%) patients, respectively. We thus suggested an algorithm featuring norepinephrine dose, serum lactate concentration and P(v-a)CO2 to predict patient outcomes and obtained an area under the curve (AUC) of 74% (63–85%). In conclusion, our findings underline that identifying relevant variables and phenotypes may help physicians recognize patient outcomes.

Hemodynamic impact of molecular adsorbent recirculating system in refractory vasoplegic shock due to calcium channel blocker poisoning

Objective: To report the hemodynamic effect of to the molecular adsorbent recirculating system (MARS™) therapy for patients in refractory vasoplegic shock due to calcium channel blocker (CCB) poisoning Methods: We report a retrospective cohort of patients who were hospitalized for CCB poisoning with refractory vasoplegic shock and treated by MARS therapy, at Amiens Hospital University, from January 2010 to December 2019. Improvement in hemodynamic was assessed by dynamic changes in mean arterial pressure (MAP) and norepinephrine levels over a 24-h period after MARS therapy. Cardiac function was assessed by transthoracic echocardiography. Results: MARS therapy was performed on seven patients for CCB poisoning. CCB poisoning included nicardipine ( n = 3, 43%) amlodipine ( n = 3, 43%), and verapamil ( n = 1, 14%). The median time to start MARS therapy was 24 [14–27] h after drug ingestion and 6 [2–9] h after ICU admission. Cardiac output was preserved for all patients. MAP values improved from 56 [43–58] to 65 [61–78] 16 mmHg ( p = 0.005). Norepinephrine dose significantly decreased from 3.2 [0.8–10] µg/kg/min to 1.2 [0.1–1.9] µg/kg/min ( p = 0.008) and lactate level decreased from 3.2 [2.4–3.4] mmol/l−1 to 1.6 [0.9–2.2] mmol/l−1 ( p = 0.008). The median length of ICU stay was 4 (2–7) days and hospital stay was 4 (4–16) days. No complication related to the MARS therapy were reported. No patient died and all were discharged from the hospital. Conclusion: We reported the largest case-series of MARS therapy for refractory vasoplegic shock due to CCB poisoning. We observed that MARS therapy was associated with an improvement of hemodynamic parameters.

Risk factors for 28-day mortality in patients with sepsis-related myocardial injury in intensive care units

Objective This study aimed to identify the risk factors for death in patients with sepsis-related myocardial injury. Methods A retrospective study was conducted in 158 patients with sepsis-related myocardial injury in a mixed medical intensive care unit from January 2009 to March 2020. The patients were divided into those who survived and those who died on the basis of whether they survived after 28 days. Demographic and clinical parameters were collected. Multivariate logistic regression was performed. Results Sixty-nine (43.7%) patients died within 28 days after admission to the intensive care unit. Multivariate logistic regression analysis showed that the oxygenation index (odds ratio [OR]: 0.979, 95% confidence interval [CI]: 0.970–0.989), acute kidney injury (OR: 4.787, 95% CI: 1.674–13.693), norepinephrine dose (OR: 1.706, 95% CI: 1.375–2.117), and abdominopelvic cavity infection (OR: 0.257, 95% CI: 0.076–0.866) were significantly associated with mortality within 28 days after admission in patients with sepsis-related myocardial injury. Conclusions Patients with sepsis-related myocardial injury have a high mortality rate. A high oxygenation index, occurrence of acute kidney injury, high norepinephrine dose, and occurrence of abdominopelvic cavity infection are independent risk factors for 28-day mortality in patients with sepsis-related myocardial injury.

Echocardiographic measure of dynamic arterial elastance predict pressure response during norepinephrine weaning: an observational study

The purpose of this study was to determine whether dynamic elastance EAdyn derived from echocardiographic measurements of stroke volume variations can predict the success of a one-step decrease of norepinephrine dose. In this prospective single-center study, 39 patients with vasoplegic syndrome treated with norepinephrine and for whom the attending physician had decided to decrease norepinephrine dose and monitored by thermodilution were analyzed. EAdyn is the ratio of pulse pressure variation to stroke volume variation and was calculated from echocardiography stroke volume variations and from transpulmonary thermodilution. Pulse pressure variation was obtained from invasive arterial monitoring. Responders were defined by a decrease in mean arterial pressure (MAP) > 10% following norepinephrine decrease. The median decrease in norepinephrine was of 0.04 [0.03–0.05] µg kg−1 min−1. Twelve patients (31%) were classified as pressure responders with a median decrease in MAP of 13% [12–15%]. EAdyn was lower in pressure responders (0.40 [0.24–0.57] vs 0.95 [0.77–1.09], p < 0.01). EAdyn was able to discriminate between pressure responders and non-responders with an area under the curve of 0.86 (CI95% [0.71 to1.0], p < 0.05). The optimal cut-off was 0.8. EAdyn calculated from the echocardiographic estimation of the stroke volume variation and the invasive arterial pulse pressure variation can be used to discriminate pressure response to norepinephrine weaning. Agreement between EAdyn calculated from echocardiography and thermodilution was poor. Echocardiographic EAdyn might be used at bedside to optimize hemodynamic treatment.

Efficacy of 4-hour rescue therapeutic plasma exchange in severe septic shock patients

Background.Early intervention for septic shock is crucial to reduce mortality and improve outcome. There is still a great debate over the exact time of therapeutic plasma exchange (TPE) administration in septic shock patients. This study aims to investigate the effect of early initiation (within 4 hours) of TPE in severe septic shock on hemodynamics & outcome.Methods. We conducted a prospective, before-after case series study on 16 septic shock patients requiring high doses of vasopressors admitted in two ICUs from Cairo, Egypt. All of our patients received TPE within 4 hours of ICU admission. The fresh frozen plasma exchange volume = 1.5 × plasma volume.Results. In the 16 patients included in the study, mean arterial pressure was significantly improved after the initial TPE (p < 0.002) and norepinephrine dose which significantly reduced post TPE (p < 0.001). In addition, norepinephrine dose to mean arterial pressure significantly improved (p < 0.001). There was reduction of a net 6 hours fluid balances following the first TPE were observed in all the patients (p < 0.03) by a mean of 757 ml. Systemic vascular resistance index was markedly improved post-TPE along with statistically improved cardiac index (p < 0.01). Stroke volume variance was also significantly decreased after the TPE sessions (p < 0.01). C-reactive protein significantly improved after TPE (P < 0.01).Conclusion. Early initiation of TPE in severe septic shock patients might improve hemodynamic measures.

708 Enteral Nutrition Initiation During Periods of Vasopressor Requirements and Elevated Lactate Levels

Introduction Nutrition is a core component of care for the critically ill burn patient. The Society for Critical Care Medicine recommends initiating enteral nutrition (EN) within 4–6 hours of injury for burn patients, while simultaneously recommending waiting until hemodynamic stability is achieved for critical care patients. The goal of this analysis was to evaluate tolerance of EN during periods of different pressor requirements and lactate levels. Methods We performed a retrospective evaluation on all burn patients admitted to our intensive care unit in 2018 who received EN. This performance improvement project was approved by our regulatory compliance division. Lactate levels and vasopressor use just prior to EN initiation, the highest EN rates and gastric residual volumes during the 24 hours after initiation, and ischemic bowel and aspiration after EN initiation were recorded. Significance was accepted at p&lt; 0.05. Results EN was initiated at 30 ± 20 hours after admission in 58 patients with the following characteristics: 47 ± 19 years old, 29 ± 24% TBSA burn, 13 mechanical ventilator days (IQR: 5–30), 15% mortality. The highest EN rate reached was 100 ± 49 mL/hr during the first 24 hours after initiation. Lactate levels were 1.9 mmol/L at the time of EN initiation (IQR: 1.6–2.4 mmol/L), with a maximum of 4.9 mmol/L. Lactate levels did not have a significant correlation with gastric residual volumes (p=0.532). Most (59%) patients did not have vasopressor requirements, but 21% required vasopressin only, 2% required norepinephrine only, and 19% required a combination of vasopressin and norepinephrine. Those who received norepinephrine received 3.3 ± 1.7 mcg/min, with a maximum of 7 mcg/min. There was a significant difference in gastric residual volumes between patients who had no vasopressor requirements compared to those who required vasopressors [13 mL (IQR: 0–200 mL) vs. 240 mL (IQR: 21–430 mL), p=0.014)]; however, the number of patients with gastric residual volumes over 500 mL was not significantly different (3% vs. 17%, p=0.149). When examining patients receiving vasopressin alone, there was a significant but weak correlation between vasopressin dose and gastric residual volumes (p=0.047, R2=0.339); however, when examining only patients receiving norepinephrine, there was no correlation between norepinephrine dose and gastric residual volumes (p=0.905, R2=0.002). There was 1 episode of aspiration and 1 episode of ischemic bowel, both of which occurred 3 days after EN initiation. EN was initiated without vasopressors running and lactate levels were normal in both cases. Conclusions The majority of patients tolerated EN initiation with vasopressor dosing of norepinephrine up to 7 mcg/min and lactate up to 4.9 mmol/L. Applicability of Research to Practice We found no indication for holding EN for lactate levels under 5 mmol/L and norepinephrine under 8 mcg/min.