Pro-inflammatory cytokines as potential predictors for intradialytic hypotension.

BACKGROUND: Intradialytic hypotension (IDH) is a common complication in maintaining hemodialysis (MHD) patients. Immune activation might be part of the mechanisms. However, the association between pro-inflammatory cytokines and blood pressure (BP) has not been deeply explored. So we aim to evaluate the potential role of pro-inflammatory cytokines in IDH. METHODS: MHD patients starting hemodialysis before January 2016 were enrolled in our retrospective study. Patients' characteristics, laboratory results, and intradialytic BP were collected. IDH was defined as nadir systolic BP ≤ 90 mmHg during hemodialysis. The definition of IDH group was that those who suffered from more than one hypotensive event during one month after the enrollment (10% of dialysis treatments). Spearman correlation analysis and logistic regression were employed to explore the relationship between pro-inflammatory cytokines and IDH. RESULTS: Among 390 patients, 72 were identified with IDH (18.5%). High levels of serum tumor necrosis factor-α (TNF-α) and interleukin-1ß (IL-1ß) were observed in the IDH group (p < 0.001). Both TNF-α and IL-1ß positively correlated with predialysis BP (p < 0.01). Receiver operating characteristic curve (ROC) analysis was used to evaluate the diagnostic accuracy of serum IL-1ß and TNF-α for IDH. The area under the curve of IL-1ß was 0.772 (95% CI: 0.708-0.836, p < 0.01), and that of TNF-α was 0.701 (95% CI: 0.620-0.781, p < 0.01). After adjusting for patients' characteristics, biochemical parameters, comorbid conditions, predialysis BP, and medications, elevated TNF-α and IL-1ß were still risk factors for IDH. CONCLUSION: Pro-inflammatory cytokines (TNF-α and IL-1ß) could be potential predictors for IDH.

Pannexin 1 channels control the hemodynamic response to hypoxia by regulating O2-sensitive extracellular ATP in blood.

Pannexin 1 (Panx1) channels export ATP and may contribute to increased concentration of the vasodilator ATP in plasma during hypoxia in vivo. We hypothesized that Panx1 channels and associated ATP export contribute to hypoxic vasodilation, a mechanism that facilitates the matching of oxygen delivery to metabolic demand of tissue. Male and female mice devoid of Panx1 (Panx1-/-) and wild-type controls (WT) were anesthetized, mechanically ventilated, and instrumented with a carotid artery catheter or femoral artery flow transducer for hemodynamic and plasma ATP monitoring during inhalation of 21% (normoxia) or 10% oxygen (hypoxia). ATP export from WT vs. Panx1-/-erythrocytes (RBC) was determined ex vivo via tonometer experimentation across progressive deoxygenation. Mean arterial pressure (MAP) was similar in Panx1-/- (n = 6) and WT (n = 6) mice in normoxia, but the decrease in MAP in hypoxia seen in WT was attenuated in Panx1-/- mice (-16 ± 9% vs. -2 ± 8%; P < 0.05). Hindlimb blood flow (HBF) was significantly lower in Panx1-/- (n = 6) vs. WT (n = 6) basally, and increased in WT but not Panx1-/- mice during hypoxia (8 ± 6% vs. -10 ± 13%; P < 0.05). Estimation of hindlimb vascular conductance using data from the MAP and HBF experiments showed an average response of 28% for WT vs. -9% for Panx1-/- mice. Mean venous plasma ATP during hypoxia was 57% lower in Panx1-/- (n = 6) vs. WT mice (n = 6; P < 0.05). Mean hypoxia-induced ATP export from RBCs from Panx1-/- mice (n = 8) was 82% lower than that from WT (n = 8; P < 0.05). Panx1 channels participate in hemodynamic responses consistent with hypoxic vasodilation by regulating hypoxia-sensitive extracellular ATP levels in blood.NEW & NOTEWORTHY Export of vasodilator ATP from red blood cells requires pannexin 1. Blood plasma ATP elevations in response to hypoxia in mice require pannexin 1. Hemodynamic responses to hypoxia are accompanied by increased plasma ATP in mice in vivo and require pannexin 1.

Central Administration of Angiotensin-(1-7) Improves Vasopressin Impairment and Hypotensive Response in Experimental Endotoxemia.

Angiotensin-(1-7) [Ang-(1-7)]/Mas receptor is a counter-regulatory axis that counteracts detrimental renin-angiotensin system (RAS) effects, especially regarding systemic inflammation, vasopressin (AVP) release, and hypothalamic-pituitary-adrenal (HPA) activation. However, it is not completely understood whether this system may control centrally or systemically the late phase of systemic inflammation. Thus, the aim of this study was to determine whether intracerebroventricular (i.c.v.) administration of Ang-(1-7) can modulate systemic inflammation through the activation of humoral pathways in late phase of endotoxemia. Endotoxemia was induced by systemic injection of lipopolysaccharide (LPS) (1.5 mg/kg, i.v.) in Wistar rats. Ang-(1-7) (0.3 nmol in 2 µL) promoted the release of AVP and attenuated interleukin-6 (IL-6) and nitric oxide (NO) levels but increased interleukin-10 (IL-10) in the serum of the endotoxemic rats. The central administration of Mas receptor antagonist A779 (3 nmol in 2 µL, i.c.v.) abolished these anti-inflammatory effects in endotoxemic rats. Furthermore, Ang-(1-7) applied centrally restored mean arterial blood pressure (MABP) without affecting heart rate (HR) and prevented vascular hyporesponsiveness to norepinephrine (NE) and AVP in animals that received LPS. Together, our results indicate that Ang-(1-7) applied centrally promotes a systemic anti-inflammatory effect through the central Mas receptor and activation of the humoral pathway mediated by AVP.

Kinetic Changes of Plasma Renin Concentrations Predict Acute Kidney Injury in Cardiac Surgery Patients.

Rationale: The renin-angiotensin-aldosterone system is a major pathway in regulating blood pressure, glomerular filtration, and fluid homeostasis. During inflammatory diseases, generation of angiotensin II might be disturbed, leading to increased renin concentrations. Cardiac surgery and the use of cardiopulmonary bypass both induce inflammatory response and cardiovascular instability, which can contribute to acute kidney injury (AKI).Objectives: To investigate whether renin concentrations are associated with hypotension and AKI.Methods: This is a single-center, prospective, observational study among patients undergoing cardiac surgery.Measurements and Main Results: The primary endpoint was the occurrence of AKI within 72 hours after cardiac surgery. A total of 197 patients were available for the primary analysis. The median renin serum concentration was 40.2 µU/ml (quartile 1 [Q1]-Q3, 9.3-144.4) at baseline and 51.3 µU/ml (Q1-Q3, 19.1-167.0) 4 hours after cardiac surgery, whereas the difference between postoperation and preoperation concentrations (Δ-renin) was 3.7 µU/ml (Q1-Q3, -22.7 to 50.9). Patients with an elevated Δ-renin developed an AKI significantly more often (43% vs. 12.2%; P < 0.001). High Δ-renin after cardiac surgery was associated with a significantly lower mean arterial pressure, longer time on vasopressors, and longer length of ICU and hospital stay. The area under the curve (AUC) of Δ-renin for the prediction of AKI (AUC, 0.817; 95% confidence interval, 0.747-0.887) was significantly greater compared with the AUC of the postoperative renin concentrations (AUC, 0.702; 95% CI, 0.610-0.793; P = 0.007).Conclusions: Elevated renin concentrations were associated with cardiovascular instability and increased AKI after cardiac surgery. Elevated renin concentrations could be used to identify high-risk patients for cardiovascular instability and AKI who would benefit from timely intervention that could improve their outcomes.

Development of a severe mesenteric traction syndrome during major abdominal surgery is associated with increased postoperative morbidity: Secondary data analysis on prospective cohorts.

PURPOSE: MTS is elicited during open abdominal surgery and is characterized by facial flushing, hypotension, and tachycardia in response to the release of prostacyclin (PGI2) to plasma. MTS seems to affect postoperative morbidity, but data from larger cohorts are lacking. We aimed to determine the impact of severe mesenteric traction syndrome (MTS) on postoperative morbidity in patients undergoing open upper gastrointestinal surgery. METHODS: The study was a secondary analysis of data from three cohorts (n = 137). The patients were graded for severity of MTS intraoperatively, and hemodynamic variables and blood samples for plasma 6-keto-PGF1α, a stable metabolite of PGI2, were obtained at defined time points. Postoperative morbidity was evaluated by the comprehensive complication index (CCI) and the Dindo-Clavien classification (DC). RESULTS: Patients undergoing either esophagectomy (n = 70), gastrectomy (n = 22), liver- (n = 23), or pancreatic resection (n = 22) were included. Severe MTS was significantly associated with increased postoperative morbidity, i.e., CCI ≥ 26.2 (OR 3.06 [95% CI 1.1-6.6]; p = 0.03) and risk of severe complications, i.e., DC ≥3b (OR 3.1 [95% CI 1.2-8.2]; p = 0.023). Furthermore, patients with severe MTS had increased length of stay (OR 10.1 [95% CI 1.9-54.3]; p = 0.007) and were more likely to be admitted to the intensive care unit (OR = 7.3 [95% CI 1.3-41.9]; p = 0.027), but there was no difference in 1-year mortality. CONCLUSION: Occurrence of severe MTS during upper gastrointestinal surgery is associated with increased postoperative morbidity as indicated by an increased rate of severe complications, length of stay, and admission to the ICU. It remains to be determined whether inhibition of MTS enhances postoperative recovery.

A Prospective, Randomized, Double-Blinded Study of the Effect of Intravenous Ondansetron on the Effective Dose in 50% of Subjects of Prophylactic Phenylephrine Infusions for Preventing Spinal Anesthesia-Induced Hypotension During Cesarean Delivery.

BACKGROUND: Ondansetron has been shown to reduce the incidence of hypotension and vasopressor requirement during spinal anesthesia for obstetric and nonobstetric surgery. However, the magnitude of this effect has not been fully quantified. In this parallel-group, randomized, double-blinded study, we determined the effective dose in 50% of subjects (ED50) of a prophylactic phenylephrine infusion for preventing hypotension in patients who received a single dose of intravenous ondansetron 4 mg or saline control before combined spinal-epidural anesthesia for elective cesarean delivery. ED50 values obtained were compared to estimate the effect of ondansetron versus placebo on vasopressor requirement. METHODS: Sixty parturients were randomly assigned to receive ondansetron (group O) or saline control (group C) 10 minutes before positioning for induction of spinal anesthesia. A prophylactic phenylephrine infusion was used to prevent hypotension. The first patient in each group received a phenylephrine infusion at the rate of 0.5 µg/kg/min. The infusion rate for each subsequent patient was varied with increments or decrements of 0.05 µg/kg/min based on the response of the previous patient, and the effective dose of the phenylephrine infusion for preventing hypotension in 50% of patients (ED50) was calculated for each group and compared using up-down sequential analysis. Probit regression was applied as a backup and sensitivity analysis was used to compare ED50 values for phenylephrine between groups by comparing calculated relative mean potency. RESULTS: The ED50 (mean [95% confidence interval (CI)]) of the rate of phenylephrine infusion was lower in group O (0.24 µg/kg/min [0.10-0.38 µg/kg/min]) compared with group C (0.32 µg/kg/min [0.14-0.47 µg/kg/min]) (P < .001). The total consumption of phenylephrine (mean ± standard deviation [SD]) until delivery was lower in group O (316.5 ± 25.9 µg) than in group C (387.7 ± 14.7 µg, P = .02). The estimate of relative median potency for phenylephrine for group O versus group C was 0.74 (95% CI, 0.37-0.95). CONCLUSIONS: Under the conditions of this study, intravenous ondansetron 4 mg reduced the ED50 of a prophylactic phenylephrine infusion by approximately 26% in patients undergoing cesarean delivery under combined spinal-epidural anesthesia.

Maternal hyperuricemia as a marker of post-spinal hypotension and uterine tone during cesarean delivery: a prospective observational study.

PURPOSE: Raised serum uric acid, a marker of oxidative stress, is known to increase vascular tone and depress myometrial contractility. A rise in serum uric acid levels has also been reported during labor, warranting its correlation with post-spinal hypotension and uterine tone. METHODS: Serum UA sample was drawn from enrolled healthy, laboring parturients. Of these, 100 women who required emergency cesarean delivery were re-sampled prior to surgery. Following spinal anesthesia we recorded episodes of hypotension (MAP < 80% of baseline), use of vasopressors and supplemental uterotonics. The primary outcome was maternal hyperuricemia (1SD > appropriate for gestation age) and its correlation with post-spinal hypotension. Secondary outcomes were total vasopressors used, duration of labor and its effect on uric acid levels, uterine tone and neonatal outcome. RESULTS: Hyperuricemia was observed in 33% of parturients. On comparing with women showing normal uric acid levels, hyperuricemic parturients experienced significantly lower incidence of post-spinal hypotension (45.5% vs. 67.2%; p value = 0.04) and lower vasopressor usage (p value = 0.06). Clinically, an increased use of supplemental uterotonics in these parturients was noted (p = 0.20). The duration of labor had no impact on uric acid levels. Neonatal outcome was unaffected. CONCLUSIONS: In healthy, normotensive parturients undergoing emergency cesarean delivery, maternal hyperuricemia is associated with lower incidence of post-spinal hypotension and reduced need of vasopressors. Elevated serum uric acid levels may also be associated with decreased uterine tone, necessitating greater requirement of supplemental uterotonics. However, further prospective trials are needed to strongly establish this association.

Neurological complications after cardiac surgery: anesthetic considerations based on outcome evidence.

PURPOSE OF REVIEW: Neurological complications after cardiac surgery remain prevalent. This review aims to discuss the modifiable and outcome-relevant risk factors based on an up-to-date literature review, with a focus on interventions that may improve outcomes. RECENT FINDINGS: There is a close relationship between intraoperative blood pressure and postoperative neurological outcomes in cardiac surgical patients based on cohort studies and randomized controlled trials. Adopting an optimal and personalized blood pressure target is essential; however, the outstanding issue is the determination of this target. Maintaining cerebral tissue oxygen saturation at least 90% patient's baseline during cardiac surgery may be beneficial; however, the outstanding issues are effective intervention protocols and quality outcome evidence. Maintaining hemoglobin at least 7.5 g/dl may be adequate for cardiac surgical patients; however, this evidence is based on the pooled results of thousands of patients. We still need to know the optimal hemoglobin level for an individual patient, which is of particular relevance during the decision-making of transfusion or not. SUMMARY: The available evidence highlights the importance of maintaining optimal and individualized blood pressure, cerebral tissue oxygen saturation and hemoglobin level in improving neurological outcomes after cardiac surgery. However, outstanding issues remain and need to be addressed via outcome-oriented further research.

Role of the Autonomic Nervous System and Vascular Endothelial Factors in the Development of Primary Arterial Hypotension in Paediatric Patients.

BACKGROUND: There is a dearth and inconsistency of data on the role of the autonomic nervous system (ANS) in the development of arterial hypotension. Also, little is known about the involvement of endothelial factors in the development of this disease. The aim of the study was to investigate the role of the ANS and endothelial factors or vasoregulators in the development of primary arterial hypotension (PAH) in children. METHODS: The cardiointervalography and clino-orthostatic test results of 113 children with PAH were compared with 88 healthy children of comparable age (7-11 years). Serum endothelial factors (nitric oxide and endothelins) of all children were measured. RESULTS: The findings revealed that children with PAH had higher activity of the sympathetic (p<0.001) and parasympathetic (p<0.001) divisions of the ANS at the initial (resting) position of clino-orthostatic test. The activity of these divisions of the autonomic nervous system correlated with the activity of a cardiac pacemaker. The change of position from horizontal into vertical was accompanied by a rise only in sympathetic activity (p<0.001). However, there was a decline in the sympathetic nervous system (p<0.001) compared to the indices of the initial (resting) position registered in the tenth minute of the vertical position. The parasympathetic division of the ANS based on heart rate variability showed high activity in all positions of the clino-orthostatic test in the patients with PAH compared with healthy children. The activity of the parasympathetic nervous system was associated with increased synthesis of endothelial factors (nitric oxide and endothelins) in blood. CONCLUSIONS: The inadequate response of the autonomic nervous system to the clino-orthostatic test in children with PAH is associated with disorders of both divisions of the autonomic nervous system as well as vascular endothelial factors.

Syncope and hypotension associated with carotid sinus hypersensitivity in a patient with nasopharyngeal carcinoma: A case report.

RATIONALE: Carotid sinus hypersensitivity (CSH) is traditionally classified into 3 subgroups: cardioinhibitory, vasodepressor, and mixed subtypes. However, the underlying mechanism of CSH in head and neck cancer is controversial. Several pathological mechanisms of CSH have been proposed: atherosclerotic noncompliance, sternocleidomastoid proprioceptive denervation, and generalized autonomic dysfunction. PATIENT CONCERNS: We reported a 75-year-old man who had recurrent syncope attacks secondary to hypotension and reduced plasma norepinephrine (NE) levels. CSH was suspected when carotid massage induced syncope-like symptom. DIAGNOSES: Nasopharynx carcinoma with regional lymph node involvement and CSH. INTERVENTIONS: On admission, dopamine was administered to maintain the blood pressure. When NE deficiency was confirmed, intravenous NE combined with oral midodrine replaced the dopamine treatment. OUTCOMES: The syncopal episodes completely resolved with periodic occurrence of hypertension. LESSONS: Our case suggests a potential role of carotid sinus in regulating the release of NE in adrenal gland and that the monitoring of catecholamine level is recommended in the CSH cases either from head and neck tumors or other mechanical manipulation of carotid sinus.

Age-Dependent Changes in AMPK Metabolic Pathways in the Lung in a Mouse Model of Hemorrhagic Shock.

The development of multiple organ failure in patients with hemorrhagic shock is significantly influenced by patient age. Adenosine monophosphate-activated protein kinase (AMPK) is a crucial regulator of energy homeostasis, which coordinates metabolic repair during cellular stress. We investigated whether AMPK-regulated signaling pathways are age-dependent in hemorrhage-induced lung injury and whether AMPK activation by 5-amino-4-imidazole carboxamide riboside (AICAR) affords lung protective effects. Male C57/BL6 young mice (3-5 mo), mature adult mice (9-12 mo), and young AMPKα1 knockout mice (3-5 mo) were subjected to hemorrhagic shock by blood withdrawing, followed by resuscitation with shed blood and lactated Ringer's solution. Plasma proinflammatory cytokines were similarly elevated in C57/BL6 young and mature adult mice after hemorrhagic shock. However, mature adult mice exhibited more severe lung edema and neutrophil infiltration, and higher mitochondrial damage in alveolar epithelial type II cells, than did young mice. No change in autophagy was observed. At molecular analysis, the phosphorylation of the catalytic subunit AMPKα1 was associated with nuclear translocation of peroxisome proliferator-activated receptor γ co-activator-α in young, but not mature, adult mice. Treatment with AICAR ameliorated the disruption of lung architecture in mice of both ages; however, effects in mature adult mice were different than young mice and also involved inhibition of nuclear factor-κB. In young AMPKα1 knockout mice, AICAR failed to improve hypotension and lung neutrophil infiltration. Our data demonstrate that during hemorrhagic shock, AMPK-dependent metabolic repair mechanisms are important for mitigating lung injury. However, these mechanisms are less competent with age.

Effect of hemorrhage rate on early hemodynamic responses in conscious sheep.

Physiological compensatory mechanisms can mask the extent of hemorrhage in conscious mammals, which can be further complicated by individual tolerance and variations in hemorrhage onset and duration. We assessed the effect of hemorrhage rate on tolerance and early physiologic responses to hemorrhage in conscious sheep. Eight Merino ewes (37.4 ± 1.1 kg) were subjected to fast (1.25 mL/kg/min) and slow (0.25 mL/kg/min) hemorrhages separated by at least 3 days. Blood was withdrawn until a drop in mean arterial pressure (MAP) of >30 mmHg and returned at the end of the experiment. Continuous monitoring includedMAP, central venous pressure, pulmonary artery pressure, pulse oximetry, and tissue oximetry. Cardiac output by thermodilution and arterial blood samples were also measured. The effects of fast versus slow hemorrhage rates were compared for total volume of blood removed and stoppage time (whenMAP < 30 mmHg of baseline) and physiological responses during and after the hemorrhage. Estimated blood volume removed whenMAPdropped 30 mmHg was 27.0 ± 4.2% (mean ± standard error) in the slow and 27.3 ± 3.2% in the fast hemorrhage (P = 0.47, pairedttest between rates). Pressure and tissue oximetry responses were similar between hemorrhage rates. Heart rate increased at earlier levels of blood loss during the fast hemorrhage, but hemorrhage rate was not a significant factor for individual hemorrhage tolerance or hemodynamic responses. In 5/16 hemorrhages MAP stopping criteria was reached with <25% of blood volume removed. This study presents the physiological responses leading up to a significant drop in blood pressure in a large conscious animal model and how they are altered by the rate of hemorrhage.

Association between Intraoperative Hypotension and Myocardial Injury after Vascular Surgery.

BACKGROUND: Postoperative myocardial injury occurs frequently after noncardiac surgery and is strongly associated with mortality. Intraoperative hypotension (IOH) is hypothesized to be a possible cause. The aim of this study was to determine the association between IOH and postoperative myocardial injury. METHODS: This cohort study included 890 consecutive patients aged 60 yr or older undergoing vascular surgery from two university centers. The occurrence of myocardial injury was assessed by troponin measurements as part of a postoperative care protocol. IOH was defined by four different thresholds using either relative or absolute values of the mean arterial blood pressure based on previous studies. Either invasive or noninvasive blood pressure measurements were used. Poisson regression analysis was used to determine the association between IOH and postoperative myocardial injury, adjusted for potential clinical confounders and multiple comparisons. RESULTS: Depending on the definition used, IOH occurred in 12 to 81% of the patients. Postoperative myocardial injury occurred in 131 (29%) patients with IOH as defined by a mean arterial pressure less than 60 mmHg, compared with 87 (20%) patients without IOH (P = 0.001). After adjustment for potential confounding factors including mean heart rates, a 40% decrease from the preinduction mean arterial blood pressure with a cumulative duration of more than 30 min was associated with postoperative myocardial injury (relative risk, 1.8; 99% CI, 1.2 to 2.6, P < 0.001). Shorter cumulative durations (less than 30 min) were not associated with myocardial injury. Postoperative myocardial infarction and death within 30 days occurred in 26 (6%) and 17 (4%) patients with IOH as defined by a mean arterial pressure less than 60 mmHg, compared with 12 (3%; P = 0.08) and 15 (3%; P = 0.77) patients without IOH, respectively. CONCLUSIONS: In elderly vascular surgery patients, IOH defined as a 40% decrease from the preinduction mean arterial blood pressure with a cumulative duration of more than 30 min was associated with postoperative myocardial injury.

Arteriovenous blood gas agreement in intensive care patients with varying levels of circulatory compromise: a pilot study.

OBJECTIVE: Venous blood gas (VBG) analysis is suggested as an alternative to arterial blood gas (ABG) analysis. In haemodynamically stable patients, there is clinically acceptable arteriovenous (AV) agreement for pH and bicarbonate (HCO3-) concentration, but in haemodynamically unstable patients, evidence is conflicting. We aimed to evaluate the level of AV agreement for the values of pH, PCO2, base excess, HCO3- and lactate between ABGs and VBGs in critically ill patients with varying degrees of hypotension. DESIGN AND SETTING: A prospective cohort study of a convenience sample of patients in an intensive care unit of a metropolitan teaching hospital. INTERVENTION: Paired ABG and central VBG samples were drawn within 5 minutes of each other from existing arterial lines and central venous lines, and analysed for AV agreement of pH, PCO2, base excess, HCO3- and lactate. The outcome of interest was AV agreement with varying levels of blood pressure (BP). Analysis was by descriptive statistics, box whisker plot and Bland-Altman bias plot analysis. RESULTS: We studied 50 patients with 117 paired ABG and VBG samples. The AV differences (venous-arterial) were: pH, -0.04; HCO3-, -0.37 mmmol/L; base excess, 0.08 mEq/ L; and lactate, 0.16 mmol/L. There was not a clinically relevant deterioration in agreement for these parameters with falling BP. CONCLUSION: In critically ill patients with varying degrees of hypotension in the ICU, there is clinically acceptable AV agreement for the values of pH, HCO3-, base excess and lactate, an agreement that does not deteriorate significantly with falling blood pressure.

Low baseline proBNP associated with increased risk of intraoperative hypotension during spinal anaesthesia for cesarean delivery.

BACKGROUND AND OBJECTIVES: Brain natriuretic peptide (BNP) has a role in the regulation of body fluid volume and blood pressure (BP). BNP remains within a normal range during spinal anaesthesia (SA) in patients undergoing cesarean delivery. However, the effect of BNP on changes in BP during the perioperative period has not been evaluated. We aimed to investigate the effect of preoperative serum BNP on the risk of hypotension during cesarean delivery with SA. DESIGN AND SETTINGS: Patients were randomly selected among the patient group who were attending routine clinic visits for pregnancy monitoring. All had a healthy pregnancy and no other acute or chronic disease by their obstetrician. The study design was cross-sectional. PATIENTS AND METHODS: Patients who had uncomplicated pregnancy process and no known medical dis.ease were selected consecutively during their last outpatient clinical examination. Baseline BP was recorded before SA. Simultaneously, blood samples were drawn for routine biochemistry and BNP. BP, SaO2, and electrocardiography were monitored during surgery. Intraoperative hypotension (IOH) was defined as >=25% decrease in mean arterial pressure (MAP) at the 5th minute of SA. RESULTS: In 41 term pregnant women, 18 of the 41 patients (43.9%) fulfilled the criteria for IOH, while 23 (56.1%) showed a decrease 13.1 (11.3%) and were classified as normotensive. Baseline BNP was significantly lower in patients with IOH compared with normotensive patients 45.7 (26.9) vs.70.2 (40.5); P=.05. Baseline BNP had no significant correlation MAP at any time point. Age, body mass index, hemoglobin, baseline MAP and heart rate were not different between patients with and without IOH. CONCLUSION: Those findings suggest that higher baseline BNP levels might have a protective role in development of hypotension in healthy term pregnant women during SA for cesarean delivery.

Serum cystatin C levels in preterm newborns in our setting: Correlation with serum creatinine and preterm pathologies.

BACKGROUND: Cystatin C (CysC) is a renal function marker that is not as influenced as creatinine (Cr) by endogenous or exogenous agents, so it is therefore proposed as a marker in preterm infants. OBJECTIVES: To determine serum CysC values in preterm infants during the first week of life, compared to Cr. To analyze alterations caused by prematurity diseases. METHOD: The design involved a longitudinal, observational study of prospective cohorts. Groups were based on gestational age (GA): Group A (24-27 weeks), Group B (28-33 weeks), Group C (34-36 weeks). Blood samples were collected at birth, within 48-72hours and after 7 days of life. STATISTICS: SPSS v.20 software was used. The statistical methods applied included chi-squared test and ANOVA. RESULTS: A total of 109 preterm infants were included in the study. CysC levels were: 1.54mg/L (±0.28) at birth; 1.38mg/L (±0.36) within 48-72hours of life; 1.50mg/L (±0.31) after 7 days (p<0.05). Cr levels were: 0.64mg/dL (±0.17) at birth; 0.64mg/dL (±0.28) within 48-72hours; 0.56mg/dL (±0.19) after 7 days (P<.05). CysC values were lower in hypotensive patients and those with a respiratory disease (P<.05), and no alterations associated with other diseases were observed. There were no differences in Cr levels associated with any disease. Creatinine levels were higher in patients ≤1.500g (P<.05). CONCLUSIONS: Serum CysC decreased within 48-72hours of life, and this decline showed significance (P<.05). The levels increased after 7 days in all 3 GA groups, and there was no difference in CysC levels among the groups. More studies in preterm infants with hypotension and respiratory disease are required. CysC is a better glomerular filtration (GF) marker in ≤1.500g preterm infants.

Effect of corticosteroids on arginine vasopressin after pediatric cardiac surgery.

INTRODUCTION: Arginine vasopressin's (AVP) efficacy in the treatment of refractory hypotension is, in part, dependent upon preinfusion endogenous AVP concentration. Corticosteroids, also commonly used to treat refractory hypotension, have been shown to suppress endogenous AVP release. We aimed to determine if corticosteroids affect endogenous AVP concentrations in children recovering from cardiac surgery. MATERIALS AND METHODS: We reviewed the records of children who underwent cardiac surgery between January 2008 and January 2009 and had AVP concentrations available as part of a prior prospective study. Doses of hydrocortisone, methylprednisolone, and dexamethasone administered within the first 48 hours after cardiopulmonary bypass were quantitated. Multivariable linear regression was performed to determine if corticosteroids had a significant effect on 48-hour plasma AVP concentration. RESULTS: Sixty-nine children with plasma AVP concentrations available were reviewed, 34 (49%) of which received corticosteroids within 48 hours after cardiopulmonary bypass. On multivariable regression, greater number of corticosteroid doses but not cumulative corticosteroid dosage was significantly associated with low 48-hour AVP concentration (ß=-4.0; 95% confidence intervals, -6.5 to -1.4). CONCLUSIONS: Children who receive multiple doses of corticosteroids after cardiac surgery, regardless of potency, are likely to have low endogenous AVP concentrations. Children who remain unstable despite corticosteroids may respond favorably to exogenous AVP therapy.

Characterizing vasopressin and other vasoactive mediators released during resuscitation of trauma patients.

BACKGROUND: We sought to perform the first characterization of vasopressin and other vasoactive mediators released during resuscitation of hypotensive trauma patients. METHODS: This institutional review board-approved study was conducted under waiver of consent. Adults with clinical evidence of acute traumatic injury and systolic blood pressure less than or equal to 90 mm Hg within 1 hour of arrival were evaluated at our Level I trauma center. Two hundred three patients were screened with 50 enrolled from February 2010 to February 2011. Demographic information was also collected. Blood samples were obtained at 0, 30, 60, 90, 120, and 240 minutes after arrival, and assays were performed for vasopressin, angiotensin II, epinephrine, and cortisol. We assessed the significance of variation in these vasoactive mediators with injury and transfusion of more than 600 mL, with adjustment for time using repeated-measures linear models in log units. RESULTS: We found that vasopressin (p = 0.005) and epinephrine (p = 0.01) increased significantly with injury, while angiotensin (p = 0.60) and cortisol (p = 0.46) did not and that vasopressin (p < 0.001) and epinephrine (p = 0.004) increased significantly in patients requiring transfusion of more than 600 mL but angiotensin II (p = 0.11) and cortisol (p = 0.90) did not. Relatively low levels of vasopressin (<30 pg/mL) were observed at least once during the first 2 hours in 88% of trauma patients, and abnormally low epinephrine levels (<100 pg/mL) were observed at least once during the first 2 hours in 18% of trauma patients. CONCLUSION: This is the first clinical trial to serially evaluate vasopressin and other vasoactive mediators following trauma during the resuscitation phase. Vasopressin, in particular, and epinephrine seem to be the key mediators produced in the human response to severe injury. A deficiency of vasopressin may contribute to intractable shock after trauma. LEVEL OF EVIDENCE: Prognostic/epidemiologic study, level III.