A basic solution for a complex problem: does treatment of metabolic acidosis slow CKD progression?

PURPOSE OF THIS REVIEW: Metabolic acidosis is frequently encountered in patients with chronic kidney disease (CKD), with increasing prevalence as kidney function worsens. Treating electrolyte disturbances is the sine qua non of Nephrologists, and alkali therapy to normalize serum bicarbonate levels and slow progression of kidney disease has been embedded in clinical practice guidelines for decades on the basis of animal models and controversial clinical trials. This review will critically appraise the literature base for this recommendation and determine whether the available evidence supports this common practice, which is a timely endeavor considering the impending demotion of metabolic acidosis treatment from recommendation to practice point in forthcoming KDIGO guidelines. RECENT FINDINGS: Earlier, open-label, studies supporting the utility of sodium bicarbonate therapy to slow progression of chronic kidney disease have been challenged by more recent, blinded, studies failing to show benefit on CKD progression. This was further demonstrated in the absence of concomitant sodium administration with the hydrochloric acid binder veverimer, which failed to demonstrate benefit on renal death, end stage kidney disease or 40% reduction in estimated glomerular filtration rate in a large multicenter trial. SUMMARY: The current body of literature does not support the routine treatment of metabolic acidosis in patients with CKD and the authors agree with the forthcoming KDIGO guidelines to de-emphasize this common practice.

Arterial Blood Gases and Acid-Base Regulation.

Disorders of acid-base status are common in the critically ill and prompt recognition is central to clinical decision making. The bicarbonate/carbon dioxide buffer system plays a pivotal role in maintaining acid-base homeostasis, and measurements of pH, PCO2, and HCO3 - are routinely used in the estimation of metabolic and respiratory disturbance severity. Hypoventilation and hyperventilation cause primary respiratory acidosis and primary respiratory alkalosis, respectively. Metabolic acidosis and metabolic alkalosis have numerous origins, that include alterations in acid or base intake, body fluid losses, abnormalities of intermediary metabolism, and renal, hepatic, and gastrointestinal dysfunction. The concept of the anion gap is used to categorize metabolic acidoses, and urine chloride excretion helps define metabolic alkaloses. Both the lungs and kidneys employ compensatory mechanisms to minimize changes in pH caused by various physiologic and disease disturbances. Treatment of acid-base disorders should focus primarily on correcting the underlying cause and the hemodynamic and electrolyte derangements that ensue. Specific therapies under certain conditions include renal replacement therapy, mechanical ventilation, respiratory stimulants or depressants, and inhibition of specific enzymes in intermediary metabolism disorders.

Electrolytes disturbances in cancer patients.

PURPOSE OF REVIEW: Hypernatremia, hyperphosphatemia, hypocalcaemia, hyperkalaemia and hypermagnesemia are electrolytes disturbances that can arise in cancer patients in relation to unique causes that are related to the cancer itself or its treatment and can lead to delay or interruption of cancer therapy. This article summarizes these main causes, the proposed pathophysiology and the recommended management for these disturbances. RECENT FINDINGS: There have been many cancer drugs approved in the field of oncology over the past several years and a subset of these drugs have been associated with electrolytes disturbances. This includes, for example, immune checkpoint inhibitor related hyperkalemia, fibroblast growth factor 23 inhibitor associated hyperphosphatemia and epidermal growth factor receptor inhibitor associated hypomagnesemia and hypocalcaemia. SUMMARY: This article provides an updated review of certain electrolytes disturbance in cancer patients and allows clinicians to have a greater awareness and knowledge of these electrolyte abnormalities in efforts to early recognition and timely management.

Bloodstream Infections in Preterm Neonates and Mortality-Associated Risk Factors.

OBJECTIVE: To investigate the association of early (±4 hours after onset of bloodstream infection) clinical and laboratory variables with episode-related mortality (<7 days). STUDY DESIGN: This 2-site retrospective study included 142 neonates born at <35 weeks of gestational age with positive blood/cerebrospinal fluid (CSF) culture at >72 hours of age from organisms other than coagulase-negative Staphylococcus. Early variables were compared between those with bloodstream infection-related mortality and survivors. Multivariable analysis was conducted for the primary outcome, and the area under the curve (AUC) was estimated for relevant variables. RESULTS: The neonates who died were of lower gestational age at disease onset. After adjusting for relevant variables, lowest mean blood pressure (MBP) (aOR, 0.10; 95% CI, 1.02-1.19) and highest base deficit (aOR, 1.18; 95% CI, 1.06-1.32) were independently associated with mortality. The AUC was 0.87 (95% CI, 0.78-0.96) for base deficit, increasing to 0.91 (95% CI, 0.83-0.99) with the addition of MBP. CONCLUSION: Low MBP and high base deficit within ±4 hours of bloodstream infection onset identify preterm neonates at risk of mortality.

Electrolyte imbalance in COVID-19 patients admitted to the Emergency Department: a case-control study.

In patients visiting the emergency department (ED), a potential association between electrolytes disturbance and coronavirus disease 2019 (COVID-19) has not been well studied. We aim to describe electrolyte disturbance and explore risk factors for COVID-19 infection in patients visiting the ED. We carried out a case-control study in three hospitals in France, including adult ED inpatients (≥ 18 years old). A total of 594 ED case patients in whom infection with COVID-19 was confirmed, were matched to 594 non-COVID-19 ED patients (controls) from the same period, according to sex and age. Hyponatremia was defined by a sodium of less than 135 mmol/L (reference range 135-145 mmol/L), hypokalemia by a potassium of less than 3.5 mmol/L (reference range 3.5-5.0 mmol/L), and hypochloremia by a chloride of less than 95 mmol/L (reference range 98-108 mmol/L). Among both case patients and controls, the median (IQR) age was 65 years (IQR 51-76), and 44% were women. Hyponatremia was more common among case patients than among controls, as was hypokalemia and hypochloremia. Based on the results of the multivariate logistic regression, hyponatremia, and hypokalemia were associated with COVID-19 among case patients overall, with an adjusted odds ratio of 1.89 [95% CI 1.24-2.89] for hyponatremia and 1.76 [95% CI 1.20-2.60] for hypokalemia. Hyponatremia and hypokalemia are independently associated with COVID-19 infection in adults visiting the ED, and could act as surrogate biomarkers for the emergency physician in suspected COVID-19 patients.

Early-Life Multiple Sevoflurane Exposures Alleviate Long-term Anxiety-Like Behaviors in Mice via the proBDNF/ERK Pathway.

Early-life multiple anesthetics exposure causes neurotoxicity and hence cognitive dysfunction on developing brain. However, the effects of early-life multiple sevoflurane exposures on emotional changes, especially upon stress, are far beyond understood. In young male C57BL6/J mice, the present study showed that 3% sevoflurane inhalation for 2 h in three consecutive days did not influence anxiety-like behaviors as measured by open field test, light dark transition, and elevated plus maze test. In addition, foot shocks stress induced both the short- and long-term anxiety-like behaviors. However, triple sevoflurane exposures ameliorated the long-term anxiety-like behaviors induced by the foot shocks. In parallel, foot shocks stress upregulated the expression of phosphorylated extracellular signal-regulated kinase (p-ERK) and brain-derived neurotrophic factor precursor (proBDNF) in the anterior cingulate cortex (ACC), which were significantly inhibited by triple sevoflurane exposures. Immunofluorescence further indicated that the increased p-ERK was mainly expressed in the proBDNF-positive staining cells. Intra-ACC injection of recombinant proBDNF protein upregulated the p-ERK expression and blocked the anxiolytic effect of sevoflurane exposure on long-term anxiety-like behaviors. Therefore, our study demonstrated that multiple sevoflurane exposures alleviate long-term anxiety-like behaviors upon acute stress in young mice by inhibiting proBDNF-ERK signaling in the ACC.

Fluid management in chronic kidney disease: what is too much, what is the distribution, and how to manage fluid overload in patients with chronic kidney disease?

PURPOSE OF REVIEW: Assessment of fluid status to reach normovolemia in patients with chronic kidney disease (CKD) continues to be a tough task. Besides clinical observation, technological methods have been introduced, yet, the best approach is still uncertain. The present review looks at fluid overload in CKD from three perspectives: the critical fluid threshold leading to adverse cardiovascular outcomes, fluid distribution and its clinical correlates, and direct effect of fluid overload on vascular function related to disturbance of the sodium-skin axis and endothelial glycocalyx dysfunction. RECENT FINDINGS: To determine fluid status, both the absolute and relative fluid overload is used as parameter in clinical practice. In addition, the definition of fluid overload is ambivalent and its relation to symptom burden has not been studied well. Studies on the impact of distribution of fluid are scarce and the limited evidence suggests differences based on the cause of CKD. So far, no standardized technologies are available to adequately determine fluid distribution. After discovering the 'third compartment' of total body sodium in skin and muscle tissue and its potential direct effect on vascular function, other biomarkers such as VEGF-C are promising. SUMMARY: We propose a multimodal clinical approach for volume management in CKD. Because there are currently no studies are available demonstrating that correction of fluid overload in CKD will lead to better outcome, these are strongly needed.

Spironolactone-furosemide combination therapy and acid-base disorders in liver cirrhosis patients
.

OBJECTIVE: Respiratory alkalosis (RA) and dilutional hyperchloremic acidosis (DHA) are the most common acid-base balance (ABB) disorders in patients with liver cirrhosis. The aims of this study were to clarify whether RA develops in relation to DHA via respiratory compensation of metabolic acidosis and whether spironolactone in combination with low-dose furosemide - diuretics known to ameliorate DHA - positively affects RA in liver cirrhosis patients. MATERIALS AND METHODS: 59 patients with advanced cirrhosis were divided into two groups. Group D consisted of individuals (urine sodium concentration (UNa+) > 20 mmol/L) who responded to combination therapy consisting of spironolactone and low-dose furosemide. The non-D group consisted of individuals (UNa+ ≤ 20 mmol/L) who either did not respond to the treatment or who were not administered it. In both groups, we examined serum and urine concentrations of electrolytes and ABB parameters, including SNa+-SCl- and SNa+/SCl- values. RESULTS: In group D, we found a statistically significant relationship between pCO2 and SHCO3-: r = 0.756 (p < 0.001) and between pCO2 and SNa+-SCl-: r = 0.522 (p = 0.001). Neither Salb nor the corrected anion gap were associated with changes in SHCO3- or pCO2 values. Although SHCO3- values were normal, abnormal pCO2 values were observed in one third of group D patients. Based on multivariable analysis, SHCO3- proved to be a statistically significant influencing factor on pCO2 values. CONCLUSION: DHA contributes to the development of RA in individuals with liver cirrhosis. Reducing DHA by means of effective diuretic therapy comprising spironolactone and furosemide has a beneficial effect on RA in such patients.

Assessing Acid-Base Status in Circulatory Failure: Relationship Between Arterial and Peripheral Venous Blood Gas Measurements in Hypovolemic Shock.

BACKGROUND AND OBJECTIVES: In severe circulatory failure agreement between arterial and mixed venous or central venous values is poor; venous values are more reflective of tissue acid-base imbalance. No prior study has examined the relationship between peripheral venous blood gas (VBG) values and arterial blood gas (ABG) values in hemodynamic compromise. The objective of this study was to examine the correlation between hemodynamic parameters, specifically systolic blood pressure (SBP) and the arterial-peripheral venous (A-PV) difference for all commonly used acid-base parameters (pH, Pco 2, and bicarbonate). DESIGN, SETTING, PARTICIPANTS, AND MEASUREMENTS: Data were obtained prospectively from adult patients with trauma. When an ABG was obtained for clinical purposes, a VBG was drawn as soon as possible. Patients were excluded if the ABG and VBG were drawn >10 minutes apart. RESULTS: The correlations between A-PV pH, A-PV Pco 2, and A-PV bicarbonate and SBP were not statistically significant (P = .55, .17, and .09, respectively). Although patients with hypotension had a lower mean arterial and peripheral venous pH and bicarbonate compared to hemodynamically stable patients, mean A-PV differences for pH and Pco 2 were not statistically different (P = .24 and .16, respectively) between hypotensive and normotensive groups. CONCLUSIONS: In hypovolemic shock, the peripheral VBG does not demonstrate a higher CO2 concentration and lower pH compared to arterial blood. Therefore, the peripheral VBG is not a surrogate for the tissue acid-base status in hypovolemic shock, likely due to peripheral vasoconstriction and central shunting of blood to essential organs. This contrasts with the selective venous respiratory acidosis previously demonstrated in central venous and mixed venous measurements in circulatory failure, which is more reflective of acid-base imbalance at the tissue level than arterial blood. Further work needs to be done to better define the relationship between ABG and both central and peripheral VBG values in various types of shock.

Increased compensatory kidney workload results in cellular damage in a short time porcine model of mixed acidemia - Is acidemia a 'first hit' in acute kidney injury?

Acute kidney injury (AKI) corrupts the outcome of about 50% of all critically ill patients. We investigated the possible contribution of the pathology acidemia on the development of AKI. Pigs were exposed to acidemia, acidemia plus hypoxemia or a normal acid-base balance in an experimental setup, which included mechanical ventilation and renal replacement therapy to facilitate biotrauma caused by extracorporeal therapies. Interestingly, extensive histomorphological changes like a tubular loss of cell barriers occurred in the kidneys after just 5 hours exposure to acidemia. The additional exposure to hypoxemia aggravated these findings. These 'early' microscopic pathologies opposed intra vitam data of kidney function. They did not mirror cellular or systemic patterns of proinflammatory molecules (like TNF-α or IL 18) nor were they detectable by new, sensitive markers of AKI like Neutrophil gelatinase-associated lipocalin. Instead, the data suggest that the increased renal proton excretion during acidemia could be an 'early' first hit in the multifactorial pathogenesis of AKI.

Combined effects of lung function, blood gases and kidney function on the exacerbation risk in stable COPD: Results from the COSYCONET cohort.

RATIONALE: Alterations of acid-base metabolism are an important outcome predictor in acute exacerbations of COPD, whereas sufficient metabolic compensation and adequate renal function are associated with decreased mortality. In stable COPD there is, however, only limited information on the combined role of acid-base balance, blood gases, renal and respiratory function on exacerbation risk grading. METHODS: We used baseline data of the COPD cohort COSYCONET, applying linear and logistic regression analyses, the results of which were implemented into a comprehensive structural equation model. As most informative parameters it comprised the estimated glomerular filtration rate (eGFR), lung function defined via forced expiratory volume in 1 s (FEV1), intrathoracic gas volume (ITGV) and (diffusing capacity for carbon monoxide (DLCO), moreover arterial oxygen content (CaO2), partial pressure of oxygen (PaCO2), base exess (BE) and exacerbation risk according to GOLD criteria. All measures were adjusted for age, gender, body-mass index, the current smoking status and pack years. RESULTS: 1506 patients with stable COPD (GOLD grade 1-4; mean age 64.5 ±â€¯8.1 y; mean FEV1 54 ±â€¯18 %predicted, mean eGFR 82.3 ±â€¯16.9 mL/min/1.73 m2) were included. BE was linked to eGFR, lung function and PaCO2 and played a role as indirect predictor of exacerbation risk via these measures; moreover, eGFR was directly linked to exacerbation risk. These associations remained significant after taking into account medication (diuretics, oral and inhaled corticosteroids), whereby corticosteroids had effects on exacerbation risk and lung function, diuretics on eGFR, BE and lung function. CONCLUSION: Even in stable COPD acid-base metabolism plays a key integrative role in COPD risk assessment despite rather small deviations from normality. It partially mediates the effects of impairments in kidney function, which are also directly linked to exacerbation risk.

The Treatment of Metabolic Acidosis: An Interactive Case-Based Learning Activity.

Introduction: Metabolic acidosis is a dangerous and potentially life-threatening condition encountered in the inpatient and emergency department setting. Metabolic acidoses due to renal failure, bicarbonate losses, or lactic acidosis are common conditions, and the appropriate medical management of each is relevant to any inpatient medical provider. Therefore, we created a learning activity that utilizes blackboard-style videos followed by an interactive case-based learning session to help the medical student recognize, diagnose, and manage common causes of metabolic acidosis. Methods: We organized this learning activity by assigning digital videos, followed by application in an interactive team-based format. We created electronic blackboard-style videos and a quiz to assess medical knowledge related to concepts discussed in the videos. Next, we created case resources that facilitate an interactive case-based teaching session so the learners could apply their knowledge and simulate the management of metabolic acidosis. Results: We implemented this activity for 34 medical students. All students viewed the videos prior to the in-class session. In a pre/post assessment of medical knowledge, we observed a significant improvement in quiz scores. Next, we successfully facilitated the case-based active learning session, allowing the assessment of higher-order cognitive skills related to management of patients with metabolic acidosis. Our medical students felt highly satisfied and competent at the completion of our course. Discussion: Our medical students rated this as an excellent learning activity. Others may find this activity useful within the context of any course or rotation related to patients with metabolic acidosis.

Spuriously Low Serum Bicarbonate Levels in Patients With Hyperlipidemia: A Report of 4 Cases.

Four patients were recently seen at our institution presenting with severe hypobicarbonatemia and elevated anion gap on serum specimens processed by an autoanalyzer using enzymatic reactions. Arterial blood gas values in each case revealed no significant acid-base disturbance and a marked discordance between arterial blood gas calculated bicarbonate levels and those reported on the basic metabolic panel. All patients had profound hyperlipidemia (triglycerides > 3,500mg/L), and ultracentrifugation of one patient's serum corrected the discordance. Lipid interference with the photometric measurement of light absorbance after enzymatic reaction in the autoanalyzer is thought to be responsible for the low reported bicarbonate values. Use of an indirect ion-specific electrode method for total carbon dioxide analysis would avoid this pitfall. Caution is advised when enzymatic autoanalyzer-calculated laboratory values are used to diagnose acid-base disturbances in patients with severe hyperlipidemia. Physicians involved in the diagnosis of acid-base disorders in hospitalized patients should always be aware of the method used by their chemistry laboratories to determine total carbon dioxide values.

Hyperchloremia and postoperative acute kidney injury: a retrospective analysis of data from the surgical intensive care unit.

BACKGROUND: Whether perioperative hyperchloremia can induce postoperative acute kidney injury (AKI) is controversial. We investigated the association between perioperative hyperchloremia and postoperative AKI in patients admitted to the intensive care unit (ICU) after surgery. METHODS: We performed a retrospective observational study of patients admitted to the surgical ICU at a single tertiary care hospital between January 2011 and June 2016. Our primary objective was to determine whether hyperchloremia or an increase in serum chloride levels was associated with postoperative AKI. Perioperative hyperchloremia was defined as serum chloride levels ≥ 110 mmol·L- 1 during postoperative days (PODs) 0-3. The increase in serum chloride levels was defined as the difference between preoperative and maximum postoperative serum chloride levels during the first 3 days after surgery. RESULTS: Of the 7991 patients included in the final analysis, 1876 (23.5%) developed hyperchloremia during PODs 0-3, and 1187 (14.9%) developed postoperative AKI. Exposure to hyperchloremia during the first 3 days after surgery was not associated with postoperative AKI (odds ratio, 1.09; 95% confidence interval, 0.80-1.49; P = 0.571). However, among patients with preoperative chronic kidney disease stage ≥ 3 (estimated glomerular filtration rate < 60 mL·min- 1·1.73·m- 2), the incidence of postoperative AKI was higher in patients with an increase > 6 mmol·L- 1 in serum chloride levels than in patients with an increase ≤ 1 mmol·L- 1 (odds ratio, 1.42; 95% confidence interval, 1.09-1.84; P = 0.009). In addition, the incidence of postoperative AKI stage ≥ 2 was not associated with exposure to hyperchloremia or with the increase in serum chloride levels during PODs 0-3, regardless of preoperative kidney function. CONCLUSIONS: Exposure to perioperative hyperchloremia is not associated with postoperative AKI in surgical ICU patients. However, in patients with moderate-to-severe chronic kidney disease (stage ≥ 3), a substantial perioperative increase in serum chloride levels may reflect a higher risk of AKI.

Retarding progression of chronic kidney disease: use of modalities that counter acid retention.

PURPOSE OF REVIEW: Acid retention because of chronic kidney disease (CKD) increases tissue acidity and accelerates progression of CKD, whereas reduction in acid retention slows progression of CKD. Herein, we describe the mechanisms through which increased tissue acidity worsens CKD, modalities for countering acid retention and their impact on progression of CKD, and current recommendations for therapy. RECENT FINDINGS: Studies in animals and humans show that increased tissue acidity raises the renal levels of endothelin, angiotensin II, aldosterone, and ammoniagenesis, thereby worsening renal fibrosis and causing progression of CKD. Measures that counter acid retention, such as providing alkali or modifying the quantity or type of dietary protein, reduce the levels of endothelin, angiotensin II, aldosterone, and ammoniagenesis, slowing progression of CKD. Alkali can be provided as NaHCO3, sodium citrate, or base in fruits and vegetables. A serum [HCO3] of 24-26 mEq/l is targeted, because higher values can be associated with adverse consequences. SUMMARY: Insights into the mechanisms through which increased tissue acidity mediates progression of CKD and the beneficial impact of ameliorating positive acid balance underlie our recommendation for modalities that counter acid retention in CKD.

Urine Ammonium, Metabolic Acidosis and Progression of Chronic Kidney Disease.

The metabolism of a typical Western diet generates 50-100 mEq of acid (H+) per day, which must be excreted in the urine for the systemic acid-base to remain in balance. The 2 major mechanisms that are responsible for the renal elimination of daily acid under normal conditions are ammonium (NH4+) excretion and titratable acidity. In the presence of systemic acidosis, ammonium excretion is intensified and becomes the crucial mechanism for the elimination of acid. The impairment in NH4+ excretion is therefore associated with reduced acid excretion, which causes excess accumulation of acid in the body and consequently results in metabolic acidosis. Chronic kidney disease (CKD) is associated with the impairment in acid excretion and precipitation of metabolic acidosis, which has an adverse effect on the progression of CKD. Recent studies suggest that the progressive decline in renal ammonium excretion in CKD is an important determinant of the ensuing systemic metabolic acidosis and is an independent factor for predicting the worsening of kidney function. While these studies have been primarily performed in hypertensive individuals with CKD, a closer look at renal NH4+ excretion in non-hypertensive individuals with CKD is warranted to ascertain its role in the progression of kidney disease.

Prevalence and predictors of intra-abdominal hypertension and compartment syndrome in surgical patients in critical care units at Kenyatta National Hospital.

BACKGROUND: Intra-abdominal hypertension (IAH) affects almost every organ sytem.If it is not detected early and corrected, mortality would be high. The prevalence of IAH and abdominal compartment syndrome (ACS) at Kenyatta National Hospital (KNH) critical care units is not known. The aim of this sudy was to determine the prevalence and factors associated with development of IAH/ACS among critically ill surgical patients. METHODS: This was a cross sectional descriptive study involving surgical patients in critical care units at KNH, carried out from March 2015 to October 2015. One hundred and thirteen critically ill and ventilated patients 13 years or older were recruited into the study. Krohn's intravesical method was used to measure intra- abdominal pressure (IAP). Measurements were done at first contact, then at 12 and 24 h. Additional parameters recorded included: laboratory tests such as serum bilirubin and total blood count as well as clinical parameters such as urine output, vital signs and peak airway pressure, among others. Frequency, means and standard deviation were used to describe the data. Categorical variables e.g. age, were analysed using Chi square test and continous variables using student 't' test and Mann Whitney test as appropriate RESULT: A total of 113 consecutive surgical patients admitted to the critical care units were recruited. Of our study population, 71.7% (by IAP max) and 67.3% (by IAP mean) had IAH. Abdominal compartment syndrome (ACS) developed in 4.4% of the population. The following factors were significant determinants of risk of IAH : amount of IV fluids over 24 h (3949.6 vs 2931.1, p = 0.003, adjusted OR 1.0 [1.0-1.002]), haemoglobin values at admission (9.9 vs 12.0, p = <0.012, adjusted OR 0.6 [0.4-0.9]), peak airway pressure (28.4 vs 17.3; p = 0.018, adjusted OR 1.6 [1.1-2.4]) and synchronised intermittent mandatory ventilation (SIMV) (60 vs 32; p = 0.041, adjusted OR 1.4 [0.78-2.04]). Of those who had IAH; age, amount of iv fluids over 24 h, fluid balance and ventilator mode were significant determinants of risk of progression to ACS . CONCLUSION: The prevalence of intraabdominal hypertension and abdominal compartment syndrome at KNH is high. Clinical parameters pertaining to fluids administration and ventilator mode are siginificant determinants.

Risk Factors for Extubation Failure in Extremely Low Birth Weight Infants.

BACKGROUND: Although antenatal steroids and early use nasal continuous positive airway pressure (NCPAP) have significantly improved outcomes of neonatal respiratory distress syndrome, intubation with ventilator support is still commonly required in extremely low birth weight (ELBW) infants. The optimal timing of extubation in ELBW infants remains unclear. METHODS: We retrospectively analyzed all ELBW preterm infants who were admitted to our neonatal intensive care unit (NICU) from January 2009 to December 2013. Demographic, ventilation, and arterial blood gas analysis results prior to and 2 hours after extubation were collected. Extubation failure was defined as reintubation due to deterioration of respiratory condition within 7 days after extubation. Risk factors for extubation failure were analyzed. RESULTS: In total, 173 ELBW infants were born and admitted to our NICU during these 5 years. Among these 173 infants, 77 (44.5%) used NCPAP only during their hospitalization (20 diagnosed with chronic lung disease (CLD), 25.9%). Among the 95 patients that required intubation, 27 patients expired so extubation was not attempted. Sixteen of 68 (23.5%) survival cases required reintubation within 7 days after extubation. We found that gestational age, birth body weight, and sex ratio did not differ between the successful extubation group and the failed extubation group. Univariate analysis showed that the failed extubation group had a lower arterial pH right before and 2 hours after extubation, with a lower bicarbonate level after extubation. Further multivariate logistic regression analysis revealed an association between poor acid-base homeostasis 2 hours after extubation (pH < 7.3 and HCO3 < 18 mM/L) and extubation failure (odds ratio 4.56 and 6.187 and 95% confidence interval: 1.263∼16.462 and 1.68∼22.791, respectively). CONCLUSION: This study shows that nearly half of ELBW infants do not require intubation. Among ELBW infants who require invasive ventilator support, those who have lower postextubation arterial pH and bicarbonate levels are at high risk of extubation failure.

Beyond bicarbonate: complete acid-base assessment in patients receiving intermittent hemodialysis.

Background: Acid-base assessments in hemodialysis patients have been limited almost entirely to measurements of total CO 2 concentration, and assumptions have been made about the presence of acid-base disorders. To gain a fuller understanding of the acid-base status of stable hemodialysis patients, we analyzed measurements of pCO 2 , pH and HCO 3 - obtained in a cohort of chronic stable hemodialysis patients over a 5-year period. Methods: We reviewed acid-base measurements taken pre-dialysis from fistula blood in 53 outpatients receiving hemodialysis thrice weekly between 2008 and 2012. In these patients, pH and pCO 2 were measured using an onsite blood gas analyzer, and HCO 3 - was computed. Relevant clinical and laboratory data were obtained from medical records. Factors affecting serum HCO 3 - were identified. Simple and mixed acid-base disorders were diagnosed using accepted rules. Results: Serum HCO 3 - was affected by age, normalized protein catabolic rate, interdialytic weight gain and length of interval between treatments. As expected, metabolic acidosis was the most common acid-base disorder, but respiratory acid-base disturbances, as simple or complex disorders, were found in 41% of the measurements. Respiratory alkalosis was seen more frequently than respiratory acidosis, but the latter disorder was more commonly associated with serious comorbidities. Conclusions: Respiratory acid-base disorders are an important component of the acid-base abnormalities seen in hemodialysis patients and are not identified by measuring total CO 2 concentration; hence, complete acid-base measurements are needed to determine the components of hemodialysis patients' acid-base status that are contributing to mortality risk.

Hyperchloremia is associated with 30-day mortality in major trauma patients: a retrospective observational study.

BACKGROUND: Chloride is important for maintaining acid-base balance, muscular activity, osmosis and immunomodulation. In patients with major trauma, chloride levels increase after fluid therapy; this is associated with poor clinical outcomes. The purpose of this study was to determine whether hyperchloremia was associated with increased mortality in patients who had sustained major trauma. METHODS: This study enrolled 266 major trauma patients by retrospective chart review, from January 2011 to December 2015. Patients were older than 16 years; were admitted to an intensive care unit; survived more than 48 h; and had sustained major trauma, defined as an injury severity score ≥ 16. Hyperchloremia was defined as a chloride level > 110mEq/L. Delta chloride (Δchloride) was defined as the difference between the serum chloride level measured 48-h post-admission and the initial level. Clinical and laboratory variables were compared between survivors (n = 235) and non-survivors (n = 31). A multivariate logistic regression analysis was performed to assess the association between hyperchloremia 48-h post-admission (hyperchloremia-48) and 30-day mortality. RESULTS: The overall 30-day mortality was 11.7 % (n = 31). Hyperchloremia-48 occurred in 65 patients (24.4 %) and the incidence was significantly different between survivors and non-survivors (19.6 vs. 61.3 %, respectively, p < 0.001). Multivariate logistic analysis identified hyperchloremia-48 and Δchloride as independent predictive factors for 30-day mortality in major trauma patients. DISCUSSION: Infusion of chloride-rich solutions, such as normal saline, is itself associated with hyperchloremia, which has been associated with poor patient outcomes. Patients receiving normal saline were more likely to suffer major postoperative complications, acute kidney injury, and infections. Moreover, large changes in serum chloride levels correlated with greater in-hospital mortality. CONCLUSION: Hyperchloremia 48-h post-admission and Δchloride was associated with 30-day mortality in major trauma patients. These indices may be useful prognostic markers.