Administration Of Bicarbonate Research Articles

Use of sodium bicarbonate and blood gas monitoring in diabetic ketoacidosis: A review.

Diabetic ketoacidosis (DKA) is a severe and too-common complication of uncontrolled diabetes mellitus. Acidosis is one of the fundamental disruptions stemming from the disease process, the complications of which are potentially lethal. Hydration and insulin administration have been the cornerstones of DKA therapy; however, adjunctive treatments such as the use of sodium bicarbonate and protocols that include serial monitoring with blood gas analysis have been much more controversial. There is substantial literature available regarding the use of exogenous sodium bicarbonate in mild to moderately severe acidosis; the bulk of the data argue against significant benefit in important clinical outcomes and suggest possible adverse effects with the use of bicarbonate. However, there is scant data to support or refute the role of bicarbonate therapy in very severe acidosis. Arterial blood gas (ABG) assessment is an element of some treatment protocols, including society guidelines, for DKA. We review the evidence supporting these recommendations. In addition, we review the data supporting some less cumbersome tests, including venous blood gas assessment and routine chemistries. It remains unclear that measurement of blood gas pH, via arterial or venous sampling, impacts management of the patient substantially enough to warrant the testing, especially if sodium bicarbonate administration is not being considered. There are special circumstances when serial ABG monitoring and/or sodium bicarbonate infusion are necessary, which we also review. Additional studies are needed to determine the utility of these interventions in patients with severe DKA and pH less than 7.0.

Positron Emission Tomography Imaging of Lesions pH Using 11C-Labeled Bicarbonate.

As acid-base imbalance is involved in many pathological processes, the capability to image tissue pH alterations in the clinic could offer new ways to detect disease and respond to treatment. In this study, the authors show that tissue pH can be imaged in vivo with 11C-labeled bicarbonate (H11CO3-) buffer and positron emission tomography (PET). H11CO3- was produced by on-column NaOH adsorption. Biodistribution of H11CO3- in normal mice was determined. In addition, uptake studies and inhibition experiments of H11CO3- in the S180 fibrosarcoma-bearing mice and the inflammatory mice were investigated with PET imaging. The tumor and inflammatory interstitial pH was measured by a needle pH microelectrode. PET imaging demonstrated the high uptake of H11CO3- in mice tumor tissues and inflammatory tissues, which showed that the average tumor or inflammatory interstitial pH was significantly lower than the surrounding tissue. Administration of sodium bicarbonate in the drinking water increased the measured tumor pH, while the uptake of H11CO3- in mice model tissues had no change. Similarly, administration with ammonium chloride (NH4Cl) decreased the pH, whereas the unchanged uptake of H11CO3- in mice model tissues was also found. However, after administration of acetazolamide, the low uptake of H11CO3- in mice model tissues was observed. H11CO3- solution is an endogenous bicarbonate buffer tracer that can be injected into patients without toxicity. H11CO3- PET can be used clinically to image pathological processes that are associated with acid-base imbalance, such as cancer and inflammation.

Abstract PCCLB-69: TRANSFUSION RELATED ACUTE HEPATIC INJURY (TRAHI) IN PEDIATRIC PATIENTS UNDERGOING THE FONTAN PROCEDURE

Aims & Objectives: The final common pathway of single ventricle patients is the Fontan procedure. One of the immediate postoperative complications is acute hepatic injury presented by marked elevation of liver enzymes (alanine transaminase (ALT) and aspartate transaminase (AST)). Aims: We aimed to determine the contribution of blood products transfusion to acute hepatic injury. Methods We retrospectively reviewed demographic, pre-, intra- and post-operative parameters including blood products transfusions and liver enzymes (Table 1). ALT and AST levels were transformed into log scale for the regression analysis. We used the Spearman correlation while adjusting for possible confounders. Propensity score was used in order to perform a stepwise weighted linear regression. Results 99 pediatric patients after the Fontan procedure were identified between 01/2009 and 12/2016. Out of the four types of blood products, transfusion of platelets was found to significantly impact post-operative levels of ALT and AST (Figure 1). Additional factors include post-operative administration of sodium bicarbonate, decreased flow through the Fontan canal and decreased urine output. Cardiopulmonary bypass time, aortic cross-clamp time, amount of post-operative bleeding and vasoactive-inotropic score did not influence liver enzymes levels (Table 2). Conclusions In pediatric patients undergoing the Fontan procedure, platelets transfusions significantly contribute to acute hepatic injury. The relation between platelets and transfusion related acute lung injury (TRALI) has been well described, but this is the first time it is being described in regards to acute hepatic injury (TRAHI). Changing platelet transfusion strategy could decrease morbidity in Fontan patients but further research is needed.

Radiocontrast agents: wrongfully accused?

Radiocontrast agents: wrongfully accused? Abstract. Since its first description over half a century ago, contrast-induced nephropathy has been considered as one of the most common causes of acute kidney injury and as a major preventable health problem. Newer data now suggest that the incidence of contrast-induced nephropathy has been clearly overestimated and that prophylactic measures, such as the administration of N-acetylcysteine, sodium bicarbonate or intravenous hydration are largely useless. Indeed, the fear of contrast-induced nephropathy has prompted withholding of clinically indicated imaging procedures and interventions in many patients or the installation of unnecessary and potentially harmful prophylactic measures. The awareness of contrast-induced nephropathy has thus likely caused more harm than benefit.

Severe lactic acidosis and hypoglycemia due to acute metformin intoxication in a dog

To report a case of severe lactic acidosis and hypoglycemia due to acute metformin intoxication in a dog. A female neutered Rat Terrier was presented for an acute onset of seizure-like episodes, weakness, and vomiting approximately 14 hours after ingestion of 198 mg/kg of metformin. The dog was found to be laterally recumbent, paddling, and unresponsive shortly before presentation. On physical exam, the dog was in hypovolemic shock and hypothermic. Blood work revealed severe lactic acidosis and hypoglycemia. The dog was volume resuscitated with intravenous crystalloids and dextrose, followed by a continuous infusion of intravenous fluids and dextrose, as well as administration of isotonic sodium bicarbonate. Repeat blood work showed minimal improvement of the hyperlactatemia for 3 hours despite resolution of hypovolemia and hypoglycemia followed by gradual improvement over the next 9 hours of hospitalization. High performance liquid chromatography/tandem mass spectrometry analysis showed markedly increased plasma metformin concentrations at 3.9 μg/mL. The dog was discharged from the hospital within 24 hours and showed no recurrence of clinical signs one year following discharge. Metformin-associated lactic acidosis and hypoglycemia is a severe complication in human patients, but has not been reported in veterinary medicine. Aggressive treatment with supportive care including IV fluids and dextrose administration resulted in resolution of the clinical signs in this patient. Metformin toxicosis should be considered in dogs with severe hyperlactatemia and hypoglycemia of unknown etiology.

Avoiding Patient Harm With Parenteral Nutrition During Electrolyte Shortages.

Purpose: We report a case of a patient with gastrointestinal dysmotility and substantial drainage losses who required parenteral nutrition (PN) and developed a non-anion gap metabolic acidosis secondary to a shortage of concurrent potassium acetate and sodium acetate PN additives. We describe how severe PN-associated metabolic consequences were averted during this acetate shortage. Summary: The patient with inability to swallow and significant weight loss was admitted to the hospital and given PN after failure to tolerate either gastric or jejunal feeding due to dysmotility and severe abdominal distension and discomfort. PN was initiated and the nasogastric and jejunal tubes were left to low intermittent suction or gravity drainage (average losses of 800 mL and 1600 mL daily, respectively) to reduce abdominal distension. The patient had been stable on PN for approximately 2 months prior to when a shortage in potassium acetate and sodium acetate occurred. As a result, potassium and sodium requirements had to be met with chloride and phosphate salts. The patient developed a non-anion gap metabolic acidosis after 11 days of acetate-free PN. Progression to severe acidemia was avoided by administration of sodium bicarbonate daily for 3 days and replacement of 0.9% sodium chloride supplemental intravenous fluid with lactated ringers solution. Conclusion: This case report illustrates that PN component shortages require clinicians to closely monitor patients who require PN. In addition, clinicians may need to use creative therapeutic strategies to avoid potential serious patient harm during PN component shortages.

Sodium bicarbonate on severe metabolic acidosis during prolonged cardiopulmonary resuscitation: a double-blind, randomized, placebo-controlled pilot study.

Sodium bicarbonate administration during cardiopulmonary resuscitation (CPR) is controversial. Current guidelines recommend sodium bicarbonate injection in patients with existing metabolic acidosis, but clinical trials, particularly, those involving patients with acidosis, are limited. We aimed to evaluate the efficacy of sodium bicarbonate administration in out-of-hospital cardiac arrest (OHCA) patients with severe metabolic acidosis during prolonged CPR. Prospective, double-blind, randomized placebo-controlled pilot trial was conducted between January 2015 and December 2015, at a single center emergency department (ED). After 10 minutes of CPR, patients who failed to achieve return of spontaneous circulation (ROSC) and with severe metabolic acidosis (pH<7.1 or bicarbonate <10 mEq/L) were enrolled. Sodium bicarbonate (n=25) or normal saline (n=25) were administered. The primary end point was sustained ROSC. The secondary end points were the change of acidosis and good neurologic survival. Sodium bicarbonate group had significant effect on pH (6.99 vs. 6.90, P=0.038) and bicarbonate levels (21.0 vs. 8.0 mEq/L, P=0.007). However, no significant differences showed between sodium bicarbonate and placebo groups in sustained ROSC (4.0% vs. 16.0%, P=0.349) or good neurologic survival at 1 month (0.0% vs. 4.0%, P=1.000). The use of sodium bicarbonate improved acid-base status, but did not improve the rate of ROSC and good neurologic survival. We could not draw a conclusion, but our pilot data could be used to design a larger trial to verify the efficacy of sodium bicarbonate. NCT02303548 (http://www.ClinicalTrials.gov).

The association of emergency department administration of sodium bicarbonate after out of hospital cardiac arrest with outcomes

BackgroundSodium bicarbonate administration is mostly restricted to in-hospital use in Taiwan. This study was conducted to investigate the effect of sodium bicarbonate on outcomes among patients with out-of-hospital cardiac arrest (OHCA). MethodsThis population-based study used a 16-year database to analyze the association between sodium bicarbonate administration for resuscitation in the emergency department (ED) and outcomes. All adult patients with OHCA were identified through diagnostic and procedure codes. The primary outcome was survival to hospital admission and secondary outcome was the rate of death within the first 30days of incidence of cardiac arrest. Cox proportional-hazards regression, logistic regression, and propensity analyses were conducted. ResultsAmong 5589 total OHCA patients, 15.1% (844) had survival to hospital admission. For all patients, a positive association was noted between sodium bicarbonate administration during resuscitation in the ED and survival to hospital admission (adjusted odds ratio [OR]: 4.47; 95% confidence interval [CI]: 3.82–5.22, p<0.001). In propensity-matched patients, a positive association was also noted (adjusted OR, 4.61; 95% CI: 3.90–5.46, p<0.001). ConclusionsAmong patients with OHCA in Taiwan, administration of sodium bicarbonate during ED resuscitation was significantly associated with an increased rate of survival to hospital admission.

CLINICAL PROFILE OF CHILDREN WITH DIABETIC KETOACIDOSIS AND RELATED CEREBRAL EDEMA IN A TERTIARY CARE HOSPITAL FROM SOUTHERN KERALA

Objective: To study the clinical profile of children admitted with diabetic ketoacidosis (DKA) in the pediatric intensive care unit (PICU) of a tertiary care teaching hospital. To assess the risk factors for the development of cerebral edema in children with DKA. Methods: This retrospective case review was conducted in the PICU of a tertiary care teaching hospital. Details of children admitted with DKA during the period from August 2012 to November 2017 were collected with respect to clinical features, lab parameters, management, and outcome. The characteristics of children with and without cerebral edema were compared. The data were then analyzed statistically using SPSS software. Results: Among the 51 cases analyzed 66.7% were females and 35.3% were newly detected cases. 51.5% of the previously diagnosed and 50% of the newly detected subjects had an infection as the precipitating event. Vomiting was the most common clinical presentation (64.7%). Mean time taken for acidosis correction was 22.65 h. 12 patients (23.53%) developed cerebral edema during the course of treatment. Neurologic deterioration developed at a median of 6 h (range 1.5–36 h) after the initiation of treatment. An increased incidence of cerebral edema was found in patients who received excess fluid boluses before starting insulin treatment (p=0.02) and newly detected cases (p=0.037). In those who developed cerebral edema the mean blood sugar value at admission was found to be significantly higher (p=0.013). No deaths or neurological sequelae were reported. Conclusions: Infections are an important precipitating factor for DKA. A significant proportion of children developed cerebral edema during treatment. New cases, excess intravenous fluid boluses, high mean blood sugar at admission, and bicarbonate administration were identified as risk factors for cerebral edema.

Acute kidney injury: Antioxidants do not PRESERVE kidney function after contrast exposure.

New data from the PRESERVE trial suggest that administration of N-acetylcysteine and/or sodium bicarbonate does not reduce the incidence of acute kidney injury in patients with chronic kidney disease undergoing angiography. Given the limitations of this study, use of these antioxidants should be considered discretionary until further data becomes available.

The effect of metabolic alkalosis on the ventilatory response in healthy subjects

BackgroundPatients with acute respiratory failure may develop respiratory acidosis. Metabolic compensation by bicarbonate production or retention results in posthypercapnic alkalosis with an increased arterial bicarbonate concentration. The hypothesis of this study was that elevated plasma bicarbonate levels decrease respiratory drive and minute ventilation. MethodsIn an intervention study in 10 healthy subjects the ventilatory response using a hypercapnic ventilatory response (HCVR) test was assessed, before and after administration of high dose sodium bicarbonate. Total dose of sodiumbicarbonate was 1000 ml 8.4% in 3 days. ResultsPlasma bicarbonate increased from 25.2 ± 2.2 to 29.2 ± 1.9 mmol/L. With increasing inspiratory CO2 pressure during the HCVR test, RR, Vt, Pdi, EAdi and VE increased. The clinical ratio ΔVE/ΔPetCO2 remained unchanged, but Pdi, EAdi and VE were significantly lower after bicarbonate administration for similar levels of inspired CO2. ConclusionThis study demonstrates that in healthy subjects metabolic alkalosis decreases the neural respiratory drive and minute ventilation, as a response to inspiratory CO2.

Propafenone Overdose-induced Arrhythmia and Subsequent Correction After Administration of Sodium Bicarbonate

Propafenone Overdose-induced Arrhythmia and Subsequent Correction After Administration of Sodium Bicarbonate

Protective Role of Pomegranate and Sodium bicarbonate on Acute Renal Failure Induced by Gentamicin In Rabbits Model

Acute renal failure ARF is common condition can be categorized as prerenal, intrinsic or postrenal causes in which the glomerular filtration rate decreases GFR over days to weeks . The aim of this study was to test whether the administration of pomegranate and sodium bicarbonate minimize the adverse health effect of acute renal failure. Methods : twenty female rabbits were assessed in to five groups ( n = 4 ) ,Group 1 : control group (C) .Group 2 : Gentamicin group ( G ): animals were injected with a single dose of Gentamicin ( 80 mg / Kg / bw ) intramuscular , daily for 10 days to induce renal failure. Group 3 : sodium bicarbonate group ( G+S ),animals were treated as in group 2 plus they received sodium bicarbonate ( 1 ml / Kg / bw ) of 8.4% by gavage daily for 10 days .Group 4 : pomegranate group ( G+P ),animals were treated as in group 2 plus they received pomegranate 500 ( mg / Kg / bw ) by gavage. Group 5 : combination group ( G+S+P ),animals were treated as in group 2 plus group 3 and group 4 for 10 days. Results : serum creatinine and blood urea levels were decreased in both groups (G+P) and (( G+S+P ) , p < 0.05 . while in group ( G+S ) they increased more effectively than the ( G) group .Serum electrolytes concentrations and serum ( pH ) shows different response , they were improved mostly in the ( G+S+P ) group, and they fluctuated in (G+S) group showing significant decreasing in serum ( Cl and Ca ) , p < 0.05 . Although the results for the hematological parameters were also improved in the combination group ( G+S+P ) but the differences were non significant between all others measured parameters and control group. Conclusions : the administration of sodium bicarbonate in Gentamicin model to induced acute renal failure inducement has adverse biological effects . but those effects were minimized by the ameliorative effects of the pomegranate administration which was helpful in speeding recovery

The effect of sodium bicarbonate and validation of beckman coulter AU680 analyzers for measuring total carbon dioxide (TCO2) concentrations in horse serum.

This study evaluated the usage of Beckman Coulter AU680 analyzers for measurement of TCO 2 in horse serum, and the effect of sodium bicarbonate administrations on serum TCO 2 levels in resting horses. Treatment of horses with sodium bicarbonate did not result in any adverse events. Mean TCO 2 concentration was significantly higher from 1 to 8 h in the sodium bicarbonate‐treated horses compared to the untreated controls. Within an hour, administration of sodium bicarbonate increased the TCO 2 level from 31.5 ± −2.5 (SD) to 34.0 ± 2.65 (SD) mmol/L and at 2–8 h post‐administration, the TCO 2 level was above the 36 mmol/L cut‐off level. In all quality control analysis of Australian standard by Beckman Coulter AU680 analyzer, the instrument slightly over estimated the TCO 2 level but the values were in close agreement with mean TCO 2 level being 38.03 with ± 0.87 mmol/L (SD). Expanded uncertainty was calculated using different levels of confidence interval. Based on 99.5% confidence interval using 0.805% expanded uncertainty using mean measured concentration of 38.05 mmol/L, it was estimated that any race samples TCO 2 level higher than 38.5 mmol/L will be indicative of sodium bicarbonate administration using Beckman Coulter AU680 analyzer in Louisiana.

Recommended oral sodium bicarbonate administration for urine alkalinization did not affect the concentration of mitomycin-C in non-muscle invasive bladder cancer patients.

ObjectiveSodium bicarbonate has been reported to maximize the efficacy of intravesical instillation of mitomycin-C (IVI-MMC) therapy by urine alkalinization in non-muscle-invasive bladder cancer (NMIBC). This study aimed to analyze the changes in MMC concentration according to urinary pH and evaluate the efficacy of sodium bicarbonate to maintain the concentration of active form of MMC during IVI-MMC.MethodsWe prospectively enrolled 26 patients with NMIBC after transurethral resection of bladder tumor. Patients with very high-risk and low-risk NMIBC were excluded. Urinary creatinine, volume, pH, and concentrations of MMC and its degraded form were measured immediately before and after IVI-MMC. The patients were administered 1.5 g of oral sodium bicarbonate during the preceding evening, in the morning, and immediately before the fourth cycle of the six-cycle IVI-MMC. The correlation between MMC concentration and urinary pH changes was explored with or without oral bicarbonate therapy.ResultsRecurrence without progression to muscle-invasive disease was noted in 4 of 26 patients in a 23.7-month follow-up. The mean urinary pH before and after the therapy increased from 6.03 to 6.50, and 6.46 to 7.24, without or with oral SB therapy, respectively. Despite this increase, the concentration of active form of MMC did not change significantly. No correlation was found between urinary pH and MMC concentration. Urine alkalinization by SB administration did not maintain the high concentration of urinary MMC.ConclusionsUrine alkalinization by sodium bicarbonate administration for IVI-MMC did not maintain the high concentration of active urinary MMC in NMIBC.

Ketones and Contention: Bicarbonate Therapy and Clinical Outcomes in Severe Diabetic Ketoacidosis

SESSION TITLE: Top Posters - Electronic session SESSION TYPE: Original Investigation Poster PRESENTED ON: Monday, October 30, 2017 at 12:00 PM - 01:30 PM PURPOSE: The current recommendations of preeminent endocrinologic societies in the United States and Europe advocate the use of bicarbonate therapy in patients with severe diabetic ketoacidosis (DKA). However, the use of bicarbonate therapy in severe DKA remains controversial, as evidence on meaningful clinical outcomes is lacking. The aim of this study was to investigate the benefits of bicarbonate therapy on clinically relevant adverse outcomes. We also examined other potential secondary benefits, such as rapidity of anion gap closure, and effects on ICU, and hospital length of stay. METHODS: We conducted a retrospective cohort study of patients with severe DKA admitted to the Intensive Care Unit utilizing the Medical Information Mart for Intensive Care III (MIMIC-III) database. Severe DKA was defined as a pH on hospital presentation of <7.0, and/or a serum bicarbonate <10mEq/L, with evidence of ketosis and hyperglycemia. The effect of bicarbonate administration on a composite endpoint of meaningful clinical outcomes including death, respiratory failure, shock, cardiac complications, renal failure requiring renal replacement therapy, as well as stroke and cerebral edema, was assessed. We also studied potential benefits of bicarbonate therapy on the time to anion gap closure, as well as ICU, and hospital length of stay (LOS). RESULTS: A total of 154 out of a possible 878 patients met study criteria for severe DKA. Of those patients, 30 received bicarbonate therapy as part of management for their disease, while 124 did not receive the intervention. The baseline characteristics of the two groups were comparable, barring differences in age, and Simplified Acute Physiology (SAPS-II) score, which were higher among the group receiving bicarbonate. On univariate analysis, there was no difference in the occurrence of composite outcome 16.67% vs 13.71% [OR 1.28, CI (0.39-3.54) P=0.69], nor a reduction in time to anion gap closure [Mean 42 hrs vs. 36 hours (p=0.6)] in those patients receiving bicarbonate, versus those that did not, respectively. Interestingly, an increased ICU [ mean 4.7 vs. 2.8 days (P 0.04)], and hospital LOS, [mean 8.6 vs. 5.3 days (P 0.007)] was noted. After adjusting for SAPS-II score and age, there was still no significant difference in composite outcome between the two groups with adjusted OR of 2.922 [ 95%CI (0.80-13.29) P 0.107] for reaching the composite outcome. CONCLUSIONS: Bicarbonate therapy in patients with severe DKA did not result in any statistically significant differences in the occurrence of composite clinical outcome, nor an improvement in time to DKA resolution. However, such intervention was associated with a longer ICU and hospital LOS. This finding may potentially be related to the severity of illness in patients who received bicarbonate therapy. CLINICAL IMPLICATIONS: While current recommendations advocate the administration of bicarbonate therapy in patients with severe DKA, there is no evidence to suggest an improvement in clinical outcomes, and may unnecessarily prolong ICU and hospital length of stay. DISCLOSURE: The following authors have nothing to disclose: Alexander Morales, Mohammed Aboelsoud, Faeq Kukhon, Mahmoud Mowafy, Muhammad Ehtisham, Venu Velagapudi, Mazen Al-Qadi No Product/Research Disclosure Information

PRENATAL DIAGNOSIS IMPROVES THE PERIOPERATIVE CONDITION OF NEONATES REQUIRING SURGICAL INTERVENTION FOR COARCTATION BUT IS ASSOCIATED WITH LONGER PREOPERATIVE STAY

Neonates with critical coarctation of the aorta (CoA) may present in extremis if unrecognized. Prenatal diagnosis permits more appropriate early management of affected neonates. We sought to determine whether, as a consequence, prenatal diagnosis improves the preoperative condition and operative course associated with critical CoA (surgery at < 30 days). We hypothesized that prenatal diagnosis of CoA would be associated with both improved preoperative condition and shorter hospital stay than postnatal diagnosis. We retrospectively compared the clinical presentation, preoperative condition and operative course of neonates prenatally (Group 1, G1) or only postnatally (Group 2, G2) diagnosed in Alberta from 2004 to 2015 with critical CoA. Cases with other left heart obstructive lesions and ventricular septal defects were included, but those with more complex heart disease were excluded. Preoperative data analysed included highest lactate and lowest arterial pH, highest creatinine and urea, the level of support required (use of inotropes, bicarbonate, oxygen, respiratory support), and pre and postoperative length of hospital stay (LOS). In total, 110 cases were included: G1-44 and G2-66. Age at surgery differed between groups (G1: median 7[1-30days] vs G2: 10 [1-30days] p = 0.05). Preoperatively, G2 had a greater incidence of metabolic acidosis with a pH < 7.29 in 5.1% vs 31% (p=0.002) and highest lactate >3.5 mmol/Lin 5.3% vs 25.5% (p=0.009) in G1 vs G2, respectively), and need for support including supplemental oxygen (24% vs 48%, G1 vs G2, respectively, p=0.028), and bicarbonate administration (0% vs 5%, G1 vs G2, p=0.001). A need for preoperative ventilation (43% vs 55%, G1 vs G2, respectively) and preop inotrope use (25.7% vs 38%) did not differ between groups. Total LOS was significantly longer in G1 patients (median 19.5 [5-72 days] vs G2 12.5 [4-58days] p=0.024) which was due to longer preoperative LOS (median 7 [1-22 days] vs 3 [0-25 days], G1 vs G2, respectively p < 0.001), as postoperative LOS did not differ. Prenatal diagnosis of critical CoA is associated with improved preoperative condition with reduced metabolic acidosis and the need for support; however, it is also associated with longer preoperative hospitalization. The factors responsible for lengthier preoperative stay among prenatally diagnosed cases are currently being explored to determine modifiable factors.

321 A Step Towards Nil Mortality in Organophosphorus Compound Poisoning: Development of an Algorithm

Tamilnadu, an agriculture-based state in India, suffered severe drought during 2014 to 2016 when the number of suicides increased among farmers. Organophosphorus compound (OPC) poisoning is a common method of committing suicide among farmers since it is easily available as pesticides. Mortality rate in OPC poisoning in India is 15%. To propose an algorithm for timely interventions in managing OPC poisoning patients that may help the physician in decisionmaking and decreasing mortality. Retrospective chart review of OPC poisoning patients between August 7, 2014 and August 6, 2016. All OPC poisoning patients above 18 years of age who were previously healthy are included. Patients who were pregnant, refusing to consent, exposed to other toxins, hospitalized elsewhere prior to ED arrival, or underwent cardiac arrest were excluded. Mortality is the main outcome measured. 108 patients were included in the study out of which 9 patients were clinically stable and did not require any intervention. 86 patients needed inotrope/vasopressor support, 91 patients had dyselectrolytemia. 59 patients required administration of sodium bicarbonate. 87 patients were intubated in the ED. 12 patients were intubated in the ICU. Minimum duration endotracheal tube required was 5 days and maximum intubated days was 8. On the ninth day, intubated patients were either extubated (26 patients) or tracheomised (73 patients). Reintubation rate was nil. 12 patients had intermittent syndrome. 28 patients had seizure, 9 patients developed signs of myocardial suppression and 4 developed ARDS. Minimum duration of hospital stay is 5 days and maximum was 38 days. Minimum duration of ICU stay was 3 days and maximum was 31 days. All 108 patients were safely discharged home and mortality was nil. This study shows resuscitation and stabilization, timely interventions like early administration of antidote, shock management, intubation and appropriate ventilator settings and proper ICU and nursing care altogether may nullify mortality resulting from organophosphorus compounds poisoning.Tabled 1INTERVENTIONINDICATIONSurface decontamination, Gastric lavage and activated charcoalAll organophosphorus compound poisoning patientsAtropineDUMBBELLSNeed for mechanical ventilationIntubation and mechanical ventilationBronchorrheaSpo2 < 94% with oxygen face maskRespiratory muscles weaknessShock refractory to fluidsGCS < 9SeizureIntermediate syndromeElectrolyte correctionDyselectrolytemia including Ca++, Mg++, K+Inotropes / vasopressorsShock refractory to fluidsCentral venous accessMultiple infusions, prolonged stayArterial accessInvasive BP monitoring, blood gasesSodium bicarbonateMetabolic acidosis with pH < 7.10AntiepilepticsSeizureTracheostomyProlonged mechanical ventilationGlucose – insulin – potassiumSigns of myocardial injury likePersistent bradycardia (refractory to atropine and dopamine)Hypotension refractory to inotropes and vasopressorsST segment changesDecrease in ejection fractionGlobal hypokinesiaGlycemic control140 - 180 mg/dl maintainedTemperature controlNormothermia maintained Open table in a new tab

Effect of sodium bicarbonate on prolonged running performance: A randomized, double-blind, cross-over study.

BackgroundThe ability to sustain intense exercise seems to be partially limited by the body’s capability to counteract decreases in both intra- and extracellular pH. While the influence of an enhanced buffering capacity via sodium bicarbonate (BICA) on short-term, high-intensity exercise performance has been repeatedly investigated, studies on prolonged endurance performances are comparatively rare, especially for running. The aim of the following study was to assess the ergogenic effects of an oral BICA substitution upon exhaustive intensive endurance running performance.MethodIn a double-blind randomized cross-over study, 18 trained runners (VO2peak: 61.2 ± 6.4 ml•min-1•kg-1) performed two exhaustive graded exercise tests and two constant load tests (30 main at 95% individual anaerobic threshold (IAT) followed by 110% IAT until exhaustion) after ingestion of either sodium bicarbonate (BICA) (0.3 g/kg) or placebo (4 g NaCl) diluted in 700 ml of water. Time to exhaustion (TTE) in the constant load test was defined as the main outcome measure. Throughout each test respiratory gas exchange measurements were conducted as well as determinations of heart rate, blood gases and blood lactate concentration.ResultsTTE in the constant load test did not differ significantly between BICA and placebo conditions (BICA: 39.6 ± 5.6 min, placebo: 39.3 ± 5.6 min; p = 0.78). While pH in the placebo test dropped to a slightly acidotic value two minutes after cessation of exercise (7.34 ± 0.05) the value in the BICA trial remained within the normal range (7.41 ± 0.06) (p < 0.001). In contrast, maximum running speed (Vmax) in the exhaustive graded exercise test was significantly higher with BICA (17.4 ± 1.0 km/h) compared to placebo (17.1 ± 1.0 km/h) (p = 0.009). The numerical difference in maximum oxygen consumption (VO2peak) failed to reach statistical significance (BICA: 61.2 ± 6.4 ml•min-1•kg-1, placebo: 59.8 ± 6.4 ml•min-1•kg-1; p = 0.31). Maximum blood lactate was significantly higher with BICA compared to the corresponding placebo test (BICA: 11.1 ± 2.3 mmol/l, placebo: 8.9 ± 3.0 mmol/l; p < 0.001). At the end of exercise, an acidotic pH value was found in both exhaustive graded exercise tests (p = 0.002). BICA caused gastrointestinal side effects in 15 patients.ConclusionMaximal performance was enhanced significantly after BICA administration. The ergogenic effect of BICA in the exhaustive graded exercise test can most likely be attributed to an increased anaerobic glycolysis that is reflected by an accumulation of lactate. However, TTE in prolonged high-intensity running was not improved. Even at the end of exercise no severe metabolic acidosis was found. Metabolic acidification as one of the dominant factors causing muscular fatigue should therefore be reconsidered.Trial registrationGerman Clinical Trials Register (DRKS) DRKS00011284.

The effect of extracellular alkalinization on lactate metabolism of breast cancer stem cells: Overview of LDH-A, LDH-B, MCT1 and MCT4 gene expression

Changes in the metabolic status of cancer cells are presumed to be correlated with the adjustment of these cells to extracellular changes. Cell glycolysis increases the production of intracellular lactate catalyzed by the lactate dehydrogenases, both LDH-A and LDH-B. An increase in intracellular lactate can affect extracellular pH balance through monocarboxylate transporters, particularly MCT1 and MCT4. This study aimed to analyze the effects of extracellular alkalinization on the lactate metabolism of human breast cancer stem cells (BCSCs). In this study, human primary BCSCs (CD24-/CD44+ cells) were treated with 100 mM sodium bicarbonate for 0.5, 24, and 48 h in DMEM F12/HEPES. After incubation, extracellular pH was measured and cells were harvested to extract the total RNA and protein. The expression of LDH-A, LDH-B, MCT1, and MCT4 mRNA genes were analyzed using qRT-PCR method. Our study shows that administration of sodium bicarbonate in the BCSC culture medium could increase extracellular pH. To balance the increase of extracellular pH, BCSCs regulated the expression of LDH-A, LDH-B, MCT1, and MCT4 genes. As the extracellular pH increases, the expression of LDH-A that converts pyruvate to lactate increased along with the increase of MCT 4 and MCT 1 expression, which act as lactate transporters. As the incubation time increases, the pH decreases, leading to the suppression of LDH-A and increase of LDH-B expression that converts lactate into pyruvate. Therefore, we suggest that the extracellular alkalinization by sodium bicarbonate in BCSCs affected the genes that regulate lactate metabolism.