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Diabetic ketoacidosis (DKA) is an acute, life-threatening metabolic complication of diabetes classically associated with hyperglycemia, metabolic acidosis, and ketosis. Though relatively uncommon, patients can also develop DKA with relative euglycemia, further complicating diagnosis. Here, we describe the case of a patient who presented with intractable vomiting secondary to diabetic gastroparesis. He was euglycemic, non-acidemic, and serum bicarbonate was within normal limits. However, labs were significant for ketonuria, an elevated anion gap, and an elevated beta-hydroxybutyrate. Given the high concern for euglycemic DKA in the setting of a competing primary metabolic alkalosis, he was transferred to the intensive care unit for intravenous insulin infusion and fluid resuscitation with significant clinical improvement and normalization of laboratory results. This serves as an important reminder that DKA can be masked by euglycemia as well as additional metabolic derangements, and should be suspected in any diabetic patient with an anion gap and/or ketosis.

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Cystinosis is a rare, genetically inherited disease that affects lysosomal storage of cysteine. It is the most common cause of Fanconi syndrome. Mutations have led to early-onset end-stage renal disease as well as other systemic organ failures. In this case, we report a 19-month-old female child who presented acutely to the outpatient clinic with nausea, vomiting, and diarrhea. The patient was previously diagnosed with unspecified renal tubular acidosis and treated with oral electrolytes. Early labs during her acute presentation showed severe hypokalemia and electrolyte imbalance, which necessitated a transfer to a pediatric ICU. Through confirmatory testing, a diagnosis of cystinosis was made. This case is an example of the recognition and treatment of a rare inherited disease.

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INTRODUCTION: Due to a COVID-related job loss resulting in financial and food insecurity, a 28-year-old woman initiated a diet consisting solely of one cup of ramen noodles daily for twenty-two months, leading to 27 kg of weight loss. Ramen noodles are low in calories and lack key nutrients, including potassium, chloride, and vitamin B12. CASE DESCRIPTION: The patient presented to the emergency department with acute, worsening weakness and paresthesias in her left wrist and hand. Exam revealed no other abnormalities aside from a cachectic appearance. Labs revealed marked hypokalemia, hypochloremia, lactic acidosis, a mixed metabolic alkalosis with respiratory acidosis, and low levels of zinc and copper. An EKG revealed a prolonged QT interval. After a neurology and psychiatry consult, the patient was admitted for failure to thrive with malnutrition, peripheral neuropathy, hypokalemia, and an acid-base disorder. An MRI of the brain was unremarkable. Studies of other nutritional deficiencies, autoimmune conditions, and sexually transmitted infections were unremarkable. The patient received food and vitamin supplementation, was monitored for re-feeding syndrome, and had a significant recovery. DISCUSSION: After stroke, spinal injury, multiple sclerosis, and the most common focal mononeuropathies were ruled out, the clinical focus turned to nutritional deficiencies, the most significant of which was hypokalemia. Prior research has shown that severe hypokalemia can lead to weakness. It has also shown that chronically insufficient dietary intake is a common cause of hypokalemia. This case, with its partial paralysis of a unilateral upper extremity, may add to the known clinical manifestations of hypokalemia. We review the role of hypokalemia and hypochloremia in acid-base dynamics. Etiologies and clinical manifestations of cobalamin, thiamine, pyridoxine, and copper deficiencies, along with lead toxicity, are also discussed. Diagnostic clarity of mononeuropathies in the context of malnutrition and hypokalemia can be aided by urine potassium levels prior to repletion, neuroimaging that includes the cervical spine, and follow-up electromyography.

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BACKGROUND: Stewart's approach is known to have better diagnostic accuracy for the identification of metabolic acid-base disturbances compared to traditional methods based either on plasma bicarbonate concentration ([HCO3-]) and anion gap (AG) or on base excess/deficit (BE). This study aimed to identify metabolic acid-base disorders using either Stewart's or traditional approaches in critically ill COVID-19 patients admitted to the ICU, to recognize potential hidden acid-base metabolic abnormalities and to assess the prognostic value of these abnormalities for patient outcome. METHODS: This was a single-center retrospective study, in which we collected data from patients with severe COVID-19 admitted to the ICU. Electronical files were used to retrieve data for arterial blood gases, serum electrolytes, and proteins and to derive [HCO3-], BE, anion gap (AG), AG adjusted for albumin (AGadj), strong ion difference, strong ion gap (SIG), and SIG corrected for water excess/deficit (SIGcorr). The acid-base status was evaluated in each patient using the BE, [HCO3-], and physicochemical approaches. RESULTS: We included 185 patients. The physicochemical approach detected more individuals with metabolic acid-base abnormalities than the BE and [HCO3-] approaches (p < 0.001), and at least one acid-base disorder was recognized in most patients. According to the physicochemical method, 170/185 patients (91.4%) had at least one disorder, as opposed to the number of patients identified using the BE 90/186 (48%) and HCO3 62/186 (33%) methods. Regarding the derived acid-base status variables, non-survivors had greater AGadj, (p = 0.013) and SIGcorr (p = 0.035) compared to survivors. CONCLUSIONS: The identification of hidden acid-base disturbances may provide a detailed understanding of the underlying conditions in patients and of the possible pathophysiological mechanisms implicated. The association of these acid-base abnormalities with mortality provides the opportunity to recognize patients at increased risk of death and support them accordingly.

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OBJECTIVE: This study aims to assess the impact of different subtypes of extreme acidosis on the mortality of critically ill patients. METHODS: This retrospective cohort study included critically ill patients who were admitted to the intensive care unit (ICU) with a pH level <7. Clinical data and blood gas analyses were collected from electronic medical records. The primary outcome was in-hospital mortality. The use of vasopressors, mechanical ventilation (MV), and renal replacement therapy (RRT), the duration of MV and RRT, and the length of ICU and hospital stay were secondary outcomes. The simplified Stewart approach to acid-base disorders was used to analyze the causes of acidosis. RESULTS: A total of 231 patients with 371 arterial blood gas analyses with pH < 7 were admitted from January 2012 to December 2021 and 222 were included in the study. Out of the 222 patients analyzed, respiratory acidosis was the primary disorder in 11.3% of patients (n = 25), metabolic acidosis in 33.8% (n = 75), and mixed acidosis in 55% (n = 122). Overall mortality was 42.8% (n = 95). No significant difference was observed in mortality among patients with respiratory, metabolic, or mixed acidosis (28%, 42.7%, and 45.9%, respectively; p = 0.26). The primary disorder affected the use of vasopressors and MV, the duration of MV, and the length of ICU and hospital stay. Patients with extreme acidosis due to unmeasured anions with lactate levels of 4 mmol/L or higher had higher mortality compared with patients with lactate levels <4 mmol/L (55.6% and 27.7%, respectively; p = 0.007). CONCLUSION: Among critically ill patients with extreme acidosis, the primary disorder is not associated with mortality, but it is associated with the use of vasopressors and MV, the duration of MV, and the length of ICU and hospital stay. Additionally, hyperlactatemia is a predictor of poor prognosis in patients with extreme acidosis.

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The light-scattering effect of hypertriglyceridemia may interfere with the photometric analysis of the electrolytes, leading to errors in laboratory values. We present a case of erroneously low bicarbonate levels due to the presence of severe hypertriglyceridemia. A 49-year-old male was admitted for knee cellulitis. A comprehensive metabolic panel showed very low bicarbonate of <5 mmol/L, and an elevated anion gap of 26 mmol/L. The lactic acid, salicylic acid, ethanol, and methanol levels were normal. The lipid panel showed a remarkably high triglyceride level of 4846 mg/dL. An arterial blood gas (ABG) showed a normal pH of 7.39 and a bicarbonate level of 28 mmol/L, which was inconsistent with the metabolic acidosis seen in the blood test. The discrepancy between acidosis seen in the metabolic panel and ABG was explained by a lab error in the measured bicarbonate levels, which occurs in the presence of elevated triglyceride levels. Most laboratories use either an enzymatic/ photometric or an indirect ion-selective electrode method to measure bicarbonate. Hyperlipidemia interferes with photometric analysis due to its light-scattering effect. An ABG analyzer uses a direct ion-selective electrode method that is free of the errors of a photometric analyzer. Knowing about conditions like hypertriglyceridemia, which can interfere with the measurement of electrolytes, is important in everyday clinical medicine, as it can prevent unnecessary investigation and intervention.

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BACKGROUND: Studies comparing venous total carbon dioxide (tCO2) and standard hydrogen carbonate (HCO3-(P,st)) has shown diverse results, and it is debatable whether these two parameters can be used interchangeably for workup of acid-base disorders in a hospital setting. METHOD: All patients with an HCO3-(P,st) requisition from any department at Odense University Hospital between 11th May 2021 and 1st June 2021 had tCO2 and HCO3-(P,st) analysed simultaneously. TCO2 was measured on Cobas® 8000, c702 module, while HCO3-(P,st) was calculated based on measurements on ABL835 Flex. RESULTS: From 1210 patients, mean (standard deviation (SD)) was 22.9 (3.7) mmol/L for tCO2 and 22.5 (2.9) mmol/L for HCO3-(P,st). TCO2 range was 10.1-42.3 mmol/L and 11.7-41.4 mmol/L for HCO3-(P,st). Linear regression showed that tCO2 (mmol/L) = -2.90 + 1.15 × HCO3-(P,st) (mmol/L) with R2 = 0.81. Bias (mean (SD) difference) between tCO2 and HCO3-(P,st)) was 0.4 (1.7) mmol/L with a -5.0-9.6 mmol/L range. Limits of agreement was -2.90-3.70 mmol/L. Comparison of classification within, above or below reference interval for tCO2 and HCO3-(P,st) showed that 984 samples (81%) retained their classification. Only one sample (0.1%) would be severely misclassified (outside the respective reference intervals) if HCO3-(P,st) was considered the gold standard. Of the samples investigated, 46.1% had a mean difference between tCO2 and HCO3-(P,st) of 0-1 mmol/L and 30.3% had 1.1-2.0 mmol/L. CONCLUSIONS: Our results indicate that venous tCO2 and venous HCO3-(P,st) can be used interchangeably in a hospital setting for workup of acid-base disorders.

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Introduction: acid-base disorders are very common in critically ill patients and contribute significantly to morbidity and mortality. The aim of this study was to identify the types of acid-base disorders at the time of admission to the intensive care unit (ICU) and its associated ICU and in-hospital mortality. Methods: we conducted a retrospective cohort study of all adult patients that were admitted to the ICU and had an arterial blood gas sample at the time of admission from 1st January 2019 to 31 December 2019. Using the traditional approach, acid-base disorders were categorised into six disorders. Variables predicting in-hospital death were identified using logistic regression. Results: a total of 375 patients were included. The median age for the entire cohort was 39 (IQR 30-52) years and 48.3% (n=181) were female. Mixed acid-base disorders were the most common at 48.8% (n=183), followed by no disorder at 24.8% (n=93), metabolic acidosis at 9.3% (n=35), metabolic alkalosis at 6.7% (n=25), respiratory acidosis 6.1% (n=23) and respiratory alkalosis at 4.3% (n=16). A total of 94 (25.0%) patients died. There were no differences in ICU (p = 0.35) or in-hospital death (p = 0.32) by acid-base disorder. Male sex (aOR: 5.8, 95% CI 1.55-21.42; p < 0.01), APACHE II score (aOR: 1.17, 95% CI 1.06-1.30; p < 0.01) and the corrected anion gap (aOR: 1.14, 95% CI 1.02-1.27; p = 0.02) were identified as predictors of in-hospital death using multivariable logistic regression. Conclusion: there was no association between acid-base disorders at the time of ICU admission and ICU or in-hospital death. Therefore, in our setting, acid-base disorders at the time of ICU admission should not be used to predict the outcome of patients requiring intensive care.

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Metabolic acidosis is a common complication among acutely unwell hospitalised patients. Untreated, it can result in undesirable cardiovascular, respiratory and neurological consequences. Metabolic acidosis can occur as an isolated entity or coexist with other acid-base disorders, making diagnosing the aetiology difficult. Accurate identification of the underlying cause is imperative for proper and timely management. A systematic approach can help simplify the assessment of patients and can aid in establishing the correct diagnosis, even in more complex cases. This article provides a practical, step-by-step guide for the assessment of adult patients with metabolic acidosis.

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Acid-base disturbances in patients with cardiopulmonary or other disorders are common and are often misinterpreted or interpreted incompletely. Treating acid-base disorders in greater detail facilitates pathophysiologic understanding and improved therapeutic planning. Understanding the ratiometric relationship between the lungs, which excrete volatile acid as carbon dioxide, and the kidneys, which contribute to maintenance of plasma bicarbonate, allows precise identification of the dominant acid-base disturbance when more than a simple disorder is present and aids in executing a measured treatment response. Concordantly, mapping paired values of the partial pressure of carbon dioxide (PCO2) and the bicarbonate concentration ([HCO3 -]) on a Cartesian coordinate system visually defines an acid-base disorder and validates the ratiometric methodology. We review and demonstrate the algebraic and logarithmic methods of arterial blood gas analysis through the example of a complex acid-base disorder, emphasizing examination of the PCO2-to-[HCO3 -] ratio.

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Objective: Acetate- and lactate-containing fluids influence the acid-base and electrolyte status. This prospective, randomized, clinical study compared two balanced crystalloid solutions regarding their influence on acid-base status, electrolytes, and lactate values, when given to dogs as a resuscitation bolus of 30 mL/kg. Material and methods: One hundred client-owned dogs presenting to the emergency service with signs of fluid deficits were randomly assigned to receive an intravenous bolus of 30 mL/kg of either a lactate- (LAC), or an acetate-containing solution (ACET). Before and after the bolus, vital parameters were assessed, and a venous blood gas analysis was performed. Results: Both solutions performed equally well in decreasing the heart rate (ACET: -10 ± 27 bpm, LAC: -12 ± 30 bpm; p = 0.737). The acetate-containing solution caused a significant decrease in plasma lactate levels (p = 0.016), anion gap (p < 0.001), and potassium (p < 0.001), and a significant increase in chloride (p < 0.001), and ionized calcium (p = 0.014). The lactate-containing solution caused a significant decrease in anion gap (p < 0.001), sodium (p = 0.016), and potassium (p = 0.001), and a significant increase in chloride (p < 0.001). ACET causes a stronger decrease in plasma lactate (p = 0.015), sodium (p = 0.039), potassium (p = 0.006), and an increase in chloride (p < 0.001), and ionized calcium (p = 0.016) compared to LAC. Conclusion: Both solutions caused mild changes in electrolyte concentrations and had minor influence on acid-base status when used for bolus therapy in dogs with fluid deficits. Further studies are needed to evaluate their influence on acid-base status, lactate, and electrolytes when used in larger volumes and for a longer time span.

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Rational treatment and thorough diagnostic classification of acid-base disorders requires quantitative understanding of the mechanisms that generate and dissipate loads of acid and base. A natural precondition for this tallying is the ability to quantify the acid content in any specified fluid. Physical chemistry defines the pH-dependent charge on any buffer species, and also on strong ions on which, by definition, the charge is pH-invariant. Based, then, on the requirement of electroneutrality and conservation of mass, it was shown in 1914 that pH can be calculated and understood on the basis of the chemical composition of any fluid. Herein we first show that this specification for [H+] of the charge-balance model directly delivers the pH-dependent buffer-capacity as defined in the literature. Next, we show how the notion of acid transport as proposed in experimental physiology can be understood as a change in strong ion difference, ΔSID. Finally, based on Brønsted-Lowry theory we demonstrate that by defining the acid content as titratable acidity, this is equal to SIDref - SID, where SIDref is SID at pH 7.4. Thereby, any chemical situation is represented as a curve in a novel diagram with titratable acidity = SIDref - SID as a function of pH. For any specification of buffer chemistry, therefore, the change in acid content in the fluid is path invariant. Since constituents of SID and titratable acidity are additive, we thereby, based on first principles, have defined a new framework for modeling acid balance across a cell, a whole organ, or the whole-body.

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Our aim was to investigate the distribution of acid-base disorders in patients with COVID-19 ARDS using both the Henderson-Hasselbalch and Stewart's approach and to explore if hypoxemia can influence acid-base disorders. COVID-19 ARDS patients, within the first 48 h of the need for a non-invasive respiratory support, were retrospectively enrolled. Respiratory support was provided by helmet continuous positive airway pressure (CPAP) or by non-invasive ventilation. One hundred and four patients were enrolled, 84% treated with CPAP and 16% with non-invasive ventilation. Using the Henderson-Hasselbalch approach, 40% and 32% of patients presented respiratory and metabolic alkalosis, respectively; 13% did not present acid-base disorders. Using Stewart's approach, 43% and 33% had a respiratory and metabolic alkalosis, respectively; 12% of patients had a mixed disorder characterized by normal pH with a lower SID. The severe hypoxemic and moderate hypoxemic group presented similar frequencies of respiratory and metabolic alkalosis. The most frequent acid-base disorders were respiratory and metabolic alkalosis using both the Henderson-Hasselbalch and Stewart's approach. Stewart's approach detected mixed disorders with a normal pH probably generated by the combined effect of strong ions and weak acids. The impairment of oxygenation did not affect acid-base disorders.

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This study aimed to describe the inflammation, hydro-electrolyte and acid-base imbalances caused by generalised peritonitis (GP) and parietal fibrinous peritonitis (PFP) after caesarean section. After clinical examination, blood was sampled from 11 cows with PFP, 30 with GP and 14 healthy cows. Serum and plasma refractometry and glutaraldehyde tests were used to evaluate the inflammation level, while hydro-electrolytes and acid-base parameters were assessed using an EPOC® device. In addition to clinical signs of dehydration (>10%), blood analysis showed a high fibrinogen concentration (PFP: 8.64 ± 8.82 g/L; GP: 7.83 ± 2.45 g/L) and fast glutaraldehyde coagulation (<3 min) indicative of severe inflammation in both diseases compared to the control group (p < 0.05). Moreover, a severe decrease in electrolytes concentration (Na+: 126.93 ± 5.79 mmol/L; K+: 3.7 ± 1.3 mmol/L; Ca++: 0.89 ± 0.12 mmol/L; Cl−: 82.38 ± 6.45 mmol/L) and a significant increase in bicarbonate (30.87 ± 8.16 mmol/L), base excess (5.71 ± 7.42 mmol/l), L-lactate (8.1 ± 4.85 mmol/L) and creatinine (3.53 ± 2.30 mg/dL) were observed in cows with GP compared to the control group (p < 0.05). In contrast, few major perturbations were noticed in PFP, where only K+ (3.64 ± 0.25 mmol/L) and Ca++ (1.06 ± 0.09 mmol/L) were significantly modified (p < 0.05). In conclusion, a high dehydration and severe inflammation are induced by PFP and GP. Nevertheless, GP causes more electrolytes and acid-base disturbances than PFP.

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The hypokalemic response to alkali infusion has been attributed to the resulting extracellular fluid (ECF) expansion, urinary potassium excretion, and internal potassium shifts, but the dominant mechanism remains uncertain. Hypertonic NaHCO3 infusion (1 N, 5 mmol/kg) to unanesthetized dogs with normal acid-base status or one of the four chronic acid-base disorders decreased plasma potassium concentration ([K+]p) at 30 min in all study groups (Δ[K+]p, - 0.16 to - 0.73 mmol/L), which remained essentially unaltered up to 90-min postinfusion. ECF expansion accounted for only a small fraction of the decrease in ECF potassium content, (K+)e. Urinary potassium losses were large in normals and chronic respiratory acid-base disorders, limited in chronic metabolic alkalosis, and minimal in chronic metabolic acidosis, yet, ongoing kaliuresis did not impact the stability of [K+]p. All five groups experienced a reduction in (K+)e at 30-min postinfusion, Δ(K+)e remaining unchanged thereafter. Intracellular fluid (ICF) potassium content, (K+)i, decreased progressively postinfusion in all groups excluding chronic metabolic acidosis, in which a reduction in (K+)e was accompanied by an increase in (K+)i. We demonstrate that hypokalemia following hypertonic NaHCO3 infusion in intact animals with acidemia, alkalemia, or normal acid-base status and intact or depleted potassium stores is critically dependent on mechanisms of internal potassium balance and not ECF volume expansion or kaliuresis. We envision that the acute NaHCO3 infusion elicits immediate ionic shifts between ECF and ICF leading to hypokalemia. Thereafter, maintenance of a relatively stable, although depressed, [K+]e requires that cells release potassium to counterbalance ongoing urinary potassium losses.

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The collecting duct is a highly adaptive terminal part of the nephron, which is essential for maintaining systemic homeostasis. Principal and intercalated cells perform different physiological tasks and exhibit distinctive morphology. However, acid-secreting A- and base secreting B-type of intercalated cells cannot be easily separated in functional studies. We used BCECF-sensitive intracellular pH (pHi ) measurements in split-opened collecting ducts followed by immunofluorescent microscopy in WT and intercalated cell-specific ClC-K2-/- mice to demonstrate that ClC-K2 inhibition enables to distinguish signals from A- and B-intercalated cells. We show that ClC-K2 Cl- channel is expressed on the basolateral side of intercalated cells, where it governs Cl- -dependent H+ /HCO3- transport. ClC-K2 blocker, NPPB, caused acidification or alkalization in different subpopulations of intercalated cells in WT but not ClC-K2-/- mice. Immunofluorescent assessment of the same collecting ducts revealed that NPPB increased pHi in AE1-positive A-type and decreased pHi in pendrin-positive B-type of intercalated cells. Induction of metabolic acidosis led to a significantly augmented abundance and H+ secretion in A-type and decreased proton transport in B-type of intercalated cells, whereas metabolic alkalosis caused the opposite changes in intercalated cell function, but did not substantially change their relative abundance. Overall, we show that inhibition of ClC-K2 can be employed to discriminate between A- and B-type of intercalated cells in split-opened collecting duct preparations. We further demonstrate that this method can be used to independently monitor changes in the functional status and abundance of A- and B-type in response to systemic acid/base stimuli.

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OBJECTIVE: To investigate the effect of three different buffered balanced crystalloid solutions on acid-base status and electrolyte concentrations in dogs with gastric dilation-volvulus (GDV) syndrome. METHODS: The study design was a prospective, randomized clinical trial of 40 dogs. The dogs were randomly assigned to one of three groups according to the fluid used: Hartmann's solution (H), Plasmalyte (PL), and Ringerfundin (RF). Hemoglobin, albumin, lactate, electrolyte, and acid-base parameters were determined before fluid administration (T0) and at the end of surgery (T1). Results were assessed by one-way ANOVA, Fisher's exact test, the Wilcoxon signed-rank test, the Kruskal-Wallis test, and a linear mixed-effect regression model. A significance level of 0.05 was used in all analyses. RESULTS: Bicarbonate and base excess (BE) levels increased and chloride concentration decreased in the PL group; in contrast, strong ion difference apparent (SIDapp) decreased and chloride concentration increased in the RF group. The mixed-effect model confirmed a significant interaction between the type of solution and time on the changes in bicarbonate, BE, anion gap (AG), SIDapp, and chloride levels. CLINICAL SIGNIFICANCE: Significantly different effects in acid-base parameters were observed in dogs after intravenous administration of H, PL, and RF. However, clinical significance of these changes is lacking, requiring further investigation in a larger randomized controlled clinical trial.

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To compare whether the diagnostic evaluation of metabolic acidosis can be improved by using a modified Story method compared to the traditional evaluation in a population of critically ill patients with shock. This prospective cohort study included shock patients admitted to the ICU of a tertiary hospital in Brazil between May 2018 and November 2019. We collected laboratory data necessary for traditional evaluation and the simplified Stewart's method. During the study period, 149 patients were included in the final analysis. Of the 17 patients with a normal SBE and AGcorrected, 13 (76.5%) presented with metabolic acidosis according to the modified Story assessment. Therefore, of the 149 patients included in the study, the traditional approach failed to identify metabolic acidosis that was identified by the modified Story assessment in 13 (8.7%) patients. In addition, the determination of the severity of metabolic acidosis also differed between the two methods by a mean of - 7.8 mEq/L. We found that a modified Story method can identify and quantify metabolic acidosis in patients with disorders that were not revealed by the traditional approach.

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INTRODUCTION: Acute exposure to nitrogen compounds combined with a massive inhalation of air pollutants can influence respiratory and cardiovascular symptoms and coagulation abnormalities in accidentally exposed healthy adults during cave detonation operations. METHODS: Italian alpine and cave rescuers widened a cave in the Abisso Luca Kralj in Trieste, Italy. Volunteers inside the cave were accidentally exposed to the fumes from an uncontrolled detonation of blasting gelatin microcharges. We performed a retrospective cohort study on the clinical data, arterial blood gas analysis, and rotational thromboelastometry parameters from the rescuers involved in the accident. RESULTS: Ninety-three healthy rescuers were involved in the uncontrolled detonation: 47 volunteers handled a mixture of nitrogen compounds (blaster group), and 46 volunteers did not (nonblaster group). After the accident, statistically significant differences (P<0.05) in arterial blood gas values were observed between the groups, with a pattern of mild respiratory acidosis with hypercapnia in the nonblaster group and severe mixed acid-base disorder with hypoxia and hypercapnia in the blaster group. Mild hyperfibrinolysis was observed in 44 volunteers in the blaster group, as were associated bleeding symptoms in 34 volunteers; no significant coagulation modifications were recorded in the nonblaster group. CONCLUSIONS: Respiratory acidosis with hypoxia, hypercapnia, a compensatory metabolic response, and mild hyperfibrinolysis were probably related to the combined effect of nitrogen compounds and the inhaled toxic products of detonation. Therefore, each element exerts a determinant effect on promoting the biological toxicity of the others.

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BACKGROUND AND AIM: Acetate or lactate buffered, balanced isotonic rehydration fluids are commonly used for fluid therapy in dogs and may influence acid-base and electrolyte status. This study aimed to assess acid-base status, electrolyte levels, and lactate levels in dehydrated dogs after receiving acetate or lactate-containing intravenous rehydration fluids. MATERIALS AND METHODS: In this prospective, randomized study, 90 dehydrated dogs were included and randomized to receive acetate [Sterofundin® ISO B. Braun Vet Care (STERO), Germany) or lactate (Ringer-Lactat-Lösung nach Hartmann B. Braun Vet Care (RL), Germany] containing intravenous fluids for rehydration. The exclusion criteria were as follows: Age <6 months, liver failure, congestive heart failure, and extreme electrolyte deviation. Physical examination, venous blood gas, and lactate levels were analyzed before and after rehydration. The two groups were compared using t-test and Chi-square test. The significance level was set at p≤0.05. RESULTS: Post-rehydration heart rate decreased in the STERO group (p<0.001) but not in the RL group (p=0.090). Lactate levels decreased in both groups STERO (p<0.001) and in group RL (p=0.014). Sodium and chloride levels increased during rehydration in group STERO (p<0.001; p<0.001) and group RL (p=0.002; p<0.001). There was a larger decrease in lactate levels in group STERO compared to group RL (p=0.047). CONCLUSION: Both solutions led to a mild increase in sodium and chloride levels and decreased lactate levels. The acetate-containing solution had an inferior effect on the decrease in lactate level.