Increased Anion Gap Research Articles

The relationship between hyperchloremia and acute kidney injury in pediatric diabetic ketoacidosis and its impact on clinical outcomes.

Diabetic ketoacidosis (DKA) is characterized by hyperglycemia, ketogenesis, and increased anion gap metabolic acidosis. Such derangements are accompanied by volume depletion as well as electrolyte disturbances. Resuscitation using traditional saline in DKA patients can exacerbate electrolyte abnormalities, in particular the production of hyperchloremia. Severe hypovolemia can result in acute kidney injury (AKI). The link between hyperchloremia and AKI is controversial. This study aimed to assess the relationship between hyperchloremia and AKI in pediatric patients with DKA and its impacts on clinical outcomes. This cross-sectional study was conducted on 70 children with DKA admitted to the pediatric intensive care unit in which all patients were subjected to detailed medical history taking and full clinical examination. Daily assessment of Na, K, urea, creatinine, chloride, arterial blood gases, and albumin/creatinine ratio (ACR) was done. AKI was defined as pRIFLE stage I and F. Hyperchloremia was detected in 65.7% of patients at admission and in 52.9% after 24h (p = 0.17). AKI was documented in 28% of patients. At admission hyperchloremia was detected in 56% of patients without AKI versus 90% of patients with AKI (p = 0.007). After 24h, hyperchloremia was detected in 48.4% patients without versus 100% of patients with AKI. Chloride was significantly positively correlated to duration of admission, creatinine, ACR, and negatively correlated to eGFR. The development of AKI in patients with DKA was accompanied by hyperchloremia, increased time to DKA resolution, and longer hospital stay. A higher resolution version of the Graphical abstract is available as Supplementary information.

Decision tree outcome prediction of acute acetaminophen exposure in the United States: A study of 30,000 cases from the National Poison Data System.

Acetaminophen is one of the most commonly used analgesic drugs in the United States. However, the outcomes of acute acetaminophen overdose might be very serious in some cases. Therefore, prediction of the outcomes of acute acetaminophen exposure is crucial. This study is a 6-year retrospective cohort study using National Poison Data System (NPDS) data. A decision tree algorithm was used to determine the risk predictors of acetaminophen exposure. The decision tree model had an accuracy of 0.839, an accuracy of 0.836, a recall of 0.72, a specificity of 0.86 and an F1_score of 0.76 for the test group and an accuracy of 0.848, a recall of 0.85, a recall of 0.74, a specificity of 0.87 and an F1_score of 0.78 for the training group. Our results showed that elevated serum levels of liver enzymes, other liver function test abnormality, anorexia, acidosis, electrolyte abnormality, increased bilirubin, coagulopathy, abdominal pain, coma, increased anion gap, tachycardia and hypotension were the most important factors in determining the outcome of acute acetaminophen exposure. Therefore, the decision tree model is a reliable approach in determining the prognosis of acetaminophen exposure cases and can be used in an emergency room or during hospitalization.

New Onset Type-1 Diabetes Mellitus in a Toddler with Sars-Cov-2 Infection Presenting In Diabetic Ketoacidosis: A Case Report

Introduction: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), though mostly sparing the lungs in children, has been found to affect other organs including the endocrine pancreas. Type 1 diabetes mellitus (T1DM) may occur through direct negative effects of the virus on beta-cell function leading to diminished insulin production. Diabetic ketoacidosis (DKA) is a known and life-threatening complication of T1DM. Case presentation: This is a case of a 3-year-old previously healthy male who presented with 4 days history of fever, with malaise and hyperpnea for one day. Review of systems was notable for increased thirst and urination, nausea, vomiting, fatigue, and visible weight loss for 4 days. Initial investigations done showed elevated blood glucose, ketonuria, increased anion gap metabolic acidosis, and positive SARS-CoV-2 polymerase chain reaction (PCR). He was immediately commenced on intravenous fluids and insulin with progressive improvement and was discharged on hospital day 6. Conclusion: Coronavirus disease-2019 (COVID-19) has impacted children most profoundly with the new post-infectious multi-inflammatory syndrome, however, it is important to remember that primary coronavirus infection is still a threat to pediatric patients, for example, and its cytotoxic effects on the pancreatic beta cells that may lead to T1DM. We, therefore, recommend that caregivers, parents, and medical professionals should have a high index of suspicion when children present with symptoms consistent with a diagnosis of T1DM during the COVID-19 pandemic so that diagnosis can be made promptly and therefore DKA prevented.

Metabole acidose met verhoogde anion gap ten gevolge van 5-oxoprolinurie bij gelijktijdig gebruik van acetaminofen en flucloxacilline

Metabolic acidosis with increased anion gap due to 5-oxoprolinuria with concomitant use of acetaminophen and flucloxacillin 5-oxoprolinuria is a relatively rare metabolic disorder in which there is accumulation of 5-oxoproline leading to a high anion gap metabolic acidosis. The acquired form is usually caused by simultaneous use of acetaminophen (also known as paracetamol) and flucloxacillin, which is not uncommon. The exact incidence and prevalence of the acquired form are not known. This disorder is most likely under-reported as the test used for diagnosis is not always performed nor easy accessible. Diagnosing 5-oxoprolinuria requires testing urine or serum of a patient for the presence of organic acids, which are highly elevated in 5-oxoprolinuria. Due to the relative rareness of the disorder, cases are easily missed. 5-oxoprolinuria should always be suspected in a patient with unexplained high anion gap metabolic acidosis and/or therapy with flucloxacillin with or without the concomitant use of acetaminophen. Treating 5-oxoprolinuria is straightforward and consists of stopping the offending drug(s) which mostly leads to a spontaneous recovery. Treatment with sodium bicarbonate and/or N-acetylcysteine are also described in the literature, but at present there is not sufficient evidence supporting their use.

Euglycemic ketoacidosis complicating empagliflozin therapy in a Bangladeshi type 2 diabetic lady

Diabetic ketoacidosis (DKA) is an acute complication of diabetes mellitus, which may occurin both type 1 and type 2 diabetic patients. It is characterized by hyperglycaemia [blood glucose levels > 250 mg/dL (13.8 mmol/ L)], metabolic acidosis (pH <7.3 or serum bicarbonate <15 mmol/L) with an increased anion gap and the presence of ketone bodies in blood or urine. A subgroup of patients may present without signs of hyperglycemia, rather present with euglycemia, posing a diagnostic challenge due to the absence of the cardinal findings of the pathophysiology in DKA. Here, we report a case of euglycemic ketoacidosis complicating a 50-year-old Bangladeshi diabetic lady receiving empagliflozin treatment. BIRDEM Med J 2021; 11(3): 243-245

New Onset Type-1 Diabetes Mellitus in a Toddler with SARS-CoV-2 Infection Presenting in Diabetic Ketoacidosis: A Case Report

<strong>Introduction:</strong> Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), though mostly sparing the lungs in children, has been found to affect other organs including the endocrine system [1, 2]. Diabetes mellitus (DM) from SARS-CoV-2 infection occurs through direct negative effects of the virus on beta cell function, [3, 4] and may rapidly progress to complications such as diabetic ketoacidosis (DKA) which can be potentially fatal [3]. We present a case of new-onset type 1 DM presenting as DKA in a toddler with SARS-CoV-2 infection. <strong>Case presentation:</strong> A 3-year-old previously healthy male presented with 4 days history of fever and generalized body weakness, and “deep breathing” of 1 day. Review of systems was notable for increased thirst and urination, nausea, vomiting, fatigue, and visible weight loss noted in the last 4 days. Initial investigations done showed elevated blood glucose (582 mg/dL), ketonuria (2+ or 80 mg/dL), increased anion gap metabolic acidosis (pH 6.95, bicarbonate &lt;6 mEq/L, lactate 2.7 mmol/L, anion gap 23), and positive SARS-CoV-2 polymerase chain reaction (Table 1). He was immediately commenced on intravenous fluids and insulin with progressive improvement. Subsequent laboratory findings include elevated HbA1c (10.0%), low insulin and low C-peptide (&lt;15 mIU/L and &lt;0.1 ng/ml respectively) suggestive of type 1 DM. Antibodies to insulin and glutamic acid decarboxylase (GAD) 65 were within normal range (&lt;0.4 U/mL and &lt;5 IU/mL respectively). Screening for celiac disease and thyroid disorders were also within normal limits. He remained otherwise asymptomatic with other coronavirus disease-2019 (COVID-19) symptoms and was discharged on hospital day 6 on subcutaneous insulin. <strong>Conclusion:</strong> The association between COVID-19 and new-onset type 1 diabetes mellitus (T1DM) is becoming increasingly prevalent. The case highlights the possibility of SARS-CoV-2 acting as an infectious precipitant for T1DM and DKA. Although the presence of multiple autoantibodies greatly increases the probability for T1DM with about 96% of affected individuals being positive for at least one of the autoantibodies, the index case did not have autoantibodies suggesting a different mechanism of pancreatic beta cell destruction. Since children have been mostly spared the respiratory symptoms in acute COVID, it is important to remember that other organ systems can be affected distinct from the post-infectious multi-inflammatory syndrome. We therefore recommend that caregivers, parents, and medical professionals should have a high index of suspicion so that diagnosis can be early and DKA potentially prevented.

A Case of Possible SARS-COV-2 Induced Beta-Cell Failure

Background: There are several known viral triggers of ketosis-prone diabetes, including SARS-1 and HHV-81,2. SARS-COV-2 can bind ACE-2 receptors on the beta-cell causing destruction and acute impairment of insulin secretion3. There is accruing evidence to suggest that COVID-19 infection can worsen preexisting diabetes or induce new disease4. Clinical Case: A 40-year-old Hispanic male presented to the ER complaining of fatigue, polyuria, and polydipsia. A screening COVID-19 PCR was positive but he denied URI symptoms. His admission labs were notable for hyperglycemia (434 mg/dL; n 71–99), metabolic acidosis (pH 7.1 [n 7.35–7.45]; HCO3 3 mmoL/L [n 21–32]), increased anion gap (27 mmoL/L; n < 12) and elevated HbA1c (7.9%; n < 5.7%). The patient’s fructosamine was also high (464 umol/L; n 200–285) and discordant from his HbA1c. There was no evidence of pancreatitis, lactic acidosis, renal impairment or hepatic dysfunction. The patient had no known medical problems, did not drink alcohol to excess, and reported good access to nutrition. He had a strong family history of T2DM, but his BMI (23.3 kg/m2) and lipid panel were normal. The DKA was managed in the medical ICU using fluids and IV insulin per protocol. The patient required 180 units of IV insulin/24-hours (2.5 units/kg/day) to maintain blood glucose 180–250 mg/dL. After 48-hours of IV insulin, he was transitioned to subcutaneous insulin and prescribed multiple daily injections at discharge. There were concerns about possible T1DM and/or glucose toxicity leading to further diagnostics. His GAD-65 (<5 [IU]/mL; n 0–5 [IU]/mL) and IA-2 (<5.4 U/mL; n <5.4 U/mL) antibodies were negative but his c-peptide was suppressed (0.64 ng/mL; n 0.8–3.85). The patient was reevaluated at three months post-discharge. His glycemic control and insulin requirements had improved but repeat c-peptide level was undetectable. He was thought to have beta-cell failure and referred to a diabetologist. Conclusion: This is a case of absolute insulin deficiency persisting for at least three months most likely attributable to acute COVID-19 infection.

Alpelisib-Induced Hyperglycemia- A Small Case Series

The phosphoinositide-3-kinase (PI3K) family consists of highly conserved enzymes that are key intermediaries in signal transduction regulating cell survival and mitogenesis. This axis has been implicated in many types of cancers. In 2019 Alpelisib (Piqray), a reversible inhibitor specific to the PI3Kα subunit, in combination with fulvestrant, was approved to treat hormone receptor positive, human epidermal growth factor receptor 2 (Her2) negative, PI3K mutated breast cancer. This approval followed SOLAR-1 trial results showing a 35% risk reduction in cancer progression or death with alpelisib-fulvestrant compared to placebo in a cohort with PI3K mutated breast cancer. PI3K also plays a critical role in the insulin signaling pathway and alpelisib has been shown to cause a dose dependent rise in plasma glucose, insulin and c-peptide. Here we present a case series of severe hyperglycemia induced by alpelisib.A 44-year-old woman with ER+/Her2(-)/PI3K positive metastatic breast cancer was started on alpelisib. Previously, HbA1C was 5.4%. Hyperglycemia developed and HbA1c rose to 9.0% within 6 months of alpelisib 300mg daily. She started metformin and empagliflozin, which she was unable to tolerate due to nausea and vomiting. Her self-monitored blood glucoses were 300-400mg/dL within hours after her morning alpelisib dose. We discontinued empagliflozin when she developed metabolic acidosis with an increased anion gap. However, prior to any dose reduction, oncology discontinued alpelisib due to evidence of cancer progression. A week later, her glucoses normalized.Second case is of a 64-year-old woman with stage IV ER+/Her2(-)/PI3K mutated breast cancer with bony metastases, who was started on alpelisib 250mg. Her prior HbA1C was 5.5%. Ten days after initiation of alpelisib, she developed grade 3 hyperglycemia (blood glucoses 200-500mg/dL). She was started on metformin 2000mg with alpelisib dosed at noon. However, she noted a marked rise in blood glucose in the afternoon, few hours following alpelisib dose. Thus, moving the alpelisib to bedtime allowed better control of glycemia by using overnight basal insulin.Similarly, a 37-year-old woman with a history of ER+/HER2(-) stage IV metastatic breast cancer to the liver, with PI3K mutation was found to have acute, severe hyperglycemia with blood glucose of 300mg/dL, despite HbA1C being only 4.7%. This was attributed to initiation of alpelisib 2 days prior to admission. Given the severity of her insulin resistance (requiring > 100 units of insulin daily), alpelisib dose was reduced from 300mg to 150mg/day. On discharge, she was placed on metformin, dulaglutide, and basal and prandial insulins. Her HbA1C rose to 9.4% within 3 months of alpelisib initiation.This case series demonstrate the unique challenges in managing alpelisib induced reversible hyperglycemia.

1,3‐Butanediol at 5% v/v best mimics the systemic and urinary concentrations of β‐hydroxybutyrate after a 24 h fast in adult rats

Ketogenic diets are trendy in the nutrition community as promoters of rapid weight loss for improved cardiometabolic health. In the absence of carbohydrates and increased consumption of fats, ketone bodies become the primary energy source via free fatty acid oxidation, and this state of ketosis mimics what occurs during starvation. β-hydroxybutyrate (βHB) is the most abundant circulating ketone body. βHB is synthesized in the liver and transported to the peripheral tissues for conversion into energy. To study the long-term consequences of enhanced βHB bioavailability, the secondary alcohol, 1,3-butanediol (1,3-BD), is commonly administered in drinking water as a precursor. After consumption, 1,3-BD is catabolized by the liver into βHB. However, the concentration of 1,3-BD that best represents the circulating concentration of βHB after fasting is currently unknown. The objective of the current work was to determine what concentration of 1,3-BD best mimics the concentration of βHB after a 24 h fast in male adult rats. To test this objective, 40-week old Wistar-Kyoto rats were administered with or without 5%, 10%, or 20% v/v 1,3-BD in drinking water. All rats had free access to food throughout the investigation, although some vehicle-treated rats were fasted for the final 24 h before study termination to serve as a positive control. While 5% and 10% 1,3-BD increased βHB in the systemic circulation 1.5-fold (p<0.05), similar to an overnight fast, which was increased 2.0-fold (p<0.05), 20% 1,3-BD increased βHB by 4.5-fold (p<0.05). On the other hand, fasting and 5% 1,3-BD did not change urinary βHB, whereas 10% and 20% 1,3-BD increased urinary βHB by 3-fold and (p<0.05) and 10-fold (p<0.05), respectively. No difference in fasting blood glucose was observed in any of the 1,3-BD groups. Rats treated with 20% 1,3-BD had a dramatic and sustained decrease in body mass as early as one week after treatment commencement (19±4 g, p<0.05). Consumption of normal chow was decreased relative to vehicle in all three groups of 1,3-BD (p<0.05), but fluid consumption and urine volume was only decreased in the 20% group (p<0.05). The 20% group, similar to the vehicle-fasting group, also presented with increased red blood cells (1012/L, vehicle-non-fasting: 9.24±0.10, vehicle-fasting: 9.82±0.26*, and 20%: 9.74±0.20*, p<0.05) and hematocrit (%, vehicle-non-fasting: 44.00±0.82, vehicle-fasting: 46.53±1.10*, and 20%: 46.73±0.78*, p<0.05), indicative of dehydration. Finally, the 20% 1,3-BD group presented with an increased anion gap (p<0.05), a clinically used marker of metabolic acidosis. In summary, our data suggests that 5% 1,3-BD best represents the circulatory and urinary concentrations of βHB after a 24 h fast, and overall, we recommend this concentration of 1,3-BD as the most optimal to understand the physiological significance of fasting-induced βHB.

POS-106 A NOT SO SWEET COMPLICATION OF DIABETES MELLITUS THERAPY(EUGLYCEMIC DKA)

Diabetic ketoacidosis (DKA) is the most feared and well-known life-threatening complication of diabetes generally due to noncompliance or an active infectious process. But, what if DKA were to take place with adequate medication adherence? Euglycemic diabetic ketoacidosis is a clinical diagnosis that encompasses an increased anion gap metabolic acidosis, ketonemia or ketonuria in the setting of normal blood glucose levels (<200 mg/dL). This entity is a diagnostic challenge as euglycemia cover-ups the underlying diabetic ketoacidosis. Seeing as how sodium-glucose cotransporter 2 (SGLT2) inhibitor use has increased following studies that demonstrate its cardioprotective and renoprotective effects a high index of clinical suspicion is warranted now more than ever, and other diagnosis must be ruled out. This is the case of a 66 y/o male patient with past medical history of type 2 diabetes mellitus on empagliflozin, insulin and metformin, arterial hypertension, major depressive disorder, dyslipidemia who was initially admitted to a psychiatric hospital for management of depression and psychosis. Two days after admission he presented with diffuse abdominal discomfort associated with nausea, vomiting, poor appetite and difficulty voiding for which he was transferred to our institution for Internal Medicine evaluation. After evaluation at the Emergency Department he was admitted to IM ward with diagnostic impression of acute prostatitis and obstructive uropathy. Initial laboratories were remarkable for WBCs at 9.4x10-3uL, no bandemia and no neutrophilia, adequate hemoglobin and platelet count. Chemistry with Glucose at 136mEq/L, Potassium at 4.5mEq/L, HCO3 at19mEq/L, normal hepatic enzymes, normal lactic acid and normal pancreatic enzymes. Laboratories the next morning revealed glucose 127 mg/dL, bicarbonate 14 mEq/L with a pure high anion gap metabolic acidosis of 23mEq/L (delta-delta of 1.1), beta-hydroxybutyrate at 65mg/dL, normal lactate 0.8 mmol/L, negative toxicology and arterial blood gases revealing metabolic acidosis with adequate respiratory compensation (pH 7.314, pCO2 31.3 mmHg and bicarbonate 15.5 mmol/L). Diagnosis of euglycemic DKA secondary to empagliflozin precipitated by acute bacterial prostatitis and decreased oral intake was made. Patient subsequently transferred to t he medical intensive care unit where crystalloid volume expansion was provided, DKA protocol with intravenous insulin infusion initiated along with D10W intravenous fluid administration. After approximately 16 hours of treatment, metabolic acidosis and anion gap normalized. Patient was successfully discharged home after completion of antibiotherapy with follow up with his primary care physician. Euglycemic DKA secondary to SGLT2i is a diagnosis often missed by physicians accustomed to seeking for elevated blood sugars. Its presentation is often vague and insidious for which cases are underreported and incidence remains unknown. Nonetheless, ketoacidosis in diabetic patients remains a medical emergency despite euglycemia. High clinical suspicion is warranted in order to begin prompt treatment and reduce hospital stay as well as associated costs.

Electrocardiographic changes in the acute hyperkalaemia produced by intragastric KCl load in rats.

What is the central question of this study? This study presents a new model for studying the rapid onset of severe, acute hyperkalaemia in rats with intact kidney function by administering an intragastric KCl load. What is the main finding and its importance? This new model of intragastric KCl load produces a reliable and reproducible model for studying the rapid onset of severe, acute hyperkalaemia in rats with intact kidney function. We report unprecedented rapid changes (30min) in ECG, blood pressure and various arterial blood analyses with this new model, providing a solid foundation for future experiments in this field. A variety of animal models have been proposed to study hyperkalaemia, but most of them have meaningful limitations when the goal is to study the effect of potassium overload on healthy kidneys. In this study, we aimed to introduce a new approach for induction of hyperkalaemia in a reliable and reproducible animal model. We used intragastric administration of potassium chloride [KCl 2.3M, 10ml/(kg body weight)] to male Holtzman rats (300-350g) to induce hyperkalaemia. The results showed that this potassium load can temporarily overwhelm the renal and extrarenal handling of this ion, causing an acute and severe hyperkalaemia that can be useful to study the effect of potassium imbalance in a variety of scenarios. Severe hyperkalaemia (>8meqiv/l) and very profound ECG alterations, characterized by lengthening waves and intervals, were seen as early as 30min after intragastric administration of KCl in rats. In addition, a transient increase in arterial blood pressure and time-dependent bradycardia were also seen after the KCl administration. No metabolic acidosis was present in the animals, and the potassium ion did not increase proportionally to chloride ion in the blood, leading to an increased anion gap. In conclusion, the results suggest that intragastric KCl loading is a reliable model to promote rapid and severe hyperkalaemia that can be used for further research on this topic.

Euglycemic Diabetic Ketoacidosis and Sodium-Glucose Cotransporter-2 Inhibitors: A Focused Review of Pathophysiology, Risk Factors, and Triggers.

Diabetic ketoacidosis (DKA) is an acute and significant life-threatening complication of diabetes. The association of sodium-glucose cotransporter-2 inhibitors (SGLT2i) with euglycemic diabetic ketoacidosis (EDKA) has been well reported. This literature review was conducted to understand the mechanism of EDKA and identify the potential risk factors and precipitants for patients taking SGLT2i. After reviewing the published literature between 2010 and 2020, 32 articles are included in the final review. The underlying mechanism is mainly enhanced lipolysis and ketone body reabsorption. SGLT2i also stimulates pancreatic alpha cells and inhibits beta cells, causing an imbalance in glucagon/insulin levels, further contributing to lipolysis and ketogenesis. Most patients were diagnosed with blood glucose less than 200 mg/dL, blood pH <7.3, increased anion gap, increased blood, or urine ketones. Perioperative fasting, pancreatic etiology, low carbohydrate or ketogenic diet, obesity, and malignancy are identified precipitants in this review. As normoglycemia can conceal the underlying acidosis, physicians should be cognizant of the EDKA diagnosis and initiate prompt treatment. Patient education on risk factors and triggers is recommended to avoid future events.

Short communication: Effects of different blood buffers administered in electrolyte solution to grain-fed veal calves experiencing diarrhea

Calf diarrhea can commonly lead to dehydration and metabolic acidosis due to the loss of fluid and electrolytes. The objective of this randomized clinical trial was to examine differences between treating male dairy calves experiencing diarrhea with either a basic bicarbonate electrolyte powder (BBP) composed of sodium bicarbonate (50.7 mmol/L); a mixed buffer powder (MBP) including sodium bicarbonate (33.8 mmol/L), sodium citrate (8.4 mmol/L), sodium acetate (6.3 mmol/L), and potassium citrate (1.9 mmol/L); or a liquid electrolyte (HAL) composed of sodium acetate (50.1 mmol/L). All 3 electrolyte solutions were standardized to provide 50 mmol/L blood buffers and a similarly strong ion difference (74.4, 74.9, and 82.6 mEq/L for BBP, MBP, and HAL, respectively). Holstein male calves (n = 80) were sourced from auction barns or local farms and delivered in 1 batch to the research facility. Calves were housed in individual pens and fed a 24% crude protein and 17% fat calf milk replacer (CMR) twice daily. Starter grain and water were offered ad libitum. Calves were randomly enrolled in 1 of the 3 treatments when experiencing either 2 consecutive days of a fecal score of 2 (runny, spreads easily) or 1 d with a fecal score of 3 (liquid devoid of solid material). Calves were blocked by the different enrollment criteria. The respective electrolyte solution was administered via esophageal tube 1 h after feeding CMR until the fecal score returned to 0 (normal consistency) or 1 (semiformed or pasty). Blood gas measurements were taken at 1, 8, and 24 h post the initial electrolyte feeding, and weight was measured at 1, 2, 7, 14, and 28 d postenrollment. Mixed repeated measure linear regression models were built to assess the effect that the electrolyte solutions had on the blood gas measurements and body weight. A total of 45 calves were enrolled in the trial with 14, 16, and 15 calves randomly assigned to the MBP, HAL, and BBP groups, respectively. As compared with BBP, MBP increased blood CO2 at 8 and 24 h, increased bicarbonate at 24 h, increased base excess at 8 and 24 h, and increased anion gap at 24 h. Calves in the BBP and HAL groups noted more severe eye recession when compared with the MBP group. Average daily gain did not differ between treatments at any time point. Although a severe dehydration challenge was not present, which should be considered a limitation of the study, MBP improved the acid-base status of calves compared with BBP, whereas HAL performed similarly to MBP.

Metabolic acidosis

Acid-base disorders due to different etiologies are frequently encountered in daily clinical practice and may result in life-threatening situations. Basic knowledge of the diagnostic and therapeutic approach of acid-base disorders is therefore essential for every clinician. Acid-base disorders should be treated according to their underlying etiology. Therefore, diagnosis of the underlying etiology is the critical step in the process of care for patients with acid-base disorders. Undirected buffering with HCO3 - should be avoided, since the application of HCO3 - might lead to severe side effects. A strict diagnostic pathway for the diagnosis of acid-base disorders is required, which should be vigorously applied:- analysis of the pH to classify acidemia or alkalemia- analysis of pCO2 and HCO3 - to classify the primary acid base disorder- analysis of the adequate regulation in order to detect additional acid-base disorders- analysis of the anion gap and the relationship of the anion gap vs. the change in HCO3 - to detect further metabolic disordersMetabolic acidosis can be divided into two main etiologies:- acidosis with addition of acid with increased anion gap,- acidosis with loss of HCO3 - with normal anion gap.

Metabolic acidosis with increased anion gap, oxaluria, and acute kidney injury: Answers.

Metabolic acidosis with increased anion gap, oxaluria, and acute kidney injury: Answers.

Metabolic acidosis with increased anion gap, oxaluria, and acute kidney injury: Questions.

Metabolic acidosis with increased anion gap, oxaluria, and acute kidney injury: Questions.

Death also have color, this time purple; Methanol

Introduction: Methanol is a colorless and odorless alcohol type that is toxic by its metabolites and is obtained by distillation of wood.Case Report: A 64-year-old female patient was admitted to our emergency department with complaints of double vision, difficulty in answering questions and drowsiness. Her extremities had pink-purple hyperemia, suggesting widespread dermatitis in both knees. It was found that dermatitis developed after the patient was applied wrapping from wood alcohol for knee pain, and the patient was diagnosed with methanol poisoning. Upon the disruption of her consciousness, an intubation decision was made and hemodialysis was performed in the anesthesia and reanimation unit of our hospital while the patient was intubated. After 3 days of her hospitalization in the intensive care unit, the patient was exitus with a development of cardiac arrest.Discussion: We aimed to remind you that in metabolic acidosis cases with increased anion gap, methanol toxicity is a reason that should not be neglected and may be fatal.

104-LB: Glucose-Insulin-Potassium (GIK) as a Proposed Treatment for Normoglycemic Diabetic Ketoacidosis: An Old Friend for a New Foe?

Introduction: Glucose, Insulin, and potassium (GIK) infusions were introduced into medical practice to reduce myocardial injury during a heart attack in 1962. Euglycemic diabetic ketoacidosis (EDKA) is a clinical triad comprising increased anion gap metabolic acidosis, ketonemia or ketonuria and blood glucose levels &amp;lt;250mg/dL. Based on common treatment delays due lack of hyperglycemia, we decided to start a new proposed protocol for patients with confirmed EDKA that included the use of GIK and compared them with historical controls before the protocol was established. GIK solution was prepared with Dextrose 5% solution 500 cc, 10 UI of short acting insulin al 10 mmol KCl. At al initial rate of 100 ml/hr. Objectives: Describe general characteristics and compare time to remission, length of ICU stay and length of hospital time between patients with SGLT2i-associated EDKA in whom GIK was used compared to standard care. Design: A Cohort study was designed to compare objectives between EDKA patients treated with a GIK-adapted protocol versus previous patients treated with standard of care of DKA. Patients and Methods: 4 Patients with EDKA treated with new protocol were compared with 7 previous patients treated with ADA recommendations for DKA. Results: 41.66% of patients were male, type 2 diabetes was initially diagnosed in 66.66% of patients. No differences in ER characteristics between standard vs. GIK group. The use of GIK as an add-on treatment to standard care was associated with a significant lower time to resolution (1.5±0.5 vs. 3.57±1.61, p&amp;lt;0.01), fewer ICU days (2.5±0.57 vs. 5.57±1.98, p&amp;lt;0.01), in-hospital days (4.5±0.577 vs. 11.85±3.43, p&amp;lt;0.01). No differences in hypoglycemic or hipo/hyperkalemia were found. Conclusions: With the wide use of SLGT2 inhibitors there has been a similar increase in the number of SGLT2i-associated EDKA. Were propose a different way of management of these patients. More research is needed in this field and entity. Disclosure D. Espinoza-Peralta: None. J. Monjardin-Rochin: None. M.E. Búrquez-González: None. L.G. Mireles-Zavala: None.

A study on mean anion gap over 6 hours after admission as a predictor of pediatric mortality in pediatric intensive care unit

&lt;p class="abstract"&gt;&lt;strong&gt;Background:&lt;/strong&gt; The aims of the study was to correlate change in anion gap at 0 and 6 hours of admission with mortality in pediatric intensive care unit (PICU).&lt;/p&gt;&lt;p class="abstract"&gt;&lt;strong&gt;Methods:&lt;/strong&gt; Fifty children up to 12 years of age, admitted in PICU were included in the study. Blood gas anion gap levels were taken at 0 and 6 hours of admission and change in anion gap was calculated. Final outcome was recorded. &lt;/p&gt;&lt;p class="abstract"&gt;&lt;strong&gt;Results:&lt;/strong&gt; Out of 50 patients enrolled in the study, 18 (36%) patients died and 32 (64%) survived. Mortality was higher in group with increased anion gap after 6 hours of admission as compared to survived. Change in anion gap was higher in expired patient as compared to survivors.&lt;/p&gt;&lt;p class="abstract"&gt;&lt;strong&gt;Conclusions:&lt;/strong&gt; Mortality was higher in group with increased anion gap after 6 hours of admission.&lt;/p&gt;

ISOVALERIC ACIDEMIA IN A NEONATE PRESENTING AS SEPSIS AND DIABETIC KETOACIDOSIS: A CASE REPORT

Isovaleric acidemia (IVA), an inborn error of leucine catabolism resulting in the accumulation of derivatives of isovaleryl-CoA that leads to hyperammonemia and ketoacidosis. IVA is clinically characterized by lethargy, vomiting, and a distinctive smell of “sweaty feet.” We report the case of a 10-day-old male neonate who presented with acute encephalopathy, hyperglycemia, increased anion gap metabolic acidosis, ketosis, and features of sepsis. After the management of acute metabolic decompensation, he was successfully treated with dietary restriction of leucine and L-carnitine supplementation. This case is of interest because of the rarity of presentation, early detection, and prompt implementation of the treatment with satisfactory outcomes.