sodium-bicarbonate and Diabetic-Ketoacidosis

Sodium-glucose co-transporter-2 (SGLT-2) inhibitors are a relatively novel class of oral medications for the treatment of Type 2 DM with a generally acceptable safety profile. However, these agents have been associated with rare events of a serious and potentially life-threatening complication named euglycemic diabetic ketoacidosis (euDKA). euDKA is not identical with the typical diabetic ketoacidosis, as it often presents with serious metabolic acidosis but only mild to moderate glucose and anion gap elevation.. We report a case of a 51-year old female with Type 2 DM treated with an SGLT-2 inhibitor, developing severe metabolic acidosis with only mild blood glucose elevation after a routine surgery. A careful evaluation of involved factors led to the diagnosis of euDKA, followed by cautious application of simple therapeutic measures that resulted in complete restoration of acidosis and glycemic control in less than 48-h.. Euglycemic ketoacidosis is a rare but rather serious complication of SGLT-2 inhibitors use, often with a multifactorial etiology. Its atypical presentation requires a high level of awareness by physicians as early recognition of this complication can quickly and safely restore acid-base balance.

Topics: Acid-Base Equilibrium; Anti-Bacterial Agents; Benzhydryl Compounds; Blood Gas Analysis; Blood Glucose; Diabetes Mellitus, Type 2; Diabetic Ketoacidosis; Female; Fluid Therapy; Glucosides; Glycerophosphates; Humans; Hypoglycemic Agents; Hysterectomy; Insulin; Middle Aged; Postoperative Complications; Sodium Bicarbonate; Sodium-Glucose Transporter 2 Inhibitors; Surgical Wound Infection

Topics: Acid-Base Equilibrium; Bicarbonates; Brain Edema; Child; Diabetic Ketoacidosis; Fatty Acids; Humans; Mitochondria; Osmolar Concentration; Oxidation-Reduction; Sodium Bicarbonate

Diabetic ketoacidosis is a common, serious acute complication in children with diabetes mellitus. Diabetic ketoacidosis can accompany new-onset type 1 diabetes mellitus or it can occur with established type 1 diabetes mellitus during the increased demands of an acute illness or with decreased insulin delivery due to omitted doses or insulin pump failure. Additionally, diabetic ketoacidosis episodes in children with type 2 diabetes mellitus are being reported with greater frequency. Although the diagnosis is usually straightforward in a known diabetes patient with expected findings, a fair proportion of patients with new-onset diabetes present in diabetic ketoacidosis. The initial management of children with diabetic ketoacidosis frequently occurs in an emergency department. Physicians must be aware that diabetic ketoacidosis is an important consideration in the differential diagnosis of pediatric metabolic acidosis. This review will acquaint emergency medicine clinicians with the pathophysiology, treatment, and potential complications of this disorder.

Topics: Ambulatory Care; Blood Urea Nitrogen; Brain Edema; Child; Contraindications; Creatinine; Critical Pathways; Diabetes Mellitus, Type 1; Diabetes Mellitus, Type 2; Diabetic Ketoacidosis; Diagnosis, Differential; Dose-Response Relationship, Drug; Electrolytes; Emergency Medicine; Emergency Service, Hospital; Fluid Therapy; Humans; Hypoglycemic Agents; Insulin; Phosphates; Potassium; Risk Management; Sodium Bicarbonate

To critically discuss the treatment of metabolic acidosis and the main mechanisms of disease associated with this disorder; and to describe controversial aspects related to the risks and benefits of using sodium bicarbonate and other therapies.. Review of PubMed/MEDLINE, LILACS and Cochrane Library databases for articles published between 1996 and 2006 using the following keywords: metabolic acidosis, lactic acidosis, ketoacidosis, diabetic ketoacidosis, cardiopulmonary resuscitation, sodium bicarbonate, treatment. Classical publications concerning the topic were also reviewed. The most recent and representative were selected, with emphasis on consensus statements and guidelines.. There is no evidence of benefits resulting from the use of sodium bicarbonate for the hemodynamic status, clinical outcome, morbidity and mortality in high anion gap metabolic acidosis associated with lactic acidosis, diabetic ketoacidosis and cardiopulmonary resuscitation. Therefore, the routine use of sodium bicarbonate is not indicated. Potential side effects must be taken into consideration. Treating the underlying disease is essential to reverse the process. The efficacy of other alternative therapies has not been demonstrated in large-scale studies.. Despite the known effects of acidemia on the organism in critical situations, a protective role of acidemia in hypoxic cells and the risk of alkalemia secondary to drug interventions are being considered. There is consensus regarding the advantages of alkali and sodium bicarbonate therapy in cases with normal anion gap; however, in the presence of high anion gap acidosis, especially lactic acidosis, diabetic acidosis and cardiopulmonary resuscitation, the use of sodium bicarbonate is not beneficial and has potential adverse effects, limiting its indication. The only points of agreement in the literature refer to the early treatment of the underlying disease and the mechanisms generating metabolic acidemia. Other promising treatment alternatives have been proposed; however, the side effects and absence of controlled studies with pediatric populations translate into lack of evidence to support the routine use of such treatments.

Topics: Acidosis; Acidosis, Lactic; Cardiopulmonary Resuscitation; Child; Diabetic Ketoacidosis; Humans; Randomized Controlled Trials as Topic; Sodium Bicarbonate

To review current concepts of physiopathology, diagnosis and treatment of diabetic ketoacidosis (DKA) in childhood, as well as preventive measures to avoid cerebral edema.. The authors selected articles from MEDLINE with the keywords diabetes, ketoacidosis, hyperglycemia and cerebral edema, and priority was given to studies including children and that contained complete texts published in English, Portuguese or Spanish. Chapters of books published in Brazil describing the treatment of DKA in pediatric intensive care unit were also reviewed. Based on the reviewed literature and on the author's experience, the most efficient and recommended measures for DKA management are presented.. Normal saline solution (NaCl 0.9%) has been increasingly used for fast replacement and hydration, as a substitute to diluted (hypotonic) solutions, as well as contraindication of sodium bicarbonate to repair metabolic acidosis in DKA. Regular insulin should be used as continuous infusion (0.1 IU/kg/h) without the need of a loading dose. For fast corrections of glucose oscillations, a practical scheme using two bags of electrolytic solutions is presented. Cerebral edema, its physiopathological mechanism and current treatment are reviewed.. Use of continuous infusion of regular insulin associated with adequate water and electrolyte replacement using isotonic solutions, besides being an effective treatment for DKA, preserves plasma osmolarity and prevents cerebral edema.

Topics: Brain Edema; Child; Contraindications; Critical Care; Dehydration; Diabetic Ketoacidosis; Fluid Therapy; Humans; Hydrogen-Ion Concentration; Hyperglycemia; Insulin; Insulin, Long-Acting; Intensive Care Units, Pediatric; Isotonic Solutions; Sodium Bicarbonate

Topics: Acidosis, Lactic; Contraindications; Diabetic Ketoacidosis; Humans; Hypoglycemic Agents; Insulin; Lactic Acid; Phenformin; Sodium Bicarbonate

Disorders of acid-base balance are commonly encountered in clinical practice and can have a substantial impact on the prognosis of the patient. Moreover, identification of a particular acid-base disturbance can provide a clue to an underlying disorder. Proper evaluation and treatment of acid-base disorders requires a systematic and analytic approach including: (1) assess the accuracy of the acid-base values using the Henderson equation or Henderson-Hasselbalch equation, (2) obtain a complete history and physical examination, (3) calculate the serum anion gap, (4) identify the primary acid-base disturbance and determine whether a simple or mixed disturbance is present, (5) examine serum electrolytes and additional laboratory data, and (6) measure urine pH and urine electrolytes and calculate the urine anion and osmolal gaps. Strict adherence to these principles will enable the clinician to diagnose the acid-base disturbance in the majority of cases. To illustrate these principles, 5 cases of patients with acid-base disturbances are analyzed.

Topics: Acid-Base Equilibrium; Acid-Base Imbalance; Adult; Aged; Carbon Dioxide; Clinical Protocols; Diabetic Ketoacidosis; Electrolytes; Ethanol; Female; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Sodium Bicarbonate

Topics: Acidosis, Lactic; Diabetic Ketoacidosis; Diagnosis, Differential; Humans; Hyperglycemic Hyperosmolar Nonketotic Coma; Insulin; Potassium; Prognosis; Sodium Bicarbonate; Sodium Chloride

The use of bicarbonates in the treatment of severe diabetic ketoacidosis remains controversial, especially regarding the benefit/risk ratio. The aim of this study was to assess the efficacy of bicarbonate therapy during severe diabetic ketoacidosis (pH <7.10).. Retrospective study.. The emergency unit of a teaching hospital.. The records of 39 patients consecutively admitted for severe diabetic ketoacidosis were analyzed (pH <7.10). The patients were divided into two groups: group 1 (n = 24; patients with bicarbonate treatment) and group 2 (n = 15; patients without bicarbonate treatment).. None.. We compared two groups of patients presenting with severe diabetic ketoacidosis (pH values between 6.83 and 7.08) treated with or without bicarbonate. A group of 24 patients received 120+/-40 mmol sodium bicarbonate. The two groups were similar at admission with regard to clinical and biological parameters. No difference could be demonstrated between the two groups concerning the clinical parameters or the normalization time of biochemical parameters. If the number of patients with hypokalemia was comparable between the two groups, the potassium supply was significantly more important in group 1 compared with group 2 (366+/-74 mmol/L vs. 188+/-109 mmol/L, respectively; p < .001).. Data from the literature and this study are not in favor of the use of bicarbonate in the treatment of diabetic ketoacidosis with pH values between 6.90 and 7.10.

Topics: Adult; Critical Care; Diabetic Ketoacidosis; Female; Fluid Therapy; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Retrospective Studies; Sodium Bicarbonate

Insulin-dependent diabetes mellitus in poor control, alcohol intake associated with extracellular fluid volume contraction, or hypoglycemia may each lead to an increased rate of production of ketoacids. Generally, several days of illness are required before ketoacidosis becomes severe. Two clinical examples are presented to suggest that a severe degree of ketoacidosis may develop over a short period of time, literally overnight. In both examples, there was the ingestion of a modest amount of ethanol. From a quantitative analysis of factors that may influence the rate of production and removal of ketoacids, the following were deduced. Contributing factors to the very rapid development of maximal ketoacidosis could include the absence of a lag period for the conversion of ethanol to acetyl-coenzyme A in the liver and an impaired ability of the brain and kidneys to oxidize ketoacids, especially if these ketoacids are produced very rapidly and/or if less metabolic work is performed by these organs. In special settings, ketoacidosis may develop more rapidly than is generally appreciated.

Topics: Adult; Alcohol Drinking; Cerebral Hemorrhage; Diabetic Ketoacidosis; Humans; Insulin; Keto Acids; Male; Sodium Bicarbonate; Sodium Chloride; Time Factors

Topics: Clinical Protocols; Diabetic Ketoacidosis; Female; Fetal Monitoring; Fluid Therapy; Humans; Insulin; Ketone Bodies; Potassium; Precipitating Factors; Pregnancy; Pregnancy in Diabetics; Pregnancy Outcome; Sodium Bicarbonate

Transport of the pediatric patients with DKA to a tertiary care center may be safely accomplished with a thorough understanding of the conditions that may require it. The patient should be acutely stabilized and standard therapeutic regimens begun prior to and during transport. Careful attention to detail and close monitoring are essential to prevent further instability and morbidity.

Topics: Bicarbonates; Critical Care; Diabetic Ketoacidosis; Fluid Therapy; Humans; Insulin; Pediatrics; Sodium; Sodium Bicarbonate; Transportation of Patients

Topics: Acidosis; Acidosis, Lactic; Alkalies; Animals; Bicarbonates; Carbonates; Diabetic Ketoacidosis; Dichloroacetic Acid; Dogs; Drug Combinations; Humans; Sodium; Sodium Bicarbonate

Topics: Acid-Base Equilibrium; Bicarbonates; Diabetic Ketoacidosis; Humans; Hydrogen-Ion Concentration; Models, Biological; Sodium; Sodium Bicarbonate

Topics: Bicarbonates; Diabetic Ketoacidosis; Diphosphoglyceric Acids; Fluid Therapy; Humans; Hydrogen-Ion Concentration; Hypokalemia; Infusions, Parenteral; Insulin; Magnesium Deficiency; Magnesium Sulfate; Phosphates; Sodium Bicarbonate; Time Factors

Diabetic ketoacidosis (DKA) is the commonest endocrine emergency encountered in clinical practice. Although in the last 3 decades the average worldwide immediate mortality has decreased from 10% to 5%, survival has not improved strikingly. The pathogenesis of DKA is currently attributed to a combination of two hormonal abnormalities--a relative insulin insufficiency and stress hormone excess (glucagon, catecholamines, cortisol and growth hormone). Withdrawal of exogenous insulin, pancreatic beta cell failure and insulin resistance are factors leading to relative insulin insufficiency. Factors leading to stress hormone excess include fasting, stress and dehydration. The combination of these two hormonal abnormalities leads to impaired carbohydrate utilization and ketonaemia which in turn results in metabolic acidosis with loss of water through acidotic breaths, rise in plasma lipids, hyperglycaemia and glycosuria leading to osmotic diuresis and further loss of water, excretion of partly neutralised ketoacids via the kidney with loss of cations (Na+ and K+). A net increase in protein catabolism which leads to an increased amino acid flux from muscle and an enhanced load of gluconeogenic precursor to the liver and a rise in blood pyruvate and lactate concentration. The prevention of either of these hormonal abnormalities will prevent the development of DKA. The successful outcome in the treatment of DKA is clearly related to the prompt recognition of the diagnosis and the precipitation factors, the severity of the initial metabolic derangements, the judicious use of fluid and electrolyte replacement, the choice, route and dosage of the insulin therapy and above all the close monitoring and meticulous clinical care of the patient throughout the entire course of the treatment. Current acceptable treatment of DKA include the following: adequate fluid replacement: low dose insulin therapy at frequent intervals; adequate potassium replacement from time of first insulin therapy with ECG monitoring; bicarbonate replacement if pH less than 7.1; broad spectrum antibiotics if infections is suspected and other supportive measures. The role of phosphate and magnesium replacement is still controversial. An awareness of the complications during the treatment of DKA including cerebral edema (paradoxical acidosis), altered central nervous system oxygenation, vascular thrombosis, shock, myocardial infarction, pancreatitis, infection, inhalation of vomitus , overhydration, un

Topics: Aged; Bicarbonates; Child; Diabetic Ketoacidosis; Electrolytes; Fluid Therapy; Humans; Insulin; Keto Acids; Ketone Bodies; Liver; Magnesium; Phosphates; Potassium; Sodium; Sodium Bicarbonate

The effect of intravenous bicarbonate on the changes in intermediary metabolites during the initial treatment of diabetic ketoacidosis was examined in 16 patients. The results were compared with the changes seen in 16 patients receiving intravenous saline. Infusion of 150 mmol (mEq) bicarbonate significantly delayed the fall in blood lactate, lactate:pyruvate ratio, and total ketone bodies observed in the saline treated group. No difference in the rate of fall of blood glucose concentration was found. There is no metabolic indication for the use of intravenous bicarbonate in the treatment of diabetic ketoacidosis.

Topics: Adolescent; Adult; Aged; Bicarbonates; Blood Glucose; Diabetic Ketoacidosis; Female; Humans; Ketone Bodies; Lactates; Male; Middle Aged; Pyruvates; Sodium Bicarbonate; Sodium Chloride

Topics: Blood Glucose; Combined Modality Therapy; Continuous Renal Replacement Therapy; Diabetes Mellitus, Type 1; Diabetic Ketoacidosis; Emergencies; Fluid Therapy; Humans; Insulin; Male; Middle Aged; Respiration, Artificial; Sodium Bicarbonate; Sodium-Glucose Transporter 2 Inhibitors

Topics: Antacids; Diabetic Coma; Diabetic Ketoacidosis; Female; Humans; Ketones; Sodium Bicarbonate; Solutions

Patients with diabetic ketoacidosis (DKA) are uniquely predisposed to mucormycosis, an angioinvasive fungal infection with high mortality. Previously, we demonstrated that Rhizopus invades the endothelium via binding of fungal CotH proteins to the host receptor GRP78. Here, we report that surface expression of GRP78 is increased in endothelial cells exposed to physiological concentrations of β-hydroxy butyrate (BHB), glucose, and iron that are similar to those found in DKA patients. Additionally, expression of R. oryzae CotH was increased within hours of incubation with DKA-associated concentrations of BHB, glucose, and iron, augmenting the ability of R. oryzae to invade and subsequently damage endothelial cells in vitro. BHB exposure also increased fungal growth and attenuated R. oryzae neutrophil-mediated damage. Further, mice given BHB developed clinical acidosis and became extremely susceptible to mucormycosis, but not aspergillosis, while sodium bicarbonate reversed this susceptibility. BHB-related acidosis exerted a direct effect on both GRP78 and CotH expression, an effect not seen with lactic acidosis. However, BHB also indirectly compromised the ability of transferrin to chelate iron, as iron chelation combined with sodium bicarbonate completely protected endothelial cells from Rhizopus-mediated invasion and damage. Our results dissect the pathogenesis of mucormycosis during ketoacidosis and reinforce the importance of careful metabolic control of the acidosis to prevent and manage this infection.

Topics: 3-Hydroxybutyric Acid; Animals; Diabetic Ketoacidosis; Disease Models, Animal; Endoplasmic Reticulum Chaperone BiP; Endothelial Cells; Fungal Proteins; Glucose; Heat-Shock Proteins; Host-Pathogen Interactions; Humans; Iron; Male; Mice; Mice, Inbred ICR; Mucormycosis; Rhizopus; Sodium Bicarbonate; Virulence

Topics: Adolescent; Diabetic Ketoacidosis; Humans; Male; Potassium Chloride; Sodium Bicarbonate

Topics: Acid-Base Equilibrium; Brain Edema; Diabetic Ketoacidosis; Humans; Sodium Bicarbonate

Topics: Acid-Base Equilibrium; Brain Edema; Diabetic Ketoacidosis; Humans; Sodium Bicarbonate

Topics: Acid-Base Equilibrium; Brain Edema; Diabetic Ketoacidosis; Humans; Sodium Bicarbonate

Topics: Acid-Base Equilibrium; Brain Edema; Diabetic Ketoacidosis; Humans; Sodium Bicarbonate

New-onset diabetes mellitus after transplant is a well-recognized complication of tacrolimus immunosuppression and commonly occurs as a form of type 2 diabetes mellitus. However, tacrolimus-associated acute pancreatitis causing diabetic ketoacidosis has not been reported in heart transplant patients. We report a 22-year-old women hospitalized owing to diabetic ketoacidosis associated with acute pancreatitis 7 months after a heart transplant. Her immunosuppression included tacrolimus. She was admitted with complaints of polydipsia, anorexia, and abdominal pain of 3 days' duration. Her initial laboratory test revealed a toxic level of tacrolimus (> 30 ng/mL), severe hyperglycemia (39 mmol/L), severe metabolic acidosis (pH 6.9), and ketonuria, although diabetes mellitus had never been diagnosed. Serum amylase and lipase levels and abdominal computed tomography suggested the presence of acute pancreatitis. After correcting the diabetic ketoacidosis and getting the tacrolimus level to the normal range, she was discharged home. Three months later, insulin was replaced with oral hypoglycemic agents. Pancreatitis can present with diabetic ketoacidosis in the recipient of a heart transplant treated with tacrolimus. Clinicians should pay more attention to tacrolimus levels and the risk of pancreatitis.

Topics: Acute Disease; Cardiomyopathy, Dilated; Diabetic Ketoacidosis; Female; Graft Rejection; Heart Transplantation; Humans; Immunosuppressive Agents; Insulin; Pancreatitis; Risk Factors; Sodium Bicarbonate; Tacrolimus; Treatment Outcome; Young Adult

We report a unique case of diabetic ketoacidosis in which a relatively low potassium level on admission was associated with consequent life-threatening and refractory arrhythmia secondary to inappropriate use of intravenous insulin and bicarbonate therapy. The latter was reversed by rapid bolus potassium injection. Although we do not advocate this approach in every case, we emphasise that a bolus injection of potassium may be life saving in such cases. The lessons from this case have led to multidisciplinary meetings and modification of the institute's diabetic ketoacidosis clinical pathway.

Topics: Adult; Diabetic Ketoacidosis; Female; Heart Arrest; Humans; Hypoglycemic Agents; Hypokalemia; Insulin; Potassium Chloride; Sodium Bicarbonate; Young Adult

Hyperkalemia generally is attributable to cell shifts or abnormal renal potassium excretion. Cell shifts account for transient increases in serum potassium levels, whereas sustained hyperkalemia generally is caused by decreased renal potassium excretion. Impaired renal potassium excretion can be caused by a primary decrease in distal sodium delivery, a primary decrease in mineralocorticoid level or activity, or abnormal cortical collecting duct function. Excessive potassium intake is an infrequent cause of hyperkalemia by itself, but can worsen the severity of hyperkalemia when renal excretion is impaired. Before concluding that a cell shift or renal defect in potassium excretion is present, pseudohyperkalemia should be excluded.

Topics: Adult; Aldosterone; Chronic Disease; Diabetes Mellitus, Type 1; Diabetic Ketoacidosis; Glomerular Filtration Rate; Humans; Hyperkalemia; Kidney; Kidney Tubules; Liddle Syndrome; Male; Potassium, Dietary; Renin-Angiotensin System; Sodium Bicarbonate

Topics: Diabetic Ketoacidosis; Humans; Infant, Newborn; Sodium Bicarbonate

Topics: Child; Diabetic Ketoacidosis; Humans; Sodium Bicarbonate

Topics: Diabetic Coma; Diabetic Ketoacidosis; Fluid Therapy; Humans; Sodium Bicarbonate

Topics: Diabetic Ketoacidosis; Humans; Infusions, Intravenous; Sodium Bicarbonate

In this teaching exercise, the goal is to demonstrate how an application of principles of physiology can reveal the basis for a severe degree of acidaemia (pH 6.81, bicarbonate <3 mmol/l (P(HCO(3))), PCO(2) 8 mmHg), why it was tolerated for a long period of time, and the issues for its therapy in an 8-year-old female with diabetic ketoacidosis. The relatively low value for the anion gap in plasma (19 mEq/l) suggested that its cause was both a direct and an indirect loss of NaHCO(3). Professor McCance suggested that ileus due to hypokalaemia might cause this direct loss of NaHCO(3), and that an excessive excretion of ketoacid anions without NH(4)(+) in the urine accounted for the indirect loss of NaHCO(3). In addition, he suspected that another factor also contributing to the severity of the acidaemia was a low input of alkali. He was also able to explain why there was a 16-h delay before there was a rise in the P(HCO(3)) once therapy began. The missing links in this interesting story, including a possible basis for the hypokalaemia, emerge during the discussion between the medical team and Professor McCance.

Topics: Acidosis; Child; Chlorine; Diabetic Ketoacidosis; Female; Humans; Hydrogen-Ion Concentration; Potassium; Sodium; Sodium Bicarbonate

To ascertain whether initial depression of conscious level in children with diabetic ketoacidosis (DKA) is related to hyperosmolality, acidosis or other factors.. In 225 episodes of DKA without evidence of cerebral edema, we examined the relationship between conscious level and initial biochemical variables. We contrasted these findings with those in 42 children who later developed cerebral oedema.. On admission, 42/225 (19%) had mild (pH 7.26-7.35); 96 (44%) moderate (pH 7.11-7.25); and 80 (37%) severe DKA (pH

Topics: Adolescent; Age Factors; Blood Glucose; Brain Edema; Child; Child, Preschool; Consciousness; Diabetes Mellitus, Type 1; Diabetic Ketoacidosis; Female; Humans; Hydrogen-Ion Concentration; Infant; Male; Multivariate Analysis; Osmolar Concentration; Sodium Bicarbonate; Unconsciousness

Acute severe metabolic acidosis associated with lactic acidosis or ketoacidosis can have severe detrimental effects on organ function, and might contribute to mortality. A general consensus exists that elimination of the cause of the acidosis is essential for treatment, but there is controversy concerning the use of base for the treatment of these disorders. Some physicians advocate administration of base when the acidosis is severe to prevent a decrease in cardiac output, whereas others oppose administration of base even when the acidosis is severe given the potential compromise of cardiac function. Nephrologists and critical care specialists are often the physicians developing recommendations for the treatment of severe acid-base disorders.. A short online survey of 20 questions was developed to assess the approach to the treatment of acute metabolic acidosis of program directors of fellowship programs and experts from the specialties of critical care and nephrology.. Although there was variability among individual physicians from both specialties, a larger percentage of nephrologists than critical care physicians queried recommended administration of base for the treatment of lactic acidosis (86% vs 67%) and ketoacidosis (60% vs 28%). Also, critical care physicians in general used a lower level of blood pH when deciding when to initiate treatment. Of the physicians who gave base, most utilized sodium bicarbonate as the form of base given.. The results of this survey indicate that the decisions whether to use base for the treatment of acute severe metabolic acidosis, and under which circumstances, vary among physicians, and indicate the need for further studies to develop evidence-based guidelines for therapy.

Topics: Acidosis; Acidosis, Lactic; Blood; Critical Care; Diabetic Ketoacidosis; Humans; Hydrogen-Ion Concentration; Nephrology; Online Systems; Sodium Bicarbonate; Surveys and Questionnaires

Topics: Adult; Cardiopulmonary Resuscitation; Diabetic Ketoacidosis; Heart Arrest; Humans; Male; Sodium Bicarbonate; Survivors; Treatment Outcome

Topics: Diabetic Ketoacidosis; Emergencies; Humans; Sodium Bicarbonate

Topics: Acid-Base Equilibrium; Diabetic Ketoacidosis; Humans; Hydrogen-Ion Concentration; Hyperglycemia; Sodium Bicarbonate

We shall illustrate that management of patients with an acid-base disorder could be improved if the acid-base analysis was based on a better understanding of basic concepts of physiology. Three concepts of acid-base physiology and their clinical implications are emphasized in a patient with diabetic ketoacidosis. First, when an acid is produced from neutral precursors in the body, there is a net increase in the number of hydrogen ions (H(+)) and new anions. The corollary is that H(+) will be removed when the accompanying anion is metabolized to a neutral end-product or is excreted in the urine with H(+) or ammonium (NH(4)(+)). Second, buffering of H(+) is beneficial if H(+) are removed by bicarbonate rather than being able to bind to proteins. This latter function depends on having a low tissue PCO(2), due to a combination of hyperventilation plus an adequate blood flow rate to vital organs. Third, the kidneys add new bicarbonate to the body when NH(4)(+) is excreted with chloride ions.

Topics: Acid-Base Equilibrium; Anions; Blood Chemical Analysis; Brain; Child; Diabetic Ketoacidosis; Female; Humans; Insulin; Kidney; Models, Biological; Protons; Sodium Bicarbonate

Topics: Diabetic Ketoacidosis; Humans; Sodium Bicarbonate

Topics: Diabetic Ketoacidosis; Humans; Hydrogen-Ion Concentration; Sodium Bicarbonate

Severe acidemia (blood pH < 7.1 to 7.2) suppresses myocardial contractility, predisposes to cardiac arrhythmias, causes venoconstriction, and can decrease total peripheral vascular resistance and blood pressure, reduce hepatic blood flow, and impair oxygen delivery. These alterations in organ function can contribute to increased morbidity and mortality. Although it seemed logical to administer sodium bicarbonate to attenuate acidemia and therefore lessen the impact on cardiac function, the routine use of bicarbonate in the treatment of the most common causes of severe acidemia, diabetic ketoacidosis, lactic acidosis, and cardiac arrest, has been an issue of great controversy. Studies of animals and patients with these disorders have reported conflicting data on the benefits of bicarbonate, showing both beneficial and detrimental effects. Alternative alkalinizing agents, tris-hydroxymethyl aminomethane and Carbicarb, have shown some promise in studies of animals and humans, and reevaluation of these buffers in the treatment of severe acidemic states seems warranted. The potential value of base therapy in the treatment of severe acidemia remains an important issue, and further studies are required to determine which patients should be administered base therapy and what base should be used.

Topics: Acidosis; Acidosis, Lactic; Animals; Arrhythmias, Cardiac; Bicarbonates; Buffers; Calcium; Carbonates; Cardiac Output; Diabetic Ketoacidosis; Drug Combinations; Heart Arrest; Humans; Myocardial Contraction; Oxygen; Potassium; Sodium Bicarbonate; Tromethamine; Vascular Resistance; Water-Electrolyte Balance

The purpose of this study was to review the emergency department management of children presenting in diabetic ketoacidosis (DKA) to determine if current recommendations for fluid therapy are practiced. A 5-year retrospective chart review was conducted of all pediatric patients admitted with DKA to the University of Alberta Hospital. Presenting clinical and laboratory data, the initial fluid therapy, and insulin dose were analyzed. The therapy was also compared between sites of initial presentation (primary, secondary, or tertiary hospital). A total of 49 cases of DKA in 37 patients were reviewed. There were no significant clinical or biochemical differences between patients presenting at the three levels of hospital. Forty-one cases (84%) were given a saline bolus and the mean fluid volume given by 1 hour was 18.3 mL/kg. In the first hour 82% of patients presenting at a primary or secondary centre and 67% of those at the tertiary centre received more than 10 mL/kg. This excessive fluid therapy was also evident after 4 hours. Fluid management of children in DKA is excessive and not in keeping with current recommendations. Education of emergency physicians is needed to reduce fluid therapy and the risk of neurologic complications.

Topics: Alberta; Blood Glucose; Child; Diabetic Ketoacidosis; Emergency Service, Hospital; Fluid Therapy; Humans; Hydrogen-Ion Concentration; Hypoglycemic Agents; Insulin; Retrospective Studies; Sodium Bicarbonate

To determine the sensitivity and specificity of the urine ketone dip test as a screening test for ketonemia in hyperglycemic patients and to compare the performance of the urine ketone dip test with the anion gap and serum bicarbonate level.. This was a prospective study conducted in an urban, university-affiliated public hospital emergency department. Inclusion criteria consisted of (1) patients with known diabetes and hyperglycemia (glucose level>200 mg/dL) and any complaint of illness, or (2) patients with hyperglycemia and symptoms of undiagnosed diabetes mellitus. Urine ketone dip test, serum ketone, and electrolyte levels were determined on all subjects. Sensitivity, specificity, and predictive values along with 95% confidence intervals (CIs) were calculated.. The study group comprised 697 patients, including 98 patients with diabetic ketoacidosis (DKA) and 88 with diabetic ketosis (DK). The sensitivity, specificity, positive, and negative predictive values of the urine ketone dip test for the detection of DKA were 99% (95% CI 97% to 100%), 69% (95% CI 66% to 73%), 35% (95% CI 29% to 41%), and 100% (95% CI 99% to 100%), respectively. For DKA and DK, the sensitivity, specificity, positive, and negative predictive values of the urine ketone dip test were 95% (95% CI 90% to 97%), 80% (95% CI 76% to 83%), 63% (95% CI 57% to 69%) and 98% (95% CI 96% to 99%). The anion gap and serum bicarbonate level were less sensitive but more specific than the urine ketone dip test for the detection of DKA and DK.. The urine ketone dip test has high sensitivity for detecting DKA and a high negative predictive value for excluding DKA in hyperglycemic patients with diabetes with any symptoms of illness. The urine ketone dip test is a better screening test for DKA and DK than the anion gap or serum bicarbonate.

Topics: Acid-Base Equilibrium; Adolescent; Adult; Aged; Aged, 80 and over; Blood Gas Analysis; Cost Savings; Diabetes Complications; Diabetic Ketoacidosis; Emergency Treatment; Female; Humans; Hyperglycemia; Ketone Bodies; Ketosis; Male; Mass Screening; Middle Aged; Prospective Studies; Reagent Strips; Reproducibility of Results; Sensitivity and Specificity; Sodium Bicarbonate

We have attempted to identify any characteristics which could be used to predict the development of cerebral edema in four children under 5 years of age with new onset insulin-dependent diabetes mellitus and diabetic ketoacidosis. We retrospectively analysed and compared the concentration of serum sodium (corrected for serum glucose value) and effective serum osmolality of these 4 children with values of 10 age-matched controls with new onset insulin-dependent diabetes mellitus who did not develop cerebral edema during treatment of diabetic ketoacidosis. The initial serum sodium values of the two groups were not statistically different. Patients who developed cerebral edema had lower initial serum glucose values and effective serum osmolality. During treatment, patients who developed cerebral edema had consistently lower mean serum sodium and osmolality than controls at each 4-h interval after the first 4 h of therapy. Serum sodium and osmolality declined progressively after the initiation of therapy in cerebral edema patients, while remaining stable in controls. These data suggest that children who develop cerebral edema during treatment for diabetic ketoacidosis initially may have a relatively normal serum osmolality and subsequently develop progressive hyponatremia and/or a trend of declining serum sodium before developing cerebral edema.

Topics: Brain Edema; Child, Preschool; Diabetes Mellitus, Type 1; Diabetic Ketoacidosis; Humans; Hyponatremia; Infant; Insulin; Prognosis; Retrospective Studies; Sodium; Sodium Bicarbonate

Although a growing body of evidence supports that alkali therapy in diabetic ketoacidosis (DKA) might be counterproductive, our knowledge about the consequences of this treatment on ketone metabolism is limited. Consequently, we performed clinical and animal studies to further examine this topic. The clinical studies assessed seven patients with DKA treated with continuous insulin infusion at a low dosage. Three of them also received sodium bicarbonate (NaHCO3), whereas the remaining four acted as controls. The group receiving NaHCO3 showed a 6-h delay in the improvement of ketosis as compared with controls. In addition, there was an increase in acetoacetate (AcAc) levels during alkali administration, followed by an increase in 3-hydroxybutyrate (3-OHB) level after its completion. Significant differences were not found between groups in the response of plasma glucose to the overall therapy. The animal study examined the effects of a NaHCO3-rich perfusate on the hepatic production of ketones with the in situ rat-liver preparation. Alkali loading resulted in an immediate increase in the AcAc level followed by increases in both the 3-OHB level and the 3-OHB/AcAc ratio after its completion. Hepatic ketogenesis increased even further, to about twice the basal level, after termination of the NaHCO3 loading. This investigation confirms that alkali administration augments ketone production and unravels an effect of bicarbonate infusion that promotes a selective build up of AcAc in body fluids. The data support that alkali therapy in DKA has nonsaltuary effects in the metabolism and plasma levels of ketones.

Topics: Adult; Animals; Blood Glucose; Diabetic Ketoacidosis; Female; Humans; Ketone Bodies; Male; Rats; Rats, Wistar; Sodium Bicarbonate

To determine if initial emergency department (ED) laboratory parameters in children with diabetic ketoacidosis (DKA) can predict the minimum duration of continuous insulin therapy and aid in ED triage.. Retrospective chart review, over a four-year period.. Tertiary care pediatric center ED.. All patients in DKA, managed with a standard hospital protocol were included. Standard therapy consisted of an intravenous infusion over an hour of normal saline or Ringer's lactate, followed by 0.45% saline (potassium acetate/ phosphate added) at 1.5 times maintenance and insulin infusion (0.1 units/kg/h). New-onset diabetic patients were excluded.. One hundred thirty-two visits (45 patients, 55.5% female) were reviewed. Three of 60 (5%) patient-visits with moderate to severe DKA (serum pH < 7.20 and serum bicarbonate concentration < 10 mmol/L) had their acidosis corrected (serum pH > or = 7.30 or serum bicarbonate concentration > or = 15 mmol/L) within four hours compared to 33 of 72 (46%) patient-visits with mild DKA (serum pH > or = 7.20 or serum bicarbonate concentration > or = 10 mmol/L) (P < 0.0001). The acidosis was corrected within six hours in 69 and 11% of the mild and moderate-severe DKA group, respectively (P < 0.0001).. Initial laboratory presentation can help predict the minimum necessary duration of therapy in pediatric patient with DKA, aid early triage decision in the ED, and select a subgroup of patients who may be considered for outpatient management.

Topics: Adolescent; Ambulatory Care; Child; Child, Preschool; Diabetic Ketoacidosis; Emergency Service, Hospital; Female; Hospitalization; Humans; Hydrogen-Ion Concentration; Insulin; Male; Predictive Value of Tests; Recurrence; Retrospective Studies; Sodium Bicarbonate; Time Factors; Triage

To examine factors determining the haemodynamic and metabolic responses to treatment of diabetic ketoacidosis with alkali, groups of anaesthetised and ventilated rats with either diabetic ketoacidosis (mean arterial pH 6.86-6.96, mean arterial blood pressure 63-67 mm Hg) or hypovolaemic shock due to blood withdrawal (mean pHa 7.25-7.27, mean arterial blood pressure 36-41 mm Hg) were treated with sodium chloride ('saline'), sodium bicarbonate or 'Carbicarb' (equimolar bicarbonate plus carbonate). In the diabetic ketoacidosis series, treatment with either alkali resulted in deterioration of mean arterial blood pressure and substantial elevation of blood lactate, despite a significant rise in myocardial intracellular pH determined by 31P-magnetic resonance spectroscopy. These effects were accompanied by falling trends in the ratios of myocardial phosphocreatine and ATP to inorganic phosphate. Erythrocyte 2,3-bisphosphoglycerate was virtually absent in animals with diabetic ketoacidosis of this severity and duration. In contrast, in shock due to blood withdrawal, infusion of saline or either alkali was accompanied by a transient elevation of mean arterial blood pressure and no significant change in the already elevated blood lactate; erythrocyte 2,3-bisphosphoglycerate was normal in these animals. The effect of alkalinization in rats with severe diabetic ketoacidosis was consistent with myocardial hypoxia, due to the combination of very low initial erythrocyte 2,3-bisphosphoglycerate, alkali-exacerbated left shift of the haemoglobin-oxygen dissociation curve and artificial ventilation. No evidence was found for any beneficial effect of 'Carbicarb' in either series of animals; 'Carbicarb' and sodium bicarbonate could be deleterious in metabolic acidosis of more than short duration.

Topics: 3-Hydroxybutyric Acid; Animals; Blood Pressure; Carbon Dioxide; Carbonates; Diabetes Mellitus, Experimental; Diabetic Ketoacidosis; Drug Combinations; Hemodynamics; Hydrogen-Ion Concentration; Hydroxybutyrates; Lactates; Magnetic Resonance Spectroscopy; Male; Partial Pressure; Rats; Rats, Wistar; Shock; Sodium Bicarbonate; Sodium Chloride; Time Factors

The effects of agents used in the treatment of metabolic acidosis could depend on the induced changes in intracellular pH (pHi). To determine the effect of sodium bicarbonate on hepatic pHi and function, this agent was infused into anesthetized rats with acute metabolic acidosis due to either diabetic ketoacidosis (DKA) or HCl infusion. Hepatic pHi was measured by 31P-magnetic resonance spectroscopy (MRS). A substantial increase in pHi occurred (from 7.13 +/- 0.08 to 7.32 +/- 0.08, P < .05) despite an increase in mixed venous PCO2. Isolated livers from normal rats or those with DKA were perfused at pH 6.8 and normal PCO2. With infusion of sodium bicarbonate, there was again an increase in pHi (delta pHi, + 0.27 +/- 0.06, P < .02) despite increases in both portal and hepatic venous PCO2. Lactate uptake was increased twofold to threefold (P < .001) by bicarbonate infusion in perfusions from both types of animals. Glucose output was increased twofold (P < .001) only in livers from normal animals.

Topics: Acidosis; Animals; Bicarbonates; Diabetic Ketoacidosis; Gluconeogenesis; Glucose; Hydrochloric Acid; Hydrogen-Ion Concentration; Lactates; Liver; Magnetic Resonance Spectroscopy; Male; Perfusion; Rats; Rats, Wistar; Sodium; Sodium Bicarbonate

Topics: Animals; Bicarbonates; Diabetes Mellitus, Experimental; Diabetic Ketoacidosis; Hydrogen; Hydrogen-Ion Concentration; Magnetic Resonance Spectroscopy; Male; Muscles; Phosphorus; Rats; Rats, Wistar; Sodium; Sodium Bicarbonate

Topics: Bicarbonates; Brain Edema; Child, Preschool; Dexamethasone; Diabetes Mellitus, Type 1; Diabetic Ketoacidosis; Humans; Infusions, Intravenous; Insulin; Intubation, Intratracheal; Male; Mannitol; Oxygen Inhalation Therapy; Sodium; Sodium Bicarbonate

Topics: Adult; Aged; Aged, 80 and over; Bicarbonates; Diabetic Ketoacidosis; Erythropoietin; Female; Humans; Hydrogen-Ion Concentration; Kidney Failure, Chronic; Male; Middle Aged; Sodium; Sodium Bicarbonate

Topics: Acidosis, Lactic; Adolescent; Adult; Aged; Bicarbonates; Blood Glucose; Diabetic Ketoacidosis; Dichloroacetic Acid; Female; Humans; Insulin; Lactates; Lactic Acid; Male; Middle Aged; Sodium; Sodium Bicarbonate; Tromethamine

To investigate the effect of low-dose versus high-dose insulin treatment of Kussmaul's coma, the authors treated 2 groups of relevant patients. Group I treated with low-dose insulin in combination with other therapeutic measures achieved a progressive decrease of glycemia within 8 hours. Complications were not registered. Group II on high-dose insulin scheme exhibited a drop in blood sugar resultant in hypoglycemia in 4, hypotonia in 2, brain edema in 1 patient. The absence of complications, availability and simplicity support the advantages of the low-dose regime which is now widely introduced into clinical practice.

Topics: Adolescent; Adult; Aged; Bicarbonates; Diabetic Coma; Diabetic Ketoacidosis; Drug Therapy, Combination; Female; Humans; Hyperglycemia; Hypoglycemia; Infusions, Intravenous; Injections, Intramuscular; Insulin; Male; Middle Aged; Sodium; Sodium Bicarbonate

Fifteen patients with diabetic ketoacidosis treated at ICU in the last eight years with low-dose intravenous insulin infusion are retrospectively revised. Diabetic ketoacidosis was the initial presentation of diabetes in 12 children. Mild infections were the usual starting factor. Only the children with shock of blood pH less than or equal to 7.10 on admission received sodium bicarbonate. The average of pH correction was 6.4 h. The average of glycemia correction (less than or equal to 250 mg/dl) was 5 h with a rate of 120 mg/dl/h. None of children had complications in the course of the treatment, except for one of them who presented cerebral edema. This procedure is a safe and efficacious treated for diabetic ketoacidosis in children.

Topics: Adolescent; Bicarbonates; Blood Glucose; Child; Child, Preschool; Diabetic Ketoacidosis; Female; Humans; Hydrogen-Ion Concentration; Infant; Insulin; Male; Retrospective Studies; Sodium; Sodium Bicarbonate

1. The effects of exogenously (NH4Cl ingestion) and endogenously (streptozotocin-diabetes) generated chronic metabolic acidosis on the abundance of rat renal mRNAs have been examined. 2. Total RNA was translated in vitro and the translation products analyzed by two-dimensional gel electrophoresis. 3. The translation product identified as phosphoenolpyruvate carboxykinase (PEPCK) increased 3.5-fold in both acidosis and diabetes. 4. This increase was not observed in diabetic rats treated with NaHCO3. 5. The abundance of one other translation product increased in acidosis. 6. That of 10 others increased in diabetes, several of which were elevated regardless of acid-base status. 7. The abundance of one translation product decreased in acidosis and diabetes but not in NaHCo3 treated diabetic rats, indicating acid-base regulation of this product. 8. The results establish that the acidosis response is limited to a small number of renal mRNAs and confirm that renal PEPCK is primarily regulated by changes in acid-base status. 9. They also indicate that diabetes affects the abundance of specific renal mRNAs through mechanisms independent of acid-base status.

Topics: Acidosis; Animals; Bicarbonates; Diabetes Mellitus, Experimental; Diabetic Ketoacidosis; Electrophoresis, Polyacrylamide Gel; In Vitro Techniques; Isoelectric Focusing; Kidney; Male; Phosphoenolpyruvate Carboxykinase (GTP); Protein Biosynthesis; Rats; Rats, Inbred Strains; RNA, Messenger; Sodium; Sodium Bicarbonate

Determination of the appropriateness of the compensatory response is essential in evaluation of any acid-base disturbance. Adequate compensation supports the presence of a single acid-base event. Inadequate compensation may indicate that a second primary acid-base event is present or, in some circumstances, that time has been inadequate for maximal physiologic compensation. When acid-base disturbances are mixed, treatment of one disorder may unmask the full pH-altering potential of the second disorder. Close monitoring of patients at risk for the development of acid-base disorders permits detection of problems at a time when intervention may prevent serious complications. Relatively inexpensive and easy-to-use chemical analytic systems to assist early diagnosis are now present in many office-based laboratories.

Topics: Acid-Base Imbalance; Acidosis; Alkalosis; Alkalosis, Respiratory; Bicarbonates; Diabetic Ketoacidosis; Humans; Potassium Chloride; Primary Health Care; Risk Factors; Sodium; Sodium Bicarbonate; Sodium Chloride

Diabetic ketoacidosis can be effectively treated by using a few properly selected tests and more physiologic administration of insulin and intravenous fluids. Insulin is given by intravenous drip at an initial rate of about 0.1 u per kg per hour. The initial hydrating fluid is 5 percent glucose in 0.45 percent saline plus 40 mEq of potassium chloride or buffered potassium phosphate, given at a rate of 250 mL per hour. Arterial blood gas measurements are not needed.

Topics: Bacterial Infections; Bicarbonates; Diabetic Ketoacidosis; Diet, Diabetic; Humans; Insulin; Phosphates; Potassium; Sodium; Sodium Bicarbonate; Sodium Chloride

Topics: Adult; Bicarbonates; Brain Edema; Diabetic Ketoacidosis; Female; Humans; Insulin; Sodium; Sodium Bicarbonate

Diabetic ketoacidosis remains a threat to the survival of an insulin-dependent diabetic. Despite improvements in the management of the condition, mortality is still substantial. In this review, we will discuss approaches to the management of the condition and ways in which incidence, as well as case fatality, might be reduced.

Topics: Bicarbonates; Brain Edema; Diabetic Ketoacidosis; Humans; Insulin; Phosphates; Respiratory Distress Syndrome; Sodium; Sodium Bicarbonate; Thrombosis

A case report of extreme acidosis associated with diabetic metabolic decompensation is described. Treatment with conventional therapy and sodium bicarbonate resulted in complete recovery.

Topics: Acid-Base Equilibrium; Acidosis, Lactic; Adult; Bicarbonates; Diabetes Mellitus, Type 1; Diabetic Ketoacidosis; Humans; Infusions, Intravenous; Lactates; Male; Sodium; Sodium Bicarbonate

Rates of recovery of plasma glucose and bicarbonate levels, arterial pH, and level of consciousness were determined in a retrospective analysis of 95 episodes of severe diabetic ketoacidosis in patients treated with conventional regimens including low-dose insulin, saline, and potassium administration. No significant differences were found between 73 episodes in 52 patients treated with sodium bicarbonate and 22 episodes in 21 patients not undergoing such treatment. In view of these observations, the potential hazards of sodium bicarbonate replacement therapy, and the fact that sodium bicarbonate is still frequently given, the use of intravenous sodium bicarbonate treatment in patients with severe diabetic ketoacidosis requires reevaluation.

Topics: Acid-Base Equilibrium; Adult; Arteries; Bicarbonates; Blood Glucose; Diabetic Ketoacidosis; Female; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Retrospective Studies; Sodium Bicarbonate

Insulin resistance in vivo and impaired insulin binding to isolated adipocytes are characteristic of diabetic ketoacidosis in the rat. To determine the respective roles of diabetes and acidaemia in the genesis of the binding defect, insulin binding to adipocytes from alkali-treated ketoacidotic diabetic and ammonium chloride acidotic rats was studied. Reversal of the acidaemia of ketoacidotic rats by sodium bicarbonate infusion (pH 6.73 +/- 0.027 to 7.35 +/- 0.027, p less than 0.001, n = 12) increased adipocyte insulin binding (0.51 +/- 0.21% to 2 x 10(5) cells/ml, n = 6 untreated versus 1.10 +/- 0.27% to 2 x 10(5) cell, n = 6 treated, p less than 0.05). Scatchard analysis showed this to be due to an increase in insulin receptor concentration. Ammonium chloride infusion caused marked metabolic acidaemia (pH 6.72 +/- 0.04, n = 12) and insulin binding to adipocytes was markedly decreased (0.81 +/- 0.12% to 2 x 10(5) cells/ml n = 6 versus 2.40 +/- 0.22% to 2 x 10(5) cells/ml, n = 6 in controls p less than 0.02), due to a change in receptor concentration. The apparent affinity of the receptor was markedly decreased in diabetic animals compared with normal controls but was unchanged in ammonium chloride acidotic animals. Thus in diabetic ketoacidosis there is both decreased affinity and number of insulin receptors partially reversible by prolonged alkali infusion. Only changes in affinity appeared to be specific for the diabetic state.

Topics: Acidosis; Adipose Tissue; Ammonium Chloride; Animals; Bicarbonates; Binding, Competitive; Diabetic Ketoacidosis; Insulin; Male; Rats; Rats, Inbred Strains; Receptor, Insulin; Sodium Bicarbonate

Topics: Bicarbonates; Diabetic Ketoacidosis; Emergencies; Humans; Insulin; Intraoperative Complications; Postoperative Care; Potassium Compounds; Sodium Bicarbonate