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Archives de Pediatrie : Organe Officiel... Jun 2010
Review
Topics: Acidosis; Acidosis, Lactic; Bicarbonates; Child; Child, Preschool; Humans; Infant; Infant, Newborn; Metabolism, Inborn Errors; Risk Factors
PubMed: 20654837
DOI: 10.1016/S0929-693X(10)70055-5 -
BMC Endocrine Disorders Apr 2023Euglycemic diabetic ketoacidosis associated with SGLT2 inhibitors is a rare, relatively new and potentially fatal clinical entity, characterized by metabolic acidosis...
BACKGROUND
Euglycemic diabetic ketoacidosis associated with SGLT2 inhibitors is a rare, relatively new and potentially fatal clinical entity, characterized by metabolic acidosis with normal or only moderately elevated glycemia. The mechanisms are not fully understood but involve increased ketogenesis and complex renal metabolic dysfunction, resulting in both ketoacidosis and hyperchloremic acidosis. We report a rare case of fatal empagliflozin-associated acidosis with profound hyperchloremia and review its pathogenesis.
CASE PRESENTATION
A patient with type 2 diabetes mellitus treated with empagliflozin underwent an elective hip replacement surgery. Since day 4 after surgery, he felt generally unwell, leading to cardiac arrest on the day 5. Empagliflozin-associated euglycemic diabetic ketoacidosis with severe hyperchloremic acidosis was identified as the cause of the cardiac arrest.
CONCLUSIONS
This unique case documents the possibility of severe SGLT2 inhibitor-associated mixed metabolic acidosis with a predominant hyperchloremic component. Awareness of this possibility and a high index of suspicion are crucial for correct and early diagnosis.
Topics: Male; Humans; Diabetic Ketoacidosis; Diabetes Mellitus, Type 2; Acidosis; Sodium-Glucose Transporter 2 Inhibitors; Heart Arrest
PubMed: 37060078
DOI: 10.1186/s12902-023-01339-w -
Journal of Nephrology 2006Clinicians should identify life-threatening issues in patients with metabolic acidosis. These threats may be present before therapy begins and/or anticipated after... (Review)
Review
Clinicians should identify life-threatening issues in patients with metabolic acidosis. These threats may be present before therapy begins and/or anticipated after therapy commences. By adding four amendments, short-comings in the commonly used clinical approaches for the diagnosis of metabolic acidosis can be overcome. First, a definition of metabolic acidosis should consider not only the concentration of bicarbonate but also the content of bicarbonate in the extra cellular fluid compartment. The latter requires a quantitative estimate of the ECF volume, which can be obtained using the hematocrit and/or the total protein concentration in plasma. Second, to determine if the basis for metabolic acidosis was the addition of acids or the loss of NaHCO 3 , one must hunt for new anions, not only in plasma, but also in the urine. Third, it is important to measure the venous as well as the arterial PCO2 to assess the capacity to buffer H+ while minimizing H + binding to intracellular proteins. Fourth, to assess the role of the kidney in a patient with metabolic acidosis, the urine osmolal gap and the concentration of creatinine in the urine should be measured to provide an estimate of the rate of excretion of ammonium.
Topics: Acid-Base Equilibrium; Acidosis; Bicarbonates; Diagnosis, Differential; Extracellular Fluid; Humans; Hydrogen-Ion Concentration; Prognosis
PubMed: 16736445
DOI: No ID Found -
British Journal of Hospital Medicine Feb 1986Metabolic acidosis is the most frequent acid-base abnormality observed in the critically ill. Although there are many different causes, in the absence of ketosis and...
Metabolic acidosis is the most frequent acid-base abnormality observed in the critically ill. Although there are many different causes, in the absence of ketosis and renal failure lactic acidosis is the most likely underlying disturbance. Controversy continues to surround the relative roles of the liver and the kidneys in the control of acid-base balance. There is no consensus concerning the use of bicarbonate in the treatment of a life-threatening metabolic acidosis.
Topics: Acidosis; Bicarbonates; Blood; Dichloroacetic Acid; Hemodynamics; Humans; Hydrogen-Ion Concentration; Renal Dialysis; Shock; Sodium; Sodium Bicarbonate; Vasodilator Agents
PubMed: 3015308
DOI: No ID Found -
Pediatric Nephrology (Berlin, Germany) Jan 2011Metabolic acidosis is common in patients with chronic kidney disease (CKD), particularly once the glomerular filtration rate (GFR) falls below 25 ml/min/1.73 m(2). It is... (Review)
Review
Metabolic acidosis is common in patients with chronic kidney disease (CKD), particularly once the glomerular filtration rate (GFR) falls below 25 ml/min/1.73 m(2). It is usually mild to moderate in magnitude with the serum bicarbonate concentration ([HCO(3)(-)]) ranging from 12 to 23 mEq/l. Even so, it can have substantial adverse effects, including development or exacerbation of bone disease, growth retardation in children, increased muscle degradation with muscle wasting, reduced albumin synthesis with a predisposition to hypoalbuminemia, resistance to the effects of insulin with impaired glucose tolerance, acceleration of the progression of CKD, stimulation of inflammation, and augmentation of β(2)-microglobulin production. Also, its presence is associated with increased mortality. The administration of base to patients prior to or after initiation of dialysis leads to improvement in many of these adverse effects. The present recommendation by the National Kidney Foundation Kidney Disease Outcomes Quality Initiative (NKF KDOQI) is to raise serum [HCO(3)(-)] to ≥ 22 mEq/l, whereas Caring for Australians with Renal Impairment (CARI) recommends raising serum [HCO(3)(-)] to >22 mEq/l. Base administration can potentially contribute to volume overload and exacerbation of hypertension as well as to metastatic calcium precipitation in tissues. However, sodium retention is less when given as sodium bicarbonate and sodium chloride intake is concomitantly restricted. Results from various studies suggest that enhanced metastatic calcification is unlikely with the pH values achieved during conservative base administration, but the clinician should be careful not to raise serum [HCO(3)(-)] to values outside the normal range.
Topics: Acidosis; Animals; Bicarbonates; Humans; Kidney Failure, Chronic; Renal Insufficiency, Chronic
PubMed: 20526632
DOI: 10.1007/s00467-010-1564-4 -
Journal of Diabetes Investigation Jul 2019A patient with mitochondrial diabetes mellitus developed diabetic ketoacidosis. During insulin treatment, although diabetic ketoacidosis improved, lactic acidosis...
A patient with mitochondrial diabetes mellitus developed diabetic ketoacidosis. During insulin treatment, although diabetic ketoacidosis improved, lactic acidosis unexpectedly worsened. This clinical course, named "switched metabolic acidosis," could reflect the unique pathophysiology of the mitochondrial disorder.
Topics: Acidosis; Aged; Diabetes Complications; Diabetes Mellitus; Female; Humans; Mitochondrial Diseases; Prognosis
PubMed: 30659759
DOI: 10.1111/jdi.12992 -
Australian Veterinary Journal Jan 2021This case report describes the clinical signs and case management of a 1-year-old neutered male Siberian Husky that accidentally ingested 635 mg/kg of oral...
CASE REPORT
This case report describes the clinical signs and case management of a 1-year-old neutered male Siberian Husky that accidentally ingested 635 mg/kg of oral acetazolamide (a carbonic anhydrase inhibitor). The dog presented with severe tachypnoea due to the development of hyperchloraemic metabolic acidosis and associated hypokalaemia that persisted for 7 days. Clinical and biochemical changes resolved with intravenous and subsequent oral supplementation of sodium bicarbonate and potassium. Complete recovery occurred within 9 days of presentation.
CONCLUSION
To the authors' knowledge, this is the first case that reports overdosage of an oral carbonic anhydrase inhibitor in a dog and subsequent recovery with adequate supplementation and supportive care.
Topics: Acetazolamide; Acidosis; Animals; Carbonic Anhydrase Inhibitors; Dog Diseases; Dogs; Male; Potassium
PubMed: 33025586
DOI: 10.1111/avj.13027 -
Annales Francaises D'anesthesie Et de... 1984
Review
Topics: Acid-Base Equilibrium; Acidosis; Adaptation, Physiological; Asphyxia Neonatorum; Bicarbonates; Buffers; Carbon Dioxide; Child; Child, Preschool; Humans; Infant; Infant, Newborn; Kidney
PubMed: 6433754
DOI: 10.1016/s0750-7658(84)80122-7 -
Paediatric and Perinatal Epidemiology Sep 2020Risks of neonatal and long-term neurological outcomes are influenced by metabolic acidosis at birth and by reduced Apgar scores, even within the normal range (7-10).
BACKGROUND
Risks of neonatal and long-term neurological outcomes are influenced by metabolic acidosis at birth and by reduced Apgar scores, even within the normal range (7-10).
OBJECTIVE
To analyse associations between metabolic acidosis at birth and risks of reduced Apgar scores within the normal range.
METHODS
In a Swedish cohort of term non-malformed infants born between 2008 and 2013, we included 81 861 infants with information from cord blood gas analyses and Apgar score values of 7-10 at 1, 5, and 10 minutes. Poisson log-linear regression analyses were used to examine associations between metabolic acidosis at birth (defined as pH <7.05 or <7.10 and base deficit ≥12) and Apgar scores of 7, 8, and 9. Adjusted risk ratio (RR) and 95% confidence intervals (C). were calculated.
RESULTS
Compared with infants without metabolic acidosis, the adjusted RR of an Apgar score of 9 at 5 minutes was 3.14 (95% CI 2.57, 3.84) in infants with metabolic acidosis (pH <7.05 as cut-off), and 10.13 (95% CI 7.63, 13.45) and 7.60 (95% CI 3.54, 16.33) for Apgar scores of 8 and 7, respectively. Corresponding RRs of Apgar scores at 10 minutes were also substantially increased. The magnitude of RDs varied, but was consistently increased. Both reduced Apgar scores and metabolic acidosis (pH <7.10) influenced neonatal morbidity.
CONCLUSIONS
Metabolic acidosis is associated with increased risks of reduced Apgar scores within the normal range. Due to international variations in the assessment of Apgar score, our findings need to be confirmed in other populations.
Topics: Acidosis; Adolescent; Adult; Apgar Score; Blood Gas Analysis; Case-Control Studies; Female; Fetal Blood; Humans; Hydrogen-Ion Concentration; Infant, Newborn; Linear Models; Male; Pregnancy; Sweden; Term Birth; Young Adult
PubMed: 32133682
DOI: 10.1111/ppe.12663 -
Journal of Nephrology Jan 2022
Topics: Acidosis; Acidosis, Renal Tubular; Endolymphatic Sac; Humans; Infant
PubMed: 34086198
DOI: 10.1007/s40620-021-01085-z