Lactic acidosis in diabetic ketoacidosis

Feenstra, Rieneke; Kiewiet, Mink K P; Boerma, E. Christiaan; Avest, Ewoud ter

doi:10.1136/bcr-2014-203594

Cited by 11 publications

(9 citation statements)

References 10 publications

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“…The positive correlation of IPG with lactate as seen in our patients support the possible role of hyperglycemia, in causing lactate elevation, possibly via glyoxalase pathway involving intermediate metabolite methylglyoxal formation and its subsequent conversion into lactate. [ 7 ] This relationship of IPG with lactate demonstrated in our study is in agreement with the findings reported in literature by other investigators.…”

Section: Discussionsupporting

confidence: 94%

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Lactic Acidosis in Diabetic Ketoacidosis

Bhat¹,

Masoodi²,

Bhat³

et al. 2021

Indian Journal of Endocrinology and Metabolism

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Purpose: The lactate level is being increasingly used as a marker of severity of illness and prognosis in multitude of critical conditions. However, its role in diabetic ketoacidosis (DKA) is not well defined. Aim: To determine the prevalence and clinical importance along with the underlying role of metformin in lactic acidosis (LA) in patients admitted with DKA. Methods: A 2-year prospective and observational study involving 62 consenting in hospital DKA patients. Plasma lactate level on arrival, its clinical significance and relationship with morbidity and mortality in patients with DKA was evaluated. Results: The prevalence of LA (lactate ≥2.5 mmol/l) among the study cohort was found to be 55% with significant LA (≥5 mmol/l) documented in 16%. The median lactate level was 2.55 mmol/l (interquartile range, 1.70–3.20). No significant difference in the severity of LA was seen with metformin use. Lactate correlated positively with initial plasma glucose (IPG) ( P = 0.001) and APACHE-II Score ( P = 0.002); correlated negatively with systolic blood pressure ( P = 0.003), pH ( P = 0.002) and severity of DKA ( P = 0.001). After controlling for AKI, APACHE II score and blood pressure, lactate continued to correlate positively with IPG ( P = 0.002). No mortality or significant morbidity was documented in the entire cohort. Conclusions: LA has a significant presence in patients with DKA; however, it is not associated with mortality or significant morbidity. Moreover, there was no significant difference in severity of LA with metformin use. Elevated lactate levels may be an adaptation to provide alternate substrate for metabolism in the presence of hypoinsulinemic state. The study results provide rationale for large well-designed studies evaluating in-depth clinical relationship of lactate in DKA.

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Section: Discussionsupporting

confidence: 94%

“…Elevated lactate is a common finding in DKA[ 5 6 ] and is generally thought to result from anaerobic glycolysis due to relative tissue hypo-perfusion and hypoxemia; however, other pathophysiological mechanisms are also thought to be responsible. [ 5 7 ]…”

Section: Introductionmentioning

confidence: 99%

Lactic Acidosis in Diabetic Ketoacidosis

Bhat¹,

Masoodi²,

Bhat³

et al. 2021

Indian Journal of Endocrinology and Metabolism

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“…Lactic acidosis is a common finding in diabetic ketoacidosis (DKA) and may be multi-factorial in origin, due to metformin use, D-lactate production in erythrocytes (discussed later) and L-lactate production due to increased anaerobic glycolysis [43]. Lactic acidosis has been described in association with hematological malignancies and solid tumors; proposed mechanisms include increased glycolytic activity of the tumor cells (Warburg effect), tumor tissue hypoxia and decreased clearance of lactate due to liver metastases [40,[44][45][46].…”

Section: Causes and Classification Of Lactic Acidosismentioning

confidence: 99%

Lactic acidosis: an update

Seheult

Fitzpatrick

Boran

2017

Clinical Chemistry and Laboratory Medicine (CCLM)

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Lactate is one of the most crucial intermediates in carbohydrate and nonessential amino acid metabolism. The complexity of cellular interactions and metabolism means that lactate can be considered a waste product for one cell but a useful substrate for another. The presence of elevated lactate levels in critically ill patients has important implications for morbidity and mortality. In this review, we provide a brief outline of the metabolism of lactate, the pathophysiology of lactic acidosis, the clinical significance of D-lactate, the role of lactate measurement in acutely ill patients, the methods used to measure lactate in blood or plasma and some of the methodological issues related to interferences in these assays, especially in the case of ethylene glycol poisoning.

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“…Insulin normally inhibits ketogenesis, hence in lack of insulin ketone products are created which can lead to metabolic acidosis. 18 Elevated lactate levels are often seen in diabetic ketoacidosis, and those are consequence of inadequate tissue perfusion (due to decrease in intravascular volume, presence of micro- and macroangiopathy, increase in glycolyzed hemoglobin, and abnormal platelet function). Further, hypoxemia stimulates process of anaerobic glycolysis where pyruvate is metabolized to lactate along with 2 molecules of adenosine triphosphate (ATP).…”

Section: Discussionmentioning

confidence: 99%

Successful Outcomes of Critically Ill Patients with Extreme Metabolic Acidosis Treated with Structured Approach: Case Series

Dragic

Momčičević

Zlojutro

et al. 2021

Clin Med Insights Case Rep

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Introduction: Hydrogen ion concentration which is expressed as pH value is in human blood maintained in narrow physiological range (7.36-7.44 in arterial blood). This range is crucial for normal functioning of most biochemical reactions. Extreme acidosis with pH < 6.8 is incompatible with life, unless pathophysiologic process is rapidly reversed. Timely, standardized, and structured approach to assessment and management of extreme critical illness is essential to maximize the chances of patient’s survival. Cases: We present a series of 3 critically ill patients admitted to Medical intensive care unit (MICU) diagnosed with extreme metabolic acidosis (pH ⩽ 6.8). Each patient was treated using Checklist for Early Recognition and Treatment of Acute Illness and INjury (CERTAIN) which is a standard decision support tool in our MICU. Causes of extreme metabolic acidosis included hemorrhagic shock, sepsis, and acute renal failure and diabetic ketoacidosis. Rapid assessment, prompt resuscitation (IV fluids, vasopressors, mechanical ventilation, and renal replacement), and application of specific causal treatment led to positive outcomes in all 3 patients. Discussion: Medical physiology textbooks set the lower limit of pH value at which life is possible to 6.8. However, examples from clinical practice show that if adequate resuscitation measures are taken early in the acute phase of the disease, the biochemical cascade of reactions that are considered irreversible (at pH ⩽ 6.8) may be reversed after all. Conclusion: Critical care approach to extreme metabolic acidosis is a prime example of applied clinical physiology where basic science and clinical practice connect. With these case series we show that timely and structured approach to critical illness shifts the boundaries of reversibility for some of the most severe physiologic derangements.

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Lactic acidosis in diabetic ketoacidosis

Cited by 11 publications

References 10 publications

Lactic Acidosis in Diabetic Ketoacidosis

Lactic Acidosis in Diabetic Ketoacidosis

Lactic acidosis: an update

Successful Outcomes of Critically Ill Patients with Extreme Metabolic Acidosis Treated with Structured Approach: Case Series

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