Lactic acidosis in diabetes mellitus in the practice of a family doctor

2020 ◽  
pp. 37-43
Author(s):  
Vsevolod Skvortsov ◽  
Ekaterina Skvortsova ◽  
Georgiy Malyakin ◽  
Elina Goliyeva
Keyword(s):  
Diabetes Mellitus ◽  
Lactic Acid ◽  
Metabolic Acidosis ◽  
Lactic Acidosis ◽  
Chronic Hypoxia ◽  
Pathological Condition ◽  
Family Doctor ◽  
The Body ◽  
Anion Gap ◽  
The Moment

Lactic acidosis is a metabolic acidosis with a large anion gap (> 10 mmol/L) and a level of lactic acid in the blood > 4 mmol/L (according to some definitions, more than 2 mmol/L). This is a critical pathological condition of the body, accompanied by acute or chronic hypoxia, and even coma. The prognosis for the development of this condition is always severe, mortality is 50–80 %. Clear criteria for the diagnosis and treatment of this pathological condition are defined at the moment. This article focuses on the main issues that endocrinologists and resuscitators may encounter when identifying this complex of symptoms.

Metabolic Acidosis

2017 ◽  
Author(s):  
Lisa Cohen ◽  
Dipal Savla ◽  
Shuchi Anand
Keyword(s):  
Metabolic Acidosis ◽  
Lactic Acidosis ◽  
The Body ◽  
Anion Gap ◽  
Plasma Sodium ◽  
Toxic Substances ◽  
Disease States ◽  
Common Causes ◽  
Total Body ◽  
Renal Tubular

Metabolic acidosis is a common clinical entity that can arise from a variety of disease states, medications, and toxic ingestions. This review covers the pathophysiology, diagnosis, and management of common presentations of metabolic acidosis. We have differentiated various causes of metabolic acidosis based on the presence of a normal or elevated anion gap (AG), the sum of serum anions unaccounted for by the measurement of plasma sodium, bicarbonate, and chloride levels. Normal AG metabolic acidosis, or non-AG metabolic acidosis, arises when there is excessive loss of bicarbonate from the gastrointestinal tract or in the urine. This review covers the development and diagnosis of non-AG metabolic acidosis, including a discussion of the spectrum of renal tubular acidosis subtypes. The treatment of non-AG metabolic acidosis is reviewed. Metabolic acidosis with an elevated AG, also called AG metabolic acidosis, develops when exogenous or endogenous nonchloride acid accumulates in the body. The most common causes of AG metabolic acidosis are lactic acidosis and ketoacidosis from starvation, heavy alcohol intake, or diabetes with total body insulin depletion. Medications, toxic substances, and uremia can also lead to AG acidosis. The mechanisms and management of these causes of metabolic acidosis with high AG are covered in detail. Key words: anion-gap acidosis, diabetic ketoacidosis, lactic acidosis, non–anion gap acidosis

scholarly journals A Rare Case of Metformin Associated Lactic Acidosis in a Type 2 Diabetic Patient With No Known Contraindications for Metformin Prescription - a Diagnostic Conundrum!

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A361-A362
Author(s):  
Rima Gandhi ◽  
Randa Abdelmasih ◽  
Alauddin El-Hag ◽  
Elis Cruz Salcedo
Keyword(s):  
Lactic Acid ◽  
Metabolic Acidosis ◽  
Lactic Acidosis ◽  
Diabetic Patient ◽  
Side Effect ◽  
Anion Gap ◽  
Type 2 Dm ◽  
History Of ◽  
Type 2 Diabetic

Abstract Introduction: Metformin is a biguanide drug primarily inhibits hepatic gluconeogenesis and improves insulin sensitivity. Lactic acidosis is a rare complication of metformin. The incidence of Metformin-associated lactic acidosis (MALA) is 6.3 per 100,000 patient-years. Metformin raises lactate levels by inhibiting the conversion of lactate and pyruvate into glucose, shunting towards anaerobic glycolysis. Although, MALA is a reported side effect, metformin is still identified as the drug of choice for Type 2 DM. Here we present a case of MALA in a Type 2 Diabetic patient to shed light on this controversial dilemma. Case Presentation: A 56-year-old African-American male with Type 2 DM and diabetic retinopathy presented after a fall and generalized weakness. Upon arrival, his blood sugar was 22 mg/dL. Patient was vitally stable with signs of dehydration. Home medications includes Metformin 1000 mg twice daily and Glipizide. Laboratory results showed an anion gap metabolic acidosis of 18 mmol/L, Lactic acid was 6.5 mmol/L with repeat of 7.6 mmol/L. Creatinine was 6.0 mg/dL with a BUN of 89 mg/dL. Baseline creatinine from 1 year prior was 1.3–1.5 mg/dL with GFR of 52 mL/min. Hemoglobin A1c was 5.9%. Sodium bicarbonate infusion in 5% dextrose in water. The patient clinically improved with closure of the anion gap and resolution of the metabolic acidosis. Metformin level was 10 mcg/mL. He was discharged on basal insulin and discontinued Metformin and Glipizide. Discussion: Metformin is the first line treatment of Type 2 DM due to its safety. The most common adverse events of Metformin include nausea, bloating, and diarrhea. MALA is a rare, yet serious side effect with a reported mortality of 45%. Higher mortality was associated with increased age, lower arterial pH, and need for mechanical ventilation and vasopressor medicationsThe following criteria should raise concern for MALA in patients with history of Metformin use; elevated lactate level, high anion gap, severe acidosis, low serum bicarbonate level and a history of renal insufficiency. Our patient met the above criteria. The treatment approach for MALA includes adequate supportive measures and correction of acidosis with the acceleration of lactic acid metabolism. Ultimately, if there is no improvement with the aforementioned strategies, then the next step is elimination of the offending agent by renal excretion or dialysis. Fortunately our patient improved with intravenous hydration and did not require advanced intervention. This case highlights the importance of the early recognition of MALA in a patient with unexplained anion gap acidosis and history of Metformin use as even with no risk factors, an episode of gastroenteritis can be enough to impair renal function which increases the risk of MALA. More importantly, it is crucial to educate patients to withhold Metformin in the setting of acute illness and volume contraction to prevent MALA.

scholarly journals Elevated lactic acid during ketoacidosis: pathophysiology and management

2019 ◽  
Vol 7 (3) ◽  
pp. 115-117 ◽  
Author(s):  
Hamda Houssein Ahmed ◽  
David De Bels ◽  
Rachid Attou ◽  
Patrick M. Honore ◽  
Sebastien Redant
Keyword(s):  
Diabetes Mellitus ◽  
Lactic Acid ◽  
Lactic Acidosis ◽  
Rare Complication ◽  
Hypovolemic Shock ◽  
Hematologic Malignancies ◽  
The Body ◽  
Type B ◽  
Acid Base Balance ◽  
Base Balance

Abstract Lactic acidosis results from an acid-base balance disorder of the body due to an excess of lactic acid. It is frequently found in critically ill patients admitted to the intensive care. The most common cause is type A, found in pathologies such as cardiogenic, septic and hypovolemic shock, trauma and severe hypoxemia. The type B is less common and arises without evidence of tissue hypoperfusion or shock. Divers etiologies have been described for this type of hyperlactatemia: Grand Mal seizures, liver failure, hematologic malignancies, congenital enzyme deficiencies, thiamine deficiencies and diabetes mellitus and also alcohol abuse, which may induce a lactic acid under-use or an increased production. The authors describe a rare complication of type 1 Diabetes Mellitus (T1DM), leading to a major and persistent expression of a type B lactic acidosis during ketoacidosis.

Metabolic Acidosis

2017 ◽  
Author(s):  
Lisa Cohen ◽  
Dipal Savla ◽  
Shuchi Anand
Keyword(s):  
Metabolic Acidosis ◽  
Lactic Acidosis ◽  
The Body ◽  
Anion Gap ◽  
Plasma Sodium ◽  
Toxic Substances ◽  
Disease States ◽  
Common Causes ◽  
Total Body ◽  
Renal Tubular

Metabolic acidosis is a common clinical entity that can arise from a variety of disease states, medications, and toxic ingestions. This review covers the pathophysiology, diagnosis, and management of common presentations of metabolic acidosis. We have differentiated various causes of metabolic acidosis based on the presence of a normal or elevated anion gap (AG), the sum of serum anions unaccounted for by the measurement of plasma sodium, bicarbonate, and chloride levels. Normal AG metabolic acidosis, or non-AG metabolic acidosis, arises when there is excessive loss of bicarbonate from the gastrointestinal tract or in the urine. This review covers the development and diagnosis of non-AG metabolic acidosis, including a discussion of the spectrum of renal tubular acidosis subtypes. The treatment of non-AG metabolic acidosis is reviewed. Metabolic acidosis with an elevated AG, also called AG metabolic acidosis, develops when exogenous or endogenous nonchloride acid accumulates in the body. The most common causes of AG metabolic acidosis are lactic acidosis and ketoacidosis from starvation, heavy alcohol intake, or diabetes with total body insulin depletion. Medications, toxic substances, and uremia can also lead to AG acidosis. The mechanisms and management of these causes of metabolic acidosis with high AG are covered in detail. Key words: anion-gap acidosis, diabetic ketoacidosis, lactic acidosis, non–anion gap acidosis

scholarly journals Profound metabolic acidosis from pyroglutamic acidemia: an underappreciated cause of high anion gap metabolic acidosis

CJEM ◽  
2010 ◽  
Vol 12 (05) ◽  
pp. 449-452 ◽  
Author(s):  
Thomas J. Green ◽  
Jan Jaap Bijlsma ◽  
David D. Sweet
Keyword(s):  
Emergency Department ◽  
Lactic Acid ◽  
Metabolic Acidosis ◽  
Ethylene Glycol ◽  
Inborn Errors Of Metabolism ◽  
Pyroglutamic Acid ◽  
Anion Gap ◽  
Emergency Patient ◽  
Inborn Errors ◽  
Chronic Ingestion

ABSTRACTThe workup of the emergency patient with a raised anion gap metabolic acidosis includes assessment of the components of “MUDPILES” (methanol; uremia; diabetic ketoacidosis; paraldehyde; isoniazid, iron or inborn errors of metabolism; lactic acid; ethylene glycol; salicylates). This approach is usually sufficient for the majority of cases in the emergency department; however, there are many other etiologies not addressed in this mnemonic. Organic acids including 5-oxoproline (pyroglutamic acid) are rare but important causes of anion gap metabolic acidosis. We present the case of a patient with profound metabolic acidosis with raised anion gap, due to pyroglutamic acid in the setting of malnutrition and chronic ingestion of acetaminophen.

scholarly journals Acidosis activates complement systemin vitro

1998 ◽  
Vol 7 (6) ◽  
pp. 417-420 ◽  
Author(s):  
Michael Emeis ◽  
Josef Sonntag ◽  
Carsten Willam ◽  
Evelyn Strauss ◽  
Matthias M. Walka ◽  
...  
Keyword(s):  
Lactic Acid ◽  
Metabolic Acidosis ◽  
Hydrochloric Acid ◽  
Lactic Acidosis ◽  
Respiratory Acidosis ◽  
Complement Components ◽  
Blood Samples ◽  
Significant Activation

We investigated thein vitroeffect of different form s of acidosis (pH 7.0) on the formation of anaphylatoxins C3a and C5a. Metabolic acidosis due to addition of hydrochloric acid (10 μ mol/ml blood) or lactic acid (5.5 μ mol/ml) to heparin blood(N=12)caused significant activation of C3a and C5a compared to control (bothp=0.002). Respiratory acidosis activated C3a(p=0.007)and C5a(p=0.003)compared to normocapnic controls. Making blood samples with lactic acidosis hypocapnic resulted in a median pH of 7.37. In this respiratory compensated metabolic acidosis, C3a and C5a were not increased. These experiments show that acidosis itself and not lactate trigger for activation of complement components C3 and C5.

Lactic and hydrochloric acids induce different patterns of inflammatory response in LPS-stimulated RAW 264.7 cells

2004 ◽  
Vol 286 (4) ◽  
pp. R686-R692 ◽  
Author(s):  
John A. Kellum ◽  
Mingchen Song ◽  
Jinyou Li
Keyword(s):  
Immune Response ◽  
Lactic Acid ◽  
Metabolic Acidosis ◽  
Dna Binding ◽  
Lactic Acidosis ◽  
Raw 264.7 Cells ◽  
Complete Medium ◽  
Raw 264.7 ◽  
Dependent Manner ◽  
No Release

Metabolic acidosis frequently complicates sepsis and septic shock and may be deleterious to cellular function. Different types of metabolic acidosis (e.g., hyperchloremic and lactic acidosis) have been associated with different effects on the immune response, but direct comparative studies are lacking. Murine macrophage-like RAW 264.7 cells were cultured in complete medium with lactic acid or HCl to adjust the pH between 6.5 and 7.4 and then stimulated with LPS ( Escherichia coli 0111:B4; 10 ng/ml). Nitric oxide (NO), IL-6, and IL-10 levels were measured in the supernatants. RNA was extracted from the cell pellets, and RT-PCR was performed to amplify corresponding mediators. Gel shift assay was also performed to assess NF-κB DNA binding. Increasing concentrations of acid caused increasing acidification of the media. Trypan blue exclusion and lactate dehydrogenase release demonstrated that acidification did not reduce cell viability. HCl significantly increased LPS-induced NO release and NF-κB DNA binding at pH 7.0 but not at pH 6.5. IL-6 and IL-10 expression (RNA and protein) were reduced with HCl-induced acidification, but IL-10 was reduced much more than IL-6 at low pH. By contrast, lactic acid significantly decreased LPS-induced NO, IL-6, and IL-10 expression in a dose-dependent manner. Lactic acid also inhibited LPS-induced NF-κB DNA binding. Two common forms of metabolic acidosis (hyperchloremic and lactic acidosis) are associated with dramatically different patterns of immune response in LPS-stimulated RAW 264.7 cells. HCl is essentially proinflammatory as assessed by NO release, IL-6-to-IL-10 ratios, and NF-κB DNA binding. By contrast, lactic acidosis is anti-inflammatory.

scholarly journals HYPERLACTATEMIA IN TREATMENT OF DIABETES TYPE 2 BY METFORMIN

2020 ◽  
Vol 23 (2) ◽  
pp. 201-205
Author(s):  
I. V. Tereshchenko
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Lactic Acid ◽  
Lactic Acidosis ◽  
Blood Lactate ◽  
Clinical Manifestations ◽  
Diabetes Type 2 ◽  
Oxygen Starvation

It was previously found that when it is treated type 2 diabetes mellitus (DM2) by metformin, hyperlactemia does not develop or occurs extremely rarely, and due to concomitant pathology. Clinicians usually do not monitor blood lactate levels. Goal: to analyze the frequency of hyperlactatemia in patients with DM2, its possible causes and role in this of metformin, clinical manifestations, ways of elimination and prevention. We observed in the dynamics of 38 patients with DM2 receiving metformin in doses of 1500–3000 mg / day. All patients were tested the level of lactate in the blood. Hyperlactatemia was detected in 6 cases (12.8% of patients), of which two patients (5.3%) showed lactic acidosis: the blood lactate level of them was 4.0 μmol/L and 4.6 μmol/L. A correlation between the level of lactic acid and the dose of metformin has not been established. All observed patients had polymorbidity and compelled polypharmacy. Hypothyroidism was observed in 42.1% of patients; in patients with lactic acidosis hypothyroidism was decompensated, i.e. it was chronic oxygen starvation of tissues. Conclusion: Observations confirmed that treatment of DM2 with metformin is rarely complicated by lactic acidosis and even moderate hyperlactatemia. Complications of diabetes, concomitant pathology and compelled polypharmacy, including metformin, disrupt the metabolism of lactic acid, its elimination, utilization in gluconeogenesis processes; in ≈12.8% of cases, the level of lactate in the blood rises. The risk of lactic acidosis, i.e. death threat occurs in ≈5.3% of patients. Along with the etiological factors of lactic acidosis widely presented in publications in patients with type 2 diabetes mellitus, in ≈42.1% of cases, lactate accumulation is promoted by hypothyroidism, the decompensation of which creates chronic oxygen starvation of tissues. To check periodically the level of lactic acid and monitor the function of the thyroid gland it is necessary in all patients with DM2, even if they are not treated with metformin.

scholarly journals Lactic Acidosis Update for Critical Care Clinicians

2001 ◽  
Vol 12 (suppl 1) ◽  
pp. S15-S19 ◽  
Author(s):  
FRIEDRICH C. LUFT
Keyword(s):  
Lactic Acid ◽  
Lactic Acidosis ◽  
Pyruvate Dehydrogenase ◽  
Case Reports ◽  
Survival Rates ◽  
Lactate Production ◽  
Type A ◽  
Individual Case ◽  
The Body ◽  
Lactate Removal

Abstract. Lactic acidosis is a broad-anion gap metabolic acidosis caused by lactic acid overproduction or underutilization. The quantitative dimensions of these two mechanisms commonly differ by 1 order of magnitude. Overproduction of lactic acid, also termed type A lactic acidosis, occurs when the body must regenerate ATP without oxygen (tissue hypoxia). Circulatory, pulmonary, or hemoglobin transfer disorders are commonly responsible. Overproduction of lactate also occurs with cyanide poisoning or certain malignancies. Underutilization involves removal of lactic acid by oxidation or conversion to glucose. Liver disease, inhibition of gluconeogenesis, pyruvate dehydrogenase (thiamine) deficiency, and uncoupling of oxidative phosphorylation are the most common causes. The kidneys also contribute to lactate removal. Concerns have been raised regarding the role of metformin in the production of lactic acidosis, on the basis of individual case reports. The risk appears to be considerably less than with phenformin and involves patients with underlying severe renal and cardiac dysfunction. Drugs used to treat lactic acidosis can aggravate the condition. NaHCO3 increases lactate production. Treatment of type A lactic acidosis is particularly unsatisfactory. NaHCO3 is of little value. Carbicarb is a mixture of Na2CO3 and NaHCO3 that buffers similarly to NaHCO3 but without net generation of CO2. The results from animal studies are promising; however, clinical trials are sparse. Dichloroacetate stimulates pyruvate dehydrogenase and improves laboratory values, but unfortunately not survival rates, among patients with lactic acidosis. Hemofiltration has been advocated for the treatment of lactic acidosis, on the basis of anecdotal experiences. However, kinetic studies of lactate removal do not suggest that removal can counteract lactate production in any meaningful way. The ideal treatment is to stop acid production by treating the underlying disorder.

Amelioration of hypoxia-induced lactic acidosis by superimposed hypercapnea or hydrochloric acid infusion

1986 ◽  
Vol 250 (4) ◽  
pp. F702-F709 ◽  
Author(s):  
S. Abu Romeh ◽  
R. L. Tannen
Keyword(s):  
Lactic Acid ◽  
Metabolic Acidosis ◽  
Lactic Acidosis ◽  
Blood Lactate ◽  
Acid Production ◽  
Lactic Acid Production ◽  
Respiratory Acidosis ◽  
Control Mechanisms ◽  
Lactate Levels ◽  
Blood Lactate Levels

Recent studies have shown that ketoacid production is exquisitely sensitive to changes in systemic pH, with a decrease inhibiting and an increase stimulating the production rate. To determine whether inhibition of net endogenous acid production is a widely applicable mechanism for the defense of acid-base homeostasis, we examined the effect of superimposed acidosis on lactic acid production by hypoxic rats. Anesthetized paralyzed mechanically ventilated rats with normocapnia increased blood lactate progressively in response to a fractional inspired O2 (FIO2) of 8% (PaO2, 35-38 mmHg) and achieved a level of 7.0 +/- 1.2 mM at 3 h. Superimposition of either mild respiratory acidosis (PCO2, 59 mmHg) or exogenous inorganic metabolic acidosis (intra-arterial HCl sufficient to decrease pH from 7.33 to 7.23) after 1 h of hypoxia dramatically diminished the rise in blood lactate. At the end of the third hour, blood lactate levels averaged 1.7 +/- 0.6 mM with superimposed respiratory acidosis and 2.7 +/- 0.4 mM with superimposed metabolic acidosis, both values being significantly less than the hypoxic controls. Termination of the superimposed respiratory acidosis resulted in a rapid increase in blood lactate levels, demonstrating the reversibility of the pH modulation of lactic acid production. Thus systemic acidosis appears to feed back in a protective fashion to inhibit net lactic acid production in rats with hypoxia-induced lactic acidosis. These findings suggest that finely tuned feedback control mechanisms that keep systemic pH within a narrow range operate under both major conditions of enhanced endogenous acid production (i.e., keto- and lactic acidosis).

Sign in / Sign up

Export Citation Format

Share Document