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• W2037421788 abstract "Metabolic acidosis is associated with increased mortality of critically ill patients. Lactic acidosis results in higher mortality than metabolic acidosis of a different etiology.1 Metformin-associated lactic acidosis (MALA) is a type of lactic acidosis with mortality as high as 50%.2 Lactate is a common metabolite that must be taken even in physiological conditions. Its daily turnover is about 10–20 mmol/kg. Lactate production is related to the production of pyruvate via glycolysis or deamination of nonessential amino acids. Utilization of lactate is determined by the rate of gluconeogenesis and oxidative phosphorylation. Lactate plays an important role in energetic metabolism both under physiological and pathological conditions.3 Hyperlactatemia, or lactic acidosis, is an alarming metabolic signal of many pathological states, and endogenous clearance of lactate is a commonly used prognostic marker of illness.4 Metformin (dimethylbiguanid), the most frequently used of the anti-diabetic agents, reduces all-cause mortality, diabetes- related death, and diabetes-related complications of patients with diabetes mellitus type 2.5 Except for being able to provide glycemic control without the risk of weight gain, metformin has a positive effect on other metabolic pathways and organ systems. The mechanism by which metformin exerts its effect is still not fully understood. Its main hypoglycemic effect is to inhibit gluconeogenesis. There is also evidence that metformin causes inhibition of complex I of the mitochondrial respiratory chain. This mechanism probably plays an important role in the antidiabetic effect of metformin as well as in the adverse effects of treatment.6 The most severe complication of metformin treatment is lactate accumulation and lactic acidosis. Metformin is exclusively eliminated in urine in its unchanged form. Every cause of increased lactate production, decreased lactate utilization, and metformin accumulation should be considered a contraindication of metformin use. A serum creatinine value greater than 133 μmol/L or creatinine clearance less than 1.0 mL/s also should be considered contraindications.7 A 63-year-old woman admitted to our intensive care unit (ICU) had a history of essential arterial hypertension complicated by hypertensive nephrosclerosis and chronic renal insufficiency. This patient had been estimated to have a serum creatinine level of 165 μmol/L and creatinine clearance of 0.34 mL/s in the last several months of ambulatory surveillance. Previously she had been treated for diabetes mellitus type 2 with insulin and metformin 850 mg 2 times daily. A few days before admission to the hospital, she had suffered a mild respiratory infection. When admitted to our ICU, the patient was somnolent, with acute respiratory failure and refractory hyperdynamic vasoplegic shock requiring high-dose catecholamines (the maximum dose of noradrenalin was 4.44 μg kg−1 min−1) in combination with continuous administration of terlipressin (0.1 mg/h). Hemodynamic monitoring was performed using a Swan-Ganz pulmonary artery catheter. The maximum value of the cardiac index was 5.6 L min−1 (m2)−1, and the systemic vascular resistance index was 843 dyne s/cm5. The echocardiogram showed normal myocardial function. Laboratory findings revealed severe metabolic acidosis: arterial blood pH was 6.54, actual base excess was −33.5 mEq/L, arterial lactate level was 21.2 mmol/L, anion gap (AG) was 47.8 mEq/L, AG corrected on serum albumin and lactate level was 28.3 mEq/L, strong ion gap was 15.2 mEq/L, and serum osmol gap was normal. The deterioration of renal function with a serum creatinine of 993 μmol/L and a serum phosphate of 5.35 mmol/L was evident. Glycemia was in the normal range at the time of admission. Severe sepsis as well as acute intoxication, mesenteric artery occlusion, or other causes were ruled out. It was concluded that MALA was the probable etiology in the course of a mild respiratory infection that progressed to chronic renal failure. The patient was treated by routine lifesaving procedures including mechanical ventilation. In the first 12 hours after admission, we administered a total of 1400 mmol sodium bicarbonate (15.6 mmol/kg) to achieve an arterial blood pH above 7.1. In the fourth hour after admission, we started continuous venovenous hemofiltration (CVVH) with high-volume hemofiltration (40 mL kg−1 h−1) using bicarbonate-buffered fluid (40 mmol/L). Marked hemodynamic improvement was reached in the first 14 hours after admission, with full withdrawal of catecholamines within 7 days. Normalization of arterial pH was achieved within 16 hours, normalization of the actual BE during 21 hours (Figure 1), and a normal serum lactate value was achieved within 39 hours (Figure 2). CVVH was completed after 53 hours. The patient was successfully weaned from mechanical ventilation on the 12th day. On the 14th day, she was discharged from the ICU, and on the 25th day, she was discharged from the hospital without any deterioration of her previous quality of life and without being dependent on hemodialysis. Arterial blood pH and aBE over 20 hours on patient's admission. Arterial blood lactate level over 36 hours on patient's admission. Lactic acidosis is a sporadic but life-threatening complication of the treatment of diabetes mellitus type 2 by metformin. The common estimated incidence of MALA is up to 5–9 cases per 100,000 patient-years, the same as the incidence of lactic acidosis in patients receiving other, nonmetformin antidiabetic agents.8, 9 A systematic review of 197 human studies of patients with diabetes mellitus 2 type treated by metformin versus nonmetformin antidiabetic drugs in a 10-year period did not show any case of lactic acidosis.10 On the other hand, intensivists have reported sporadic MALA cases. In almost 100% of these cases, MALA occurred in the context of violating the contraindications for metformin use or of metformin intoxication.11 The treatment for MALA-induced metabolic acidosis including still-controversial alkalinization is the same as that for severe metabolic acidosis of another cause.12 Hypernatremia is one of the complications of the administration of natrium bicarbonate. In our case, mild hypernatremia lasted for the first 24 hours. The maximum value was 154 mmol/L, and normal values were achieved promptly after CVVH was initiated. Renal replacement therapy is a very effective tool for the treatment of severe metabolic acidosis,13, 14 preferably as a continuous method in a situation of hemodynamic instability. Metformin is a non-protein- bound hydrophilic compound, but its sieving factor is not reported in the literature. The efficacy of CVVH in the treatment of MALA has not been proved by clinical or experimental study, but sporadic references from clinical practice show this method is beneficial.15, 16 Moreover, a highly positive SIG confirmed the contribution of renal failure to severe acidosis in our case. Although the role of acid-base balance normalization using natrium bicarbonate administration to reach hemodynamic stabilization clearly has not been established, the rapid hemodynamic improvement in our patient strongly supports this idea. We consider CVVH the most important part of the complex treatment our patient received. To our knowledge, only a few articles in the literature have reported a lower arterial blood pH caused by metabolic acidosis in a patient who survived. There was a case report of combined uncompensated respiratory acidosis and lactic acidosis with an arterial blood pH of 6.38 related to metformin use and hypothermia (core body temperature 29°C) in a 62-year-old man17; a second case report explained the neardrowning cardiac arrest of a 24-year-old man with hypothermia and metabolic acidosis whose arterial blood pH was 6.33.18 The lowest arterial blood pH reported in the literature (6.30) was described as occurring in an 84-year-old man and related to metformin use, but more data are not available.19 A review of MALA cases in the literature until 1999 showed only two patients with a pH (undetermined) under 6.70, both of whom died.10 Our patient suffered from life-threatening MALA in the context of 2 metformin therapy contraindication violations: chronic renal insufficiency and timely noninterruption of metformin use at the time of acute infection. MALA was complicated by hyperdynamic vasoplegic circulatory shock. The cornerstone of the treatment of our patient was high-volume isovolemic CVVH using bicarbonate-buffered fluid along with support or replacement of vital functions and withdrawal of metformin use. In our opinion, alkalinization by natrium bicarbonate was necessary until CVVH took effect and it was not complicated by a serious hypernatremia because of following CVVH." @default.
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• W2037421788 title "How Severe Acidosis Can a Human Survive? Successful Hemofiltration Use" @default.
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