Metabolic acidosis is a primary reduction of bicarbonate (HCO3-), which typically occurs with a decrease of the compensatory Carbondioxid partial pressure (PCO2). The pH can be significantly lower or even below the normal range. Metabolic acidosis are classified according to presence or absence of anions not measured in the serum in acidosis with normal anion, or in with a large anion acidosis. Causes the accumulation of ketones and lactic acid, kidney failure, taking medication or ingestion of toxins (large anion gap) and HCO 3 – loss through the kidneys or the gastrointestinal tract (normal anion gap). Symptoms and clinical signs in severe cases, nausea and vomiting, lethargy and Hyperpnea. The diagnosis is made by clinical and ABG and measurement of serum electrolytes. The underlying cause must be treated. I.v. Administration of sodium bicarbonate may be indicated at very low pH values.
(See also acid-base regulation and acid-base disturbances).
Metabolic acidosis is a primary reduction of bicarbonate (HCO3-), which typically occurs with a decrease of the compensatory Carbondioxid partial pressure (PCO2). The pH can be significantly lower or even below the normal range. Metabolic acidosis are classified according to presence or absence of anions not measured in the serum in acidosis with normal anion, or in with a large anion acidosis. Causes the accumulation of ketones and lactic acid, kidney failure, taking medication or ingestion of toxins (large anion gap) and HCO 3 – loss through the kidneys or the gastrointestinal tract (normal anion gap). Symptoms and clinical signs in severe cases, nausea and vomiting, lethargy and Hyperpnea. The diagnosis is made by clinical and ABG and measurement of serum electrolytes. The underlying cause must be treated. I.v. Administration of sodium bicarbonate may be indicated at very low pH values. (. See also acid-base regulation and acid-base disturbances) aetiology metabolic acidosis is an acid accumulation due to increased acid production or acid uptake Decreased acid excretion Gastrointestinal or renal HCO3 – loss acidemia (arterial pH <7.35) occurs when the acid load exceeding the respiratory compensation capability. The causes are judged by their effects on the divided anion (the anion gap and see Table: Causes of metabolic acidosis). Clinical Calculator: anion gap causes of metabolic acidosis cause Examples Large anion gap ketoacidosis Diabetes Chronic alcoholism malnutrition fasting lactic acidosis Primary (due to physiological processes) shock hypoxia due to lung disease seizures alcohol (chronic abuse) Lactic acidosis ((by exogenous toxins) carbon monoxide iron cyanide isoniazid toluene initially large gap; subsequent excretion of metabolites normalizes the gap) HIV nucleoside reverse transcriptase inhibitors Biguanides (rare except with acute renal failure) Propofol T-Milchsäuremethylester generation Bacterial Überwucherungs- / short bowel syndrome renal failure - metabolized to acids toxins methanol (formate) ethylene glycol (oxalate ) paraldehyde (acetate, chloroacetate) salicylates rhabdomyolysis - Normal anion gap (hyperchloremic acidosis) Gastrointestinal bicarbonate (HCO3 -) - loss colostomy diarrhea intestinal fistulas ileostomy use of ion exchange resins, calcium chloride (CaCl2) magnesium sulfate (MgSO4) urological procedures ureterosigmoidostomy urostomy Renal HCO3- loss tubulointerstitial renal disease Renal tubular acidosis, types 1, 2 and 4 hyperparathyroidism acetazolamide infusion Parenteral Arginine lysine ammonium chloride (NH 4 Cl) Rapide sodium chloride (NaCl) infusion, Other hypoaldosteronism hyperkalemia toluene (late) acidosis with high anion gap The most common causes of metabolic acidosis with high anion gap are: ketoacidosis Lactic acidosis kidney failure intake of toxins The ketoacidosis is a common complication of type -1 diabetes mellitus (see diabetic ketoacidosis), but also occurs in chronic alcoholism (see alcoholic ketoacidosis, malnutrition and to a lesser extent on fasting. In these circumstances, the body from glucose metabolism on the metabolism of free fatty acids (FFA) to. FFAs are (all unmeasured anions) is transformed in the liver into ketone acids, acetoacetate and beta-hydroxybutyrate. Ketoacidosis is a rare manifestation of congenital isovalerischen and methylmalonischen acidemia. Lactic acidosis is the most common in hospitalized patients cause of metabolic acidosis. Lactate accumulation results from a combination of excess formation and reduced utilization of lactate. An excess lactate production occurs during periods of anaerobic metabolism. The most serious form occurs during the various types of shock. A reduced recovery usually occurs in hepatocellular dysfunction by the reduced perfusion of the liver or as part of a general shocks. Diseases and medications that affect mitochondrial function, can cause lactic acidosis. Renal failure causes acidosis with an anion gap by reduced excretion of acids and a decreased HCO3 - reabsorption. The accumulation of sulfates, phosphates, urates and Hippuraten is responsible for the large anion gap. Toxins can have acidic metabolites or cause lactic acidosis. Rhabdomyolysis is a rare cause of metabolic acidosis and one suspects that the acidosis due to the release of protons and anions directly from the muscle entsteht.Azidosen with normal anion gap The most common causes of acidosis with normal anion gap are Gastrointestinal or renal HCO 3 - loss Impaired renal the acid excretion metabolic acidosis with a normal anion gap is also called hyperchloraemic acidosis because renal chloride (Cl) instead of HCO3- reabsorb. Many of the secretions of the gastrointestinal tract are rich in HCO3- (e.g., biliary, pancreatic and intestinal fluids.); Losses due to diarrhea, a drainage tube or fistulas can cause acidosis. (In the colon sigmoideum redirection of the ureter obstruction or by cystectomy) secreted in the ureterosigmoidostomy and loses the colon HCO3- in exchange for Cl- in the urine and absorbed ammonia from urine, the + dissociates into NH3 and H +. Ion exchange resins rarely cause HCO3 - loss by a bond of HCO3-. In renal tubular acidosis is either the H + secretion (Type 1 and 4) or the HCO3 - absorption (type 2) impaired. Impaired Säureexkretion and a normal anion gap also occur in the early stage of renal insufficiency on in the tubulointerstitial kidney disease and taking carbonic anhydrase inhibitors (eg. As acetazolamide). Symptoms and discomfort symptoms and complaints (see Table: Clinical effects of acid-base disturbances) are caused primarily by the underlying disease. A mild acidemia is asymptomatic in itself. A more severe acidemia (pH <7.10) can cause nausea, vomiting and malaise. Symptoms may occur even at higher pH values ??when the acidosis develops quickly. The most characteristic symptom is a Hyperpnea (long, deep breaths at normal frequency), which points to a compensatory increase in alveolar ventilation. This Hyperpnea is not accompanied by a feeling of dyspnea. Tips and risks caused by metabolic acidosis Hyperpnea caused no feeling of breathlessness. Severe, acute acidemia predisposes to cardiac disorders with hypotension and shock, ventricular arrhythmias and coma. A chronic acidemia causes Demineralisationsstörungen of the bones (eg. As rickets, osteomalacia, osteopenia). Clinical Calculator: Arterial blood gas interpretation TreeCalc diagnosis ABG and serum electrolytes calculate anion gap and delta gap Winters formula for calculating compensatory changes tests for finding the cause The recognition of metabolic acidosis and adequate respiratory compensation are discussed in acid-base disorders: diagnosis. The determination of the cause of metabolic acidosis begins with the anion gap. The cause of an elevated anion may be clinically apparent (e. B. hypovolemic shock, missed hemodialysis). If this is not the case, the laboratory values ??for glucose, BUN, creatinine and lactate should be determined and the blood will be tested for possible toxins. The salicylate levels can be determined in most laboratories, the values ??for methanol and ethylene glycol often, but not; an indication of the possible occurrence of these substances is the occurrence of an osmolar gap. The calculated serum osmolarity (2 [sodium] + [glucose] / 18 + BUN / 2.8 + blood alcohol level / 5) is subtracted from the measured osmolarity. A difference of> 10 indicates the presence of an osmotically active substance which is in the case of acidosis with a large anion of methanol or ethylene glycol. Although the intake of ethanol may cause an osmolar gap and a mild acidosis, you should not consider the cause of a severe metabolic acidosis that. If the anion gap normal and not a cause (. Eg severe diarrhea) is obvious that electrolytes should determined in the urine and the anion gap is calculated in the urine as follows: [sodium] + [potassium] – [chloride]. Normal values ??of the anion in the urine are 30-50mEq / l (also in patients with losses via the gastrointestinal tract); an increase speaks for renal HCO3- losses (for the evaluation of renal tubular acidosis, renal tubular acidosis: Diagnosis). In addition, if a metabolic acidosis, a delta gap is calculated (the anion) to identify concomitant metabolic alkalosis and the winter formula (diagnosis) is used to see if the respiratory compensation is appropriate or a second acid base disturbance reflects. Clinical Calculator: Winter equation for the expected pCO2 value of clinical calculator: Urine anion gap treatment treating the cause of sodium bicarbonate (NaHCO3) Primarily for severe acidosis you give it with caution Treatment depends on the underlying cause. When kidney failure and sometimes even with intoxication with ethylene glycol, methanol, and salicylates are required hemodialysis. For the therapy acidemia with NaHCO3 there is a clear indication only under certain circumstances; in other circumstances it may be probably harmful. When the metabolic acidosis from a HCO3 – loss or accumulation of inorganic acids derived (as in a normal acidosis with anion gap), treatment with HCO3- generally safe and appropriate. However, the acidosis caused by the accumulation of organic acids (such as at a acidosis with large anion gap), the use of HCO3- is judged uneven. This therapy option does not reduce the mortality rate significantly and includes various possible risks After treating the underlying cause lactate and ketone acids are rückmetabolisiert to HCO3-. The exogenous supply of HCO3- can therefore lead to an “excessive” metabolic alkalosis. In any case, HCO 3 – lead (by inhibiting the respiratory drive) surrender hypercapnia also sodium and volume overload, hypokalemia and. In addition, an intracellular acidosis is not corrected, since HCO3- can not diffuse through cell membranes. Acidosis may even paradoxically deteriorate since a part of the supplied HCO3- in Carbondioxid (CO2) is converted, which can diffuse into the cells and H + and HCO3- is hydrolyzed. Despite these and other controversies, most experts recommend in case of severe metabolic acidosis (pH <7.10) yet i.v. Administration of HCO3-. H. Treatment requires performing two calculations. The first determined to be up to which value HCO3- raised. This is calculated by the cashier bleaching equation. The value for [H +] is assumed to be 63 nmol / l, (is [H +] of 79 nmol / l, pH ? 7.10 the target for a high Anionenlückeazidose) coincides with a pH of 7.20. 63 = 24 × PCO2 / or HCO3- desired HCO3- = 0.38 × PCO2 HCO3- The amount which is required to achieve these values ??is: NaHCO3 required (mEq) = (desired [HCO3-] - observed [HCO3- ]) x 0.4 x body weight (kg) This quantity NaHCO3 is added over several hours. Blood pH and HCO3 - piegel should be checked 30 minutes to 1 hour after administration. This allows an intermediate equilibration with extravascular HCO 3. Alternatives to NaHCO3 include tromethamine: an amino alcohol which buffers both metabolic (H +) and respiratory (carbonic acid [H2CO3]) acids Carbicarb, an equimolar mixture of NaHCO3 and carbonate (which consumes CO2 and HCO3- generated) dichloroacetate, the oxidation of lactate improves These options compared to NaHCO3 alone no documented benefit and each may cause further complications. The K + deficiency, which is common in metabolic acidosis should be constant verification of the K + in the serum and are treated depending on the severity of oral or parenteral administration of potassium chloride. Summary An metabolic acidosis may be caused by the accumulation of acids, which is caused by increased production of acid or gain, decreased acid excretion or by loss of HCO3- via the gastrointestinal tract or via the kidneys. Metabolic acidosis are then categorized whether the anion gap is large or normal. Causes of acidosis with high anion gap are usually ketoacidosis, lactic acidosis, renal failure, or the inclusion of certain toxins cause of acidosis with normal anion gap is mostly HCO3 - loss from the gastrointestinal tract or through the kidneys Calculate the delta gap to identify concomitant metabolic alkalosis and apply they winter in the formula to see whether the respiratory compensation is appropriately reflects a second acid-base disturbance. Treat the underlying cause. kAHCO3 when acidosis is caused due to a change in HCO3 (Normal anion gap acidosis) appears Intravenous NaHCO3 is controversial (at acidosis with high anion gap can also, if the pH value is <7.00, with a target pH value are contemplated of ? 7.10). Lactic acidosis Lactic acidosis is a metabolic acidosis with high anion gap due to high blood lactate. Lactic acidosis resulting from an overproduction or reduced metabolism of lactate or both. (See also acid-base regulation and acid-base disturbances.) Lactate is a normal by-product of the glucose and amino acid metabolism. There are two main types of lactic acidosis Lactic acidosis Type A lactic acidosis Type B Type T-lactic acids acidosis is an unusual way. Lactic acidosis Type A The most severe form, lactic acidosis, type A, occurs when there is an overproduction of lactic acid in the ischemic tissue, to produce during an O2 deficiency ATP. The overproduction typically occurs during the tissue hypoperfusion in hypovolemic, cardiac or septic shock and is exacerbated by a reduced lactate metabolism in the liver underperfused. Lactic acidosis can The Type B lactic acidosis occurs during normal tissue perfusion general (and thus normal ATP production) and is less threatening even at primary hypoxia on the floor of a lung disease and auftreten.Laktatazidose some hemoglobinopathies type B. The lactate production can be increased by local relative hypoxia, as with heavy use of the muscles, cancer and the use of certain medications or toxins (eg effort, seizures, hypothermic shivering.) (See Table: Causes of metabolic acidosis). Among the drugs include nucleoside reverse transcriptase inhibitors and biguanides, phenformin and (to a lesser extent) metformin; although phenformin was taken in much of the world from the market, it can be still sourced from China (including as a component of some Chinese proprietary medicines). The metabolism can be obtained by a liver disease or a thiamine deficiency reduces sein.Laktatazidose type d The D-Lactic acidosis is an unusual form of lactic acidosis, absorbs at the D-lactic acid, a product of the bacterial carbohydrate metabolism in the colon of patients with jejunoilealem bypass or intestinal resection, systemic becomes. It remains in the circulation, as the lactate dehydrogenase in humans only L-lactate metabolize kann.Symptome and complaints The Symptoms depend on the underlying cause from (eg., Septic shock, intake of toxins) Diagnostic ABG and serum electrolytes calculate anion gap and Delta gap blood lactate levels, the findings of types A and B of lactic acidosis are like other metabolic acidosis. Diagnosis requires blood pH <7.35 and lactate> 5 to 6 mmol / l. Less extreme lactate and pH changes are referred to as hyperlactatemia. In the D-lactic acidosis, the anion is lower than that due to the decrease of the bicarbonate (HCO3-) expected and there may be a gap in the urine occur osmolar (difference between calculated and measured osmolarity). Typical laboratory lactate tests are not sensitive to T-Milchsäuremethylester. Namely T-Milchsäuremethylester are levels available and sometimes necessary to determine the cause of acidosis in patients with multiple possible causes, including intestinal problems to klären.Therapie treating the cause, the treatment of types A and B of lactic acidosis is similar to the treatment of other metabolic acidosis. Treating the cause is of utmost importance. Bicarbonate is potentially dangerous when acidosis with high anion gap, but can be considered when the pH is <7.00, with a target pH of ? 7.10. At d-lactic acidosis is the treatment in the i.v. Administration of fluids, in carbohydrate restriction, and sometimes in orally administered antibiotics (eg. As metronidazole).