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Correction Of Metabolic Acidosis

Treatment Of Metabolic Acidosis.

Treatment Of Metabolic Acidosis.

1. Curr Opin Crit Care. 2003 Aug;9(4):260-5. (1)Departemente d'Anesthesie Reanimation Est, Hopital Saint Roch-5, rue Pierre Devoluy, F-06006, Nice. [email protected] Metabolic acidosis is characterized by a decrease of the blood pH associated witha decrease in the bicarbonate concentration. This may be secondary to a decrease in the strong ion difference or to an increase in the weak acids concentration,mainly the inorganic phosphorus. From a conceptual point of view, two types ofnontoxic metabolic acidosis must be differentiated: the mineral metabolicacidosis that reveals the presence of an excess of nonmetabolizable anions, andthe organic metabolic acidosis that reveals an excess of metabolizable anions.Significance and consequences of these two types of acidosis are radicallydifferent. Mineral acidosis is not caused by a failure in the energy metabolicpathways, and its treatment is mainly symptomatic by correcting the blood pH(alkali therapy) or accelerating the elimination of excessive mineral anions(renal replacement therapy). On the other hand, organic acidosis gives evidencethat a severe underlying metabolic distress is in process. No reliable argumentexists to prove that this acidosis is harmful under these conditions in humans.Experimental data even show that hypoxic cells are able to survive only if themedium is kept acidic. The management of an acute organic metabolic acidosis istherefore primarily based on the cause of the acidosis, and no scientificargument exists to justify the correction of the acid-base imbalance in thiscontext. Continue reading >>

Correcting Metabolic Acidosis - Is It Beneficial? Is It Safe?

Correcting Metabolic Acidosis - Is It Beneficial? Is It Safe?

Correcting metabolic acidosis - is it beneficial? Is it safe? Summarized from Aschner JL, Poland RL. Sodium bicarbonate: basically useless therapy. Pediatrics 2008; 122: 831-35. Metabolic acidosis is the most common disturbance of acid-base balance among the critically ill of all ages, usually due to increased lactate production consequent on inadequate tissue perfusion and/or hypoxemia. The condition is characterized by primary reduction in bicarbonate and pH revealed during arterial blood gas analysis. For more than 50 years, standard care of patients suffering metabolic acidosis, whatever its cause, has included iv administration of the base sodium bicarbonate to correct the acidosis. Although sodium bicarbonate is certainly effective in restoring pH towards normal, in recent years doubt has been cast on the notion that it is necessary to artificially restore pH, and controversy has surrounded the ritual administration of sodium bicarbonate to patients with metabolic acidosis. This controversy is revisited in a recently published paper from two US pediatricians who robustly argue that sodium bicarbonate has no benefit and may cause harm to neonates. A major plank of their argument is the lack of evidence that bicarbonate is beneficial. The treatment was introduced before evidence-based medicine was the norm and the few randomized trials that have been conducted in more recent times have in general failed to show benefit. The article includes an historical perspective on bicarbonate use, and a critical assessment of the rationale for bicarbonate therapy. There follows a brief overview of metabolic acidosis in neonates and a discussion of current evidence about the potential risks and questionable evidence of benefit of bicarbonate therapy for neonates specifically. E Continue reading >>

5.6 Metabolic Acidosis - Correction

5.6 Metabolic Acidosis - Correction

The most important approach to managing a metabolic acidosis is to treat the underlying disorder. Then with supportive management, the body will correct the acid-base disorder. Accurate analysis & diagnosis is essential to ensure the correct treatment is used. Fortunately, in most cases this is not particularly difficult in principle. Remember though that a patient with a severe metabolic acidosis may be very seriously ill and even with optimal management the patient may not survive. The ECLS Approach to Management of Metabolic Acidosis 1. Emergency: Emergency management of immediately life-threatening conditions always has the highest priority. For example, intubation and ventilation for airway or ventilatory control; cardiopulmonary resuscitation; severe hyperkalaemia 2. Cause: Treat the underlying disorder as the primary therapeutic goal. Consequently, accurate diagnosis of the cause of the metabolic acidosis is very important. In some cases (e.g. methanol toxicity) there may be a substantial delay become the diagnosis can be confirmed so management must be based on suggestive evidence otherwise it will be too late. 3. Losses Replace losses (e.g. of fluids and electrolytes) where appropriate. Other supportive care (oxygen administration) is useful. In most cases, IV sodium bicarbonate is NOT necessary, NOT helpful, and may even be harmful so is not generally recommended. 4. Specifics There are often specific problems or complications associated with specific causes or specific cases which require specific management. For example: Ethanol blocking treatment with methanol ingestion; rhabdomyolysis requires management for preventing acute renal failure; haemodialysis can remove some toxins. Some examples of specific treatments for underlying disorders: Fluid, insulin a Continue reading >>

Metabolic Acidosis - Endocrine And Metabolic Disorders - Merck Manuals Professional Edition

Metabolic Acidosis - Endocrine And Metabolic Disorders - Merck Manuals Professional Edition

(Video) Overview of Acid-Base Maps and Compensatory Mechanisms By James L. Lewis, III, MD, Attending Physician, Brookwood Baptist Health and Saint Vincent’s Ascension Health, Birmingham Metabolic acidosis is primary reduction in bicarbonate (HCO3−), typically with compensatory reduction in carbon dioxide partial pressure (Pco2); pH may be markedly low or slightly subnormal. Metabolic acidoses are categorized as high or normal anion gap based on the presence or absence of unmeasured anions in serum. Causes include accumulation of ketones and lactic acid, renal failure, and drug or toxin ingestion (high anion gap) and GI or renal HCO3− loss (normal anion gap). Symptoms and signs in severe cases include nausea and vomiting, lethargy, and hyperpnea. Diagnosis is clinical and with ABG and serum electrolyte measurement. The cause is treated; IV sodium bicarbonate may be indicated when pH is very low. Metabolic acidosis is acid accumulation due to Increased acid production or acid ingestion Acidemia (arterial pH < 7.35) results when acid load overwhelms respiratory compensation. Causes are classified by their effect on the anion gap (see The Anion Gap and see Table: Causes of Metabolic Acidosis ). Lactic acidosis (due to physiologic processes) Lactic acidosis (due to exogenous toxins) Toluene (initially high gap; subsequent excretion of metabolites normalizes gap) HIV nucleoside reverse transcriptase inhibitors Biguanides (rare except with acute kidney injury) Normal anion gap (hyperchloremic acidosis) Renal tubular acidosis, types 1, 2, and 4 The most common causes of a high anion gap metabolic acidosis are Ketoacidosis is a common complication of type 1 diabetes mellitus (see diabetic ketoacidosis ), but it also occurs with chronic alcoholism (see alcoholic ketoacidos Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

OVERVIEW a metabolic acidosis is an abnormal primary process or condition leading to an increase in fixed acids in the blood -> resulting in a fall in arterial plasma bicarbonate CAUSES pathophysiological mechanism: (i) A gain of strong acid (ii) A loss of base the gain of strong acid may be endogenous (eg ketoacids from lipid metabolism) or exogenous (NH4Cl infusion). bicarbonate loss may occur via the bowel (diarrhoea, small bowel fistulas) or via the kidneys (carbonic anhydrase inhibitors, renal tubular acidosis). CLASSIFICATION high anion gap Lactate Toxins – methanol, metformin, phenformin, paraldehyde, propylene glycol, pyroglutamic acidosis, iron, isoniazid, ethanol, ethylene glycol, salicylates, solvents Ketones Renal Normal anion gap Chloride Acetazolamide and Addisons GI causes – diarrhoea, vomiting, fistulas (pancreatic, ureterostomies, small bowel, ileostomies) Extras – RTA MAINTENANCE the disorder is maintained as long as the primary cause persists. in many cases the acid-base disturbance tends to increase in severity while the problem causing it persists though this is not absolute. EFFECTS Respiratory Effects hyperventilation (Kussmaul respirations) – this is the compensatory response shift of oxyhaemoglobin dissociation curve (ODC) to the right – due to the acidosis occurs rapidly decreased 2,3 DPG levels in red cells (shifting the ODC back to the left) -> after 6 hours of acidosis, the red cell levels of 2,3 DPG have declined enough to shift the oxygen dissociation curve (ODC) back to normal. Cardiovascular Effects depression of myocardial contractility sympathetic overactivity resistance to the effects of catecholamines peripheral arteriolar vasodilatation venoconstriction of peripheral veins vasoconstriction of pulmonary arteries (increased Continue reading >>

Metabolic Acidosis In Emergency Medicine Treatment & Management

Metabolic Acidosis In Emergency Medicine Treatment & Management

Emergency Department Care The initial therapeutic goal for patients with severe acidemia is to raise the systemic pH above 7.1-7.2, a level at which dysrhythmias become less likely and cardiac contractility and responsiveness to catecholamines will be restored. Metabolic acidosis can be reversed by treating the underlying condition or by replacing the bicarbonate. The decision to give bicarbonate should be based upon the pathophysiology of the specific acidosis, the clinical state of the patient, and the degree of acidosis. [10] Treating the underlying conditions in high AG states usually is sufficient in reversing the acidosis. Treatment with bicarbonate is unnecessary, except in extreme cases of acidosis when the pH is less than 7.1-7.2. For all cases of diabetic ketoacidosis, the role of bicarbonate is controversial, regardless of the pH or bicarbonate level. In hyperchloremic acidosis, the central problem is with the reabsorption or regeneration of bicarbonate. In these conditions, therapy with bicarbonate makes physiologic sense and is prudent in patients with severe acidosis. Caution with bicarbonate therapy is indicated because of its potential complications, including the following: Continue reading >>

What Is Metabolic Acidosis?

What Is Metabolic Acidosis?

Metabolic acidosis happens when the chemical balance of acids and bases in your blood gets thrown off. Your body: Is making too much acid Isn't getting rid of enough acid Doesn't have enough base to offset a normal amount of acid When any of these happen, chemical reactions and processes in your body don't work right. Although severe episodes can be life-threatening, sometimes metabolic acidosis is a mild condition. You can treat it, but how depends on what's causing it. Causes of Metabolic Acidosis Different things can set up an acid-base imbalance in your blood. Ketoacidosis. When you have diabetes and don't get enough insulin and get dehydrated, your body burns fat instead of carbs as fuel, and that makes ketones. Lots of ketones in your blood turn it acidic. People who drink a lot of alcohol for a long time and don't eat enough also build up ketones. It can happen when you aren't eating at all, too. Lactic acidosis. The cells in your body make lactic acid when they don't have a lot of oxygen to use. This acid can build up, too. It might happen when you're exercising intensely. Big drops in blood pressure, heart failure, cardiac arrest, and an overwhelming infection can also cause it. Renal tubular acidosis. Healthy kidneys take acids out of your blood and get rid of them in your pee. Kidney diseases as well as some immune system and genetic disorders can damage kidneys so they leave too much acid in your blood. Hyperchloremic acidosis. Severe diarrhea, laxative abuse, and kidney problems can cause lower levels of bicarbonate, the base that helps neutralize acids in blood. Respiratory acidosis also results in blood that's too acidic. But it starts in a different way, when your body has too much carbon dioxide because of a problem with your lungs. Continue reading >>

Metabolic Acidosis And Alkalosis

Metabolic Acidosis And Alkalosis

Page Index Metabolic Acidosis. Metabolic Alkalosis Emergency Therapy Treating Metabolic Acidosis Calculating the Dose Use Half the Calculated Dose Reasons to Limit the Bicarbonate Dose: Injected into Plasma Volume Fizzes with Acid Causes Respiratory Acidosis Raises Intracellular PCO2 Subsequent Residual Changes Metabolic Acidosis. The following is a brief summary. For additional information visit: E-Medicine (Christie Thomas) or Wikepedia Etiology: There are many causes of primary metabolic acidosis and they are commonly classified by the anion gap: Metabolic Acidosis with a Normal Anion Gap: Longstanding diarrhea (bicarbonate loss) Uretero-sigmoidostomy Pancreatic fistula Renal Tubular Acidosis Intoxication, e.g., ammonium chloride, acetazolamide, bile acid sequestrants Renal failure Metabolic Acidosis with an Elevated Anion Gap: lactic acidosis ketoacidosis chronic renal failure (accumulation of sulfates, phosphates, uric acid) intoxication, e.g., salicylates, ethanol, methanol, formaldehyde, ethylene glycol, paraldehyde, INH, toluene, sulfates, metformin. rhabdomyolysis For further details visit: E-Medicine (Christie Thomas). Treating Severe Metabolic Acidosis. The ideal treatment for metabolic acidosis is correction of the underlying cause. When urgency dictates more rapid correction, treatment is based on clinical considerations, supported by laboratory evidence. The best measure of the level of metabolic acidosis is the Standard Base Excess (SBE) because it is independent of PCO2. If it is decided to administer bicarbonate, the SBE and the size of the treatable space are used to calculate the dose required: Metabolic Alkalosis Etiology: Primary Metabolic alkalosis may occur from various causes including: Loss of acid via the urine, stools, or vomiting Transfer of Continue reading >>

Sodium Bicarbonate Therapy In Patients With Metabolic Acidosis

Sodium Bicarbonate Therapy In Patients With Metabolic Acidosis

The Scientific World Journal Volume 2014 (2014), Article ID 627673, 13 pages Nephrology Division, Hospital General Juan Cardona, Avenida Pardo Bazán, s/n, Ferrol, 15406 A Coruña, Spain Academic Editor: Biagio R. Di Iorio Copyright © 2014 María M. Adeva-Andany et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Metabolic acidosis occurs when a relative accumulation of plasma anions in excess of cations reduces plasma pH. Replacement of sodium bicarbonate to patients with sodium bicarbonate loss due to diarrhea or renal proximal tubular acidosis is useful, but there is no definite evidence that sodium bicarbonate administration to patients with acute metabolic acidosis, including diabetic ketoacidosis, lactic acidosis, septic shock, intraoperative metabolic acidosis, or cardiac arrest, is beneficial regarding clinical outcomes or mortality rate. Patients with advanced chronic kidney disease usually show metabolic acidosis due to increased unmeasured anions and hyperchloremia. It has been suggested that metabolic acidosis might have a negative impact on progression of kidney dysfunction and that sodium bicarbonate administration might attenuate this effect, but further evaluation is required to validate such a renoprotective strategy. Sodium bicarbonate is the predominant buffer used in dialysis fluids and patients on maintenance dialysis are subjected to a load of sodium bicarbonate during the sessions, suffering a transient metabolic alkalosis of variable severity. Side effects associated with sodium bicarbonate therapy include hypercapnia, hypokalemia, ionized hypocalcemia, and QTc inter Continue reading >>

Acidosis

Acidosis

When your body fluids contain too much acid, it’s known as acidosis. Acidosis occurs when your kidneys and lungs can’t keep your body’s pH in balance. Many of the body’s processes produce acid. Your lungs and kidneys can usually compensate for slight pH imbalances, but problems with these organs can lead to excess acid accumulating in your body. The acidity of your blood is measured by determining its pH. A lower pH means that your blood is more acidic, while a higher pH means that your blood is more basic. The pH of your blood should be around 7.4. According to the American Association for Clinical Chemistry (AACC), acidosis is characterized by a pH of 7.35 or lower. Alkalosis is characterized by a pH level of 7.45 or higher. While seemingly slight, these numerical differences can be serious. Acidosis can lead to numerous health issues, and it can even be life-threatening. There are two types of acidosis, each with various causes. The type of acidosis is categorized as either respiratory acidosis or metabolic acidosis, depending on the primary cause of your acidosis. Respiratory acidosis Respiratory acidosis occurs when too much CO2 builds up in the body. Normally, the lungs remove CO2 while you breathe. However, sometimes your body can’t get rid of enough CO2. This may happen due to: chronic airway conditions, like asthma injury to the chest obesity, which can make breathing difficult sedative misuse deformed chest structure Metabolic acidosis Metabolic acidosis starts in the kidneys instead of the lungs. It occurs when they can’t eliminate enough acid or when they get rid of too much base. There are three major forms of metabolic acidosis: Diabetic acidosis occurs in people with diabetes that’s poorly controlled. If your body lacks enough insulin, keton Continue reading >>

Bicarbonate Therapy In Severe Metabolic Acidosis

Bicarbonate Therapy In Severe Metabolic Acidosis

Abstract The utility of bicarbonate administration to patients with severe metabolic acidosis remains controversial. Chronic bicarbonate replacement is obviously indicated for patients who continue to lose bicarbonate in the ambulatory setting, particularly patients with renal tubular acidosis syndromes or diarrhea. In patients with acute lactic acidosis and ketoacidosis, lactate and ketone bodies can be converted back to bicarbonate if the clinical situation improves. For these patients, therapy must be individualized. In general, bicarbonate should be given at an arterial blood pH of ≤7.0. The amount given should be what is calculated to bring the pH up to 7.2. The urge to give bicarbonate to a patient with severe acidemia is apt to be all but irresistible. Intervention should be restrained, however, unless the clinical situation clearly suggests benefit. Here we discuss the pros and cons of bicarbonate therapy for patients with severe metabolic acidosis. Metabolic acidosis is an acid-base disorder characterized by a primary consumption of body buffers including a fall in blood bicarbonate concentration. There are many causes (Table 1), and there are multiple mechanisms that minimize the fall in arterial pH. A patient with metabolic acidosis may have a normal or even high pH if there is another primary, contravening event that raises the bicarbonate concentration (vomiting) or lowers the arterial Pco2 (respiratory alkalosis). Metabolic acidosis differs from “acidemia” in that the latter refers solely to a fall in blood pH and not the process. A recent online survey by Kraut and Kurtz1 highlighted the uncertainty over when to give bicarbonate to patients with metabolic acidosis. They reported that nephrologists will prescribe therapy at a higher pH compared with Continue reading >>

Treatment Of Acute Non-anion Gap Metabolic Acidosis

Treatment Of Acute Non-anion Gap Metabolic Acidosis

Treatment of acute non-anion gap metabolic acidosis Medical and Research Services VHAGLA Healthcare System, Division of Nephrology, VHAGLA Healthcare System Correspondence to: Jeffrey A. Kraut; E-mail: [email protected] Search for other works by this author on: Clinical Kidney Journal, Volume 8, Issue 1, 1 February 2015, Pages 9399, Jeffrey A. Kraut, Ira Kurtz; Treatment of acute non-anion gap metabolic acidosis, Clinical Kidney Journal, Volume 8, Issue 1, 1 February 2015, Pages 9399, Acute non-anion gap metabolic acidosis, also termed hyperchloremic acidosis, is frequently detected in seriously ill patients. The most common mechanisms leading to this acidbase disorder include loss of large quantities of base secondary to diarrhea and administration of large quantities of chloride-containing solutions in the treatment of hypovolemia and various shock states. The resultant acidic milieu can cause cellular dysfunction and contribute to poor clinical outcomes. The associated change in the chloride concentration in the distal tubule lumen might also play a role in reducing the glomerular filtration rate. Administration of base is often recommended for the treatment of acute non-anion gap acidosis. Importantly, the blood pH and/or serum bicarbonate concentration to guide the initiation of treatment has not been established for this type of metabolic acidosis; and most clinicians use guidelines derived from studies of high anion gap metabolic acidosis. Therapeutic complications resulting from base administration such as volume overload, exacerbation of hypertension and reduction in ionized calcium are likely to be as common as with high anion gap metabolic acidosis. On the other hand, exacerbation of intracellular acidosis due to the excessive generation of carbon dioxide migh Continue reading >>

Approach To The Adult With Metabolic Acidosis

Approach To The Adult With Metabolic Acidosis

INTRODUCTION On a typical Western diet, approximately 15,000 mmol of carbon dioxide (which can generate carbonic acid as it combines with water) and 50 to 100 mEq of nonvolatile acid (mostly sulfuric acid derived from the metabolism of sulfur-containing amino acids) are produced each day. Acid-base balance is maintained by pulmonary and renal excretion of carbon dioxide and nonvolatile acid, respectively. Renal excretion of acid involves the combination of hydrogen ions with urinary titratable acids, particularly phosphate (HPO42- + H+ —> H2PO4-), and ammonia to form ammonium (NH3 + H+ —> NH4+) [1]. The latter is the primary adaptive response since ammonia production from the metabolism of glutamine can be appropriately increased in response to an acid load [2]. Acid-base balance is usually assessed in terms of the bicarbonate-carbon dioxide buffer system: Dissolved CO2 + H2O <—> H2CO3 <—> HCO3- + H+ The ratio between these reactants can be expressed by the Henderson-Hasselbalch equation. By convention, the pKa of 6.10 is used when the dominator is the concentration of dissolved CO2, and this is proportional to the pCO2 (the actual concentration of the acid H2CO3 is very low): TI AU Garibotto G, Sofia A, Robaudo C, Saffioti S, Sala MR, Verzola D, Vettore M, Russo R, Procopio V, Deferrari G, Tessari P To evaluate the effects of chronic metabolic acidosis on protein dynamics and amino acid oxidation in the human kidney, a combination of organ isotopic ((14)C-leucine) and mass-balance techniques in 11 subjects with normal renal function undergoing venous catheterizations was used. Five of 11 studies were performed in the presence of metabolic acidosis. In subjects with normal acid-base balance, kidney protein degradation was 35% to 130% higher than protein synthesi Continue reading >>

Metabolic Acidosis Treatment & Management

Metabolic Acidosis Treatment & Management

Approach Considerations Treatment of acute metabolic acidosis by alkali therapy is usually indicated to raise and maintain the plasma pH to greater than 7.20. In the following two circumstances this is particularly important. When the serum pH is below 7.20, a continued fall in the serum HCO3- level may result in a significant drop in pH. This is especially true when the PCO2 is close to the lower limit of compensation, which in an otherwise healthy young individual is approximately 15 mm Hg. With increasing age and other complicating illnesses, the limit of compensation is likely to be less. A further small drop in HCO3- at this point thus is not matched by a corresponding fall in PaCO2, and rapid decompensation can occur. For example, in a patient with metabolic acidosis with a serum HCO3- level of 9 mEq/L and a maximally compensated PCO2 of 20 mm Hg, a drop in the serum HCO3- level to 7 mEq/L results in a change in pH from 7.28 to 7.16. A second situation in which HCO3- correction should be considered is in well-compensated metabolic acidosis with impending respiratory failure. As metabolic acidosis continues in some patients, the increased ventilatory drive to lower the PaCO2 may not be sustainable because of respiratory muscle fatigue. In this situation, a PaCO2 that starts to rise may change the plasma pH dramatically even without a significant further fall in HCO3-. For example, in a patient with metabolic acidosis with a serum HCO3- level of 15 and a compensated PaCO2 of 27 mm Hg, a rise in PaCO2 to 37 mm Hg results in a change in pH from 7.33 to 7.20. A further rise of the PaCO2 to 43 mm Hg drops the pH to 7.14. All of this would have occurred while the serum HCO3- level remained at 15 mEq/L. In lactic acidosis and diabetic ketoacidosis, the organic anion can r Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Metabolic acidosis is a condition that occurs when the body produces excessive quantities of acid or when the kidneys are not removing enough acid from the body. If unchecked, metabolic acidosis leads to acidemia, i.e., blood pH is low (less than 7.35) due to increased production of hydrogen ions by the body or the inability of the body to form bicarbonate (HCO3−) in the kidney. Its causes are diverse, and its consequences can be serious, including coma and death. Together with respiratory acidosis, it is one of the two general causes of acidemia. Terminology : Acidosis refers to a process that causes a low pH in blood and tissues. Acidemia refers specifically to a low pH in the blood. In most cases, acidosis occurs first for reasons explained below. Free hydrogen ions then diffuse into the blood, lowering the pH. Arterial blood gas analysis detects acidemia (pH lower than 7.35). When acidemia is present, acidosis is presumed. Signs and symptoms[edit] Symptoms are not specific, and diagnosis can be difficult unless the patient presents with clear indications for arterial blood gas sampling. Symptoms may include chest pain, palpitations, headache, altered mental status such as severe anxiety due to hypoxia, decreased visual acuity, nausea, vomiting, abdominal pain, altered appetite and weight gain, muscle weakness, bone pain, and joint pain. Those in metabolic acidosis may exhibit deep, rapid breathing called Kussmaul respirations which is classically associated with diabetic ketoacidosis. Rapid deep breaths increase the amount of carbon dioxide exhaled, thus lowering the serum carbon dioxide levels, resulting in some degree of compensation. Overcompensation via respiratory alkalosis to form an alkalemia does not occur. Extreme acidemia leads to neurological and cardia Continue reading >>

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