diabetestalk.net

Metabolic Acidosis Pathophysiology

Metabolic Acidosis: Pathophysiology, Diagnosis And Management

Metabolic Acidosis: Pathophysiology, Diagnosis And Management

Jeffrey A. Kraut, MD is Chief of Dialysis in the Division of Nephrology at the Greater Los Angeles Veterans Administration Healthcare System, Professor of Medicine at the David Geffen School of Medicine at UCLA, and an investigator at the UCLA Membrane Biology Laboratory, Los Angeles, CA, USA. He completed his nephrology training at the TuftsNew England Medical Center where he performed basic research examining the mechanisms regulating acid excretion by the kidney. His present research is focused on delineating the mechanisms contributing to cellular damage with various acidbase disturbances, including metabolic acidosis, with the goal of developing newer treatment strategies. Nicolaos E. Madias, MD is Chairman of the Department of Medicine at St. Elizabeth's Medical Center in Boston, and Maurice S. Segal, MD Professor of Medicine at Tufts University School of Medicine, Boston, MA, USA. He completed his nephrology training at TuftsNew England Medical Center. He has previously served as Chief of the Division of Nephrology at TuftsNew England Medical Center, Established Investigator of the American Heart Association, member of the Internal Medicine and Nephrology Boards of the American Board of Internal Medicine, and Executive Academic Dean and Dean ad interim of Tufts University School of Medicine. His research interests are focused on acidbase and electrolyte physiology and pathophysiology. Nature Reviews Nephrology volume 6, pages 274285 (2010) Metabolic acidosis is characterized by a primary reduction in serum bicarbonate (HCO3) concentration, a secondary decrease in the arterial partial pressure of carbon dioxide (PaCO2) of 1 mmHg for every 1 mmol/l fall in serum HCO3 concentration, and a reduction in blood pH. Acute forms (lasting minutes to several days) and chro Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Metabolic acidosis occurs when the body produces too much acid. It can also occur when the kidneys are not removing enough acid from the body. There are several types of metabolic acidosis. Diabetic acidosis develops when acidic substances, known as ketone bodies, build up in the body. This most often occurs with uncontrolled type 1 diabetes. It is also called diabetic ketoacidosis and DKA. Hyperchloremic acidosis results from excessive loss of sodium bicarbonate from the body. This can occur with severe diarrhea. Lactic acidosis results from a buildup of lactic acid. It can be caused by: Alcohol Cancer Exercising intensely Liver failure Medicines, such as salicylates Other causes of metabolic acidosis include: Kidney disease (distal renal tubular acidosis and proximal renal tubular acidosis) Poisoning by aspirin, ethylene glycol (found in antifreeze), or methanol Continue reading >>

Metabolic Acidosis | Pathway Medicine

Metabolic Acidosis | Pathway Medicine

Metabolic Acidosis is a pathophysiological category of acidosis that refers to any cause of decreased ECF pH not due to a ventilatory defect (i.e. Respiratory Acidosis). Although the primary metabolic disturbance can cause a significant decrease in blood pH, respiratory compensatory mechanisms can largely correct the pH over several hours. The fundamental primary disturbance in a metabolic acidosis is a decrease in the levels of ECF bicarbonate concentration ([HCO3-]). Decreased bicarbonate results in an misalignment of the Henderson-Hasselbalch Equation for the bicarbonate buffer which largely determines the pH of the extracellular fluid. Mathematically, the reduced ECF pH results from an increase in the ratio between the partial pressure of arterial carbon dioxide (PaCO2) relative to the ECF concentration of bicarbonate ([HCO3-]). More colloquially, metabolic acidoses are caused by a pathologic consumption of the weak base form of the bicarbonate buffer, that is bicarbonate (HCO3-), resulting in a decrease in ECF pH. Metabolic Acidoses can be compensated by the actions of the lungs which serve to realign the bicarbonate buffer Henderson-Hasselbalch Equation over a period of hours. As described in Respiratory Acid-Base Control , the lungs respond to acidosis by increasing alveolar ventilation , essentially a physiological hyperventilation, which in turn reduces the PaCO2. The decreased PaCO2 realigns the Henderson-Hasselbalch Equation for the bicarbonate buffer and thus largely corrects the ECF pH. Consequently, a respiratory-compensated metabolic acidosis is characterized by decreased levels of ECF bicarbonate (caused by the primary metabolic disturbance) as well as decreased levels of PaCO2 (caused by the respiratory compensation). More colloquially, the lungs compe Continue reading >>

Metabolic Acidosis: Pathophysiology, Diagnosis And Management

Metabolic Acidosis: Pathophysiology, Diagnosis And Management

Abstract | Metabolic acidosis is characterized by a primary reduction in serum bicarbonate (HCO3 concentration, a secondary decrease in the arterial partial pressure of carbon dioxide (PaCO2) of ~1 mmHg for concentration, and a reduction in blood pH. Acute forms (lasting minutes to several days) and chronic forms (lasting weeks to years) of the disorder can occur, for which the underlying cause/s and resulting adverse effects may differ. Acute forms of metabolic acidosis most frequently result from the overproduction of organic acids such as ketoacids or lactic acid; by contrast, chronic metabolic acidosis often reflects bicarbonate wasting and/or impaired renal acidification. The calculation of the serum ] + [Cl]), aids diagnosis by classifying the disorders into categories of normal (hyperchloremic) anion gap or elevated anion gap. These categories can overlap, however. Adverse effects of acute metabolic acidosis primarily include decreased cardiac output, arterial dilatation with hypotension, altered oxygen delivery, decreased ATP production, predisposition to arrhythmias, and impairment of the immune response. The main adverse effects of chronic metabolic acidosis are increased muscle degradation and abnormal bone metabolism. Using base to treat acute metabolic acidosis is controversial because of a lack of definitive benefit and because of potential complications. By contrast, the administration of base for the treatment of chronic metabolic acidosis is associated with improved cellular Kraut, J. A. & Madias, N. E. Nat. Rev. Nephrol. 6, 274285 (2010); publshed online 23 March 2010; doi:10.1038/nrneph.2010.33 Metabolic acidosis is characterized by a primary reduc- tion in the serum concentration of bicarbonate (HCO3 a secon dary decrease in the arterial partial pre Continue reading >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Diabetic ketoacidosis is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis. Hyperglycemia causes an osmotic diuresis with significant fluid and electrolyte loss. DKA occurs mostly in type 1 diabetes mellitus (DM). It causes nausea, vomiting, and abdominal pain and can progress to cerebral edema, coma, and death. DKA is diagnosed by detection of hyperketonemia and anion gap metabolic acidosis in the presence of hyperglycemia. Treatment involves volume expansion, insulin replacement, and prevention of hypokalemia. Diabetic ketoacidosis (DKA) is most common among patients with type 1 diabetes mellitus and develops when insulin levels are insufficient to meet the body’s basic metabolic requirements. DKA is the first manifestation of type 1 DM in a minority of patients. Insulin deficiency can be absolute (eg, during lapses in the administration of exogenous insulin) or relative (eg, when usual insulin doses do not meet metabolic needs during physiologic stress). Common physiologic stresses that can trigger DKA include Some drugs implicated in causing DKA include DKA is less common in type 2 diabetes mellitus, but it may occur in situations of unusual physiologic stress. Ketosis-prone type 2 diabetes is a variant of type 2 diabetes, which is sometimes seen in obese individuals, often of African (including African-American or Afro-Caribbean) origin. People with ketosis-prone diabetes (also referred to as Flatbush diabetes) can have significant impairment of beta cell function with hyperglycemia, and are therefore more likely to develop DKA in the setting of significant hyperglycemia. SGLT-2 inhibitors have been implicated in causing DKA in both type 1 and type 2 DM. Continue reading >>

Acid-base Physiology

Acid-base Physiology

8.4.1 Is this the same as normal anion gap acidosis? In hyperchloraemic acidosis, the anion-gap is normal (in most cases). The anion that replaces the titrated bicarbonate is chloride and because this is accounted for in the anion gap formula, the anion gap is normal. There are TWO problems in the definition of this type of metabolic acidosis which can cause confusion. Consider the following: What is the difference between a "hyperchloraemic acidosis" and a "normal anion gap acidosis"? These terms are used here as though they were synonymous. This is mostly true, but if hyponatraemia is present the plasma [Cl-] may be normal despite the presence of a normal anion gap acidosis. This could be considered a 'relative hyperchloraemia'. However, you should be aware that in some cases of normal anion-gap acidosis, there will not be a hyperchloraemia if there is a significant hyponatraemia. In a disorder that typically causes a high anion gap disorder there may sometimes be a normal anion gap! The anion gap may still be within the reference range in lactic acidosis. Now this can be misleading to you when you are trying to diagnose the disorder. Once you note the presence of an anion gap within the reference range in a patient with a metabolic acidosis you naturally tend to concentrate on looking for a renal or GIT cause. 1. One possibility is the increase in anions may be too low to push the anion gap out of the reference range. In lactic acidosis, the clinical disorder can be severe but the lactate may not be grossly high (eg lactate of 6mmol/l) and the change in the anion gap may still leave it in the reference range. So the causes of high anion gap acidosis should be considered in patients with hyperchloraemic acidosis if the cause of the acidosis is otherwise not apparent. Continue reading >>

Metabolic Acidosis: Pathophysiology, Diagnosis And Management.

Metabolic Acidosis: Pathophysiology, Diagnosis And Management.

Nat Rev Nephrol. 2010 May;6(5):274-85. doi: 10.1038/nrneph.2010.33. Epub 2010 Mar 23. Metabolic acidosis: pathophysiology, diagnosis and management. Division of Nephrology, Veterans Administration Greater Los Angeles Healthcare System, 11301 Wilshire Boulevard, Los Angeles, CA 90073, USA. Metabolic acidosis is characterized by a primary reduction in serum bicarbonate (HCO(3)(-)) concentration, a secondary decrease in the arterial partial pressure of carbon dioxide (PaCO(2)) of approximately 1 mmHg for every 1 mmol/l fall in serum HCO(3)(-) concentration, and a reduction in blood pH. Acute forms (lasting minutes to several days) and chronic forms (lasting weeks to years) of the disorder can occur, for which the underlying cause/s and resulting adverse effects may differ. Acute forms of metabolic acidosis most frequently result from the overproduction of organic acids such as ketoacids or lactic acid; by contrast, chronic metabolic acidosis often reflects bicarbonate wasting and/or impaired renal acidification. The calculation of the serum anion gap, calculated as [Na(+)] - ([HCO(3)(-)] + [Cl(-)]), aids diagnosis by classifying the disorders into categories of normal (hyperchloremic) anion gap or elevated anion gap. These categories can overlap, however. Adverse effects of acute metabolic acidosis primarily include decreased cardiac output, arterial dilatation with hypotension, altered oxygen delivery, decreased ATP production, predisposition to arrhythmias, and impairment of the immune response. The main adverse effects of chronic metabolic acidosis are increased muscle degradation and abnormal bone metabolism. Using base to treat acute metabolic acidosis is controversial because of a lack of definitive benefit and because of potential complications. By contrast, the ad 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 >>

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 >>

A Comprehensive Review Of Metabolic Acidosis

A Comprehensive Review Of Metabolic Acidosis

A comprehensive review of metabolic acidosis Summarized from Kraut J, Madias N. Metabolic acidosis: pathophysiology diagnosis and management. Nat Rev Nephrol 2010; 6: 274-85 Arterial blood gas analysis is used to assess and monitor patient acid-base status. Disturbance of acid-base balance is classified to one of four main types depending on the pH, pCO2(a) and bicarbonate results generated during blood gas analysis; the four types are respiratory acidosis, respiratory alkalosis, metabolic acidosis and metabolic alkalosis. A recent review article focuses on one of these disturbances, metabolic acidosis, which is characterized by primary decrease in bicarbonate and compensatory decrease in pCO2(a). pH may be either reduced (if compensation is incomplete) or normal (if compensation is complete). This wide-ranging, comprehensive review includes discussion of epidemiology, pathophysiology, clinical consequences and management of metabolic acidosis. The authors distinguish acute metabolic acidosis (lasting hours/days) from the much less common, chronic metabolic acidosis, which can last for years. Acute metabolic acidosis is a common feature of serious illness; a study quoted in the review suggests it affects around two thirds of all patients admitted to intensive care. In broad terms metabolic acidosis arises as a result of net loss of bicarbonate or excessive addition of acid. Discussion of pathophysiology includes detailed consideration of the role of the kidney in regulating acid-base balance, focusing particularly on mechanisms involved in the maintenance of sufficient bicarbonate in blood to buffer metabolic acids. Distinguishing pure metabolic acidosis from a mixed respiratory/metabolic acidosis on the basis of the hypoventilatory response (i.e. magnitude of the redu Continue reading >>

Metabolic Acidosis: Pathophysiology, Diagnosis And Management: Pathophysiology Of Metabolic Acidosis

Metabolic Acidosis: Pathophysiology, Diagnosis And Management: Pathophysiology Of Metabolic Acidosis

Recommendations for the treatment of acute metabolic acidosis Gunnerson, K. J., Saul, M., He, S. & Kellum, J. Lactate versus non-lactate metabolic acidosis: a retrospective outcome evaluation of critically ill patients. Crit. Care Med. 10, R22-R32 (2006). Eustace, J. A., Astor, B., Muntner, P M., Ikizler, T. A. & Coresh, J. Prevalence of acidosis and inflammation and their association with low serum albumin in chronic kidney disease. Kidney Int. 65, 1031-1040 (2004). Kraut, J. A. & Kurtz, I. Metabolic acidosis of CKD: diagnosis, clinical characteristics, and treatment. Am. J. Kidney Dis. 45, 978-993 (2005). Kalantar-Zadeh, K., Mehrotra, R., Fouque, D. & Kopple, J. D. Metabolic acidosis and malnutrition-inflammation complex syndrome in chronic renal failure. Semin. Dial. 17, 455-465 (2004). Kraut, J. A. & Kurtz, I. Controversies in the treatment of acute metabolic acidosis. NephSAP 5, 1-9 (2006). Cohen, R. M., Feldman, G. M. & Fernandez, P C. The balance of acid base and charge in health and disease. Kidney Int. 52, 287-293 (1997). Rodriguez-Soriano, J. & Vallo, A. Renal tubular acidosis. Pediatr. Nephrol. 4, 268-275 (1990). Wagner, C. A., Devuyst, O., Bourgeois, S. & Mohebbi, N. Regulated acid-base transport in the collecting duct. Pflugers Arch. 458, 137-156 (2009). Boron, W. F. Acid base transport by the renal proximal tubule. J. Am. Soc. Nephrol. 17, 2368-2382 (2006). Igarashi, T., Sekine, T. & Watanabe, H. Molecular basis of proximal renal tubular acidosis. J. Nephrol. 15, S135-S141 (2002). Sly, W. S., Sato, S. & Zhu, X. L. Evaluation of carbonic anhydrase isozymes in disorders involving osteopetrosis and/or renal tubular acidosis. Clin. Biochem. 24, 311-318 (1991). Dinour, D. et al. A novel missense mutation in the sodium bicarbonate cotransporter (NBCe1/ SLC4A4) Continue reading >>

Metabolic Acidosis: Pathophysiology, Diagnosis And Management

Metabolic Acidosis: Pathophysiology, Diagnosis And Management

Jeffrey A. Kraut, MD is Chief of Dialysis in the Division of Nephrology at the Greater Los Angeles Veterans Administration Healthcare System, Professor of Medicine at the David Geffen School of Medicine at UCLA, and an investigator at the UCLA Membrane Biology Laboratory, Los Angeles, CA, USA. He completed his nephrology training at the TuftsNew England Medical Center where he performed basic research examining the mechanisms regulating acid excretion by the kidney. His present research is focused on delineating the mechanisms contributing to cellular damage with various acidbase disturbances, including metabolic acidosis, with the goal of developing newer treatment strategies. Nicolaos E. Madias, MD is Chairman of the Department of Medicine at St. Elizabeth's Medical Center in Boston, and Maurice S. Segal, MD Professor of Medicine at Tufts University School of Medicine, Boston, MA, USA. He completed his nephrology training at TuftsNew England Medical Center. He has previously served as Chief of the Division of Nephrology at TuftsNew England Medical Center, Established Investigator of the American Heart Association, member of the Internal Medicine and Nephrology Boards of the American Board of Internal Medicine, and Executive Academic Dean and Dean ad interim of Tufts University School of Medicine. His research interests are focused on acidbase and electrolyte physiology and pathophysiology. Nature Reviews Nephrology volume 6, pages 274285 (2010) Metabolic acidosis is characterized by a primary reduction in serum bicarbonate (HCO3) concentration, a secondary decrease in the arterial partial pressure of carbon dioxide (PaCO2) of 1 mmHg for every 1 mmol/l fall in serum HCO3 concentration, and a reduction in blood pH. Acute forms (lasting minutes to several days) and chro Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find one of our health articles more useful. See also separate Lactic Acidosis and Arterial Blood Gases - Indications and Interpretations articles. Description Metabolic acidosis is defined as an arterial blood pH <7.35 with plasma bicarbonate <22 mmol/L. Respiratory compensation occurs normally immediately, unless there is respiratory pathology. Pure metabolic acidosis is a term used to describe when there is not another primary acid-base derangement - ie there is not a mixed acid-base disorder. Compensation may be partial (very early in time course, limited by other acid-base derangements, or the acidosis exceeds the maximum compensation possible) or full. The Winter formula can be helpful here - the formula allows calculation of the expected compensating pCO2: If the measured pCO2 is >expected pCO2 then additional respiratory acidosis may also be present. It is important to remember that metabolic acidosis is not a diagnosis; rather, it is a metabolic derangement that indicates underlying disease(s) as a cause. Determination of the underlying cause is the key to correcting the acidosis and administering appropriate therapy[1]. Epidemiology It is relatively common, particularly among acutely unwell/critical care patients. There are no reliable figures for its overall incidence or prevalence in the population at large. Causes of metabolic acidosis There are many causes. They can be classified according to their pathophysiological origin, as below. The table is not exhaustive but lists those that are most common or clinically important to detect. Increased acid Continue reading >>

Pathogenesis, Consequences, And Treatment Of Metabolic Acidosis In Chronic Kidney Disease

Pathogenesis, Consequences, And Treatment Of Metabolic Acidosis In Chronic Kidney Disease

The content on the UpToDate website is not intended nor recommended as a substitute for medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health care professional regarding any medical questions or conditions. The use of this website is governed by the UpToDate Terms of Use ©2018 UpToDate, Inc. All topics are updated as new evidence becomes available and our peer review process is complete. INTRODUCTION — Most individuals produce approximately 15,000 mmol (considerably more with exercise) of carbon dioxide and 50 to 100 meq of nonvolatile acid each day. Acid-base balance is maintained by normal elimination of carbon dioxide by the lungs (which affects the partial pressure of carbon dioxide [PCO2]) and normal excretion of nonvolatile acid by the kidneys (which affects the plasma bicarbonate concentration). The hydrogen ion concentration of the blood is determined by the ratio of the PCO2 and plasma bicarbonate concentration. (See "Simple and mixed acid-base disorders", section on 'Introduction'.) Acidosis associated with chronic kidney disease (CKD) will be discussed in this topic. An overview of simple acid-base disorders and renal tubular acidosis, as well as the approach to patients with metabolic acidosis, are presented elsewhere. (See "Simple and mixed acid-base disorders" and "Overview and pathophysiology of renal tubular acidosis and the effect on potassium balance" and "Approach to the adult with metabolic acidosis" and "Approach to the child with metabolic acidosis".) ACID-BASE BALANCE IN CHRONIC KIDNEY DISEASE — Acid-base balance is normally maintained by the renal excretion of the daily acid load (about 1 meq/kg per day, derived mostly from the generation of sulfuric acid during the metabolism of sulf Continue reading >>

Acidosis And Alkalosis Pathophysiology

Acidosis And Alkalosis Pathophysiology

This video is to help understand the difference between Acidosis and Alkalosis. Acidosis is excessive blood acidity caused by an overabundance of acid in the blood or a loss of bicarbonate from the blood (metabolic acidosis), or by a buildup of carbon dioxide in the blood that results from poor lung function or slow breathing (respiratory acidosis). Blood acidity increases when people ingest substances that contain or produce acid or when the lungs do not expel enough carbon dioxide. People with metabolic acidosis have nausea, vomiting, and fatigue and may breathe faster and deeper than normal. People with respiratory acidosis have headache and confusion, and breathing may appear shallow, slow, or both. Tests on blood samples show there is too much acid. If an increase in acid overwhelms the bodys pH buffering systems, the blood will become acidic. As blood pH drops, the parts of the brain that regulate breathing are stimulated to produce faster and deeper breathing. Breathing faster and deeper increases the amount of carbon dioxide exhaled. The kidneys also try to compensate by excreting more acid in the urine. However, both mechanisms can be overwhelmed if the body continues to produce too much acid, leading to severe acidosis and eventually coma. Metabolic acidosis develops when the amount of acid in the body is increased through ingestion of a substance that is, or can be broken down (metabolized) to, an acidsuch as wood alcohol (methanol), antifreeze (ethylene glycol), or large doses of aspirin ). Metabolic acidosis can also occur as a result of abnormal metabolism. The body produces excess acid in the advanced stages of shock and in poorly controlled type 1 diabetes mellitus. Even the production of normal amounts of acid may lead to acidosis when the kidneys are Continue reading >>

More in ketosis