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Diabetic Ketoacidosis: Maintaining Glucose Control

Diabetic Ketoacidosis: Maintaining Glucose Control

The metabolic chain reaction that precedes diabetic ketoacidosis can occur rapidly, and this potentially life-threatening condition requires swift recognition and treatment. Two critical words in a diabetic’s vocabulary are “management” and “control.” When a patient with diabetes fails to manage food intake and loses control of blood sugar levels, hyperglycemia follows. In most cases, blood sugar levels elevate slightly, which prompts the individual with diabetes to take action to lower those levels. Under some conditions, blood sugar rises precipitously, which is usually caused by 1 or more of the following1-3 : • Developing or fulminant infection (especially Klebsiella pneumonia) or illness • Serious disruption of insulin treatment • New onset of diabetes • Physical or emotional stress • Adverse drug reaction (especially to corticosteroids, pentamidine, thiazides, sympathomimetics, or secondgeneration antipsychotics4 ) Acute, life-threatening diabetic ketoacidosis (DKA) can develop rapidly. Table 11,2 describes criteria usually used to define DKA. We typically associate this metabolic abnormality with type 1 diabetes, but it also occurs in some patients with type 2 diabetes, with infection or an adverse drug reaction as the primary causes. As blood sugar rises in DKA, the patient becomes dehydrated and metabolic changes produce acidosis.1,2,4,5 Pathophysiology DKA usually occurs when absolute or relative insulin deficiency leads to increased counter-regulatory hormones (ie, glucagon, cortisol, growth hormone, epinephrine). These hormones enhance hepatic glucose production (gluconeogenesis), glycogenolysis, and lipolysis, all of which increase free fatty acids (FFAs) in circulation. With insulin unavailable, the liver turns to FFAs as an alternative Continue reading >>

Ketoacidosis

Ketoacidosis

Kamel S. Kamel MD, FRCPC, Mitchell L. Halperin MD, FRCPC, in Fluid, Electrolyte and Acid-Base Physiology (Fifth Edition), 2017 Introduction Although ketoacidosis is a form of metabolic acidosis because of the addition of acids, it is discussed separately in this chapter to emphasize the metabolic and biochemical issues required to understand the clinical aspects of this disorder (see margin note). We discuss the metabolic setting that is required to allow for the formation of ketoacids in the liver at a high rate and what sets the limit on the rate of production. Removal of ketoacids occurs mainly in the brain and kidneys. We examine what sets the limit on the rate of removal of ketoacids by these organs. We believe that understanding the biochemical and metabolic aspects of ketoacidsis provides the clinician with a better understanding of this disorder and allows for a better design of therapy in the individual patient with ketoacidosis. Relevant to the pathophysiology of this case, the soft drinks the patient consumed contained a large quantity of glucose, fructose, and caffeine. Ketoacids • A ketone is an organic compound that has a keto group (C=O) on an internal carbon atom. • Acetone is a ketone but not an acid. • Only acetoacetic acid is a ketoacid. β-Hydroxybutyric acid has a hydroxyl group (C–OH) on its internal carbon, so it is a hydroxy acid and not a ketoacid. Abbreviations β-HB, beta hydroxybutyrate anion AcAc, acetoacetate anion ADP, adenosine diphosphate ATP, adenosine triphosphate NAD+, nicotinamide adenine dinucleotide NADH,H+, reduced form of NAD+ FAD, flavin adenine dinucleotide FADH2, hydroxyquinone form of FAD EABV, effective arterial blood volume PAnion gap, plasma anion gap PGlucose, concentration of glucose in plasma POsmolal gap, plasm Continue reading >>

The Influence Of Blood Hydrogen Ion Concentration On The Level Of Consciousness In Diabetic Ketoacidosis

The Influence Of Blood Hydrogen Ion Concentration On The Level Of Consciousness In Diabetic Ketoacidosis

The prognosis of diabetic ketoacidosis has undergone incredibly remarkable evolution since the discovery of insulin nearly a century ago. The incidence and economic burden of diabetic ketoacidosis have continued to rise but its mortality has decreased to less than 1% in good centers. Improved outcome is attributable to a better understanding of the pathophysiology of the disease and widespread application of treatment guidelines. In this review, we present the changes that have occurred over the years, highlighting the evidence behind the recommendations that have improved outcome. We begin with a discussion of the precipitants and pathogenesis of DKA as a prelude to understanding the rationale for the recommendations. A brief review of ketosis-prone type 2 diabetes, an update relating to the diagnosis of DKA and a future perspective are also provided. Diabetic ketoacidosis continues to be a threatening illness with a high mortality rate. Because children, juveniles and young adults are particularly affected, this often life-threatening disease presents a real diabetological emergency. The following article describes the epidemiological and pathophysiological correlations, as well as the genesis and triggers of ketoacidosis. The second part of the paper deals with monitoring and management of ketoacidosis in relation to single therapeutic interventions such as fluid replacement, insulin therapy, electrolyte replacement and therapy of acidosis. Special attention is drawn to the avoidance of therapeutic complications, which often contribute to high morbidity and mortality. A concept for the careful normalization of hyperglycemia and acidosis while avoiding complications is also discussed. Background: Extreme hyperglycemia (serum glucose 800 mg/dL or 44.4 mmol/L) is infre Continue reading >>

Diabetic Ketoacidosis: A Serious Complication

Diabetic Ketoacidosis: A Serious Complication

A balanced body chemistry is crucial for a healthy human body. A sudden drop in pH can cause significant damage to organ systems and even death. This lesson takes a closer look at a condition in which the pH of the body is severely compromised called diabetic ketoacidosis. Definition Diabetic ketoacidosis, sometimes abbreviated as DKA, is a condition in which a high amount of acid in the body is caused by a high concentration of ketone bodies. That definition might sound complicated, but it's really not. Acidosis itself is the state of too many hydrogen ions, and therefore too much acid, in the blood. A pH in the blood leaving the heart of 7.35 or less indicates acidosis. Ketones are the biochemicals produced when fat is broken down and used for energy. While a healthy body makes a very low level of ketones and is able to use them for energy, when ketone levels become too high, they make the body's fluids very acidic. Let's talk about the three Ws of ketoacidosis: who, when, and why. Type one diabetics are the group at the greatest risk for ketoacidosis, although the condition can occur in other groups of people, such as alcoholics. Ketoacidosis usually occurs in type one diabetics either before diagnosis or when they are subjected to a metabolic stress, such as a severe infection. Although it is possible for type two diabetics to develop ketoacidosis, it doesn't happen as frequently. To understand why diabetic ketoacidosis occurs, let's quickly review what causes diabetes. Diabetics suffer from a lack of insulin, the protein hormone responsible for enabling glucose to get into cells. This inability to get glucose into cells means that the body is forced to turn elsewhere to get energy, and that source is fat. As anyone who exercises or eats a low-calorie diet knows, fa Continue reading >>

Diagnosis And Treatment Of Diabetic Ketoacidosis And The Hyperglycemic Hyperosmolar State

Diagnosis And Treatment Of Diabetic Ketoacidosis And The Hyperglycemic Hyperosmolar State

Go to: Pathogenesis In both DKA and HHS, the underlying metabolic abnormality results from the combination of absolute or relative insulin deficiency and increased amounts of counterregulatory hormones. Glucose and lipid metabolism When insulin is deficient, the elevated levels of glucagon, catecholamines and cortisol will stimulate hepatic glucose production through increased glycogenolysis and enhanced gluconeogenesis4 (Fig. 1). Hypercortisolemia will result in increased proteolysis, thus providing amino acid precursors for gluconeogenesis. Low insulin and high catecholamine concentrations will reduce glucose uptake by peripheral tissues. The combination of elevated hepatic glucose production and decreased peripheral glucose use is the main pathogenic disturbance responsible for hyperglycemia in DKA and HHS. The hyperglycemia will lead to glycosuria, osmotic diuresis and dehydration. This will be associated with decreased kidney perfusion, particularly in HHS, that will result in decreased glucose clearance by the kidney and thus further exacerbation of the hyperglycemia. In DKA, the low insulin levels combined with increased levels of catecholamines, cortisol and growth hormone will activate hormone-sensitive lipase, which will cause the breakdown of triglycerides and release of free fatty acids. The free fatty acids are taken up by the liver and converted to ketone bodies that are released into the circulation. The process of ketogenesis is stimulated by the increase in glucagon levels.5 This hormone will activate carnitine palmitoyltransferase I, an enzyme that allows free fatty acids in the form of coenzyme A to cross mitochondrial membranes after their esterification into carnitine. On the other side, esterification is reversed by carnitine palmitoyltransferase I Continue reading >>

Role Of Beta-hydroxybutyric Acid In Diabetic Ketoacidosis: A Review

Role Of Beta-hydroxybutyric Acid In Diabetic Ketoacidosis: A Review

Go to: Diabetic ketoacidosis (DKA), a complication of diabetes mellitus, is a severe metabolic disease that often requires intensive treatment. Diagnosis of ketosis associated with DKA can be difficult due to variability in the metabolic state of DKA patients. Recognition of the clinical signs and definitive diagnosis are essential for proper treatment. This article reviews the formation of ketoacids during DKA and the role of β-hydroxybutyric acid in the diagnosis and monitoring of DKA. Go to: Introduction Diabetic ketoacidosis (DKA) is a severe and life threatening metabolic disease caused by an absolute or relative deficiency of insulin in the body (1). A disease of middle-aged dogs and cats, DKA occurs as a complication of diabetes mellitus (1). The clinical presentation can range from ketotic patients that are eating, drinking, and maintaining hydration on their own to the more common ketoacidotic patients that are dehydrated and have other signs such as vomiting, anorexia, and lethargy (1). The intensity of treatment is therefore variable and depends on the severity of clinical signs and the degree of metabolic derangement. Most DKA patients require intensive, in-hospital treatment. Go to: Pathophysiology Decreased insulin production by pancreatic beta cells, decreased activity of insulin receptors at the cellular level, or both, are responsible for the abnormal glucose metabolism and resulting hyperglycemia (1,2). One consequence of this disregulated glucose metabolism is that glucose transport from serum into the cells is inadequate, leading to cellular starvation (1–3). In order to satisfy its cellular energy requirements and maintain cellular integrity, the body utilizes adipose tissue as the main energy source (1,4). This is a protective mechanism designed Continue reading >>

Diabetic Ketoacidosis - Now@nejm Now@nejm

Diabetic Ketoacidosis - [email protected] [email protected]

Posted by Carla Rothaus February 6th, 2015 The latest review in the Fluids and Electrolytes series focuses on the safe removal of excess hydrogen ions, the administration of sodium bicarbonate, and the possible contribution of intracellular acidosis to the development of cerebral edema in patients with diabetic ketoacidosis .Several of the issues facing clinicians who care for patients with diabetic ketoacidosis are related to acid-basedisorders. How do changes in extracellular fluid volume affect assessment of the severity of diabeticketoacidosis? Because of hyperglycemia-induced osmotic diuresis and natriuresis, patients with diabetic ketoacidosis usually present with a marked contraction of the extracellular fluid volume. This factor affects the assessment of their acid-base status and in some cases their therapy. Determination of the severity of metabolic acidemia is usually based on the extent of the decrease in the plasma bicarbonate concentration. Nevertheless, as shown in the equation below, the plasma bicarbonate concentration may be only moderately reduced when there is both a large deficit of bicarbonate in the extracellular fluid and a severe contraction of the volume of extracellularfluid. Extracellular fluid bicarbonate concentration [HCO3] = extracellular fluid HCO3 content (divided by) extracellular fluidvolume. It is important to adjust for changes in the volume of extracellular fluid when using the ratio of the increase in the plasma anion gap to the decrease in the plasma bicarbonate concentration to gauge the magnitude of the acidload. What subgroups of patients with diabetic ketoacidosis may benefit from treatment with sodiumbicarbonate? Most patients with diabetic ketoacidosis do not require the administration of sodium bicarbonate, since infused Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic ketoacidosis is a state of insulin deficiency, characterised by rapid onset, extreme metabolic acidosis, a generally intact sensorium, and only mild hyperglycaemia. DKA comes up frequently in the CICM SAQs, but usually as an ABG interpretation exercise. This chapter focuses on the medical side of DKA, including its causes, manifestations, complications, and management strategies. Questions which have required such thinking have included the following: Question 1 from the second paper of 2016 (differences between HONK and DKA) Question 17 from the first paper of 2014 (differences between HONK and DKA) Question 2 from the second paper of 2009 (general approach to management) Question 15 from the second paper of 2000 (whether or not saline is appropriate) Definition of diabetic ketoacidosis How does one discriminate between DKA and HONK even when in about 30% of instances the two disorders coexist? Arbitrary definitions exist, proposed by the American Diabetes Association. In summary: DKA presents with acidosis as the major feature HONK presents with hyperglycaemia as the major feature Discriminating Between HONK and DKA Domain Features suggestive of DKA Features suggestive of HONK Demographic Young Known Type 1 diabetic Elderly Known Type 2 diabetic History Rapid clinical course History of noncompliance with insulin Abdominal pain Shortness of breath Prolonged course History of noncompliance with oral antihyperglycaemic agents and insulin Polydipsia, polyuria, weight loss Neurological symptoms Examination Tachypnoea Normal level of consciousness, or only slightly decreased Coma Seizures Biochemistry Severe acidosis Severe ketosis Mild hyperglycaemia Renal function normalises rapidly Mild acidosis Little ketosis; mainly lactate is raised Severe hyperglycaemia Esta 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 >>

Difficult Diabetic Ketoacidotics - Bsava2012 - Vin

Difficult Diabetic Ketoacidotics - Bsava2012 - Vin

School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, USA Diabetic ketoacidosis (DKA) is a severe form of complicated diabetes mellitus (DM) which requires emergency care. Ketones are synthesised from fatty acids as a substitute form of energy, because glucose has not effectively entered into the cells. Excess ketoacids result in acidosis and severe electrolyte abnormalities, which can be life threatening. The median age of dogs with DKA is 8 years (range, 8 months to 16 years). Specific breed or sex has not been shown to increase the risk of DKA in dogs. Concurrent disease increases the risk of DKA, as does the state of newly diagnosed, yet untreated, DM. Clinical Signs and Physical Examination Findings Clinical signs and physical examination findings may be attributed to chronic untreated diabetes mellitus, presence of concurrent disease and the acute onset of DKA. The most common clinical signs of dogs with DKA are polyuria and polydipsia, lethargy, inappetence or anorexia, vomiting and weight loss. Common abnormalities noted on physical examination of dogs with DKA are subjectively overweight or underweight body condition, dehydration, cranial organomegaly, abdominal pain, cardiac murmur, mental dullness, dermatological abnormalities, dyspnoea, coughing, or abnormal lung sounds and cataracts. Approximately 50% of dogs with DKA have a non-regenerative anaemia (which is not associated with hypophosphataemia), left shift neutrophilia or thrombocytosis. Persistent hyperglycaemia is apparent in all dogs with DKA, unless they are insulin treated. Alkaline phosphatase activity is elevated in almost all dogs with DKA. Alanine aminotransferase activity, aspartate aminotransferase activity and cholesterol concentration are increased in about half of th Continue reading >>

Severe Hyperkalaemia In Association With Diabetic Ketoacidosis In A Patient Presenting With Severe Generalized Muscle Weakness

Severe Hyperkalaemia In Association With Diabetic Ketoacidosis In A Patient Presenting With Severe Generalized Muscle Weakness

Diabetic ketoacidosis (DKA) is an acute, life‐threatening metabolic complication of diabetes mellitus. Hyperglycaemia, ketosis (ketonaemia or ketonuria) and acidosis are the cardinal features of DKA [1]. Other features that indicate the severity of DKA include volume depletion, acidosis and concurrent electrolyte disturbances, especially abnormalities of potassium homeostasis [1,2]. We describe a type 2 diabetic patient presenting with severe generalized muscle weakness and electrocardiographic evidence of severe hyperkalaemia in association with DKA and discuss the related pathophysiology. A 65‐year‐old male was admitted because of impaired mental status. He was a known insulin‐treated diabetic on quinapril (20 mg once daily) and was taking oral ampicillin 500 mg/day because of dysuria which had started 5 days prior to admission. He was disoriented in place and time with severe generalized muscle weakness; he was apyrexial (temperature 36.4°C), tachycardic (120 beats/min) and tachypneic (25 respirations/min) with cold extremities (supine blood pressure was 100/60 mmHg). An electrocardiogram (ECG) showed absent P waves, widening of QRS (‘sine wave’ in leads I, II, V5 and V6), depression of ST segments and tall peaked symmetrical T waves in leads V3–V6 (Figure 1). Blood glucose was 485 mg/dl, plasma creatinine 5.1 mg/dl (reference range (r.r.) 0.6–1.2 mg/dl, measured by the Jaffe method), urea 270 mg/dl (r.r. 11–54 mg/dl), albumin 4.2 g/dl (r.r. 3.4–4.7 g/dl), sodium 136 mmol/l (r.r. 135–145 mmol/l), chloride 102 mmol/l (r.r. 98–107 mmol/l), potassium 8.3 mmol/l (r.r. 3.5–5.4 mmol/l), phosphorus 1.6 mmol/l (r.r. 0.8–1.45 mmol/l) and magnesium 0.62 mmol/l (r.r. 0.75–1.25 mmol/l). A complete blood count revealed leukocytosis (12 090/µl with Continue reading >>

Relationship Between The Concentration Of H+-ions And The Efficiency Of Insulin In The Treatment Of Diabetic Ketoacidosis.

Relationship Between The Concentration Of H+-ions And The Efficiency Of Insulin In The Treatment Of Diabetic Ketoacidosis.

Relationship between the concentration of H+-ions and the efficiency of insulin in the treatment of diabetic ketoacidosis. Ionescu-Trgovite C, et al. Endokrinologie. 1980. The efficiency of insulin (decrease of the blood glucose per unit of insulin administered) was assessed in 610 cases of diabetic ketoacidosis (316 females, 274 males, aged 3 to 72 years) in terms of the degree of plasma acidemia. The 610 cases were grouped into 4 ketoacidosis stages, defined according to pH values as incipient, pH > 7.35 (77 cases); moderate, pH 7.31-7.35 (163 cases); advanced, 7.21-7.30 (160 cases); severe, pH < 7.20 (210 cases). The mean [H+]-ion concentration recorded on admission in the 4 stages of ketoacidosis was 41 nEq/1, 46 nEq/1, 53 nEq/1, and 91 nEq/1, respectively. The efficiency of insulin for the first 2 hours of treatment (interval during which acidemia was only partly corrected) was comparable in the four ketoacidosis stages, i.e. 31.1 mg/l, 32.9 mg/l, 29.5 mg/l and, respectively 28.9 mg/l per unit of insulin injected as a bolus. The somewhat lower efficiency of insulin in the advanced and severe cases of ketoacidosis appears to be due to vascular collapse encountered in 38 cases (6 advanced ketoacidosis and 32 severe ketoacidosis), since in these patients the fall in blood glucose per unit insulin was only 15.8 mg/l. Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetes mellitus is the name given to a group of conditions whose common hallmark is a raised blood glucose concentration (hyperglycemia) due to an absolute or relative deficiency of the pancreatic hormone insulin. In the UK there are 1.4 million registered diabetic patients, approximately 3 % of the population. In addition, an estimated 1 million remain undiagnosed. It is a growing health problem: In 1998, the World Health Organization (WHO) predicted a doubling of the worldwide prevalence of diabetes from 150 million to 300 million by 2025. For a very tiny minority, diabetes is a secondary feature of primary endocrine disease such as acromegaly (growth hormone excess) or Cushing’s syndrome (excess corticosteroid), and for these patients successful treatment of the primary disease cures diabetes. Most diabetic patients, however, are classified as suffering either type 1 or type 2 diabetes. Type 1 diabetes Type 1 diabetes, which accounts for around 15 % of the total diabetic population, is an autoimmune disease of the pancreas in which the insulin-producing β-cells of the pancreas are selectively destroyed, resulting in an absolute insulin deficiency. The condition arises in genetically susceptible individuals exposed to undefined environmental insult(s) (possibly viral infection) early in life. It usually becomes clinically evident and therefore diagnosed during late childhood, with peak incidence between 11 and 13 years of age, although the autoimmune-mediated β-cell destruction begins many years earlier. There is currently no cure and type 1 diabetics have an absolute life-long requirement for daily insulin injections to survive. Type 2 diabetes This is the most common form of diabetes: around 85 % of the diabetic population has type 2 diabetes. The primary prob Continue reading >>

2.6 Regulation Of Intracellular Hydrogen Ion Concentration

2.6 Regulation Of Intracellular Hydrogen Ion Concentration

2.6 Regulation of Intracellular Hydrogen Ion Concentration The most important [H+] for the body is the intracellular [H+] Why? Because of its profound effects on metabolism and other cell processes which occur due to the effects of [H+] on the degree of ionisation of intracellular compounds. Specifically: Small molecule effect: Intracellular trapping function -due to the ionisation of metabolic intermediates. Large molecule effect: Effects on protein function: The function of many intracellular proteins (esp the activities of enzymes) is altered by effects on the ionisation of amino acid residues (esp histidine residues) In assessment of acid-base disorders, the clinician is always looking from the outside in. Ease of sampling: Arterial blood is easy to sample. It is much more difficult to obtain an intracellular sample Arterial blood gives results which can be considered a sort of 'average value'. It would be more difficult to find an intracellular sample that could be considered to be 'representative' of all ICF. The basis of the clinical approach is to use the extracellular results to make inferences about intracellular conditions. Both carbon dioxide and the fixed acids are produced intracellularly and move down concentration gradients to the ECF. Carbon dioxide crosses cell membranes very easily and it is important to realise that CO2 can move in or out depending on the gradient across the cell membrane. In diabetic ketoacidosis (DKA), the ketoacids are produced in the liver and not in every cell in the body. The intracellular alkalinising effect of the compensatory hypocapnia that occurs will however affect every cell and not just the hepatocytes. Does this mean that DKA produces an extracellular rise in [H+] but the opposite change in most tissues (excluding the Continue reading >>

Potassium Balance In Acid-base Disorders

Potassium Balance In Acid-base Disorders

INTRODUCTION There are important interactions between potassium and acid-base balance that involve both transcellular cation exchanges and alterations in renal function [1]. These changes are most pronounced with metabolic acidosis but can also occur with metabolic alkalosis and, to a lesser degree, respiratory acid-base disorders. INTERNAL POTASSIUM BALANCE Acid-base disturbances cause potassium to shift into and out of cells, a phenomenon called "internal potassium balance" [2]. An often-quoted study found that the plasma potassium concentration will rise by 0.6 mEq/L for every 0.1 unit reduction of the extracellular pH [3]. However, this estimate was based upon only five patients with a variety of disturbances, and the range was very broad (0.2 to 1.7 mEq/L). This variability in the rise or fall of the plasma potassium in response to changes in extracellular pH was confirmed in subsequent studies [2,4]. Metabolic acidosis — In metabolic acidosis, more than one-half of the excess hydrogen ions are buffered in the cells. In this setting, electroneutrality is maintained in part by the movement of intracellular potassium into the extracellular fluid (figure 1). Thus, metabolic acidosis results in a plasma potassium concentration that is elevated in relation to total body stores. The net effect in some cases is overt hyperkalemia; in other patients who are potassium depleted due to urinary or gastrointestinal losses, the plasma potassium concentration is normal or even reduced [5,6]. There is still a relative increase in the plasma potassium concentration, however, as evidenced by a further fall in the plasma potassium concentration if the acidemia is corrected. A fall in pH is much less likely to raise the plasma potassium concentration in patients with lactic acidosis Continue reading >>

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