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Why Do You Get Hyperkalemia In Dka?

Hyperkalaemia In Adults

Hyperkalaemia In Adults

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 the Dietary Potassium article more useful, or one of our other health articles. Description Hyperkalaemia is defined as plasma potassium in excess of 5.5 mmol/L[1]. The European Resuscitation Guidelines further classify hyperkalaemia as: Mild - 5.5-5.9 mmol/L. Moderate - 6.0-6.4 mmol/L. Severe - >6.5 mmol/L. Potassium is the most abundant intracellular cation - 98% of it being located intracellularly. Hyperkalaemia has four broad causes: Renal causes - eg, due to decreased excretion or drugs. Increased circulation of potassium - can be exogenous or endogenous. A shift from the intracellular to the extracellular space. Pseudohyperkalaemia. Epidemiology The time of greatest risk is at the extremes of life. Reported incidence in hospitals is 1-10%, with reduced renal function causing a five-fold increase in risk in patients on potassium-influencing drugs[2]. Men are more likely than women to develop hyperkalaemia, whilst women are more likely to experience hypokalaemia. Renal causes Acute kidney injury (AKI). Chronic kidney disease (CKD): Normally all potassium that is ingested is absorbed and excretion is 90% renal and 10% alimentary. Most excretion by the gut is via the colon and in CKD this can maintain a fairly normal blood level of potassium. It seems likely that the elevated potassium levels in CKD trigger the excretion of potassium via the colon[3]. Patients with CKD must be careful of foods rich in potassium. Hyperkalaemic renal tubular acidosis. Mineralocorticoid deficiency. Medicines that interfere with potassium excretion - eg, amiloride, spironolac Continue reading >>

Why Is There Hyperkalemia In Diabetic Ketoacidosis?

Why Is There Hyperkalemia In Diabetic Ketoacidosis?

Lack of insulin, thus no proper metabolism of glucose, ketones form, pH goes down, H+ concentration rises, our body tries to compensate by exchanging K+ from inside the cells for H+ outside the cells, hoping to lower H+ concentration, but at the same time elevating serum potassium. Most people are seriously dehydrated, so are in acute kidney failure, thus the kidneys aren’t able to excrete the excess of potassium from the blood, compounding the problem. On the other hand, many in reality are severely potassium depleted, so once lots of fluid so rehydration and a little insulin is administered serum potassium will plummet, so needs to be monitored 2 hourly - along with glucose, sodium and kidney function - to prevent severe hypokalemia causing fatal arrhythmias, like we experienced decades ago when this wasn’t so well understood yet. In practice, once the patient started peeing again, we started adding potassium chloride to our infusion fluids, the surplus potassium would be peed out by our kidneys so no risk for hyperkalemia. Continue reading >>

Why Is There Hyperkalemia In Diabetic Ketoacidosis?

Why Is There Hyperkalemia In Diabetic Ketoacidosis?

Diabetic ketoacidosis is a complicated condition which can be caused if you are unable to effectively treat and manage your diabetes. In this condition, ketones are accumulated in the blood which can adversely affect your health. It can be a fatal condition and may cause a lot of complications. One such complication in diabetic ketoacidosis is the onset of hyperkalemia or the high levels of potassium in the blood. In this article, we shall try to understand as to why hyperkalemia is caused in diabetic ketoacidosis? So, read on “Why is There Hyperkalemia in Diabetic Ketoacidosis?” What is Diabetic Ketoacidosis and Hyperkalemia? Diabetic ketoacidosis is a serious complication that is faced by many patients suffering from diabetes. In this condition, excess blood acids called ketones are produced by the body. The above condition should not be taken lightly and should be immediately treated as the same can cause diabetic coma, and eventually the death of the patient. Hyperkalemia refers to abnormally high levels of potassium in the blood of an individual. For a healthy individual, the level of potassium is around 3.5 to 5 milliequivalents per liter. If you have potassium levels higher than that, that is somewhere in between 5.1 to 6 milliequivalents per liter, then you have a mild level of hyperkalemia. Similarly, if the level of potassium in your blood is somewhere between 6.1 to 7 milliequivalents per liter, you have moderate hyperkalemia. Anything above that, you may be suffering from what is known as severe hyperkalemia. Relation Between Diabetic Ketoacidosis and Hyperkalemia There appears to be a strong relationship between hyperkalemia and diabetic ketoacidosis. In the paragraph that follows, we shall try to analyze and understand the same: If you have diabetes an Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Practice Essentials Diabetic ketoacidosis (DKA) is an acute, major, life-threatening complication of diabetes that mainly occurs in patients with type 1 diabetes, but it is not uncommon in some patients with type 2 diabetes. This condition is a complex disordered metabolic state characterized by hyperglycemia, ketoacidosis, and ketonuria. Signs and symptoms The most common early symptoms of DKA are the insidious increase in polydipsia and polyuria. The following are other signs and symptoms of DKA: Nausea and vomiting; may be associated with diffuse abdominal pain, decreased appetite, and anorexia History of failure to comply with insulin therapy or missed insulin injections due to vomiting or psychological reasons or history of mechanical failure of insulin infusion pump Altered consciousness (eg, mild disorientation, confusion); frank coma is uncommon but may occur when the condition is neglected or with severe dehydration/acidosis Signs and symptoms of DKA associated with possible intercurrent infection are as follows: See Clinical Presentation for more detail. Diagnosis On examination, general findings of DKA may include the following: Characteristic acetone (ketotic) breath odor In addition, evaluate patients for signs of possible intercurrent illnesses such as MI, UTI, pneumonia, and perinephric abscess. Search for signs of infection is mandatory in all cases. Testing Initial and repeat laboratory studies for patients with DKA include the following: Serum electrolyte levels (eg, potassium, sodium, chloride, magnesium, calcium, phosphorus) Note that high serum glucose levels may lead to dilutional hyponatremia; high triglyceride levels may lead to factitious low glucose levels; and high levels of ketone bodies may lead to factitious elevation of creatinine levels. Continue reading >>

Causes And Evaluation Of Hyperkalemia In Adults

Causes And Evaluation Of Hyperkalemia In Adults

INTRODUCTION Hyperkalemia is a common clinical problem. Potassium enters the body via oral intake or intravenous infusion, is largely stored in the cells, and is then excreted in the urine. The major causes of hyperkalemia are increased potassium release from the cells and, most often, reduced urinary potassium excretion (table 1). This topic will review the causes and evaluation of hyperkalemia. The clinical manifestations, treatment, and prevention of hyperkalemia, as well as a detailed discussion of hypoaldosteronism (an important cause of hyperkalemia), are presented elsewhere. (See "Clinical manifestations of hyperkalemia in adults" and "Treatment and prevention of hyperkalemia in adults" and "Etiology, diagnosis, and treatment of hypoaldosteronism (type 4 RTA)".) BRIEF REVIEW OF POTASSIUM PHYSIOLOGY An understanding of potassium physiology is helpful when approaching patients with hyperkalemia. Total body potassium stores are approximately 3000 meq or more (50 to 75 meq/kg body weight) [1]. In contrast to sodium, which is the major cation in the extracellular fluid and has a much lower concentration in the cells, potassium is primarily an intracellular cation, with the cells containing approximately 98 percent of body potassium. The intracellular potassium concentration is approximately 140 meq/L compared with 4 to 5 meq/L in the extracellular fluid. The difference in distribution of the two cations is maintained by the Na-K-ATPase pump in the cell membrane, which pumps sodium out of and potassium into the cell in a 3:2 ratio. The ratio of the potassium concentrations in the cells and the extracellular fluid is the major determinant of the resting membrane potential across the cell membrane, which sets the stage for the generation of the action potential that is e Continue reading >>

Management Of Diabetic Ketoacidosis

Management Of Diabetic Ketoacidosis

Diabetic ketoacidosis is an emergency medical condition that can be life-threatening if not treated properly. The incidence of this condition may be increasing, and a 1 to 2 percent mortality rate has stubbornly persisted since the 1970s. Diabetic ketoacidosis occurs most often in patients with type 1 diabetes (formerly called insulin-dependent diabetes mellitus); however, its occurrence in patients with type 2 diabetes (formerly called non–insulin-dependent diabetes mellitus), particularly obese black patients, is not as rare as was once thought. The management of patients with diabetic ketoacidosis includes obtaining a thorough but rapid history and performing a physical examination in an attempt to identify possible precipitating factors. The major treatment of this condition is initial rehydration (using isotonic saline) with subsequent potassium replacement and low-dose insulin therapy. The use of bicarbonate is not recommended in most patients. Cerebral edema, one of the most dire complications of diabetic ketoacidosis, occurs more commonly in children and adolescents than in adults. Continuous follow-up of patients using treatment algorithms and flow sheets can help to minimize adverse outcomes. Preventive measures include patient education and instructions for the patient to contact the physician early during an illness. Diabetic ketoacidosis is a triad of hyperglycemia, ketonemia and acidemia, each of which may be caused by other conditions (Figure 1).1 Although diabetic ketoacidosis most often occurs in patients with type 1 diabetes (formerly called insulin-dependent diabetes mellitus), more recent studies suggest that it can sometimes be the presenting condition in obese black patients with newly diagnosed type 2 diabetes (formerly called non–insulin-depe Continue reading >>

Hyperkalemia (high Blood Potassium)

Hyperkalemia (high Blood Potassium)

How does hyperkalemia affect the body? Potassium is critical for the normal functioning of the muscles, heart, and nerves. It plays an important role in controlling activity of smooth muscle (such as the muscle found in the digestive tract) and skeletal muscle (muscles of the extremities and torso), as well as the muscles of the heart. It is also important for normal transmission of electrical signals throughout the nervous system within the body. Normal blood levels of potassium are critical for maintaining normal heart electrical rhythm. Both low blood potassium levels (hypokalemia) and high blood potassium levels (hyperkalemia) can lead to abnormal heart rhythms. The most important clinical effect of hyperkalemia is related to electrical rhythm of the heart. While mild hyperkalemia probably has a limited effect on the heart, moderate hyperkalemia can produce EKG changes (EKG is a reading of theelectrical activity of the heart muscles), and severe hyperkalemia can cause suppression of electrical activity of the heart and can cause the heart to stop beating. Another important effect of hyperkalemia is interference with functioning of the skeletal muscles. Hyperkalemic periodic paralysis is a rare inherited disorder in which patients can develop sudden onset of hyperkalemia which in turn causes muscle paralysis. The reason for the muscle paralysis is not clearly understood, but it is probably due to hyperkalemia suppressing the electrical activity of the muscle. Common electrolytes that are measured by doctors with blood testing include sodium, potassium, chloride, and bicarbonate. The functions and normal range values for these electrolytes are described below. Hypokalemia, or decreased potassium, can arise due to kidney diseases; excessive losses due to heavy sweating 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 >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Definition: A hyperglycemic, acidotic state caused by insulin deficiency. The disease state consists of 3 parameters: Hyperglycemia (glucose > 250 mg/dl) Acidosis Ketosis Epidemiology Incidence of ~ 10,000 cases/year in US Mortality rate: 2-5% (prior to insulin was 100%) (Lebovitz 1995) Pathophysiology Insulin deficiency leads to serum glucose rise Increased glucose load in kidney leads to increased glucose in urine and osmotic diuresis Osmotic diuresis is accompanied by loss of electrolytes including sodium, magnesium, calcium and potassium Volume depletion leads to impaired glomerular filtration rate (GFR) Inability to properly metabolize glucose results in fatty acid breakdown with resultant ketone bodies (acetoacetate + beta-hydroxybutyrate) Causes: An acute insult leads to decompensation of a chronic disease. Can also be first manifestation of new onset diabetes (particularly in children). Below are common triggers Infection (particularly sepsis) Myocardial ischemia or infarction Medication non-compliance Clinical Presentation History Polydipsia, polyuria, polyphagia Weakness Weight loss Nausea/Vomiting Abdominal Pain Physical Examination Acetone odor on breath (“fruity” smell) Kussmaul’s respirations – deep fast breathing (tachypnea and hyperpnea) Tachycardia Hypotension Altered mental status Abdominal tenderness Diagnostic Testing Definitive diagnosis is established by laboratory criteria as detailed above (hyperglycemia, ketosis and acidosis) Essential Diagnostic Tests Serum glucose Typically > 350 mg/dL Euglycemic DKA (< 300 mg/dL) reported in up to 18% of patients Blood gas Patients will exhibit an anion gap metabolic Electrolytes: hypo/hyper/normokalemia, hyponatremia Arterial or venous blood gas can be used (Savage 2011) Urinalysis Glucosuria Ketonur Continue reading >>

Hyperkalemia

Hyperkalemia

Objectives The objectives of this module will be to: Describe the classic presentation of a patient with hyperkalemia. Name the electrocardiographic manifestations of hyperkalemia. List the principles of managing a patient with hyperkalemia. Introduction Hyperkalemia is a metabolic abnormality seen frequently in the Emergency Department. The most common condition leading to hyperkalemia is missed dialysis in a patient with end stage renal disease (ESRD), but many other conditions can predispose an individual to hyperkalemia, such as acute renal failure, extensive burns, trauma, or severe rhabdomyolysis or severe acidosis. Other conditions that can be associated with hyperkalemia are acute digoxin toxicity and adrenal insufficiency. In rare circumstances, hyperkalemia can become so significant that cardiac dysrhythmias and subsequent death can occur; therefore, rapid identification and appropriate treatment are paramount to properly treating this condition. Initial Actions and Primary Survey The primary survey should focus on assessing airway, breathing and circulation. Since many patients with severe hyperkalemia will have renal dysfunction, some may be fluid overloaded and may present with pulmonary edema and respiratory distress. Traditionally, the electrocardiogram (ECG) has been used as a surrogate marker for clinically significant hyperkalemia. Patients suspected of having hyperkalemia (chronic renal failure, severe diabetic ketoacidosis, etc.) should be placed on a cardiac monitor and a 12-lead electrocardiogram should be performed immediately. Concurrently, intravenous access should be obtained and a blood sample should be sent to the laboratory for a basic metabolic profile. Differential Diagnosis Hyperkalemia Pseudohyperkalemia Thrombocytosis Erythrocytosis Leu Continue reading >>

Diabetic Ketoacidosis Producing Extreme Hyperkalemia In A Patient With Type 1 Diabetes On Hemodialysis

Diabetic Ketoacidosis Producing Extreme Hyperkalemia In A Patient With Type 1 Diabetes On Hemodialysis

Hodaka Yamada1, Shunsuke Funazaki1, Masafumi Kakei1, Kazuo Hara1 and San-e Ishikawa2[1] Division of Endocrinology and Metabolism, Jichi Medical University Saitama Medical Center, Saitama, Japan [2] Division of Endocrinology and Metabolism, International University of Health and Welfare Hospital, Nasushiobara, Japan Summary Diabetic ketoacidosis (DKA) is a critical complication of type 1 diabetes associated with water and electrolyte disorders. Here, we report a case of DKA with extreme hyperkalemia (9.0 mEq/L) in a patient with type 1 diabetes on hemodialysis. He had a left frontal cerebral infarction resulting in inability to manage his continuous subcutaneous insulin infusion pump. Electrocardiography showed typical changes of hyperkalemia, including absent P waves, prolonged QRS interval and tented T waves. There was no evidence of total body water deficit. After starting insulin and rapid hemodialysis, the serum potassium level was normalized. Although DKA may present with hypokalemia, rapid hemodialysis may be necessary to resolve severe hyperkalemia in a patient with renal failure. Patients with type 1 diabetes on hemodialysis may develop ketoacidosis because of discontinuation of insulin treatment. Patients on hemodialysis who develop ketoacidosis may have hyperkalemia because of anuria. Absolute insulin deficit alters potassium distribution between the intracellular and extracellular space, and anuria abolishes urinary excretion of potassium. Rapid hemodialysis along with intensive insulin therapy can improve hyperkalemia, while fluid infusions may worsen heart failure in patients with ketoacidosis who routinely require hemodialysis. Background Diabetic ketoacidosis (DKA) is a very common endocrinology emergency. It is usually associated with severe circulatory 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 >>

Electrolyte And Acid–base Disturbances In Patients With Diabetes Mellitus

Electrolyte And Acid–base Disturbances In Patients With Diabetes Mellitus

Electrolyte disturbances are common in patients with diabetes mellitus. This review highlights the ways in which specific electrolytes may be influenced by the dysregulation of glucose homeostasis. Disclosure forms provided by the authors are available with the full text of this article at NEJM.org. No potential conflict of interest relevant to this article was reported. From the Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas (B.F.P.); and the Biomedical Research Department, Diabetes and Obesity Research Division, Cedars–Sinai Medical Center, Beverly Hills, CA (D.J.C.). Address reprint requests to Dr. Palmer at the Department of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390, or at [email protected] Continue reading >>

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Introduction Diabetic ketoacidosis (DKA) is a severe form of complicated diabetes mellitus (DM) which requires emergency care. Ketones are synthesized from fatty acids as a substitute form of energy, because glucose is not effectively entered into the cells. Excess keto-acids results in acidosis and severe electrolyte abnormalities, which can be life threatening. Pathophysiology Ketone bodies are synthesized as an alternative source of energy, when intracellular glucose concentration can not meet metabolic demands. Ketone bodies are synthesized from acetyl-CoA which is a product of mitochondrial ß-oxidation of fatty acids. Synthesis of acetyl-CoA is facilitated by decreased insulin concentration and increased glucagon concentration. In non-diabetics acetyl-CoA and pyruvate enter the citric acid cycle to form ATP. However, in diabetics, production of pyruvate by glycolysis is decreased. The activity of the citric acid cycle is therefore diminished resulting in decreased utilization of Acetyl-CoA. The net effect of increased production and decreased utilization of acetyl-CoA is an increase in the concentration of acetyl-CoA which is the precursor for ketone body synthesis.1 The three ketone bodies synthesized from acetyl-CoA include beta hydroxybutyrate, acetoacetate, and acetone. Acetoacetate and beta-hydroxybutyrate are anions of moderately strong acids. Therefore, accumulation of these ketone bodies results in ketotic acidosis. Metabolic acidosis and the electrolyte abnormalities which ensue are important determinants in the outcome of patients with DKA.2 One of the beliefs regarding the pathophysiology of DKA had been that individuals that develop DKA have zero or undetectable endogenous insulin concentration. However, in a study that included 7 dogs with DKA it was Continue reading >>

Management Of Diabetic Ketoacidosis In Children And Adolescents

Management Of Diabetic Ketoacidosis In Children And Adolescents

Objectives After completing this article, readers should be able to: Describe the typical presentation of diabetic ketoacidosis in children. Discuss the treatment of diabetic ketoacidosis. Explain the potential complications of diabetic ketoacidosis that can occur during treatment. Introduction Diabetic ketoacidosis (DKA) represents a profound insulin-deficient state characterized by hyperglycemia (>200 mg/dL [11.1 mmol/L]) and acidosis (serum pH <7.3, bicarbonate <15 mEq/L [15 mmol/L]), along with evidence of an accumulation of ketoacids in the blood (measurable serum or urine ketones, increased anion gap). Dehydration, electrolyte loss, and hyperosmolarity contribute to the presentation and potential complications. DKA is the most common cause of death in children who have type 1 diabetes. Therefore, the best treatment of DKA is prevention through early recognition and diagnosis of diabetes in a child who has polydipsia and polyuria and through careful attention to the treatment of children who have known diabetes, particularly during illnesses. Presentation Patients who have DKA generally present with nausea and vomiting. In individuals who have no previous diagnosis of diabetes mellitus, a preceding history of polyuria, polydipsia, and weight loss usually can be elicited. With significant ketosis, patients may have a fruity breath. As the DKA becomes more severe, patients develop lethargy due to the acidosis and hyperosmolarity; in severe DKA, they may present with coma. Acidosis and ketosis cause an ileus that can lead to abdominal pain severe enough to raise concern for an acutely inflamed abdomen, and the elevation of the stress hormones epinephrine and cortisol in DKA can lead to an elevation in the white blood cell count, suggesting infection. Thus, leukocytosi Continue reading >>

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