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Why Is Potassium High In Ketoacidosis

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Tweet Diabetic ketoacidosis (DKA) is a dangerous complication faced by people with diabetes which happens when the body starts running out of insulin. DKA is most commonly associated with type 1 diabetes, however, people with type 2 diabetes that produce very little of their own insulin may also be affected. Ketoacidosis is a serious short term complication which can result in coma or even death if it is not treated quickly. Read about Diabetes and Ketones What is diabetic ketoacidosis? DKA occurs when the body has insufficient insulin to allow enough glucose to enter cells, and so the body switches to burning fatty acids and producing acidic ketone bodies. A high level of ketone bodies in the blood can cause particularly severe illness. Symptoms of DKA Diabetic ketoacidosis may itself be the symptom of undiagnosed type 1 diabetes. Typical symptoms of diabetic ketoacidosis include: Vomiting Dehydration An unusual smell on the breath –sometimes compared to the smell of pear drops Deep laboured breathing (called kussmaul breathing) or hyperventilation Rapid heartbeat Confusion and disorientation Symptoms of diabetic ketoacidosis usually evolve over a 24 hour period if blood glucose levels become and remain too high (hyperglycemia). Causes and risk factors for diabetic ketoacidosis As noted above, DKA is caused by the body having too little insulin to allow cells to take in glucose for energy. This may happen for a number of reasons including: Having blood glucose levels consistently over 15 mmol/l Missing insulin injections If a fault has developed in your insulin pen or insulin pump As a result of illness or infections High or prolonged levels of stress Excessive alcohol consumption DKA may also occur prior to a diagnosis of type 1 diabetes. Ketoacidosis can occasional Continue reading >>

Hyperkalemia In Diabetic Ketoacidosis.

Hyperkalemia In Diabetic Ketoacidosis.

Abstract Patients with diabetic ketoacidosis tend to have somewhat elevated serum K+ concentrations despite decreased body K+ content. The hyperkalemia was previously attributed mainly to acidemia. However, recent studies have suggested that "organic acidemias" (such as that produced by infusing beta-hydroxybutyric acid) may not cause hyperkalemia. To learn which, if any, routinely measured biochemical indices might correlate with the finding of hyperkalemia in diabetic ketoacidosis, we analyzed the initial pre-treatment values in 131 episodes in 91 patients. Serum K+ correlated independently and significantly (p less than 0.001) with blood pH (r = -0.39), serum urea N (r = 0.38) and the anion gap (r = 0.41). The mean serum K+ among the men was 5.55 mmol/l, significantly higher than among the women, 5.09 mmol/l (p less than 0.005). Twelve of the 16 patients with serum K+ greater than or equal to 6.5 mmol/l were men, as were all eight patients with serum K+ greater than or equal to 7.0 mmol/l. Those differences paralleled a significantly higher mean serum urea N concentration among the men (15.1 mmol/l) than the women (11.2 mmol/l, p less than 0.01). The greater tendency to hyperkalemia among the men in this series may have been due partly to their greater renal dysfunction during the acute illness. However, other factors that were not assessed, such as cell K+ release associated with protein catabolism, and insulin deficiency per se, may also have affected serum K+ in these patients. Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic Ketoacidosis This is a life threatening, medical emergency. This is the most common way for new type 1 diabetics to present. Ketogenesis Ketogenesis occurs when there is insufficient glucose supply and glycogen stores are exhausted (such as prolonged fasting): The liver takes fatty acids and converts them to ketones. Ketones are water soluble fatty acids that can be used as fuel. They can cross the blood brain barrier and be used by the brain as fuel. Producing ketones is normal and not harmful in healthy patients when under fasting conditions or low carbohydrate, high fat diets. Ketones levels can be measured in the urine (dip stick) and blood (by ketone meter). People in ketosis (producing ketones) have a characteristic acetone smell to their breath. Ketone acids (ketones) are buffered in normal patients, so the blood does not become acidotic. When underlying pathology (i.e. Type 1 Diabetes) causes extreme hyperglycaemic ketosis, this results in a metabolic acidosis that is life threatening (see below). Diabetic Ketoacidosis Pathophysiology When there is no insulin, the cells of the body cannot take glucose from the blood and use it for fuel Therefore, the cells think the body is being fasted and has no glucose supply Meanwhile, the level of glucose in the blood keeps rising (hyperglycaemia) Ketoacidosis Because the cells in the body have no fuel and think they are starving, they initiate the process of ketogenesis, so that they have a usable fuel Over time, the patient gets higher and higher glucose and ketones levels Initially, the kidney produces bicarbonate to counteract the acidic blood and maintain a normal pH Over time, the ketone acids uses up the bicarbonate and the blood starts to become acidic (ketoacidosis) Dehydration The hyperglycaemia overwhelm 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: Malaise, generalized weakness, and fatigability Nausea and vomiting; may be associated with diffuse abdominal pain, decreased appetite, and anorexia Rapid weight loss in patients newly diagnosed with type 1 diabetes 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) Serum or capillary beta-hydroxybutyrate levels Urine and blood cultures if intercurrent infection is suspected ECG Continue reading >>

The Power Of Potassium

The Power Of Potassium

We’ve talked about several different minerals in past blog entries. Potassium is the mineral of choice for this week’s post for several reasons, and it’s a mineral that people with kidney problems should be sure to pay close attention to. What potassium does in the body First, let’s explore what potassium does in the body. This mineral is often referred to as an “electrolyte.” Electrolytes are electrically charged particles, called ions, which our cells use to maintain voltage across our cell membranes and carry electrical impulses, such as nerve impulses, to other cells. (Bet you didn’t think you had all this electrical activity in your body, did you?) Some of the main electrolytes in our bodies, besides potassium, are sodium, chloride, calcium, and magnesium. Your kidneys help regulate the amount of electrolytes in the body. Potassium’s job is to help nerve conduction, help regulate your heartbeat, and help your muscles contract. It also works to maintain proper fluid balance between your cells and body fluids. The body is a fine-tuned machine in that, as long as it’s healthy and functioning properly, things will work as they should. This means that, as long as your kidneys are working up to par, they’ll regulate the amount of potassium that your body needs. However, people with diabetes who have kidney disease need to be especially careful of their potassium intake, as levels can get too high in the body when the kidneys don’t work as they should. Too much potassium is just as dangerous as too little. Your physician can measure the amount of potassium in your blood with a simple blood test. A normal, or “safe” level of potassium is between 3.7 and 5.2 milliequivalents per liter (mEq/L). Levels below or above this range are a cause for concer Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Professor of Pediatric Endocrinology University of Khartoum, Sudan Introduction DKA is a serious acute complications of Diabetes Mellitus. It carries significant risk of death and/or morbidity especially with delayed treatment. The prognosis of DKA is worse in the extremes of age, with a mortality rates of 5-10%. With the new advances of therapy, DKA mortality decreases to > 2%. Before discovery and use of Insulin (1922) the mortality was 100%. Epidemiology DKA is reported in 2-5% of known type 1 diabetic patients in industrialized countries, while it occurs in 35-40% of such patients in Africa. DKA at the time of first diagnosis of diabetes mellitus is reported in only 2-3% in western Europe, but is seen in 95% of diabetic children in Sudan. Similar results were reported from other African countries . Consequences The latter observation is annoying because it implies the following: The late diagnosis of type 1 diabetes in many developing countries particularly in Africa. The late presentation of DKA, which is associated with risk of morbidity & mortality Death of young children with DKA undiagnosed or wrongly diagnosed as malaria or meningitis. Pathophysiology Secondary to insulin deficiency, and the action of counter-regulatory hormones, blood glucose increases leading to hyperglycemia and glucosuria. Glucosuria causes an osmotic diuresis, leading to water & Na loss. In the absence of insulin activity the body fails to utilize glucose as fuel and uses fats instead. This leads to ketosis. Pathophysiology/2 The excess of ketone bodies will cause metabolic acidosis, the later is also aggravated by Lactic acidosis caused by dehydration & poor tissue perfusion. Vomiting due to an ileus, plus increased insensible water losses due to tachypnea will worsen the state of dehydr 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 >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Snap Shot A 12 year old boy, previously healthy, is admitted to the hospiral after 2 days of polyuria, polyphagia, nausea, vomting and abdominal pain. Temp is 37, BP 103/63, HR 112, RR 30. Physical exam shows a lethargic boy. Glucose is 534, Potasium is 5.9; WBC 16,000, pH is 7.13, PCO2 is 20 mmHg, PO2 is 90 mmHg. Introduction Results from absolute deficiency in insulin surge in counterregulatory homones (glucagon, growth hormone, catecholamine) results in hyperglycemia and ketonemia Most common in type I diabetes Precipitated by infections drugs (steroids, thiazide diuretics) noncompliance pancreatitis Presentation Symptoms vomiting abdominal pain fruity, acetone odor severely dehydrated cerebral edema associated with high mortality in pediatric patients Evaluation Diagnostic criteria blood glucose levels > 250 mg/dL Arterial pH < 7.3 expect to see an increase in free calcium since the excess hydrogen displaces calcium from albumin Serum bicarbonate < 15mEq/L Moderate ketonuria and ketonemia Labs show: Treatment Fluids Insulin with glucose give insulin until ketones are gone, even after glucose normalizes or is below normal Replace potasium for hypokalemia caused by too much potassium being secreted in the urine as a result of the glucosuria labs may show pseudo-hyperkalemia due to transcellular shift of potassium out of the cells to balance the H being transfered into the cells give in the form of potassium phosphate rather than potasium chloride Aggresive electrolyte replacement give phosphate supplementation to prevent respiratory paralysis If mental status changes (headache, obtundation, coma) occur during treatment likely due to cerebral edema give mannitol Follow anion gap to monitor improvement 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 >>

Diabetic Ketoacidosis-induced Hyperkalemia

Diabetic Ketoacidosis-induced Hyperkalemia

Abstract We report the biochemical data of 22 hospital admissions because of untreated diabetic ketoacidosis. Fifty percent of admitted patients showed an initial serum potassium between 4.6 and 6.0 mEq/1 whereas severe hyperkalemia (value>6.1 mEq/l) occurred in 32%. Initial potassium levels show a slight negative correlation with pH but a stronger correlation (p<0.001) was found between the initial serum potassium and glucose values. We suggest that hyperglycemia due to insulinopenia must be one of the factors in the pathogenesis of this hyperkalemia. Preview Unable to display preview. Download preview PDF. Continue reading >>

Understanding And Treating Diabetic Ketoacidosis

Understanding And Treating Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a serious metabolic disorder that can occur in animals with diabetes mellitus (DM).1,2 Veterinary technicians play an integral role in managing and treating patients with this life-threatening condition. In addition to recognizing the clinical signs of this disorder and evaluating the patient's response to therapy, technicians should understand how this disorder occurs. DM is caused by a relative or absolute lack of insulin production by the pancreatic b-cells or by inactivity or loss of insulin receptors, which are usually found on membranes of skeletal muscle, fat, and liver cells.1,3 In dogs and cats, DM is classified as either insulin-dependent (the body is unable to produce sufficient insulin) or non-insulin-dependent (the body produces insulin, but the tissues in the body are resistant to the insulin).4 Most dogs and cats that develop DKA have an insulin deficiency. Insulin has many functions, including the enhancement of glucose uptake by the cells for energy.1 Without insulin, the cells cannot access glucose, thereby causing them to undergo starvation.2 The unused glucose remains in the circulation, resulting in hyperglycemia. To provide cells with an alternative energy source, the body breaks down adipocytes, releasing free fatty acids (FFAs) into the bloodstream. The liver subsequently converts FFAs to triglycerides and ketone bodies. These ketone bodies (i.e., acetone, acetoacetic acid, b-hydroxybutyric acid) can be used as energy by the tissues when there is a lack of glucose or nutritional intake.1,2 The breakdown of fat, combined with the body's inability to use glucose, causes many pets with diabetes to present with weight loss, despite having a ravenous appetite. If diabetes is undiagnosed or uncontrolled, a series of metab Continue reading >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Snap Shot A 12 year old boy, previously healthy, is admitted to the hospital after 2 days of polyuria, polyphagia, nausea, vomiting and abdominal pain. Vital signs are: Temp 37C, BP 103/63 mmHg, HR 112, RR 30. Physical exam shows a lethargic boy. Labs are notable for WBC 16,000, Glucose 534, K 5.9, pH 7.13, PCO2 is 20 mmHg, PO2 is 90 mmHg. Introduction Complication of type I diabetes result of ↓ insulin, ↑ glucagon, growth hormone, catecholamine Precipitated by infections drugs (steroids, thiazide diuretics) noncompliance pancreatitis undiagnosed DM Presentation Symptoms abdominal pain vomiting Physical exam Kussmaul respiration increased tidal volume and rate as a result of metabolic acidosis fruity, acetone odor severe hypovolemia coma Evaluation Serology blood glucose levels > 250 mg/dL due to ↑ gluconeogenesis and glycogenolysis arterial pH < 7.3 ↑ anion gap due to ketoacidosis, lactic acidosis ↓ HCO3- consumed in an attempt to buffer the increased acid hyponatremia dilutional hyponatremia glucose acts as an osmotic agent and draws water from ICF to ECF hyperkalemia acidosis results in ICF/ECF exchange of H+ for K+ moderate ketonuria and ketonemia due to ↑ lipolysis β-hydroxybutyrate > acetoacetate β-hydroxybutyrate not detected with normal ketone body tests hypertriglyceridemia due to ↓ in capillary lipoprotein lipase activity activated by insulin leukocytosis due to stress-induced cortisol release H2PO4- is increased in urine, as it is titratable acid used to buffer the excess H+ that is being excreted Treatment Fluids Insulin with glucose must prevent resultant hypokalemia and hypophosphatemia labs may show pseudo-hyperkalemia prior to administartion of fluid and insulin due to transcellular shift of potassium out of the cells to balance the H+ be Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

What Is It? Diabetic ketoacidosis is a potentially fatal complication of diabetes that occurs when you have much less insulin than your body needs. This problem causes the blood to become acidic and the body to become dangerously dehydrated. Diabetic ketoacidosis can occur when diabetes is not treated adequately, or it can occur during times of serious sickness. To understand this illness, you need to understand the way your body powers itself with sugar and other fuels. Foods we eat are broken down by the body, and much of what we eat becomes glucose (a type of sugar), which enters the bloodstream. Insulin helps glucose to pass from the bloodstream into body cells, where it is used for energy. Insulin normally is made by the pancreas, but people with type 1 diabetes (insulin-dependent diabetes) don't produce enough insulin and must inject it daily. Your body needs a constant source of energy. When you have plenty of insulin, your body cells can get all the energy they need from glucose. If you don't have enough insulin in your blood, your liver is programmed to manufacture emergency fuels. These fuels, made from fat, are called ketones (or keto acids). In a pinch, ketones can give you energy. However, if your body stays dependent on ketones for energy for too long, you soon will become ill. Ketones are acidic chemicals that are toxic at high concentrations. In diabetic ketoacidosis, ketones build up in the blood, seriously altering the normal chemistry of the blood and interfering with the function of multiple organs. They make the blood acidic, which causes vomiting and abdominal pain. If the acid level of the blood becomes extreme, ketoacidosis can cause falling blood pressure, coma and death. Ketoacidosis is always accompanied by dehydration, which is caused by high Continue reading >>

Serum Potassium In Lactic Acidosis And Ketoacidosis

Serum Potassium In Lactic Acidosis And Ketoacidosis

This article has no abstract; the first 100 words appear below. METABOLIC acidosis has been thought to elevate serum potassium concentration.1 , 2 However, hyperkalemia was not found in recent studies in patients with postictal lactic acidosis3 or in dogs infused with lactic acid4 , 5 or 3-hydroxybutyric acid5 — observations that raise questions about the association between metabolic acidosis and hyperkalemia: Does metabolic acidosis cause hyperkalemia or is the latter an epiphenomenon? Does metabolic acidosis (or acidemia) cause hyperkalemia only when acidosis is due to excess "mineral acids," and not to excess organic acids? With the hope of providing some clarification of these questions, I have reviewed initial laboratory data and clinical findings in . . . We are indebted to Dr. Henry Hoberman, of the Department of Biochemistry, Albert Einstein College of Medicine, for the lactate and 3-hydroxybutyrate analyses. From the Department of Medicine, Albert Einstein College of Medicine, and the Bronx Municipal Hospital Center (address reprint requests to Dr. Fulop at the Department of Medicine, Bronx Municipal Hospital Center, Pelham Parkway South and Eastchester Road, Bronx, NY 10461). Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

The Facts Diabetic ketoacidosis (DKA) is a condition that may occur in people who have diabetes, most often in those who have type 1 (insulin-dependent) diabetes. It involves the buildup of toxic substances called ketones that make the blood too acidic. High ketone levels can be readily managed, but if they aren't detected and treated in time, a person can eventually slip into a fatal coma. DKA can occur in people who are newly diagnosed with type 1 diabetes and have had ketones building up in their blood prior to the start of treatment. It can also occur in people already diagnosed with type 1 diabetes that have missed an insulin dose, have an infection, or have suffered a traumatic event or injury. Although much less common, DKA can occasionally occur in people with type 2 diabetes under extreme physiologic stress. Causes With type 1 diabetes, the pancreas is unable to make the hormone insulin, which the body's cells need in order to take in glucose from the blood. In the case of type 2 diabetes, the pancreas is unable to make sufficient amounts of insulin in order to take in glucose from the blood. Glucose, a simple sugar we get from the foods we eat, is necessary for making the energy our cells need to function. People with diabetes can't get glucose into their cells, so their bodies look for alternative energy sources. Meanwhile, glucose builds up in the bloodstream, and by the time DKA occurs, blood glucose levels are often greater than 22 mmol/L (400 mg/dL) while insulin levels are very low. Since glucose isn't available for cells to use, fat from fat cells is broken down for energy instead, releasing ketones. Ketones accumulate in the blood, causing it to become more acidic. As a result, many of the enzymes that control the body's metabolic processes aren't able Continue reading >>

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