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Potassium Shift In Dka

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes mellitus.[1] Signs and symptoms may include vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion, and occasionally loss of consciousness.[1] A person's breath may develop a specific smell.[1] Onset of symptoms is usually rapid.[1] In some cases people may not realize they previously had diabetes.[1] DKA happens most often in those with type 1 diabetes, but can also occur in those with other types of diabetes under certain circumstances.[1] Triggers may include infection, not taking insulin correctly, stroke, and certain medications such as steroids.[1] DKA results from a shortage of insulin; in response the body switches to burning fatty acids which produces acidic ketone bodies.[3] DKA is typically diagnosed when testing finds high blood sugar, low blood pH, and ketoacids in either the blood or urine.[1] The primary treatment of DKA is with intravenous fluids and insulin.[1] Depending on the severity, insulin may be given intravenously or by injection under the skin.[3] Usually potassium is also needed to prevent the development of low blood potassium.[1] Throughout treatment blood sugar and potassium levels should be regularly checked.[1] Antibiotics may be required in those with an underlying infection.[6] In those with severely low blood pH, sodium bicarbonate may be given; however, its use is of unclear benefit and typically not recommended.[1][6] Rates of DKA vary around the world.[5] In the United Kingdom, about 4% of people with type 1 diabetes develop DKA each year, while in Malaysia the condition affects about 25% a year.[1][5] DKA was first described in 1886 and, until the introduction of insulin therapy in the 1920s, it was almost univ Continue reading >>

Diabetic Emergencies-diagnosis And Clinical Management: Diabetic Ketoacidosis In Adults, Part 2

Diabetic Emergencies-diagnosis And Clinical Management: Diabetic Ketoacidosis In Adults, Part 2

Hyperglycemia Hyperglycemia in DKA is the result of reduced glucose uptake and utilization from the liver, muscle, and fat tissue and increased gluconeogenesis as well as glycogenolysis. The lack of insulin results in an increase in gluconeogenesis, primarily in the liver but also in the kidney, and increased glycogenolysis in liver and muscle.8,9 In addition, the inhibitory effect of insulin on glucagon secretion is abolished and plasma glucagon levels increase. The increase of glucagon aggravates hyperglycemia by enhancing gluconeogenesis and glycogenolysis. In parallel, the increased concentrations of the other counter-regulatory hormones enhance further gluconeogenesis. In addition to increased gluconeogenesis, in DKA there is excess production of substances which are used as a substrate for endogenous glucose production. Thus, the amino acids glutamine and alanine increase because of enhanced proteolysis and reduced protein synthesis.8,9 Hyperglycemia-induced osmotic diuresis leads to dehydration, hyperosmolality, electrolyte loss (Na+, K +, Mg 2 +, PO 4 3+, Cl−, and Ca+), and eventually decline in glomerular filtration rate. With decline in renal function, glucosuria diminishes and hyperglycemia worsens. Dehydration results in augmentation of plasma osmolality, which results in water movement out of the cells to the extracellular space. Osmotic diuresis caused by hyperglycemia results in loss of sodium in urine; in addition, the excess of glucagon aggravates hyponatremia because it inhibits reabsorption of sodium in the kidneys. With impaired insulin action and hyperosmolality, utilization of potassium by skeletal muscles is markedly decreased leading to intracellular potassium deficiency. Potassium is also lost due to osmotic diuresis. In addition, metabolic ac Continue reading >>

Electrolyte Imbalance In Diabetic Ketoacidosis

Electrolyte Imbalance In Diabetic Ketoacidosis

If you have diabetes, it's important to be familiar with diabetic ketoacidosis (DKA). DKA is a serious complication of diabetes that occurs when lack of insulin and high blood sugar lead to potentially life-threatening chemical imbalances. The good news is DKA is largely preventable. Although DKA is more common with type 1 diabetes, it can also occur with type 2 diabetes. High blood sugar causes excessive urination and spillage of sugar into the urine. This leads to loss of body water and dehydration as well as loss of important electrolytes, including sodium and potassium. The level of another electrolyte, bicarbonate, also falls as the body tries to compensate for excessively acidic blood. Video of the Day Insulin helps blood sugar move into cells, where it is used for energy production. When insulin is lacking, cells must harness alternative energy by breaking down fat. Byproducts of this alternative process are called ketones. High concentrations of ketones acidify the blood, hence the term "ketoacidosis." Acidosis causes unpleasant symptoms like nausea, vomiting and rapid breathing. Bicarbonate is an electrolyte that normally counteracts blood acidity. In DKA, the bicarbonate level falls as ketone production increases and acidosis progresses. Treatment of DKA includes prompt insulin supplementation to lower blood sugar, which leads to gradual restoration of the bicarbonate level. Potassium may be low in DKA because this electrolyte is lost due to excessive urination or vomiting. When insulin is used to treat DKA, it can further lower the blood potassium by pushing it into cells. Symptoms associated with low potassium include fatigue, muscle weakness, muscle cramps and an irregular heart rhythm. Severely low potassium can lead to life-threatening heart rhythm abnorm Continue reading >>

Acute Complications Of Diabetes - Diabetic Ketoacidosis

Acute Complications Of Diabetes - Diabetic Ketoacidosis

- [Voiceover] Oftentimes we think of diabetes mellitus as a chronic disease that causes serious complications over a long period of time if it's not treated properly. However, the acute complications of diabetes mellitus are often the most serious, and can be potentially even life threatening. Let's discuss one of the acute complications of diabetes, known as diabetic ketoacidosis, or DKA for short, which can occur in individuals with type 1 diabetes. Now recall that type 1 diabetes is an autoimmune disorder. And as such, there's an autoimmune destruction of the beta cells in the pancreas, which prevents the pancreas from producing and secreting insulin. Therefore, there is an absolute insulin deficiency in type 1 diabetes. But what exactly does this mean for the body? To get a better understanding, let's think about insulin requirements as a balancing act with energy needs. Now the goal here is to keep the balance in balance. As the energy requirements of the body go up, insulin is needed to take the glucose out of the blood and store it throughout the body. Normally in individuals without type 1 diabetes, the pancreas is able to produce enough insulin to keep up with any amount of energy requirement. But how does this change is someone has type 1 diabetes? Well since their pancreas cannot produces as much insulin, they have an absolute insulin deficiency. Now for day-to-day activities, this may not actually cause any problems, because the small amount of insulin that is produced is able to compensate and keep the balance in balance. However, over time, as type 1 diabetes worsens, and less insulin is able to be produced, then the balance becomes slightly unequal. And this results in the sub-acute or mild symptoms of type 1 diabetes such as fatigue, because the body isn Continue reading >>

Emergency Management Of Diabetic Ketoacidosis In Adults

Emergency Management Of Diabetic Ketoacidosis In Adults

Diabetic ketoacidosis (DKA) is a potentially fatal metabolic disorder presenting most weeks in most accident and emergency (A&E) departments.1 The disorder can have significant mortality if misdiagnosed or mistreated. Numerous management strategies have been described. Our aim is to describe a regimen that is based, as far as possible, on available evidence but also on our experience in managing patients with DKA in the A&E department and on inpatient wards. A literature search was carried out on Medline and the Cochrane Databases using “diabetic ketoacidosis” as a MeSH heading and as textword. High yield journals were hand searched. Papers identified were appraised in the ways described in the Users’ guide series published in JAMA. We will not be discussing the derangements in intermediary metabolism involved, nor would we suggest extrapolating the proposed regimen to children. Although some of the issues discussed may be considered by some to be outwith the remit of A&E medicine it would seem prudent to ensure that A&E staff were aware of the probable management of such patients in the hours after they leave the A&E department. AETIOLOGY AND DEFINITION DKA may be the first presentation of diabetes. Insulin error (with or without intercurrent illness) is the most common precipitating factor, accounting for nearly two thirds of cases (excluding those where DKA was the first presentation of diabetes mellitus).2 The main features of DKA are hyperglycaemia, metabolic acidosis with a high anion gap and heavy ketonuria (box 1). This contrasts with the other hyperglycaemic diabetic emergency of hyperosmolar non-ketotic hyperglycaemia where there is no acidosis, absent or minimal ketonuria but often very high glucose levels (>33 mM) and very high serum sodium levels (>15 Continue reading >>

Myths In Dka Management

Myths In Dka Management

Anand Swaminathan, MD, MPH (@EMSwami) is an assistant professor and assistant program director at the NYU/Bellevue Department of Emergency Medicine in New York City. Review questions are available at the end of this post. Background Each year, roughly 10,000 patients present to the Emergency Department in diabetic ketoacidosis (DKA). Prior to the advent of insulin, the mortality rate of DKA was 100% although in recent years, that rate has dropped to approximately 2-5%.1 Despite clinical advances, the mortality rate has remained constant over the last 10 years. With aggressive resuscitative measures and appropriate continued management this trend may change. DKA is defined as: Hyperglycemia (glucose > 250 mg/dl) Acidosis (pH < 7.3) Ketosis In the absence of insulin, serum glucose rises leading to osmotic diuresis. This diuresis leads to loss of electrolytes including sodium, magnesium, calcium and phosphorous. The resultant volume depletion leads to impaired glomerular filtration rate (GFR) and acute renal failure. In patients with DKA, fatty acid breakdown produces 2 different ketone bodies, first acetoacetate, which then further converts to beta-hydroxybutyrate, the latter being the ketone body largely produced in DKA patients. With this background in mind, let’s take a look at four urban legends in the management of DKA and the evidence that dispels these legends. Here’s our case: Although this presentation likely represents DKA, a blood gas is typically obtained to confirm the diagnosis. Often, the question arises as to whether an arterial or venous blood gas is adequate. Urban Legend #1 – An ABG is necessary for the diagnosis and treatment of DKA ABG gets you pH, PaO2, PaCO2, HCO3, Lactate, electrolytes and O2Sat VBG gets all this except for PaO2 (but we have 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 >>

Pem Pearls: Treatment Of Pediatric Diabetic Ketoacidosis And The Two-bag Method

Pem Pearls: Treatment Of Pediatric Diabetic Ketoacidosis And The Two-bag Method

Insulin does MANY things in the body, but the role we care about in the Emergency Department is glucose regulation. Insulin allows cells to take up glucose from the blood stream, inhibits liver glucose production, increases glycogen storage, and increases lipid production. When insulin is not present, such as in patients with Type 1 diabetes mellitus (DM), all of the opposite effects occur. A lack of insulin causes the following downstream effects: Prevents glucose from being used as an energy source – Free fatty acids are used instead and produce ketoacids during metabolism. Causes a surge of stress hormones and induces gluconeogenesis – When blood glucose levels are elevated, the kidneys cannot absorb all of the glucose from the urine, and the extra glucose in the urine causes polyuria, even in the setting of dehydration. In addition, acidosis causes potassium to shift out of cells into the blood, and the combination of this with dehydration causes the body to preferentially retain sodium at the expense of potassium.1,2 When insulin homeostasis is disrupted and decompensates, patients are at risk for developing diabetic ketoacidosis (DKA). All of the following criteria are required for a diagnosis of DKA: Hyperglycemia (glucose >200 mg/dL) Acidosis (pH <7.3 or bicarb <15 mmol/L) Ketosis (by urine or blood test) Treatment is based on a simple principle: return the body’s glucose regulation to its normal state and replace all of the things the body consumed while insulin-deficient. While bolus insulin is common in the treatment of DKA in adults, it is relatively contraindicated in the pediatric patient. Dehydration and secondary sympathetic activation can interfere with local tissue perfusion and may cause irregular and unpredictable absorption. Step 1: Correction 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 >>

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 >>

How Iv Insulin Can Kill Your Patient

How Iv Insulin Can Kill Your Patient

You have a patient that comes up to your unit with a blood sugar of 952. The labs are sent off and the patient is found to be in severe diabetic ketoacidosis (DKA). The doctor puts in the orders for serial lab work, fluid boluses, electrolyte replacements, and an insulin drip. As a newer nurse, you are familiar with labs, boluses, your replacement protocols, but have never administered insulin through an IV. What nursing interventions do you need to perform to safely care for this patient? How Does Insulin Work? Insulin is a hormone created by the pancreas. It allows your body to use glucose to provide the body's cells with the necessary energy they need. Insulin production from the pancreas is based off of your blood sugar levels. If you are getting hyperglycemic, the pancreas is signaled and insulin is released into the bloodstream. Insulin then signals different cells to absorb the glucose and use it as energy or store it for later use. When insulin facilitates glucose being pulled into a cell, a potassium cation is also pulled from extracellular fluid (meaning the bloodstream) into the intracellular fluid. How does this affect our patients? Initially, patients in DKA have an increased extracellular potassium level due to the hyperglycemia and acidosis they are experiencing. This potassium level is quickly decreased as blood glucose is pulled into the cells. Administration As with all critical care medications, be sure to check your hospital's policy for administration. I have seen two main situations in which IV insulin (meaning regular insulin, not Lantus, Aspart, etc.) is given. Treatment of DKA: It seems like each hospital has a different protocol they use to manage DKA patients with. Commonly patients are treated with a bolus of regular insulin IV and then place Continue reading >>

Episode 63 – Pediatric Dka

Episode 63 – Pediatric Dka

Pediatric DKA was identified as one of key diagnoses that we need to get better at managing in a massive national needs assessment conducted by the fine folks at TREKK – Translating Emergency Knowledge for Kids – one of EM Cases’ partners who’s mission is to improve the care of children in non-pediatric emergency departments across the country. You might be wondering – why was DKA singled out in this needs assessment? It turns out that kids who present to the ED in DKA without a known history of diabetes, can sometimes be tricky to diagnose, as they often present with vague symptoms. When a child does have a known history of diabetes, and the diagnosis of DKA is obvious, the challenge turns to managing severe, life-threatening DKA, so that we avoid the many potential complications of the DKA itself as well as the complications of treatment – cerebral edema being the big bad one. The approach to these patients has evolved over the years, even since I started practicing, from bolusing insulin and super aggressive fluid resuscitation to more gentle fluid management and delayed insulin drips, as examples. There are subtleties and controversies in the management of DKA when it comes to fluid management, correcting serum potassium and acidosis, preventing cerebral edema, as well as airway management for the really sick kids. In this episode we‘ll be asking our guest pediatric emergency medicine experts Dr. Sarah Reid, who you may remember from her powerhouse performance on our recent episodes on pediatric fever and sepsis, and Dr. Sarah Curtis, not only a pediatric emergency physician, but a prominent pediatric emergency researcher in Canada, about the key historical and examination pearls to help pick up this sometimes elusive diagnosis, what the value of serum Continue reading >>

Hyperglycemic Crisis: Regaining Control

Hyperglycemic Crisis: Regaining Control

CE credit is no longer available for this article. Expired July 2005 Originally posted April 2004 VERONICA CRUMP, RN, BSN VERONICA CRUMP is a nurse on the surgical unit of Morristown Memorial Hospital in Morristown, N.J. She's also a subacute care nurse in the hospital's rehabilitation division. KEY WORDS: hyperosmolar hyperglycemic syndrome (HHS), diabetic ketoacidosis (DKA), hepatic glucose production, proteolysis, hepatic gluconeogenesis, ketone bodies, metabolic acidosis, hyperkalemia, hypokalemia When a patient presents with markedly high blood glucose levels, the consequences can be fatal. Here's how to get your patient through the crisis. Edith Schafer, age 71, has just been admitted to your ICU with pneumonia, which she developed at home. She has a history of Type 2 diabetes. In addition to a temperature of 102° F (38.9° C), she has rapid, shallow breathing and dry, flushed skin. Her blood pressure is 96/70 mm Hg, and she's so lethargic that she's unable to keep her eyes open. Her lab results show a serum glucose level of 900 mg/dL. In addition to the pneumonia, Mrs. Schafer is suffering from hyperosmolar hyperglycemic syndrome (HHS). Severe hyperglycemia is a complication of both Type 1 and Type 2 diabetes. It can indicate HHS or diabetic ketoacidosis (DKA), another life-threatening condition. HHS tends to occur in patients with Type 2 diabetes, like Mrs. Schafer, while Type 1 diabetics are more likely to develop DKA. However, DKA can occur in Type 2 diabetes as well.1 HHS and DKA can be set off by infection, stress, missed medication, and other causes. In Mrs. Schafer's case, the trigger was pneumonia, a common cause of hyperglycemia in patients with diabetes. No matter what the cause, though, a case of HHS or DKA can turn deadly if not caught in time. The m 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 >>

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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