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Why Are Dka Patients Hypokalemic

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 >>

Board Review: Diabetic Ketoacidosis And Total Body Potassium

Board Review: Diabetic Ketoacidosis And Total Body Potassium

A 23 y/o M with a PMHx of Type 1 DM arrives to your ED reporting nausea, vomiting and elevated blood sugars on his home monitor. His initial blood work indicates he is in DKA. For which of the following potassium levels should initiation of an insulin drip be delayed for potassium repletion? (scroll down for the answer) a) < 3.0 mEq/L b) < 3.3 mEq/L c) < 3.5 mEq/L d) < 3.8 mEq/L e) < 4.0 mEq/L The correct answer is b) < 3.3 mEq/L Following the American Diabetes Association guidelines for the treatment of DKA, patients with hypokalemia on initial labs of 3.3 mEq/L or less must have potassium replacement with a delay in insulin treatment until the potassium concentration is restored to > 3.3 mEq/L Patients in DKA are low in total body potassium and their serum concentration is falsely elevated due to extracellular shift. On average, patients will have a potassium deficit of 3-5 mEq/kg. Treatment with insulin will cause a shift of potassium intracellularly which can lead to severe hypokalemia and cardiac dysrhythmia. All DKA patients will require potassium replacement to prevent hypokalemia. Generally 20mEq of potassium in each liter of fluid given will maintain a normal serum potassium concentration. The ADA Guidelines for DKA can be found here: A Core review of Hypokalemia in the ED was recently posted on emDOCs by Dr. Swaminathan, see it here: 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 >>

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 >>

Profound Hypokalemia Associated With Severe Diabetic Ketoacidosis

Profound Hypokalemia Associated With Severe Diabetic Ketoacidosis

Go to: Abstract Hypokalemia is common during the treatment of diabetic ketoacidosis (DKA); however, severe hypokalemia at presentation prior to insulin treatment is exceedingly uncommon. A previously healthy 8-yr-old female presented with new onset type 1 diabetes mellitus, severe DKA (pH = 6.98), and profound hypokalemia (serum K = 1.3 mmol/L) accompanied by cardiac dysrhythmia. Insulin therapy was delayed for 9 h to allow replenishment of potassium to safe serum levels. Meticulous intensive care management resulted in complete recovery. This case highlights the importance of measuring serum potassium levels prior to initiating insulin therapy in DKA, judicious fluid and electrolyte management, as well as delaying and/or reducing insulin infusion rates in the setting of severe hypokalemia. Keywords: diabetic ketoacidosis, hypokalemia, insulin, low-dose insulin drip, pediatric Nearly one third of children with newly diagnosed type 1 diabetes present in diabetic ketoacidosis (DKA). Higher proportions of young children and those from disadvantaged socioeconomic groups present with DKA (1). DKA is the leading cause of mortality among children with diabetes, and electrolyte abnormalities are a recognized complication of DKA contributing to morbidity and mortality (2, 3). Total body potassium deficiency of 3-6 mEq/kg is expected at presentation of DKA due to osmotic diuresis, emesis, and secondary hyperaldosteronism; however, pretreatment serum potassium levels are usually not low due to the extracellular shift of potassium that occurs with acidosis and insulin deficiency (3, 4). After insulin treatment is initiated, potassium shifts intracellularly and serum levels decline. Replacement of potassium in intravenous fluids is the standard of care in treatment of DKA to prevent Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Abbas E. Kitabchi, PhD., MD., FACP, FACE Professor of Medicine & Molecular Sciences and Maston K. Callison Professor in the Division of Endocrinology, Diabetes & Metabolism UT Health Science Center, 920 Madison Ave., 300A, Memphis, TN 38163 Aidar R. Gosmanov, M.D., Ph.D., D.M.Sc. Assistant Professor of Medicine, Division of Endocrinology, Diabetes & Metabolism, The University of Tennessee Health Science Center, 920 Madison Avenue, Suite 300A, Memphis, TN 38163 Clinical Recognition Omission of insulin and infection are the two most common precipitants of DKA. Non-compliance may account for up to 44% of DKA presentations; while infection is less frequently observed in DKA patients. Acute medical illnesses involving the cardiovascular system (myocardial infarction, stroke, acute thrombosis) and gastrointestinal tract (bleeding, pancreatitis), diseases of endocrine axis (acromegaly, Cushing`s syndrome, hyperthyroidism) and impaired thermo-regulation or recent surgical procedures can contribute to the development of DKA by causing dehydration, increase in insulin counter-regulatory hormones, and worsening of peripheral insulin resistance. Medications such as diuretics, beta-blockers, corticosteroids, second-generation anti-psychotics, and/or anti-convulsants may affect carbohydrate metabolism and volume status and, therefore, could precipitateDKA. Other factors: psychological problems, eating disorders, insulin pump malfunction, and drug abuse. It is now recognized that new onset T2DM can manifest with DKA. These patients are obese, mostly African Americans or Hispanics and have undiagnosed hyperglycemia, impaired insulin secretion, and insulin action. A recent report suggests that cocaine abuse is an independent risk factor associated with DKA recurrence. Pathophysiology In Continue reading >>

Hypokalemic Respiratory Arrest In Diabetic Ketoacidosis

Hypokalemic Respiratory Arrest In Diabetic Ketoacidosis

THE OCCURRENCE of life-threatening hypokalemic hypoventilatory respiratory failure requiring intubation and respiratory support in diabetic ketoacidosis (DKA) is exceedingly rare. In none of the reported cases have serum phosphate levels been assessed within 12 hours of respiratory failure and in only one case have serial arterial blood gas measurements been performed to document hypoventilation.1 The recent documentation of severe hypophosphatemia as a cause of hypoventilation and the fact that decrements in serum phosphate and serum potassium levels frequently parallel one another in DKA call into question the importance of hypokalemia to the respiratory response in DKA. We report a case of DKA in a young, otherwise healthy man whose treatment was complicated by severe hypokalemia and a hypoventilatory respiratory arrest without severe hypophosphatemia. We further discuss issues relating to the assessment and treatment of the hypokalemic patient with DKA at risk for ventilatory failure. Report of a Case Continue reading >>

Prevalence Of Hypokalemia In Ed Patients With Diabetic Ketoacidosis

Prevalence Of Hypokalemia In Ed Patients With Diabetic Ketoacidosis

Abstract Objective Although patients with diabetic ketoacidosis (DKA) are expected to have total body potassium depletion, measured levels may be normal or elevated due to extracellular shifts of potassium secondary to acidosis. Because insulin therapy decreases serum potassium levels, which creates potential to precipitate a fatal cardiac arrhythmia in a patient with hypokalemia, the American Diabetes Association (ADA) recommends obtaining a serum potassium level before giving insulin. Although the ADA guidelines are clear, the evidence on which they are based is largely anecdotal. The purpose of this study was to estimate the prevalence of hypokalemia in patients with DKA before initiation of fluid resuscitation and insulin therapy. This is a prospective cross-sectional descriptive study of patients with a capillary blood glucose level of 250 mg/dL or higher (at risk for DKA) seen in an urban county emergency department over a 1-year period. Those who consented provided basic demographic information and had a venous blood gas and chemistry panel drawn. Diabetic ketoacidosis and hypokalemia were defined using ADA recommendations. The mean age in our sample was 40.2 years, and 81% of patients were Hispanic. Of 503 analyzable patients with hyperglycemia, 54 (10.7%) met all criteria for DKA. Of patients with DKA, 3 (5.6%) of 54 (95% confidence interval, 1.2%-15.4%) had hypokalemia. Two of these patients had values of 3.0 mmol/L, and 1 had a value of 2.8 mmol/L. Conclusion Hypokalemia was observed in 5.6% of patients with DKA. These findings support the ADA recommendation to obtain a serum potassium before initiating intravenous insulin therapy in a patient with DKA. Continue reading >>

Hyperglycemic Crises In Diabetes

Hyperglycemic Crises In Diabetes

Ketoacidosis and hyperosmolar hyperglycemia are the two most serious acute metabolic complications of diabetes, even if managed properly. These disorders can occur in both type 1 and type 2 diabetes. The mortality rate in patients with diabetic ketoacidosis (DKA) is <5% in experienced centers, whereas the mortality rate of patients with hyperosmolar hyperglycemic state (HHS) still remains high at ∼15%. The prognosis of both conditions is substantially worsened at the extremes of age and in the presence of coma and hypotension (1–10). This position statement will outline precipitating factors and recommendations for the diagnosis, treatment, and prevention of DKA and HHS. It is based on a previous technical review (11), which should be consulted for further information. PATHOGENESIS Although the pathogenesis of DKA is better understood than that of HHS, the basic underlying mechanism for both disorders is a reduction in the net effective action of circulating insulin coupled with a concomitant elevation of counterregulatory hormones, such as glucagon, catecholamines, cortisol, and growth hormone. These hormonal alterations in DKA and HHS lead to increased hepatic and renal glucose production and impaired glucose utilization in peripheral tissues, which result in hyperglycemia and parallel changes in osmolality of the extracellular space (12,13). The combination of insulin deficiency and increased counterregulatory hormones in DKA also leads to the release of free fatty acids into the circulation from adipose tissue (lipolysis) and to unrestrained hepatic fatty acid oxidation to ketone bodies (β-hydroxybutyrate [β-OHB] and acetoacetate), with resulting ketonemia and metabolic acidosis. On the other hand, HHS may be caused by plasma insulin concentrations that are in Continue reading >>

Patient With Severe Dka, Look At The Ecg

Patient With Severe Dka, Look At The Ecg

This patient presented with severe DKA. Here is the ECG: The computer and physician reader wrote: "ST depression, consider subendocardial injury." The computer read the QT as 365 ms and the QTc as 424 ms. What else? I read the QT interval as somewhere between 480 and 580 ms, depending on the complex, with a QTc (Bazett correction) of 630 - 763 ms. There is a very prominent U-wave and some of what may appear to be a QT interval is a QU interval. So the real QT is shorter, but the computer does not mention the U-wave, and the U-wave is as important as the T-wave in predicting cardiac dysrhythmias. This is an extremely dangerous ECG. The K returned at 1.9 mEq/L. This is extremely low for DKA. K in DKA is usually high from shifting out of cells, and will go lower as it shifts into cells during treatment. Therefore, hypokalemia in the setting of DKA is truly life threatening and must be treated aggressively. When the ECG shows the effects of hypokalemia, it is particularly dangerous. In spite of aggressive K replacement, the patient went into ventricular fibrillation. Discussion See this post:STEMI with Life-Threatening Hypokalemia and Incessant Torsades de Pointes I could find very little literature on the treatment of severe life-threatening hypokalemia. There is particularly little on how to treat when the K is less than 2.0, and/or in the presence of acute MI. Here are the American Heart Association Guidelines: Treatment of Hypokalemia "The treatment of hypokalemia consists of minimizing further potassium loss and providing potassium replacement. IV administration of potassium is indicated when arrhythmias are present or hypokalemia is severe (potassium level of less than 2.5 mEq/L). Gradual correction of hypokalemia is preferable to rapid correction unless the patient i Continue reading >>

Correction Of Critical Hypokalemia

Correction Of Critical Hypokalemia

I recently assisted in the management of a patient who presented in DKA with critical acidosis and hypokalemia. This presents a variety of therapeutic challenges: what to do about insulin, which treats the acidemia but worsens the hypokalemia? How can I safely supplement potassium as aggressively as possible? In contrast to the previously-posted recommendations from Micromedex, a protocol from the Bon Secours system in Richmond, VA presents the most clinically useful summary we have come across. ___ *If potassium < 3 meq/liter and the patient is symptomatic 40 meq/hour may be administered to intensive care patients. Hourly serum potassium determinations should be drawn to avoid severe hyperkalemia and/or cardiac arrest. Symptoms of hypokalemia include: fatigue, malaise, generalized muscle weakness, respiratory failure, paralysis; EKG changes include T wave flattening or inversion, U waves, or ST segment depression, and arrhythmia’s. Recommended maximum dose should not usually exceed 10 meq/hour or 200 meq for a 24 hour period if the serum potassium level is greater than 2.5 meq/liter per product package insert ___ Additionally, there is literature† to support providing a baseline rate of 40 mEq/hr (through a central line) with hourly supplementation using “runs” of up to 40 mEq (through a central line). Patients having their potassium replaced this aggressively should be on a monitor and have hourly electrolyte checks. Regarding the benefit/drawback of using insulin in DKA patients, the ADA strongly recommends withholding insulin when K < 3.3. If you want to disregard this recommendation, which I do (seems overly cautious), remember you can slow the insulin infusion rather than stop it. The key is to keep a very close eye on your blood gas/chemistry. †Murthy, 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 >>

Hypokalemia During Treatment Of Diabetic Ketoacidosis: Clinical Evidence For An Aldosterone-like Action Of Insulin

Hypokalemia During Treatment Of Diabetic Ketoacidosis: Clinical Evidence For An Aldosterone-like Action Of Insulin

Study design In this prospective observational study of patients with DKA admitted to the PCCU, blood and timed urine samples were collected for measurement of sodium (Na+), K+, and creatinine concentrations and for calculations of Na+ and K+ balances. K+ excretion rate was expressed as urine K+-to-creatinine ratio and fractional excretion of K+. Results Of 31 patients, 25 (81%) developed hypokalemia (plasma K+ concentration <3.5 mmol/L) in the PCCU at a median time of 24 hours after therapy began. At nadir plasma K+ concentration, urine K+-to-creatinine ratio and fractional excretion of K+ were greater in patients who developed hypokalemia compared with those without hypokalemia (19.8 vs 6.7, P = .04; and 31.3% vs 9.4%, P = .004, respectively). Patients in the hypokalemia group received a continuous infusion of intravenous insulin for a longer time (36.5 vs 20 hours, P = .015) and greater amount of Na+ (19.4 vs 12.8 mmol/kg, P = .02). At peak kaliuresis, insulin dose was higher in the hypokalemia group (median 0.07, range 0-0.24 vs median 0.025, range 0-0.05 IU/kg; P = .01), and there was a significant correlation between K+ and Na+ excretion (r = 0.67, P < .0001). Conclusions Hypokalemia was a delayed complication of DKA treatment in the PCCU, associated with high K+ and Na+ excretion rates and a prolonged infusion of high doses of insulin. 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 >>

Hypokalemia

Hypokalemia

Hypokalemia, also spelled hypokalaemia, is a low level of potassium (K+) in the blood serum.[1] Normal potassium levels are between 3.5 and 5.0 mmol/L (3.5 and 5.0 mEq/L) with levels below 3.5 mmol/L defined as hypokalemia.[1][2] Mildly low levels do not typically cause symptoms.[3] Symptoms may include feeling tired, leg cramps, weakness, and constipation.[1] It increases the risk of an abnormal heart rhythm, which are often too slow, and can cause cardiac arrest.[1][3] Causes of hypokalemia include diarrhea, medications like furosemide and steroids, dialysis, diabetes insipidus, hyperaldosteronism, hypomagnesemia, and not enough intake in the diet.[1] It is classified as severe when levels are less than 2.5 mmol/L.[1] Low levels can also be detected on an electrocardiogram (ECG).[1] Hyperkalemia refers to a high level of potassium in the blood serum.[1] The speed at which potassium should be replaced depends on whether or not there are symptoms or ECG changes.[1] Mildly low levels can be managed with changes in the diet.[3] Potassium supplements can be either taken by mouth or intravenously.[3] If given by intravenous, generally less than 20 mmol are given over an hour.[1] High concentration solutions (>40 mmol/L) should be given in a central line if possible.[3] Magnesium replacement may also be required.[1] Hypokalemia is one of the most common water–electrolyte imbalances.[4] It affects about 20% of people admitted to hospital.[4] The word "hypokalemia" is from hypo- means "under"; kalium meaning potassium, and -emia means "condition of the blood".[5] Play media Video explanation Signs and symptoms[edit] Mild hypokalemia is often without symptoms, although it may cause elevation of blood pressure,[6] and can provoke the development of an abnormal heart rhythm. Se Continue reading >>

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