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Hypokalemia In Dka Treatment

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 >>

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 Ketoacidosistreatment & Management

Diabetic Ketoacidosistreatment & Management

Diabetic KetoacidosisTreatment & Management Author: Osama Hamdy, MD, PhD; Chief Editor: Romesh Khardori, MD, PhD, FACP more... Managing diabetic ketoacidosis (DKA) in an intensive care unit during the first 24-48 hours always is advisable. When treating patients with DKA, the following points must be considered and closely monitored: Correction of fluid loss with intravenous fluids Correction of electrolyte disturbances, particularly potassium loss Treatment of concurrent infection, if present It is essential to maintain extreme vigilance for any concomitant process, such as infection, cerebrovascular accident, myocardial infarction, sepsis, or deep venous thrombosis . It is important to pay close attention to the correction of fluid and electrolyte loss during the first hour of treatment. This always should be followed by gradual correction of hyperglycemia and acidosis. Correction of fluid loss makes the clinical picture clearer and may be sufficient to correct acidosis. The presence of even mild signs of dehydration indicates that at least 3 L of fluid has already been lost. Patients usually are not discharged from the hospital unless they have been able to switch back to their daily insulin regimen without a recurrence of ketosis. When the condition is stable, pH exceeds 7.3, and bicarbonate is greater than 18 mEq/L, the patient is allowed to eat a meal preceded by a subcutaneous (SC) dose of regular insulin. Insulin infusion can be discontinued 30 minutes later. If the patient is still nauseated and cannot eat, dextrose infusion should be continued and regular or ultrashort-acting insulin should be administered SC every 4 hours, according to blood glucose level, while trying to maintain blood glucose values at 100-180 mg/dL. The 2011 JBDS guideline recommends the Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is an acute, life-threatening complication of diabetes mellitus. DKA occurs predominantly in patients with type 1 (insulin-dependent) diabetes mellitus, but 10% to 30% of cases occur in newly diagnosed type 2 (noninsulin-dependent) diabetes mellitus, especially in African Americans and Hispanics. 1 , 2 Between 1993 and 2003, the yearly rate of U.S. ED visits for DKA was 64 per 10,000 with a trend toward an increased rate of visits among the African American population compared with the Caucasian population. 3 Europe has a comparable incidence. A better understanding of the pathophysiology of DKA and an aggressive, uniform approach to its diagnosis and management have reduced mortality to <5% of reported episodes in experienced centers. 4 However, mortality is higher in the elderly due to underlying renal disease or coexisting infection and in the presence of coma or hypotension. Figure 220-1 illustrates the complex relationships between insulin and counterregulatory hormones. DKA is a response to cellular starvation brought on by relative insulin deficiency and counterregulatory or catabolic hormone excess ( Figure 220-1 ). Insulin is the only anabolic hormone produced by the endocrine pancreas and is responsible for the metabolism and storage of carbohydrates, fat, and protein. Counterregulatory hormones include glucagon, catecholamines, cortisol, and growth hormone. Complete or relative absence of insulin and the excess counterregulatory hormones result in hyperglycemia (due to excess production and underutilization of glucose), osmotic diuresis, prerenal azotemia, worsening hyperglycemia, ketone formation, and a wide-anion-gap metabolic acidosis. 4 Ingested glucose is the primary stimulant of insulin release from the cells of the pancreas 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

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 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 >>

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

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

Hypokalemia during Treatment of Diabetic Ketoacidosis: Clinical Evidence for an Aldosterone-Like Action of Insulin Get rights and content To investigate whether the development of hypokalemia in patients with diabetic ketoacidosis (DKA) treated in the pediatric critical care unit (PCCU) could be caused by increased potassium (K+) excretion and its association with insulin treatment. 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+. 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). 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 >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

In diabetes, blood glucose is not able to reach the body cells where it can be utilized to produce energy. In such cases, the cells start to break down fat to produce energy. This process produces a chemical called ketone.[1] The buildup of ketones makes the blood more acidic. When the blood ketone level gets too high, a condition develops called diabetic ketoacidosis (DKA). It is a serious condition that can lead to coma or even death. DKA can happen to anyone with diabetes though it is more common in people with type 1 diabetes.[2] In this article, well explore the causes, symptoms treatment options, and complications of this life-threatening condition. DKA results from inadequate insulin levels that cause the cells to burn fat for energy. Ketones are released into the blood when fats are broken down. In people with diabetes, an underlying problem often triggers the onset of DKA. The following problems or conditions may contribute to DKA: An illness where the body produces higher levels of stress hormones like cortisol or adrenalin; these illnesses have a countereffect on the action of insulin (conditions like pneumonia or a urinary tract infection are common culprits) Inadequate insulin due to missed doses or more requirements Less food intake (this could be caused by sickness, fasting, or an eating disorder; bulimia, for example, produces excess ketones) Medications like corticosteroids and diuretics Symptoms of DKA typically evolve over a period of 24 hours. Some symptoms to be aware of include the following: Long, deep labored breathing (affected person may be gasping for breath) Check your blood glucose levels if you develop these symptoms. If your blood glucose levels are above 240mg/dl (13.3mmol/L), check for ketone levels using a blood or urine ketone testing 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 >>

Respiratory Failure In Diabetic Ketoacidosis

Respiratory Failure In Diabetic Ketoacidosis

Respiratory failure in diabetic ketoacidosis Number of Hits and Downloads for This Article Jul 25, 2015 (publication date) through Mar 31, 2018 Baishideng Publishing Group Inc, 7901 Stoneridge Drive, Suite 501, Pleasanton, CA 94588, USA Copyright The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved. World J Diabetes.Jul 25, 2015;6(8): 1009-1023 Published online Jul 25, 2015.doi: 10.4239/wjd.v6.i8.1009 Respiratory failure in diabetic ketoacidosis Nikifor K Konstantinov, Mark Rohrscheib, Emmanuel I Agaba, Richard I Dorin, Glen H Murata, Antonios H Tzamaloukas Nikifor K Konstantinov, University of New Mexico School of Medicine, Albuquerque, NM 87122, United States Mark Rohrscheib, Division of Nephrology, Department of Medicine, University of New Mexico School of Medicine, Albuquerque, NM 87122, United States Emmanuel I Agaba, Division of Nephrology, Department of Medicine, University of Jos Medical School, Jos, Plateau State 930001, Nigeria Richard I Dorin, Section of Endocrinology, Medicine Service, Raymond G. Murphy Veterans Affairs Medical Center, Albuq-uerque, NM 78108, United States Glen H Murata, Section of Informatics, Medicine Service, Raymond G. Murphy Veterans Affairs Medical Center, Albuq-uerque, NM 78108, United States Antonios H Tzamaloukas, Section of Nephrology, Medicine Service, Raymond G. Murphy Veterans Affairs Medical Center, Albuq-uerque, NM 78108, United States Richard I Dorin, Glen H Murata, Antonios H Tzamaloukas, Department of Medicine, University of New Mexico School of Medicine, Albuquerque, NM 87108, United States Author contributions: Konstantinov NK reviewed the literature, contributed to the writing of the report and constructed its figure; Rohrscheib M, Agaba EI, Dorin RI and Murata GH made critical changes i Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Print Overview Diabetic ketoacidosis is a serious complication of diabetes that occurs when your body produces high levels of blood acids called ketones. The condition develops when your body can't produce enough insulin. Insulin normally plays a key role in helping sugar (glucose) — a major source of energy for your muscles and other tissues — enter your cells. Without enough insulin, your body begins to break down fat as fuel. This process produces a buildup of acids in the bloodstream called ketones, eventually leading to diabetic ketoacidosis if untreated. If you have diabetes or you're at risk of diabetes, learn the warning signs of diabetic ketoacidosis — and know when to seek emergency care. Symptoms Diabetic ketoacidosis signs and symptoms often develop quickly, sometimes within 24 hours. For some, these signs and symptoms may be the first indication of having diabetes. You may notice: Excessive thirst Frequent urination Nausea and vomiting Abdominal pain Weakness or fatigue Shortness of breath Fruity-scented breath Confusion More-specific signs of diabetic ketoacidosis — which can be detected through home blood and urine testing kits — include: High blood sugar level (hyperglycemia) High ketone levels in your urine When to see a doctor If you feel ill or stressed or you've had a recent illness or injury, check your blood sugar level often. You might also try an over-the-counter urine ketones testing kit. Contact your doctor immediately if: You're vomiting and unable to tolerate food or liquid Your blood sugar level is higher than your target range and doesn't respond to home treatment Your urine ketone level is moderate or high Seek emergency care if: Your blood sugar level is consistently higher than 300 milligrams per deciliter (mg/dL), or 16.7 mill Continue reading >>

Canine Diabetic Ketoacidosis - Acvim 2008 - Vin

Canine Diabetic Ketoacidosis - Acvim 2008 - Vin

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. 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 -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 shown that 5 of 7 dogs with DK 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 >>

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 >>

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