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Dka Hypokalemia

Hypokalemia In Diabetic Ketoacidosis Is Less Common Than Previously Reported

Hypokalemia In Diabetic Ketoacidosis Is Less Common Than Previously Reported

, Volume 10, Issue2 , pp 177180 | Cite as Hypokalemia in diabetic ketoacidosis is less common than previously reported [K+]<3.5mmol/L is reported to occur in approximately 4% of patients with diabetic ketoacidosis (DKA.) Therefore, the American Diabetes Association (ADA) and Joint British Diabetes Societies (JBDS) recommend the assessment of [K+] before the initiation of insulin treatment to avoid the precipitation of morbid hypokalemia. The purpose of this study was to assess the incidence of hypokalemia in patients presenting to the emergency department (ED) with DKA. This was a multicenter retrospective, cross-sectional study at EDs with a combined annual adult census of 155,000. Adult patients diagnosed with DKA in the ED, or who were admitted from the ED and subsequently diagnosed with DKA as determined from the hospital electronic database between January 2008 and December 2008, were included for analysis if they had the following initial laboratory values: (1) serum glucose >13.9mmol/L (250mg/dL), (2) serum bicarbonate <18mmol/L (18mEq/L) or anion gap >15, and (3) evidence of ketonaemia or ketonuria. 537 patients were diagnosed with DKA in the ED at the participating institutions during the reference period. The median [K+] was 4.9mmol/L (IQR 4.3, 5.5). There were a total of seven patients with an initial 3.3<[K+]<3.5mmol/L, but none with a [K+]<3.3mmol/L. Thus, no patients in our study sample required potassium supplementation before the initiation of insulin treatment. The incidence of hypokalemia in our sample of patients with DKA was much less than previously reported, with no cases requiring potassium supplementation before insulin administration. Diabetic KetoacidosisHypokalemiaInsulinPotassium Timothy Jang, Vijai Chauhan, and Rosanne Naunheim conceived of Continue reading >>

Hypothermia And Hypokalemia In A Patient With Diabetic Ketoacidosis

Hypothermia And Hypokalemia In A Patient With Diabetic Ketoacidosis

We present the case of a 36-year-old man with type-1 diabetes who was hospitalized with diabetic ketoacidosis (DKA). On admission, he had hypothermia, hypokalemia and combined metabolic and respiratory alkalosis, in addition to hyperglycemia. Hypothermia, hypokalemia and metabolic alkalosis, with a concurrent respiratory alkalosis, are not commonly seen in DKA. After admission, intravenous infusion of 0.45% saline was administered, which resulted in the development of pure metabolic acidosis. After starting insulin infusion, hypokalemia and hypophosphatemia became evident and finally resulted in massive rhabdomyolysis. Hyperkalemia accompanying oliguric acute kidney injury (AKI) warranted initiation of hemodialysis (HD) on Day-five. On the 45th hospital day, his urine output started to increase and a total of 22 HD sessions were required. We believe that in this case severe dehydration, hypothermia and hypokalemia might have contributed to the initial symptoms of DKA as well as the prolongation of AKI. How to cite this article: Saito O, Saito T, Sugase T, Kusano E, Nagata D. Hypothermia and hypokalemia in a patient with diabetic ketoacidosis. Saudi J Kidney Dis Transpl 2015;26:580-3 Diabetic ketoacidosis (DKA) is a combination of the biochemical triad of hyperglycemia, ketonemia and metabolic acidosis. [1] Initial hypokalemia in DKA is a rare finding, with an incidence of 4-10%. [2] Hypothermia is rarely seen in patients with DKA, and the prognosis of this association is poor, with a mortality of 60% in the Western countries. [3] Also, combined metabolic and respiratory alkalosis is rarely seen in DKA, with an incidence of 7.5%. [4] We herewith report the case of a 36-year-old man with type-1 diabetes who was admitted to the hospital with DKA in association with hypothe 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 >>

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)

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 >>

Initial Potassium Replacement In Diabetic Ketoacidosis: The Unnoticed Area Of Gap

Initial Potassium Replacement In Diabetic Ketoacidosis: The Unnoticed Area Of Gap

Initial Potassium Replacement in Diabetic Ketoacidosis: The Unnoticed Area of Gap We are experimenting with display styles that make it easier to read articles in PMC. The ePub format uses eBook readers, which have several "ease of reading" features already built in. The ePub format is best viewed in the iBooks reader. You may notice problems with the display of certain parts of an article in other eReaders. Generating an ePub file may take a long time, please be patient. Initial Potassium Replacement in Diabetic Ketoacidosis: The Unnoticed Area of Gap Diabetic ketoacidosis is an acute complication of diabetes mellitus (DM). It affects all the types of DM and hence is a continuous threat for all the diabetes patients ( 1 ). DKA is a well-studied disease. Among the precipitating causes, mostly reported factors are non-compliance of patients with the antidiabetic treatment, and infection; others, however, may not have any precipitating cause ( 1 , 2 ). The progress of disease is very simple; lack of insulin causes hyperglycemia and inability of glucose to enter the cell. In-turn, triglycerides are broken down to free fatty acids which are used as a source of energy ( 1 , 3 , 4 ). In due process, the end-product of this metabolic derangement, i.e., ketones, cause acidification of blood causing major disruption in homeostasis. Similar to pathophysiology, the treatment of DKA is also simple and encompasses administration of insulin to achieve euglycaemia, and administration of crystalloid or colloidal solution to attain euvolaemia and euelectrolytaemia ( 1 3 ). Nevertheless, by the time patient reports for medical attention, these simple derangements and the rectification pathway have had gone significant derailment with potassium being the most affected ion throughout the 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 >>

162: Incidence Of Hypokalemia In Patients Presenting To The Emergency Department With Diabetic Ketoacidosis

162: Incidence Of Hypokalemia In Patients Presenting To The Emergency Department With Diabetic Ketoacidosis

Hypokalemia is reported to occur in approximately 3 to 4 percent of patients with diabetic ketoacidosis (DKA). To prevent complications of severe hypokalemia, the American Diabetes Association (ADA) treatment guidelines recommend ensuring that serum potassium levels are > 3.3 mEq/L prior to initiation of insulin in the treatment of DKA. To access this article, please choose from the options below Society Members, full access to the journal is a member benefit. Use your society credentials to access all journal content and features 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 >>

Prevalence And Potential Risk Factors Of Hypokalemia In Pediatric Patients With Diabetic Ketoacidosis

Prevalence And Potential Risk Factors Of Hypokalemia In Pediatric Patients With Diabetic Ketoacidosis

Aims To examine the local prevalence of hypokalemia in patients with diabetic ketoacidosis (DKA), both at presentation and during treatment, and to investigate the potential risk factors leading to significant hypokalemia during treatment of DKA. Methods Retrospective review of 114 consecutive patient-episodes. Univariate analyses were performed to study any difference in mean between the group with nadir of potassium (Kn) >= 3.0mmol/L from group with Kn < 3.0mmol/L for predictors concerning patients’ demographics, the baseline characteristics, the therapies for DKA (including average insulin infusion rate before Kn), and the pace of recovery from DKA. Predictors deemed statistical significant in univariate analyses were subjected to multivariate analysis. Results The period prevalence of hypokalemia at presentation and during treatment of DKA were 13.8% and 92.5% respectively. Univariate analysis showed patients who were younger, with lower mean body weight, lower mean plasma bicarbonate at presentation, lower mean serum potassium level at presentation, higher urine output per unit body weight (in the first 24 hours of admission), higher amount of potassium supplement given before Kn, shorter time lag of starting potassium supplements (as reference to time of start of insulin) and longer duration of metabolic acidosis were independently associated with risk of developing Kn < 3.0mmol/L. Multivariate analysis showed that duration of metabolic acidosis was the sole risk factor for having Kn < 3.0mmol/L. Conclusions In our cohort, the longer duration of metabolic acidosis predicts significant hypokalemia during DKA treatment, which could have represented a persistent accumulation of free fatty acid and an on-going stimulus for aldosterone secretion, hence kaliuresis-rel 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 >>

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

Abstract Objectives: 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. 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 >>

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

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 >>

How Is Hypokalemia Treated In Diabetic Ketoacidosis (dka) Treated?

How Is Hypokalemia Treated In Diabetic Ketoacidosis (dka) Treated?

How is hypokalemia treated in diabetic ketoacidosis (DKA) treated? Hypokalemia is a complication that is precipitated by failing to rapidly address the total body potassium deficit brought out by rehydration and insulin treatment, which not only reduces acidosis but directly facilitates potassium reentry into the cell. Glaser NS, Marcin JP, Wootton-Gorges SL, et al. Correlation of clinical and biochemical findings with diabetic ketoacidosis-related cerebral edema in children using magnetic resonance diffusion-weighted imaging. J Pediatr. 2008 Jun 25. [Medline] . Umpierrez GE, Jones S, Smiley D, et al. Insulin analogs versus human insulin in the treatment of patients with diabetic ketoacidosis: a randomized controlled trial. Diabetes Care. 2009 Jul. 32(7):1164-9. [Medline] . [Full Text] . Herrington WG, Nye HJ, Hammersley MS, Watkinson PJ. Are arterial and venous samples clinically equivalent for the estimation of pH, serum bicarbonate and potassium concentration in critically ill patients?. Diabet Med. 2012 Jan. 29(1):32-5. [Medline] . Mrozik LT, Yung M. Hyperchloraemic metabolic acidosis slows recovery in children with diabetic ketoacidosis: a retrospective audit. Aust Crit Care. 2009 Jun 26. [Medline] . Bowden SA, Duck MM, Hoffman RP. Young children (12 yr) with type 1 diabetes mellitus have low rate of partial remission: diabetic ketoacidosis is an important risk factor. Pediatr Diabetes. 2008 Jun. 9(3 Pt 1):197-201. [Medline] . Potenza M, Via MA, Yanagisawa RT. Excess thyroid hormone and carbohydrate metabolism. Endocr Pract. 2009 May-Jun. 15(3):254-62. [Medline] . Taylor SI, Blau JE, Rother KI. SGLT2 Inhibitors May Predispose to Ketoacidosis. J Clin Endocrinol Metab. 2015 Aug. 100 (8):2849-52. [Medline] . Zargar AH, Wani AI, Masoodi SR, et al. Causes of mortality Continue reading >>

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