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Why Are Dka Patients Hypokalemic

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 (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 >>

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 >>

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 >>

Prime Pubmed | Profound Hypokalemia Associated With Severe Diabetic Ketoacidosi

Prime Pubmed | Profound Hypokalemia Associated With Severe Diabetic Ketoacidosi

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. Davis, Shanlee M., et al. "Profound Hypokalemia Associated With Severe Diabetic Ketoacidosis." Pediatric Diabetes, vol. 17, no. 1, 2016, pp. 61-5. Davis SM, Maddux AB, Alonso GT, et al. Profound hypokalemia associated with severe diabetic ketoacidosis. Pediatr Diabetes. 2016;17(1):61-5. Davis, S. M., Maddux, A. B., Alonso, G. T., Okada, C. R., Mourani, P. M., & Maahs, D. M. (2016). Profound hypokalemia associated with severe diabetic ketoacidosis. Pediatric Diabetes, 17(1), pp. 61-5. doi:10.1111/pedi.12246. Davis SM, et al. Profound Hypokalemia Associated With Severe Diabetic Ketoacidosis. Pediatr Diabetes. 2016;17(1):61-5. PubMed PMID: 25430801. * Article titles in AMA citation format should be in sentence-case TY - JOURT1 - Profound hypokalemia associated with severe diabetic ketoacidosis.AU - Davis,Shanlee M,AU - Maddux,Aline B,AU - Alonso,Guy T,AU - Okada,Carol R,AU - Mourani,Peter M,AU - Maahs,David M,Y1 - 2014/11/27/PY - 2014/07/09/receivedPY - 2014/10/29/revisedPY - 2014/10/30/acceptedPY - 2 Continue reading >>

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An Error Occurred Setting Your User Cookie

An Error Occurred Setting Your User Cookie This site uses cookies to improve performance. If your browser does not accept cookies, you cannot view this site. There are many reasons why a cookie could not be set correctly. Below are the most common reasons: You have cookies disabled in your browser. You need to reset your browser to accept cookies or to ask you if you want to accept cookies. Your browser asks you whether you want to accept cookies and you declined. To accept cookies from this site, use the Back button and accept the cookie. Your browser does not support cookies. Try a different browser if you suspect this. The date on your computer is in the past. If your computer's clock shows a date before 1 Jan 1970, the browser will automatically forget the cookie. To fix this, set the correct time and date on your computer. You have installed an application that monitors or blocks cookies from being set. You must disable the application while logging in or check with your system administrator. This site uses cookies to improve performance by remembering that you are logged in when you go from page to page. To provide access without cookies would require the site to create a new session for every page you visit, which slows the system down to an unacceptable level. This site stores nothing other than an automatically generated session ID in the cookie; no other information is captured. In general, only the information that you provide, or the choices you make while visiting a web site, can be stored in a cookie. For example, the site cannot determine your email name unless you choose to type it. Allowing a website to create a cookie does not give that or any other site access to the rest of your computer, and only the site that created the cookie can read it. 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 >>

How I Treat Electrolyte Disturbances In Diabetic Ketoacidosis

How I Treat Electrolyte Disturbances In Diabetic Ketoacidosis

Proceeding of the NAVC North American Veterinary Conference Reprinted in the IVIS website with the permission of the NAVC Close window to return to IVIS Small Animal – Critical Care Nishi Dhupa, BVM, DACVIM, DACVECC College of Veterinary Medicine Cornell University, Ithaca, NY INTRODUCTION Diabetic ketoacidosis (DKA) results from an absolute or relative insulin deficiency in conjunction with glucagon and stress hormone excess. It is crucial to identify underlying disease factors contributing to stress in these patients. Stress factors include changes in environment, dehydration and concomitant disease. Commonly associated diseases include renal disease, urinary tract and other infection, and pancreatitis; in cats, hepatic lipidosis is also commonly seen. DKA is characterized by hyperglycemia, dehydration, ketonemia, metabolic acidosis and multiple electrolyte abnormalities. Treatment must be intensive and directed towards the correction of fluid, electrolyte and acid-base abnormalities as well as the correction of abnormal carbohydrate metabolism. The treatment itself (particularly the correction of acid-base imbalance with sodium bicarbonate therapy and the use of insulin therapy) may exacerbate the electrolyte abnormalities, and careful monitoring and aggressive treatment of these abnormalities is critical. Without treatment, DKA is fatal and it should be considered a medical emergency. The mortality rate for DKA is 25-30 %, even with aggressive treatment. CLINICAL SIGNS Clinical signs seen in dogs and cats with ketoacidosis include polyuria, polydipsia, weight loss, anorexia, vomiting, diarrhea, lethargy, weakness, dehydration, obtundation and hyper- or hypoventilation. These clinical signs may develop in various combinations and are usually severe in the keto Continue reading >>

What Causes Potassium And Sodium Loss In Diabetic Ketoacidosis (dka)?

What Causes Potassium And Sodium Loss In Diabetic Ketoacidosis (dka)?

What causes potassium and sodium loss in diabetic ketoacidosis (DKA)? Glucosuria leads to osmotic diuresis, dehydration and hyperosmolarity. Severe dehydration, if not properly compensated, may lead to impaired renal function. Hyperglycemia, osmotic diuresis, serum hyperosmolarity, and metabolic acidosis result in severe electrolyte disturbances. The most characteristic disturbance is total body potassium loss. This loss is not mirrored in serum potassium levels, which may be low, within the reference range, or even high. Potassium loss is caused by a shift of potassium from the intracellular to the extracellular space in an exchange with hydrogen ions that accumulate extracellularly in acidosis. Much of the shifted extracellular potassium is lost in urine because of osmotic diuresis. Patients with initial hypokalemia are considered to have severe and serious total body potassium depletion. High serum osmolarity also drives water from intracellular to extracellular space, causing dilutional hyponatremia. Sodium also is lost in the urine during the osmotic diuresis. 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 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 >>

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 >>

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 >>

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 >>

Successful Use Of Renal Replacement Therapy For Refractory Hypokalemia In A Diabetic Ketoacidosis Patient

Successful Use Of Renal Replacement Therapy For Refractory Hypokalemia In A Diabetic Ketoacidosis Patient

Volume 2019 |Article ID 6130694 | 3 pages | Successful Use of Renal Replacement Therapy for Refractory Hypokalemia in a Diabetic Ketoacidosis Patient 1Department of Medicine, Saint Josephs University Medical Center, 703 Main St, Paterson, NJ, USA 2New York Medical College, Valhalla, NY, USA A 39-year-old African-American female presented to the emergency department with a seven-day history of right upper quadrant abdominal pain accompanied by nausea, vomiting, and diarrhea. She was noted to be alert and following commands, but tachypneic with Kussmaul respirations; and initial laboratory testing supported a diagnosis of diabetic ketoacidosis (DKA) and hypokalemia. To avoid hypokalemia-induced arrhythmias, insulin administration was withheld until a serum potassium (K) level of 3.3 mEq/L could be achieved. Efforts to increase the patients potassium level via intravenous repletion were ineffectual; hence, an attempt was made at more aggressive potassium repletion via hemodialysis using a 4 mEq/L K dialysate bath. The patient was started on Aldactone and continuous veno-venous hemodialysis (CVVH) with ongoing low-dose insulin infusion. This regimen was continued over 24 h resulting in normalization of the patients potassium levels, resolution of acidosis, and improvement in mental status. Upon resolution of her acidemia, the patient was transitioned from insulin infusion to treatment with a subcutaneous insulin aspart and insulin detemir, and did not experience further hypokalemia. Considering our success, we propose CVVH as a tool for potassium repletion when aggressive intravenous (IV) repletion has failed. Hospitalizations for diabetic ketoacidosis (DKA) have soared in incidence over the recent years, increasing 54.9% from 19.5 to 30.2 hospitalizations per 1,000 people Continue reading >>

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