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Why Are Dka Patients Hypokalemic

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 >>

Review Of Diabetic Ketoacidosis Management

Review Of Diabetic Ketoacidosis Management

Review of Diabetic Ketoacidosis Management Department of Clinical Health Professions Department of Clinical Health Professions ABSTRACT: Diabetic ketoacidosis (DKA) is a medical emergency caused by insulin deficiency. It is characterized by hyperglycemia, metabolic acidosis, and ketoacidosis. DKA arises from lack of insulin, with or without a precipitating event that leads to a cascade of pathophysiological changes. The goals of DKA treatment are to normalize volume status, hyperglycemia, electrolytes, and ketoacidosis. Pharmacists in community or ambulatory-care settings can assist in preventing DKA, while inpatient pharmacists play a role in management of DKA. Diabetic ketoacidosis (DKA) is a serious medical emergency caused by insulin deficiency that takes a significant toll on the U.S. healthcare system.1,2 There are over 500,000 hospital days per year and $2.4 billion in medical costs attributed to DKA alone. DKA has high rates of morbidity and mortality, especially in younger type 1 diabetic patients. It is the most common cause of death for those under the age of 24 years with type 1 diabetes.3 It is estimated that 27% to 37% of patients with DKA are newly diagnosed with diabetes, usually type 1.1 Trauma, infection, or surgery may increase the risk of DKA in patients with type 2 diabetes.3 Mortality with DKA is generally associated with the underlying illness or comorbidity.1,3,4 Generally, DKA may be characterized by significant hyperglycemia, metabolic acidosis, and ketoacidosis. However, DKA may present in various ways, from euglycemia to severe hyperglycemia with or without dehydration and coma.3-5 The treatment approach for each patient is highly individualized based on a patients clinical factors.5 Simply put, DKA is caused by too little insulin and a resp 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 >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Snap Shot A 12 year old boy, previously healthy, is admitted to the hospiral after 2 days of polyuria, polyphagia, nausea, vomting and abdominal pain. Temp is 37, BP 103/63, HR 112, RR 30. Physical exam shows a lethargic boy. Glucose is 534, Potasium is 5.9; WBC 16,000, pH is 7.13, PCO2 is 20 mmHg, PO2 is 90 mmHg. Introduction Results from absolute deficiency in insulin surge in counterregulatory homones (glucagon, growth hormone, catecholamine) results in hyperglycemia and ketonemia Most common in type I diabetes Precipitated by infections drugs (steroids, thiazide diuretics) noncompliance pancreatitis Presentation Symptoms vomiting abdominal pain fruity, acetone odor severely dehydrated cerebral edema associated with high mortality in pediatric patients Evaluation Diagnostic criteria blood glucose levels > 250 mg/dL Arterial pH < 7.3 expect to see an increase in free calcium since the excess hydrogen displaces calcium from albumin Serum bicarbonate < 15mEq/L Moderate ketonuria and ketonemia Labs show: Treatment Fluids Insulin with glucose give insulin until ketones are gone, even after glucose normalizes or is below normal Replace potasium for hypokalemia caused by too much potassium being secreted in the urine as a result of the glucosuria labs may show pseudo-hyperkalemia due to transcellular shift of potassium out of the cells to balance the H being transfered into the cells give in the form of potassium phosphate rather than potasium chloride Aggresive electrolyte replacement give phosphate supplementation to prevent respiratory paralysis If mental status changes (headache, obtundation, coma) occur during treatment likely due to cerebral edema give mannitol Follow anion gap to monitor improvement 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 >>

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 >>

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 >>

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 >>

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 >>

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 >>

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 >>

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 >>

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 >>

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 >>

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 >>

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