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Dka Potassium Replacement

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: Evaluation And Treatment

Diabetic Ketoacidosis: Evaluation And Treatment

Diabetic ketoacidosis is characterized by a serum glucose level greater than 250 mg per dL, a pH less than 7.3, a serum bicarbonate level less than 18 mEq per L, an elevated serum ketone level, and dehydration. Insulin deficiency is the main precipitating factor. Diabetic ketoacidosis can occur in persons of all ages, with 14 percent of cases occurring in persons older than 70 years, 23 percent in persons 51 to 70 years of age, 27 percent in persons 30 to 50 years of age, and 36 percent in persons younger than 30 years. The case fatality rate is 1 to 5 percent. About one-third of all cases are in persons without a history of diabetes mellitus. Common symptoms include polyuria with polydipsia (98 percent), weight loss (81 percent), fatigue (62 percent), dyspnea (57 percent), vomiting (46 percent), preceding febrile illness (40 percent), abdominal pain (32 percent), and polyphagia (23 percent). Measurement of A1C, blood urea nitrogen, creatinine, serum glucose, electrolytes, pH, and serum ketones; complete blood count; urinalysis; electrocardiography; and calculation of anion gap and osmolar gap can differentiate diabetic ketoacidosis from hyperosmolar hyperglycemic state, gastroenteritis, starvation ketosis, and other metabolic syndromes, and can assist in diagnosing comorbid conditions. Appropriate treatment includes administering intravenous fluids and insulin, and monitoring glucose and electrolyte levels. Cerebral edema is a rare but severe complication that occurs predominantly in children. Physicians should recognize the signs of diabetic ketoacidosis for prompt diagnosis, and identify early symptoms to prevent it. Patient education should include information on how to adjust insulin during times of illness and how to monitor glucose and ketone levels, as well as i Continue reading >>

Episode 63 – Pediatric Dka

Episode 63 – Pediatric Dka

Pediatric DKA was identified as one of key diagnoses that we need to get better at managing in a massive national needs assessment conducted by the fine folks at TREKK – Translating Emergency Knowledge for Kids – one of EM Cases’ partners who’s mission is to improve the care of children in non-pediatric emergency departments across the country. You might be wondering – why was DKA singled out in this needs assessment? It turns out that kids who present to the ED in DKA without a known history of diabetes, can sometimes be tricky to diagnose, as they often present with vague symptoms. When a child does have a known history of diabetes, and the diagnosis of DKA is obvious, the challenge turns to managing severe, life-threatening DKA, so that we avoid the many potential complications of the DKA itself as well as the complications of treatment – cerebral edema being the big bad one. The approach to these patients has evolved over the years, even since I started practicing, from bolusing insulin and super aggressive fluid resuscitation to more gentle fluid management and delayed insulin drips, as examples. There are subtleties and controversies in the management of DKA when it comes to fluid management, correcting serum potassium and acidosis, preventing cerebral edema, as well as airway management for the really sick kids. In this episode we‘ll be asking our guest pediatric emergency medicine experts Dr. Sarah Reid, who you may remember from her powerhouse performance on our recent episodes on pediatric fever and sepsis, and Dr. Sarah Curtis, not only a pediatric emergency physician, but a prominent pediatric emergency researcher in Canada, about the key historical and examination pearls to help pick up this sometimes elusive diagnosis, what the value of serum Continue reading >>

Diabetic Ketoacidosis (dka) Myths

Diabetic Ketoacidosis (dka) Myths

Recently, I was asked to give a lecture to both my residents and nurses at the University of Texas Health Science Center at San Antonio (UTHSCSA) on some common DKA myths. Now this topic was originally covered by my good friend Anand Swaminathan on multiple platforms and I did ask his permission to create this blogpost with the idea of improving patient care and wanted to express full disclosure of that fact. I specifically covered four common myths that I still see people doing in regards to DKA management: We should get ABGs instead of VBGs After Intravenous Fluids (IVF), Insulin is the Next Step Once pH <7.1, Patients Need Bicarbonate Therapy We Should Bolus Insulin before starting the infusion DKA Myths Case: 25 y/o female with PMH of Type I DM who presents via EMS with AMS. Per EMS report, the patient ran out of her insulin 3 days ago….. Vital Signs: BP 86/52 HR 136 RR 30 O2Sat 97% on room air Temp 99.1 Accucheck: CRITICAL HIGH EMS was not able to establish IV access, so decided to just bring her to the ED due to how sick she looks. Your nurses are on point today and get you two large bore 18G IVs and start to draw blood work to send to the lab. You state I need a blood gas, and the nurse turns to you and asks do you need an ABG or VBG? Myth #1: We should get ABGs instead of VBGs in DKA So you do a literature review and come across two studies that specifically look at ABG vs VBG in an ED population: Study #1: Kelly AM et al. Review Article – Can Venous Blood Gas Analysis Replace Arterial in Emergency Medical Care. Emery Med Australas 2010; 22: 493 – 498. PMID: 21143397 For pH, 3 studies of patients with DKA (265 patients) were reviewed showing a weighted mean difference of 0.02 pH units. Only one study, which was the largest study (200 patients) reported 95% Continue reading >>

My Site - Chapter 15: Hyperglycemic Emergencies In Adults

My Site - Chapter 15: Hyperglycemic Emergencies In Adults

Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) should be suspected in ill patients with diabetes. If either DKA or HHS is diagnosed, precipitating factors must be sought and treated. DKA and HHS are medical emergencies that require treatment and monitoring for multiple metabolic abnormalities and vigilance for complications. A normal blood glucose does not rule out DKA in pregnancy. Ketoacidosis requires insulin administration (0.1 U/kg/h) for resolution; bicarbonate therapy should be considered only for extreme acidosis (pH7.0). Note to readers: Although the diagnosis and treatment of diabetic ketoacidosis (DKA) in adults and in children share general principles, there are significant differences in their application, largely related to the increased risk of life-threatening cerebral edema with DKA in children and adolescents. The specific issues related to treatment of DKA in children and adolescents are addressed in the Type 1 Diabetes in Children and Adolescents chapter, p. S153. Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are diabetes emergencies with overlapping features. With insulin deficiency, hyperglycemia causes urinary losses of water and electrolytes (sodium, potassium, chloride) and the resultant extracellular fluid volume (ECFV) depletion. Potassium is shifted out of cells, and ketoacidosis occurs as a result of elevated glucagon levels and absolute insulin deficiency (in the case of type 1 diabetes) or high catecholamine levels suppressing insulin release (in the case of type 2 diabetes). In DKA, ketoacidosis is prominent, while in HHS, the main features are ECFV depletion and hyperosmolarity. Risk factors for DKA include new diagnosis of diabetes mellitus, insulin omission, infection, myocardial infarc Continue reading >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Tweet Diabetic ketoacidosis (DKA) is a dangerous complication faced by people with diabetes which happens when the body starts running out of insulin. DKA is most commonly associated with type 1 diabetes, however, people with type 2 diabetes that produce very little of their own insulin may also be affected. Ketoacidosis is a serious short term complication which can result in coma or even death if it is not treated quickly. Read about Diabetes and Ketones What is diabetic ketoacidosis? DKA occurs when the body has insufficient insulin to allow enough glucose to enter cells, and so the body switches to burning fatty acids and producing acidic ketone bodies. A high level of ketone bodies in the blood can cause particularly severe illness. Symptoms of DKA Diabetic ketoacidosis may itself be the symptom of undiagnosed type 1 diabetes. Typical symptoms of diabetic ketoacidosis include: Vomiting Dehydration An unusual smell on the breath –sometimes compared to the smell of pear drops Deep laboured breathing (called kussmaul breathing) or hyperventilation Rapid heartbeat Confusion and disorientation Symptoms of diabetic ketoacidosis usually evolve over a 24 hour period if blood glucose levels become and remain too high (hyperglycemia). Causes and risk factors for diabetic ketoacidosis As noted above, DKA is caused by the body having too little insulin to allow cells to take in glucose for energy. This may happen for a number of reasons including: Having blood glucose levels consistently over 15 mmol/l Missing insulin injections If a fault has developed in your insulin pen or insulin pump As a result of illness or infections High or prolonged levels of stress Excessive alcohol consumption DKA may also occur prior to a diagnosis of type 1 diabetes. Ketoacidosis can occasional Continue reading >>

Management Of Diabetic Ketoacidosis In Children And Adolescents

Management Of Diabetic Ketoacidosis In Children And Adolescents

Objectives After completing this article, readers should be able to: Describe the typical presentation of diabetic ketoacidosis in children. Discuss the treatment of diabetic ketoacidosis. Explain the potential complications of diabetic ketoacidosis that can occur during treatment. Introduction Diabetic ketoacidosis (DKA) represents a profound insulin-deficient state characterized by hyperglycemia (>200 mg/dL [11.1 mmol/L]) and acidosis (serum pH <7.3, bicarbonate <15 mEq/L [15 mmol/L]), along with evidence of an accumulation of ketoacids in the blood (measurable serum or urine ketones, increased anion gap). Dehydration, electrolyte loss, and hyperosmolarity contribute to the presentation and potential complications. DKA is the most common cause of death in children who have type 1 diabetes. Therefore, the best treatment of DKA is prevention through early recognition and diagnosis of diabetes in a child who has polydipsia and polyuria and through careful attention to the treatment of children who have known diabetes, particularly during illnesses. Presentation Patients who have DKA generally present with nausea and vomiting. In individuals who have no previous diagnosis of diabetes mellitus, a preceding history of polyuria, polydipsia, and weight loss usually can be elicited. With significant ketosis, patients may have a fruity breath. As the DKA becomes more severe, patients develop lethargy due to the acidosis and hyperosmolarity; in severe DKA, they may present with coma. Acidosis and ketosis cause an ileus that can lead to abdominal pain severe enough to raise concern for an acutely inflamed abdomen, and the elevation of the stress hormones epinephrine and cortisol in DKA can lead to an elevation in the white blood cell count, suggesting infection. Thus, leukocytosi Continue reading >>

Hyperglycemic Crises In Diabetes

Hyperglycemic Crises In Diabetes

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

Diabetic Ketoacidosis Treatment & Management

Diabetic Ketoacidosis Treatment & Management

Approach Considerations 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: 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 ultra–short-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 intravenous infusion of insulin at a weight-based fixed rate until ketosis has subsided. Should blood glucose fall below 14 mmol/L (250 mg/dL), 10% glucose should be added to allow for the continuation of fixed-rate insulin infusion. [19, 20] In established patient Continue reading >>

Myths In Dka Management

Myths In Dka Management

Anand Swaminathan, MD, MPH (@EMSwami) is an assistant professor and assistant program director at the NYU/Bellevue Department of Emergency Medicine in New York City. Review questions are available at the end of this post. Background Each year, roughly 10,000 patients present to the Emergency Department in diabetic ketoacidosis (DKA). Prior to the advent of insulin, the mortality rate of DKA was 100% although in recent years, that rate has dropped to approximately 2-5%.1 Despite clinical advances, the mortality rate has remained constant over the last 10 years. With aggressive resuscitative measures and appropriate continued management this trend may change. DKA is defined as: Hyperglycemia (glucose > 250 mg/dl) Acidosis (pH < 7.3) Ketosis In the absence of insulin, serum glucose rises leading to osmotic diuresis. This diuresis leads to loss of electrolytes including sodium, magnesium, calcium and phosphorous. The resultant volume depletion leads to impaired glomerular filtration rate (GFR) and acute renal failure. In patients with DKA, fatty acid breakdown produces 2 different ketone bodies, first acetoacetate, which then further converts to beta-hydroxybutyrate, the latter being the ketone body largely produced in DKA patients. With this background in mind, let’s take a look at four urban legends in the management of DKA and the evidence that dispels these legends. Here’s our case: Although this presentation likely represents DKA, a blood gas is typically obtained to confirm the diagnosis. Often, the question arises as to whether an arterial or venous blood gas is adequate. Urban Legend #1 – An ABG is necessary for the diagnosis and treatment of DKA ABG gets you pH, PaO2, PaCO2, HCO3, Lactate, electrolytes and O2Sat VBG gets all this except for PaO2 (but we have Continue reading >>

Actrapid: Eight Steps For Managing Diabetic Ketoacidosis

Actrapid: Eight Steps For Managing Diabetic Ketoacidosis

Diabetic Ketoacidosis (DKA) is a potentially life threatening condition that occurs when excessive amounts of ketones are released into the bloodstream as a result of the body breaking down lipids, instead of utilising glucose as the energy source. This process is known as gluconeogenesis and occurs when the body does not have sufficient insulin to allow the uptake of glucose from the bloodstream into the cells. It is observed primarily in people with type one diabetes (insulin dependent), but it can occur in type two diabetes (non-insulin dependent) under certain circumstances. To understand the symptoms of DKA and therefore how to manage it effectively, it is important to understand the pathophysiology of hyperglycaemia which is explained in the flowchart below: The further down this flowchart the patient gets, the more serious their symptoms become. For this reason, there are varying degrees of severity with DKA: Mild pH 7.25 – 7.30, bicarbonate decreased to 15–18 mmol/L, the person is alert Moderate pH 7.00 – 7.25, bicarbonate 10–15 mmol/L, drowsiness may be present Severe pH below 7.00, bicarbonate below 10 mmol/L, stupor or coma may occur A.C.T.R.A.P.I.D. To remember the principles involved in managing a patient with DKA, remember the acronym ACTRAPID. Airway, breathing, circulation Commence fluid resuscitation Treat potassium Replace insulin Acidosis management Prevent complications Information for patients Discharge Airway, Breathing, Circulation As Per Any Emergency DKA patients need to have their airway, breathing and circulation assessed immediately. A decreased level of consciousness may lead to an unprotected airway and compromised breathing. The osmotic diuresis can cause a significant loss of fluid, leading to severe dehydration and circulatory co Continue reading >>

Diabetic Ketoacidosis And Hyperosmolar Hyperglycemic State In Adults: Treatment

Diabetic Ketoacidosis And Hyperosmolar Hyperglycemic State In Adults: Treatment

INTRODUCTION Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS, also known as hyperosmotic hyperglycemic nonketotic state [HHNK]) are two of the most serious acute complications of diabetes. They are part of the spectrum of hyperglycemia, and each represents an extreme in the spectrum. The treatment of DKA and HHS in adults will be reviewed here. The epidemiology, pathogenesis, clinical features, evaluation, and diagnosis of these disorders are discussed separately. DKA in children is also reviewed separately. (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Epidemiology and pathogenesis".) (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Clinical features, evaluation, and diagnosis".) Continue reading >>

68..............................................................................................................................................................................navc Clinician’s Brief / April 2011 / Diagnostic Tree

68..............................................................................................................................................................................navc Clinician’s Brief / April 2011 / Diagnostic Tree

1. IV Isotonic Crystalloid Therapy • Shock fluid therapy is warranted if cardiovascular instability is present: Full shock dose of fluids is 90 mL/kg; start with ¼ to 1/3 dose and reassess until stable • Correct dehydration, provide maintenance needs, and replace ongoing losses over 6 to 24 hours: - % dehydration × body weight (kg) × 1000 plus - 20 mL/kg/day (insensible losses) plus - 20 to 40 mL/kg/day (maintenance sensible losses) plus - Account for vomiting, diarrhea, & polyuria (ongoing sensible losses) Alice Huang, VMD, & J. Catharine Scott-Moncrieff, Vet MB, MS, MA, Diplomate ACVIM & ECVIM Purdue University Canine Diabetic Ketoacidosis D i a gno s t i c Tre e / ENDOCRINOLOGY Peer Reviewed Physical Examination • Polyuria • Weight loss • Polydipsia • Vomiting • Polyphagia • Lethargy Patient may have only 1 or more of these signs. Laboratory Results • Blood glucose (BG): Hyperglycemia (> 200 mg/dL) • Blood gas (venous or arterial): Metabolic acidosis • Urine dipstick: Glucosuria; ketonuria or ketonemia Serum ketones can be measured if urine is unavailable. Diabetic Ketoacidosis Treatment 2. Electrolyte Supplementation (see Table 1, page 70) • Monitor serum potassium Q 4–6 H until within reference interval and stable; then Q 12–24 H • Monitor serum phosphorus Q 4–6 H until > 1.5; then Q 6–24 H • When supplementing potassium and phosphorus concurrently, take into account the amount of potassium contained in the potassium phosphate • Consider magnesium supplementation in instances of refractory hypokalemia 3. Regular Insulin • Continuous rate infusion (CRI) protocol:1 - Add 2.2 U/kg of regular insulin to 250 mL of 0.9% saline - Allow 50 Continue reading >>

Management Of Diabetic Ketoacidosis (dka)

Management Of Diabetic Ketoacidosis (dka)

Management of Acute Diabetic Ketoacidosis (DKA) Below is the link to the care pathway for the management of diabetic ketoacidosis in adults. Specific guidelines exist for the management of DKA in children. In patients aged 13-16 years presenting with DKA, the management of DKA should be discussed with relevant paediatric staff. Diagnosis Severe uncontrolled diabetes with: Hyperglycaemia (blood glucose >14mmol/L, usually but not exclusively) Metabolic acidosis (H+ >45mEq/L or HCO3- <18mmol/L or pH <7.3 on venous gases) Ketonaemia (>3mmol/L) / ketonuria (>++) Severity criteria One or more of the following may indicate severe DKA and should be considered for level 2 care (MHDU if available). It may also be necessary to consider a surgical cause for the deterioration. Blood ketones >6mmol/L Bicarbonate level <5mmol/L Venous / artierial pH <7.1 Hypokalaemia on admission (<3.5mmol/L) GCS <12 or abnormal AVPU scale Oxygen saturation <92% on air (assuming normal baseline respiratory function) Systolic BP <90mmHg, pulse >100bpm or <60bpm Anion gap >16 [anion gap = (Na+ + K+) – (Cl- + HCO3-)] Cerebral oedema The care pathways for the emergency management of DKA should be used for all eligible patients. Complete pathways for 0–4 hours and 4 hours–discharge for each DKA episode. These provide instruction on fluid balance, insulin and potassium replacement. Please note there are DKA order sets on TrakCare (DKA baseline and DKA continuing care). The care pathways are available within relevant departments or online at NHSGGC Managed Clinical Networks / Diabetes MCN / Clinical Guidelines and Protocols / DKA Care Pathway. Supplementary notes as per care pathway 0–4 hours Continue background SC insulin (glargine, levemir, degludec, isophane insulin) while on fixed rate intravenou Continue reading >>

Diabetic Ketoacidosis: Difference Between Potassium Determined By Blood Gas Analysis

Diabetic Ketoacidosis: Difference Between Potassium Determined By Blood Gas Analysis

ORIGINAL ARTICLE versus plasma measurement Cetoacidose diabética: diferença entre as concentrações do potássio na gasometria sanguínea versus potássio plasmático Fernando César RoblesI; Daniel Laguna NetoI; Fábio Guirado DiasI; Márcia SpressãoI; Priscila Nascimbeni MatosI; José Antônio CordeiroII; Antônio Carlos PiresI IDepartament of Endocrinology and Metabology, School of Medicine of São Jose do Rio Preto (Famerp), São Jose do Rio Preto, SP, Brazil IIDepartament of Epidemiology and Collective Health Famerp, São Jose do Rio Preto, SP, Brazil ABSTRACT OBJECTIVE: To evaluate the accuracy of potassium concentrations measured by blood gas analysis (PBG) compared with laboratory serum potassium (LSP), in the initial care of patients with diabetic ketoacidosis (DKA). SUBJECTS AND METHODS: Fifty three patients with diabetes mellitus were evaluated in a retrospective analysis. PBG was carried out using the Radiometer ABL 700 (Radiometer Copenhagen®), and results were compared with LSP ADVIA 1650 Chemistry system (Siemens®), the gold standard method. Both methods are based on potentiometry. RESULTS: Mean PBG was 3.66 mmol/L and mean LSP was 4.79 mmol/L. Mean difference between PBG and LSP was -1.13 mmol/L (p < 0.0005, 95% CI, -1.39 to -0,86). Lin concordance correlation coefficient was rc = 0.28 (95% CIb, 0.10 to 0.45), demonstrating low concordance between the methods. CONCLUSION: Although PBG measurement is faster and easier, it should not be used as a surrogate for LSP in the clinical treatment of DKA. Keywords: Diabetic ketoacidosis; serum potassium concentration; blood gas analysis of potassium. RESUMO OBJETIVO: Avaliar a acurácia da mensuração da concentração de potássio realizado nos analisa-dores de gasometria sanguínea (PGS) em relação ao p Continue reading >>

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