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Paradoxical Hyperkalemia In Dka

Dka, “answers”

Dka, “answers”

1. When you are suspicious for DKA do you obtain a VBG or an ABG? How good is a VBG for determining acid/base status? Diabetic ketoacidosis (DKA) is defined by five findings: acidosis (pH < 7.30, serum bicarbonate (HCO3) < 18 mEq/L, the presence of ketonuria or ketonemia, an anion gap > 10 mEq/L, and a plasma glucose concentration > 250 mg/dl. It is one of the most serious complications of diabetes seen in the emergency department. The mortality rate of hospitalized DKA patients is estimated to be between 2-10% (Lebovitz, 1995). As a result, its prompt recognition is vital to improving outcomes in these patients. As a result, emergency physicians have long relied on the combination of hyperglycemia and anion gap metabolic acidosis to help point them in the correct diagnostic direction. In the assessment of the level of acidosis in a DKA patient, an arterial blood gas (ABG) has long been thought of as much more accurate than a venous blood gas (VBG) and thus necessary in evaluating a DKA patient’s pH and HCO3 level, two values often used to direct treatment decisions. An ABG is more painful, often time-consuming and labor intensive as it may involve multiple attempts. In addition, ABGs can be complicated by radial artery aneurysms, radial nerve injury and compromised blood supply in patients with peripheral vascular disease or inadequate ulnar circulation. A VBG is less painful, can obtained at the time of IV placement, and is therefore less time consuming. But is it good enough to estimate acid/base status in these patients? Brandenburg, et al. compared arterial and venous blood gas samples in DKA patients taken at the exact same time prior to treatment and found a mean difference in pH between the arterial and venous samples to be only 0.03, with a Pearson’s correl Continue reading >>

Sodium Bicarbonate

Sodium Bicarbonate

Indications Metabolic Acidosis Diabetic Ketoacidosis (DKA) (see Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic State) Indications: pH <6.9-7.0 (however, evidence for this recommendation is lacking) Patients with Hemodynamic Compromise (Due to Impaired Myocardial Contractility and Vasodilation) or Life-Threatening Hyperkalemia May Particularly Benefit from Bicarbonate Administration to Correct the pH Lactic Acidosis (see Lactic Acidosis) Adverse Effects of Acidemia: these (selected adverse effects) provide a rationale for administering bicarbonate with pH <7.1 Arrhythmias Arterial Vasodilation and Venoconstriction Decreased Left Ventricular Contractility Impaired Responsiveness to Catecholamine Vasopressors (Nat Rev Nephrol, 2012) [MEDLINE] Indications: pH <7.1 (however, evidence for this recommendation is lacking) This is due to the fact that at pH <7.1, small changes in pCO2 and serum bicarbonate result in large changes in the serum pH Clinical Efficacy: neither of these trials demonstrated clinical benefit with bicarbonate administration in patients with pH >7.1 Trial of Sodium Bicarbonate in Critically Ill Patients with Lactic Acidosis (Ann Intern Med, 1990) [MEDLINE] Sodium Bicarbonate Did Not Improve Hemodynamics in Critically Ill Patients with Metabolic Acidosis and Hyperlactatemia Sodium Bicarbonate Did Not Increase the Cardiovascular Response to Infused Catecholamines in in Critically Ill Patients with Metabolic Acidosis and Hyperlactatemia Sodium Bicarbonate Decreased Plasma Ionized Calcium and Increased the pCO2 Trial of Sodium Bicarbonate in Lactic Acidosis (Crit Care Med, 1991) [MEDLINE] Administration of sodium bicarbonate did not improve hemodynamic variables in patients with lactic acidosis, but did not worsen tissue oxygenation Non-Anion Gap Metabo Continue reading >>

Severe Hyperkalemia In Two Patients With Diabetes After Cosyntropin Administration

Severe Hyperkalemia In Two Patients With Diabetes After Cosyntropin Administration

Abstract Some patients with diabetes mellitus are at increased risk for the development of hyperkalemia. Included in this group are patients with glucose-induced hyperkalemia who may have renal insufficiency, hyporeninemic hypoaldosteronism, or other impediments to the release or action of aldosterone. In an unusual demonstration of this abnormality, two patients with diabetes, who form the basis of our report, became markedly hyperglycemic and hyperkalemic after cosyntropin administration. To our knowledge, this complication of adrenocorticotropic hormone (ACTH) stimulation testing has not been previously reported. It should therefore be emphasized that the use of cosyntropin as a diagnostic agent can provoke severe hyperglycemia and hyperkalemia in a susceptible subgroup of patients with diabetes mellitus. To access this article, please choose from the options below 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 >>

A Patient With Hyperkalemia And Metabolic Acidosis

A Patient With Hyperkalemia And Metabolic Acidosis

First page preview Copyright © 1990 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved. Continue reading >>

Diabetic Emergencies: Diabetic Ketoacidosis In Childhood And Adolescence, Part 3 Of 3

Diabetic Emergencies: Diabetic Ketoacidosis In Childhood And Adolescence, Part 3 Of 3

Severe acidosis is reversible by fluid and insulin replacement. Insulin stops lipolysis and further ketone production and allows ketoacids to be metabolized, generating bicarbonate.4 Moreover, treatment of hypovolemia improves tissue perfusion and renal function, thereby increasing the excretion of organic acids. Controlled trials have shown no clinical benefit from bicarbonate administration 3,4 and there are well-recognized serious adverse effects, including paradoxical CNS acidosis 28,29 and hypokalemia from rapid acidosis correction. 30,31 Nevertheless, there may be selected patients who may profit from cautious alkali administration, such as patients with severe acidemia (arterial pH < 6.9) in whom decreased cardiac contractility and peripheral vasodilatation can further impair tissue perfusion, and patients with life-threatening hyperkalemia. 4,32…. If bicarbonate is considered necessary, cautiously give 1-2 mmol/kg over 60 minutes. 3,4 Follow-up management — transition to per os fluid intake and SC insulin injections Oral fluids should be introduced only when substantial clinical improvement has occurred and when oral fluids are well tolerated; IV fluid administration should then be reduced. The most convenient time to change to SC insulin is just before a mealtime, provided that ketoacidosis has resolved (venous pH > 7.3 and serum bicarbonate > 18 mmol/L), plasma glucose is < 200 mg/dl (11.1 mmol/L), and oral fluid intake is well tolerated. To prevent rebound hyperglycemia, the first SC insulin injection should be given 15-30 minutes (with rapid-acting insulin analog) or 1-2 hours (with regular insulin) before stopping the insulin infusion to allow sufficient time for the insulin to be absorbed. With intermediate or long-acting insulin the overlap should be Continue reading >>

Dynamic Changes In Serum Phosphorus Levels In Diabetic Ketoacidosis

Dynamic Changes In Serum Phosphorus Levels In Diabetic Ketoacidosis

Abstract The dynamic changes in serum phosphorus levels in 69 episodes of ketoacidosis in 48 diabetic patients were retrospectively evaluated. The mean age was 41 ± 2 years (mean ± SEM), and the duration of diabetes mellitus was 7 ± 1 years. The serum phosphorus levels determined within the first six hours of admission were analyzed. Before initiation of therapy, the incidence of hyperphosphatemia was 94.7 percent. At the end of 12 hours, the mean serum phosphorus level fell from 9.2 ± 0.6 to 2.8 ± 0.3 mg/dl. Before therapy, the serum phosphorus level correlated positively with the serum glucose level, the effective plasma osmolality, and anion gaps, and correlated negatively with the serum chloride level. It is concluded that hyperphosphatemia is common in diabetic ketoacidosis before therapy. The increase in serum phosphorus is likely to be due to a transcellular shift. Potential factors responsible for the shift are serum glucose, through its osmotic effect, and the organic anions. To access this article, please choose from the options below Continue reading >>

3,518 Possible Causes For Hyperkalemia + Ketonuria + Ketosis + Bicarbonate Increased + Metabolic Acidosis In Usa

3,518 Possible Causes For Hyperkalemia + Ketonuria + Ketosis + Bicarbonate Increased + Metabolic Acidosis In Usa

Acidosis Hyperkalemia Bicarbonate Increased Ketonuria Ketosis It is due to the accumulation of ketoacids (via excessive ketosis) and reflects a severe shift from glycolysis to lipolysis for energy needs.[en.wikipedia.org] Causes: Metabolic Acidosis and Elevated Anion Gap (Mnemonic: "MUD PILERS") Methanol , Metformin Uremia Diabetic Ketoacidosis (DKA), Alcohol ic ketoacidosis or starvation ketosis[fpnotebook.com] An increase in the production of other acids may also produce metabolic acidosis.[en.wikipedia.org] Hyperkalemia (hyperpotassemia) is the presence of an abnormally high concentration of potassium in the blood. Ketosis is a condition characterized by elevated levels of ketone bodies (β-hydroxybutyric acid, acetoacetic acid, acetone) in the body. Acidosis Bicarbonate Decreased Bicarbonate Wasting Renal Tubular Acidosis Chronic Lactic Acidosis Distal Renal Tubular Acidosis Episodic Lactic Acidosis Episodic Metabolic Acidosis Hyperchloremic Metabolic Acidosis Hyperchloremic Metabolic Acidosis - HCO3 15.5 +- 2.0 mM Hyperkalemic Metabolic Acidosis Incomplete Distal Renal Tubular Acidosis Increased Basal Metabolic Rate Ketosis Is Exacerbated by Protein Ingestion Lactic Acidosis Lactic Acidosis May Be Mild Lactic Acidosis during Infection Lactic Acidosis in E3 Deficiency Metabolic Acidosis due to Renal Bicarbonate Loss Metabolic Acidosis in Infancy Mild Hyperchloremic Metabolic Acidosis Mild Metabolic Acidosis No Lactic Acidosis Persistent Lactic Acidosis Proximal Renal Tubular Acidosis Renal Tubular Acidosis Respiratory Acidosis Severe Lactic Acidosis Severe Metabolic Acidosis Transient Metabolic Acidosis that Resolves in Infancy List represents a sample of symptoms, diseases, and other queries. Updated weekly. Hungry Bones Syndrome Altitude Sickness Cavernous Sinus T Continue reading >>

Step 2: Endo

Step 2: Endo

Endo 1 Question Answer What are the anti-islet antibodies present in patients of Type 1 DM? Anti-insulin (IAA), anti-islet cell cyoplasm (ICA), anti-glutamic acid decarboxylase (GAD), anti-tyrosine phosphatase (IA-2) Symogmi affect has __________ Glc levels at 3am, and ________ Glc levels in the morning. Low at 3am, high in the morning. (due to stress hormone release) Dawn Phenomenon is when Glc is (low/high) all night. What is its cause? high, due to not taking NPH insulin before bed How do you treat Symogmi affect? No NPH before bed, or eat a snack before bed What HLAs is DM1 associated with? DR3, DR4, DQ HbA1c indicates hyperglycemia for past ____ months. It is used to monitor __________. 3; compliance with therapy Nausea and vomiting in child with no GI symptoms/no diarrhea is usually ______. DKA How do you treat gastroparesis due to diabetic neuropathy? (3 drugs) DA agonist (metaclopramide), Bethanachol, Erythromycin (increases motility) During exercise, DM1 patients should take (less/more) insulin medication. less What is the best SCREENING test for diabetes mellitus: Random glucose, Fasting glucose, Oral Glucose Tolerance Test? Fasting glucose What is the best DEFINITIVE test for diabetes mellitus (after initial screening): Random glucose, Fasting glucose, Oral Glucose Tolerance Test? Oral Glucose Tolerance Test Fasting glucose is taken after an ____hour fast. Reading must be over ______mg/dL, on ____ separate tests to be considered positive 8hr fast, 126 mg/dL, 2 separate times OGTT is positive if the measurement is over ______mg/dL. Test is administered _____hours after a _____g load of glucose. 200 mg/dL, 2 hours, 75g load What skin condition is often associated with DM? aconthosis nigricans True/False: if mother has gestational diabetes, the offspring will ha Continue reading >>

Management Of Adult Diabetic Ketoacidosis

Management Of Adult Diabetic Ketoacidosis

Authors Gosmanov AR, Gosmanova E, Dillard-Cannon E Accepted for publication 13 May 2014 Checked for plagiarism Yes Peer reviewer comments 2 Aidar R Gosmanov,1 Elvira O Gosmanova,2 Erika Dillard-Cannon3 1Division of Endocrinology, Diabetes and Metabolism, 2Division of Nephrology, Department of Medicine, 3Department of Microbiology, Immunology, and Biochemistry, University of Tennessee Health Science Center, Memphis, TN, USA Abstract: Diabetic ketoacidosis (DKA) is a rare yet potentially fatal hyperglycemic crisis that can occur in patients with both type 1 and 2 diabetes mellitus. Due to its increasing incidence and economic impact related to the treatment and associated morbidity, effective management and prevention is key. Elements of management include making the appropriate diagnosis using current laboratory tools and clinical criteria and coordinating fluid resuscitation, insulin therapy, and electrolyte replacement through feedback obtained from timely patient monitoring and knowledge of resolution criteria. In addition, awareness of special populations such as patients with renal disease presenting with DKA is important. During the DKA therapy, complications may arise and appropriate strategies to prevent these complications are required. DKA prevention strategies including patient and provider education are important. This review aims to provide a brief overview of DKA from its pathophysiology to clinical presentation with in depth focus on up-to-date therapeutic management. Keywords: DKA treatment, insulin, prevention, ESKD Letter about this article has been published In 2009, there were 140,000 hospitalizations for diabetic ketoacidosis (DKA) with an average length of stay of 3.4 days.1 The direct and indirect annual cost of DKA hospitalizations is 2.4 billion Continue reading >>

Endocrinology

Endocrinology

Start Quiz! Xray findings decreased bone density with thinning of cortex and pseudofractures (Looser zones) 1) Post-surgical (most common cause) 2) Autoimmune 3) Congenital absence or maldevelopment of the parathyroid glands (eg DiGeorge syndrome) 4) Defective calcium-sensing receptor on the parathyroid glands 5) Non-autoimmune destruction of parathyroid gland due to infiltrative diseases (hemochromatosis, Wilson disease, neck irradiation) Continue reading >>

Treatment And Prevention Of Hyperkalemia In Adults

Treatment And Prevention Of Hyperkalemia In Adults

INTRODUCTION Hyperkalemia is a common clinical problem that is most often a result of impaired urinary potassium excretion due to acute or chronic kidney disease (CKD) and/or disorders or drugs that inhibit the renin-angiotensin-aldosterone system (RAAS). Therapy for hyperkalemia due to potassium retention is ultimately aimed at inducing potassium loss [1,2]. In some cases, the primary problem is movement of potassium out of the cells, even though the total body potassium may be reduced. Redistributive hyperkalemia most commonly occurs in uncontrolled hyperglycemia (eg, diabetic ketoacidosis or hyperosmolar hyperglycemic state). In these disorders, hyperosmolality and insulin deficiency are primarily responsible for the transcellular shift of potassium from the cells into the extracellular fluid, which can be reversed by the administration of fluids and insulin. Many of these patients have a significant deficit in whole body potassium and must be monitored carefully for the development of hypokalemia during therapy. (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Treatment", section on 'Potassium replacement'.) The treatment and prevention of hyperkalemia will be reviewed here. The causes, diagnosis, and clinical manifestations of hyperkalemia are discussed separately. (See "Causes and evaluation of hyperkalemia in adults" and "Clinical manifestations of hyperkalemia in adults".) DETERMINING THE URGENCY OF THERAPY The urgency of treatment of hyperkalemia varies with the presence or absence of the symptoms and signs associated with hyperkalemia, the severity of the potassium elevation, and the cause of hyperkalemia. Our approach to therapeutic urgency is as follows (algorithm 1): Continue reading >>

Is Bicarbonate Ever Indicated In Dka? – Dr. E. Sosa

Is Bicarbonate Ever Indicated In Dka? – Dr. E. Sosa

Diabetic ketoacidosis (DKA) is characterized by hyperglycemia, elevated serum ketones, and metabolic acidosis. To explain briefly, this disorder results from dysfunctional glucose metabolism in the context of insulin underproduction and/or insensitivity. Unable to utilize glucose, cells begin to consume fatty acids via anaerobic metabolism, leading to the buildup of acidic ketone bodies and other electrolyte abnormalities. Some common precipitants of this acutely life-threatening condition include infection and noncompliance with insulin therapy in known diabetics. DKA is often how new-onset diabetics initially present, but it can also be found in patients with acute pancreatitis, MI, and CVA. Nevertheless, the complexity of metabolic derangements that come with DKA can be formidable to manage, regardless of the precipitating insult.1 Resuscitation of a DKA patient involves aggressive fluid replacement and insulin administration, all while continuously managing sodium, potassium, chloride, phosphate, and bicarbonate shifts. For this review, we will focus on the management of low bicarbonate levels in metabolic acidosis. Since bicarbonate will be very low in severe cases, many physicians treat this metabolic acidosis with intravenous sodium bicarbonate, hoping to reverse the acidosis more quickly. However, this practice is controversial.2 There are three major adverse effects to consider when using bicarbonate: 1) When given continuously, the acidemic drive to blow off CO2 via hyperventilation is blunted. In the hypercapnic state that results, CO2 crosses the blood-brain barrier preferentially, leading to a paradoxical drop in cerebral pH and neurologic deterioration.3 2) It can actually slow ketone clearance by about 6 hours, causing a more refractory acidosis. Animal s Continue reading >>

Pediatric Diabetic Ketoacidosis

Pediatric Diabetic Ketoacidosis

Pediatric Diabetic Ketoacidosis Authors: Katia M. Lugo-Enriquez, MD, FACEP, Faculty, Florida Hospital Emergency Medicine Residency Program, Orlando, FL. Nick Passafiume, MD, Florida Hospital Emergency Medicine Residency Program, Orlando, FL. Peer Reviewer: Richard A. Brodsky, MD, Pediatric Emergency Medicine, St. Christopher's Hospital for Children, Assistant Professor, Drexel University, Philadelphia, PA. Children with diabetes, especially type 1, remain at risk for developing diabetic ketoacidosis (DKA). This may seem confounding in a modern society with such advanced medical care, but the fact remains that children who are type 1 diabetics have an incidence of DKA of 8 per 100 patient years.1 In fact, Neu and colleagues have noted in a multicenter analysis of 14,664 patients in Europe from 1995 to 2007 that there was no significant change in ketoacidosis presenting at diabetes onset in children.2 In children younger than 19 years old, DKA is the admitting diagnosis in 65% of all hospital admissions of patients with diabetes mellitus.3 This article reviews the presentation, diagnostic evaluation, treatment, and potential complications associated with pediatric DKA. — The Editor Introduction The overall mortality rate for children in DKA is not unimpressive: The range is 0.15% to 0.31%.4 Besides death, one of the most feared repercussions of DKA in children is cerebral edema, an entity that occurs approximately 1% of the time.5,6 Cerebral edema, with the exception of a few case reports in some young adults, has largely been a complication of treatment in the pediatric population, and the exact factors have yet to be completely determined. The mortality associated with cerebral edema may approach 20% to 50%, and the incidence of neurologic morbidity is significant and Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

I. Review of normal lipid metabolism Triglycerides in adipose ==lipolysis==> Long-chain FAs Long-chain FAs==hepatic beta-oxidation==>Acetyl CoA Acetyl CoA==hepatic ketogenesis==>ketone bodies Ketone bodies are Beta-hydroxybutyrate and Acetoacetate Beta-OHB is oxidized to AcAc-; their relative concentrations depend on redox state of cell; Beta-OHB predominates in situation favoring reductive metabolism (e.g. decreased tissue perfusion, met. acidosis, catabolic states--like DKA!) Typical ratio Beta-OHB:AcAc- is 3:1; us. increases in DKA II. Hormonal influences on glucose and lipid metabolism Insulin In liver, increases glu uptake from portal blood; stimulates glycogenesis, inhibits glycogenolysis and gluconeogenesis In skeletal muscle, increases glu uptake from blood, stimulates protein synth, inhibits proteolysis In adipose tissue, required for glu and lipoprotein uptake from blood; stimulates lipogenesis, inhibits lipolysis Tissues which don't require insulin to transport glucose into cells: brain, renal medulla, formed blood elements Counterregulatory hormones: glucagon (major player in DKA), epi/norepi, cortisol, growth hormone (no acute effects, only over days-weeks) Glucagon: increases hepatic beta-oxidation, ketogenesis, gluconeogenesis and glycogenolysis; decreases hepatic FA synth. Epi/Norepi: increase hepatic gluconeogenesis & glycogenolysis; increases adipose lipolysis; decreases peripheral glu utilization Cortisol: major effect is decreased peripheral glu utiliz; little effect on production Growth hormone: increases hepatic gluconeogenesis and glycogenolysis; increases adipose lipolysis In high counterreg. hormone states (see above), require high levels of insulin to avoid progressive hyperglycemia and ketoacidosis--glucagon levels in DKA are 5-6 x nl* III. Pa Continue reading >>

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