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Paradoxical Hyperkalemia In Dka

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 >>

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 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

Go to: Abstract 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. Learning points: 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. Go to: Background Diabetic ketoacidosis (DKA) is a very common endocrinology emergency. It is usually associated with severe circulatory volume depletion. Management of fluids, metabolic acidosis and electrolyte disorders is mandatory. In DKA, mild-to-moderate elevation of serum potassium is usually seen despite total body potassium wasting (1). After intravenous insulin infusion to treat DKA, even if the initial serum 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 >>

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 >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Figure 3. Timeline in DKA management. GCS:Glascow Coma Scale, CBC:Complete Blood Counting, ECG:Electrocardiogram, HR:Heart Rate, BP:Blood Pressure, BUN:Blood Urea Nitrogen, Cr: Creatinine, WBC:White Blood Cell, CRP:C-reactive protein, CE:Cerebral edema (adapted from reference 165) Figure 4. A 15 years old male patient firstly diagnosed T1DM with DKA infected by rhino-orbita-cerebral mucormycozis (Picture from the reference [218]) 1. Introduction A chronic autoimmune destruction of the pancreatic beta cells results in decreasing endogenous insulin secretion and the clinical manifestation of type 1 diabetes mellitus (T1DM). The clinical onset of the disease is often acute in children and adolescents and diabetic ketoacidosis (DKA) is present in 20-74% of the patients [1-7]. DKA is a serious condition that requiring immediate intervention. Even with appropriate intervention, DKA is associated with significant morbidity and possible mortality in diabetic patients in the pediatric age group [8]. Young age and female sex have been associated with an increased frequency of DKA [3,9]. The triad of uncontrolled hyperglycemia, metabolic acidosis and increased total body ketone concentration characterizes DKA [10]. In addition to possible acute complications, it may also influence the later outcome of diabetes [11]. 2. Epidemiology Worldwide, an estimated 65 000 children under 15 years old develop T1DM each year, and the global incidence in children continues to increase at a rate of 3% a year [12,13]. The current incidence in the UK is around 26/100 000 per year [14]. Patterson et al. were aimed to establish 15-year incidence trends for childhood T1DM in European centres with EURODIAB study. 29 311 new cases of T1DM were diagnosed in children before their 15th birthday during a 1 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 >>

Diabetic Ketoacidosis | Tintinallis Emergency Medicine: A Comprehensive Study Guide, 8e | Accessmedicine | Mcgraw-hill Medical

Diabetic Ketoacidosis | Tintinallis Emergency Medicine: A Comprehensive Study Guide, 8e | Accessmedicine | Mcgraw-hill Medical

Diabetic ketoacidosis (DKA) is an acute, life-threatening complication of diabetes mellitus. DKA occurs predominantly in patients with type 1 (insulin-dependent) diabetes mellitus, but 10% to 30% of cases occur in newly diagnosed type 2 (noninsulin-dependent) diabetes mellitus, especially in African Americans and Hispanics. 1 , 2 Between 1993 and 2003, the yearly rate of U.S. ED visits for DKA was 64 per 10,000 with a trend toward an increased rate of visits among the African American population compared with the Caucasian population. 3 Europe has a comparable incidence. A better understanding of the pathophysiology of DKA and an aggressive, uniform approach to its diagnosis and management have reduced mortality to <5% of reported episodes in experienced centers. 4 However, mortality is higher in the elderly due to underlying renal disease or coexisting infection and in the presence of coma or hypotension. Figure 225-1 illustrates the complex relationships between insulin and counterregulatory hormones. DKA is a response to cellular starvation brought on by relative insulin deficiency and counterregulatory or catabolic hormone excess ( Figure 225-1 ). Insulin is the only anabolic hormone produced by the endocrine pancreas and is responsible for the metabolism and storage of carbohydrates, fat, and protein. Counterregulatory hormones include glucagon, catecholamines, cortisol, and growth hormone. Complete or relative absence of insulin and the excess counterregulatory hormones result in hyperglycemia (due to excess production and underutilization of glucose), osmotic diuresis, prerenal azotemia, worsening hyperglycemia, ketone formation, and a wide-anion-gap metabolic acidosis. 4 Insulin deficiency. Pathogenesis of diabetic ketoacidosis secondary to relative insulin def Continue reading >>

Drug Treatment For Diabetic Ketoacidosis

Drug Treatment For Diabetic Ketoacidosis

Insulin (regular insulin; insulin aspart; insulin lispro; insulin glulisine; isophane insulin [NPH]; lente insulin; ultralente insulin; insulin glargine; insulin detemir; insulin lispro, insulin lispro protamine; insulin aspart, insulin aspart protamine; regular insulin, isophane insulin [NPH]; semilente insulin; protamine zinc insulin [PZI]) Corrects insulin deficiency and overcomes insulin resistance. Allows shift of glucose into cells and suppresses hepatic glucose production Initial bolus of 0.15 U/kg, then 0.1 U/kg·h iv. Hold insulin until K is >3.3 mEq/L Correct hyperglycemia and stop ketogenesis Hypoglycemia, hypokalemia. Low-dose insulin less likely to cause hypoglycemia or hypokalemia Once blood glucose level is ~200 mg/dL, switch fluids to include dextrose 5%-10%. Target blood glucose to 150-200 mg/dL. Once DKA is resolved (blood glucose 200 mg/dL, bicarbonate 18 mEq/L, pH >7.30) subcutaneous insulin therapy with multiple dose insulin can begin at 0.5-0.8 U/kg·d. Overlap therapy for 1-2 h before stopping iv regular insulin. If patient is unable to eat, continue iv insulin therapy Potassium Replace potassium deficit Replace at rate of 20-30 mEq/h if K is <3.3 mEq/L. Use 20 mEq/h if >3.3 and <5.0-5.5 mEq/L Reverse hypokalemia and associated complications Risk of over treatment leading to hyperkalemia. Use cautiously in anuric patients and only if K+ is <3.3 mEq/L Monitor potassium at least every 2 hours until normal. KCl is most common form of potassium replacement. Can use 2/3 KCl and 1/3 KPO4 to prevent excessive Cl levels Sodium bicarbonate Corrects metabolic acidosis If pH is <6.9 give 100 mmol NaHCO3 in 400 mL water at 200 mL/h. If pH is 6.9 to 7.0, give 50 mmol of NaHCO3 in 200 mL sterile water at 200 mL/h, repeat every 2 hours until pH is >7 By correcti Continue reading >>

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 >>

Topics By Science.gov

Topics By Science.gov

Bellazzini, Marc A; Meyer, Tom Hyperkalemia-induced electrocardiogram changes such as dysrhythmias and altered T wave morphology are well described in the medical literature. Pseudo-infarction hyperkalemia-induced changes are less well known, but present a unique danger for the clinician treating these critically ill patients. This article describes a case of pseudo anteroseptal myocardial infarction in a type 1 diabetic with hyperkalemia. The most common patterns of pseudo-infarct and their associated potassium concentrations are then summarized from a literature review of 24 cases. ... urine test is positive, contact your child's diabetes health care team. Tests done by a lab or hospital can confirm whether a child has diabetic ketoacidosis , if necessary. Some ... blood for ketones. Ask the diabetes health care team if such a meter is a good ... Katz, J. R.; Edwards, R.; Khan, M.; Conway, G. S. 1996-01-01 Diabetes in acromegaly is usually non-insulin dependent and is secondary to insulin resistance caused by growth hormone excess. Diabetic ketoacidosis is a result of relative insulin deficiency and is a rare feature of acromegaly. We describe a case of acromegaly presenting with diabetic ketoacidosis. We demonstrate that growth hormone excess can cause diabetic ketoacidosis in the presence of relative, but not absolute insulin deficiency. PMID:8944212 Gupta, Arvin; Rohrscheib, Mark; Tzamaloukas, Antonios H 2008-10-01 A patient on hemodialysis for end-stage renal disease secondary to diabetic nephropathy was admitted in a coma with Kussmaul breathing and hypertension (232/124 mmHg). She had extreme hyperglycemia (1884 mg/dL), acidosis (total CO(2) 4 mmol/L), hyperkalemia (7.2 mmol/L) with electrocardiographic abnormalities, and hypertonicity (330.7 mOsm/kg). Initial t 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 >>

Usmle Endocrine I

Usmle Endocrine I

Home > Preview Clinical Features: coarse facial features, arthralgias, uncontrolled hypertension, enlargement of the digits·, carpal tunnel syndrome. This condition is caused by excessive secretion of growth hormone (GH), usually due to a pituitary somatotroph adenoma. Other common features include malocclusion of the jaw, hyperhidrosis, heart failure, macroglossia, and local mass-effect symptoms (eg, headache, visual field defects). GH stimulates hepatic insulin-like growth factor 1 (IGF-1) secretion, which is responsible for most of the clinical manifestations of acromegaly. IGF-1 levels in acromegaly are consistently elevated throughout the day. In contrast, GH levels can fluctuate widely and cannot be used alone to diagnose acromegaly. As a result, IGF-1 is the preferred initial test. Patients with elevated IGF-1 should undergo confirmatory testing with an oral glucose suppression test Once acromegaly is confirmed with a glucose suppression test, patients should have an MRI of the brain to identify a pituitary mass. Acromegaly causes concentric myocardial hypertrophy leading to diastolic dysfunction, along with left ventricular dilation and global hypokinesis. This cardiomyopathy is worsened by concurrent hypertension, obstructive sleep apnea , and valvular heart disease, which are common in acromegaly. Complications include heart failure (eg, dyspnea, crackles at bases) and arrhythmias. Cardiovascular disease is the leading cause of death in patients with acromegaly, but normalization of growth hormone levels following successful treatment markedly reduces cardiovascular mortality. a congenital cardiomyopathy that should be distinguished from myocardial hypertrophy due to other cardiovascular diseases (eg, hypertensive, valvular, ischemic) - is characterized by as 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 >>

Search This Resource

Search This Resource

Introduction Diabetic ketoacidosis (DKA) is a severe form of complicated diabetes mellitus (DM) which requires emergency care. Ketones are synthesized from fatty acids as a substitute form of energy, because glucose is not effectively entered into the cells. Excess keto-acids results in acidosis and severe electrolyte abnormalities, which can be life threatening. Pathophysiology Ketone bodies are synthesized as an alternative source of energy, when intracellular glucose concentration can not meet metabolic demands. Ketone bodies are synthesized from acetyl-CoA which is a product of mitochondrial ß-oxidation of fatty acids. Synthesis of acetyl-CoA is facilitated by decreased insulin concentration and increased glucagon concentration. In non-diabetics acetyl-CoA and pyruvate enter the citric acid cycle to form ATP. However, in diabetics, production of pyruvate by glycolysis is decreased. The activity of the citric acid cycle is therefore diminished resulting in decreased utilization of Acetyl-CoA. The net effect of increased production and decreased utilization of acetyl-CoA is an increase in the concentration of acetyl-CoA which is the precursor for ketone body synthesis.1 The three ketone bodies synthesized from acetyl-CoA include beta hydroxybutyrate, acetoacetate, and acetone. Acetoacetate and beta-hydroxybutyrate are anions of moderately strong acids. Therefore, accumulation of these ketone bodies results in ketotic acidosis. Metabolic acidosis and the electrolyte abnormalities which ensue are important determinants in the outcome of patients with DKA.2 One of the beliefs regarding the pathophysiology of DKA had been that individuals that develop DKA have zero or undetectable endogenous insulin concentration. However, in a study that included 7 dogs with DKA it was Continue reading >>

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