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Dka Hypernatremia

Pulmcrit- Dominating The Acidosis In Dka

Pulmcrit- Dominating The Acidosis In Dka

Management of acidosis in DKA is an ongoing source of confusion. There isn’t much high-quality evidence, nor will there ever be (1). However, a clear understanding of the physiology of DKA may help us treat this rationally and effectively. Physiology of ketoacidosis in DKA Ketoacidosis occurs due to an imbalance between insulin dose and insulin requirement: Many factors affect the insulin requirement: Individuals differ in their baseline insulin resistance and insulin requirements. Physiologic stress (e.g. hypovolemia, inflammation) increases the level of catecholamines and cortisol, which increases insulin resistance. Hyperglycemia and metabolic acidosis themselves increase insulin resistance (Souto 2011, Gosmanov 2014). DKA treatment generally consists of two phases: first, we must manage the ketoacidosis. Later, we must prepare the patient to transition back to their home insulin regimen. During both phases, success depends on balancing insulin dose and insulin requirement. Phase I (Take-off): Initial management of the DKA patient with worrisome acidosis Let’s start by considering a patient who presents in severe DKA with worrisome acidosis. This is uncommon. Features that might provoke worry include the following: bicarbonate < 7 mEq/L pH < 7 (if measured; there is generally little benefit from measuring pH) clinically ill-appearing (e.g., dyspnea, marked Kussmaul respirations) These patients generally have severe metabolic acidosis with respiratory compensation. This creates two concerns: If the metabolic acidosis worsens, they may decompensate. The patient is depending on respiratory compensation to maintain their pH. If they should fatigue and lose the ability to hyperventilate, their pH would drop. It is important to reverse the acidosis before the patient m Continue reading >>

Diabetic Ketoacidosis In Children And Adolescents: An Update And Revised Treatment Protocol

Diabetic Ketoacidosis In Children And Adolescents: An Update And Revised Treatment Protocol

Standardized pediatric-specific treatment is required to ensure safe correction of metabolic derangements associated with DKA. ABSTRACT: British Columbia has an estimated 150 to 200 new cases of type 1 diabetes in children annually. In these cases, 10% to 20% of patients will present in diabetic ketoacidosis (DKA). DKA is associated with significant fluid and biochemical derangements, necessitating a thoughtful, structured approach to its management. Recent gains have been made in knowledge about the pathophysiology and medical care of DKA and its most significant complication, cerebral edema. In response, BC Children’s Hospital has devised an updated medical protocol for managing DKA in infants, children, and adolescents that conforms to new international consensus guidelines. The protocol assists the medical practitioner in calculating fluid and electrolyte replacement needs for individual patients and outlines a plan for initial assessment and ongoing monitoring. Accompanying resources have also been developed to aid nursing, laboratory, and pharmacy colleagues to ensure that all children presenting with DKA in this province are managed following scientifically established guidelines. Canada has one of the highest rates of type 1 diabetes (T1D) in the world. The estimated incidence of T1D in Canadian children aged 0 to 14 years is 21.7 per 100000 per year.[1] Using 2008 census data,[2] prevalence in this age group in British Columbia is estimated to be about 1029 established cases of T1D or about 150 new cases per year. Much publicity has been given to the rising incidence of type 2 diabetes (T2D) in youth and young adults in North America, a phenomenon that we are also observing in our province, but the fact that there has also been a 2% to 3% annual increase in t Continue reading >>

Does Fluid Choice Make Any Difference In Dka?

Does Fluid Choice Make Any Difference In Dka?

Your patient is a 21 year-old female with a history of type 1 diabetes mellitus who was brought to the ED by her boyfriend for diminished responsiveness. In a stupor, she is unable to give any history. Her vitals are: BP 102/66, pulse 120, respiratory rate 24, temperature 98.9 oral, and O2 saturation 98% on room air. Her finger stick glucose is >500 mg/dl. She looks dry and is somnolent (GCS 9). Pupils are equal, round, and reactive. Neck is supple. She is protecting her airway well, her lungs are clear, and you hear no murmurs. Her belly is soft, and you see no signs of trauma or exanthema. Her skin tents when you pinch it. She is moving all extremities in response to noxious stimulus. As the rest of her labs (including serum osmolality and cultures, of course!) are sent off, her boyfriend tells you that she has not been taking her medications over the past 2 weeks and has had symptoms consistent with polydipsia and polyuria most noticeably over the past few days. A rapid shock panel returns with a glucose level of >500 mg/dl, pH 7.2, bicarbonate 10, and a urine dipstick shows large ketones. These confirm your suspicion of diabetic ketoacidosis (DKA). You wait for further results to decide whether a full sepsis work-up and antibiotics are necessary. In the meantime, you look at the bag of normal saline (0.9% saline solution) that is already hanging and you wonder, “Am I sure this is really the best solution to resuscitate a patient with DKA?” Consensus for Resuscitation in DKA Diabetic ketoacidosis is one of the diseases for which emergency physicians are expected to have a plan to quickly put into action. The basics should be familiar: Manage the patient’s ABCs, place an IV, put the patient on a monitor to check vitals frequently, and start with an intravenous f 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 >>

Diabetic Ketoacidosis And Hyperosmolar Hyperglycemia — A Brief Review

Diabetic Ketoacidosis And Hyperosmolar Hyperglycemia — A Brief Review

Diabetic Ketoacidosis and Hyperosmolar Hyperglycemia — A Brief Review SPECIAL FEATURE By Richard J. Wall, MD, MPH, Pulmonary Critical Care & Sleep Disorders Medicine, Southlake Clinic, Valley Medical Center, Renton, WA. Dr. Wall reports no financial relationships relevant to this field of study. Financial Disclosure: Critical Care Alert's editor, David J. Pierson, MD, nurse planner Leslie A. Hoffman, PhD, RN, peer reviewer William Thompson, MD, executive editor Leslie Coplin, and managing editor Neill Kimball report no financial relationships relevant to this field of study. INTRODUCTION Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are two of the most common and serious acute complications of diabetes mellitus. DKA is responsible for more than 500,000 hospital days annually in the United States, at an estimated annual cost of $2.4 billion. Both conditions are part of the spectrum of uncontrolled hyperglycemia, and there is sometimes overlap between them. This article will discuss and compare the two conditions, with a focus on key clinical features, diagnosis, and treatment. DIAGNOSTIC FEATURES In DKA, there is an accumulation of ketoacids along with a high anion gap metabolic acidosis (see Table below).1 The acidosis usually evolves quickly over a 24-hour period. The pH is often < 7.20 and initial bicarbonate levels are often < 20 mEq/L. DKA patients (especially children) often present with nausea, vomiting, hyperventilation, and abdominal pain. Blood sugar levels in DKA tend to be 300-800 mg/dL, but they are sometimes much higher when patients present in a comatose state. In HHS, there is no (or little) ketonemia but the plasma osmolality may reach 380 mOsm/kg, and as a result, patients often have neurologic complications such as coma. Bica Continue reading >>

Management Of Diabetic Ketoacidosis In The Picu

Management Of Diabetic Ketoacidosis In The Picu

DKA - A common PICU diagnosis Incidence 4.6 – 8 per 1000 person years among people with diabetes Pediatric mortality rate is 1-2% DKA causes profound dehydration Hyperglycemia leads to osmotic diuresis Often 10-15% down from baseline weight Profound urinary free water and electrolyte loss Free water follows glucose into urine Electrolytes follow free water into urine Electrolyte abnormalities Pseudo-hyponatremia with hyperglycemia Sodium should rise with correction of glucose Profound total-body K+ depletion Urinary loss, decreased intake, emesis Initial K+ may be high due to acidosis, low insulin Aggressive K+ replacement necessary to prevent arrhythmias Phosphate, magnesium, calcium require replacement Initial DKA management - ED Resuscitation aimed at shock reversal Begin with 10-20 mL/kg NS bolus, may repeat if signs of shock persist Bolus fluids only necessary if signs of shock present Avoid overly-aggressive fluid resuscitation Concern for inciting cerebral edema, though no clear data Initial DKA management - ED NEVER give bicarbonate Increases risk of cerebral edema Begin insulin infusion at 0.1 units/kg/hr Should be initiated prior to leaving ED SQ or bolus insulin not indicated Pre-PICU arrival Order several bags of dextrose-containing and non-dextrose-containing IVF pre-PICU arrival Often takes pharmacy 1 hour to custom-make IVF No dextrose-containing fluids stocked in PICU Fluid Management - PICU 3 components to replacement fluids Deficit (often 10-15% total body water deficit) Ongoing losses (polyuria, emesis) Maintenance Possible to calculate the above, or give: 1.5X maintenance if moderately dehydrated 2X maintenance if severely dehydrated Isotonic fluid with potassium NS + 20 mEq/L KCl + 20 mEq/L KPhos Start with 40 mEq/L of potassium if K+ < 5 K+ Continue reading >>

Fluid Management In Diabetic Ketoacidosis

Fluid Management In Diabetic Ketoacidosis

Young people with insulin dependent diabetes mellitus are three times more likely to die in childhood than the general population.1 Despite advances in management over the past 20 years, the incidence of mortality associated with diabetic ketoacidosis (DKA) remains unchanged. Cerebral oedema is the predominant cause of this mortality; young children are particularly at risk, with an incidence of 0.7–1% of episodes of DKA.2,3 The mortality appears to be greatest among patients at first presentation,1,3,4 if there has been a long history of symptoms prior to admission,3 and during the first 24 hours of treatment.4 In a recently published retrospective multicentre analysis of children with DKA, low pco2 levels and high serum sodium concentration at presentation were identified as particular risk factors for the development of cerebral oedema, together with bicarbonate therapy.5 However, in the accompanying editorial, Dunger and Edge point out that this may simply be revealing an association between severe DKA and dehydration and the risk of cerebral oedema.6 The pathogenesis of cerebral oedema remains poorly understood but there may be many contributing factors.7 The aim of management of DKA is to restore metabolic homoeostasis while minimising the risks of complications including hypoglycaemia, hypokalaemia, cardiac failure, and in children the development of cerebral oedema. How best to achieve this remains contentious, with particular controversy centred on optimal fluid management. The most appropriate volume, type, and rate of fluid to be given have all been the subject of debate. A survey in 1994 of UK paediatricians found a threefold variation in the amount of fluid recommended within the first 12 hours.8 Since then national guidelines have been developed by the B Continue reading >>

1. Start Iv Fluids (1 L Of 0.9% Nacl Per Hr Initially) 2. If Serum K+ Is <3.3 Meq/l Hold Insulin

1. Start Iv Fluids (1 L Of 0.9% Nacl Per Hr Initially) 2. If Serum K+ Is <3.3 Meq/l Hold Insulin

DKA Diagnostic Criteria (See page 3 for more details):  Blood glucose >250 mg/dl,  Arterial pH <7.3,  Bicarbonate ≤18 mEq/l,  Anion Gap Acidosis  Moderate ketonuria or ketonemia.  Give 40 mEq/h until K ≥ 3.3 mEq/L 3. Initiate DKA Order Set Phase I 4. Start insulin 0.14 units/kg/hr IV infusion (calculate dose) RN will titrate per DKA protocol Insulin Potassium Bicarbonate IVF Look for the Cause - Insulin deficiency - Infection/Inflammation (PNA, UTI, pancreatitis, cholecystitis) - Ischemia/Infarction (myocardial, cerebral, gut) - Intoxication (EtOH, drugs) - Iatrogenic (drugs, lack of insulin) - Pregnancy DKA/HHS Pathway Phase 1 (Adult) Approved by Diabetes Steering Committee, MMC, 2015 Initiate and continue insulin gtt until serum glucose reaches 250 mg/dl. RN will titrate per protocol to achieve target. When sugar < 250 mg/dl proceed to DKA Phase II (reverse side) DKA/HHS Pathway Phase 2 (Adult) Non-ICU Patients Phase 2: Blood sugar now less than 250mgd/dl. If Anion Gap Normalized* If Anion Gap Elevated* Critical Illness (ICU) Follow guidelines to the right when gap has normalized.* Approved by Glycemic Steering Committee, MMC, 2015  Transition to DKA Order Set Phase 2  Discontinue Phase 1 insulin infusion order and DKA nursing titration protocol from phase 1.  Change to fixed dose insulin infusion at suggested rate of 2.5 units/hr (Adjust as needed for individual patient with typical dose range of 0.02 to 0.05 units/kg/hr based on drip rate and response in phase 1). Do not discontinue insulin therapy.  Start dextrose containing IV fluid such as D5 ½ NS and adjust dextrose to goal blood sugar 150- 200.  Continue to check labs regularly.  Reevaluate for underlying causes a Continue reading >>

Diabetic Ketoacidosis And Cerebral Edema

Diabetic Ketoacidosis And Cerebral Edema

Elliot J. Krane, M.D. Departments of Pediatrics and Anesthesiology Stanford University Medical Center Introduction In 1922 Banting and Best introduced insulin into clinical practice. A decade later the first reported case of cerebral edema complicating diabetic ketoacidosis (DKA) was reported by Dillon, Riggs and Dyer writing in the pathology literature. While the syndrome of cerebral edema complicating DKA was either not seen, ignored, or was unrecognized by the medical community until 3 decades later when the complication was again reported by Young and Bradley at the Joslin Clinic, there has since been a flurry of case reports in the 1960's and 1970's and basic and clinical research from the 1970's to the 1990's leading to our present day acceptance of this as a known complication of DKA, or of the management of DKA. In fact, we now recognize that the cerebral complications of DKA (including much less frequent cerebral arterial infarctions, venous sinus thrombosis, and central nervous system infections) are the most common cause of diabetic-related death of young diabetic patients (1), accounting for 31% of deaths associated with DKA and 20% of all diabetic deaths, having surpassed aspiration, electrolyte imbalance, myocardial infarction, etc. Furthermore, diabetes mellitus remains an important cause of hospitalization of young children. The prevalence rate of diabetes continues to grow in all Western developed nations, nearly doubling every decade, resulting in 22,000 hospital admissions in children under 15 years of age for diabetes in the United States in 1994, the majority of which were due to ketoacidosis. With approximately 4 hospital admissions of children for DKA per 100,000 population per year (2), every PICU located in a major metropolitan center will conti 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 >>

Severe Hypercalcemia In Diabetic Ketoacidosis: A Case Report

Severe Hypercalcemia In Diabetic Ketoacidosis: A Case Report

A 12-year-old boy presented to a district hospital with diabetic ketoacidosis (DKA): pH, 6.97; base excess, −27.5 mmol/L; bicarbonate, 2.5 mmol/L; glucose 29 mmol/L. A urinalysis showed 4+ ketones (≥160 mg/dL). Standard DKA management according to U.K. guidelines was instituted (1). Fluid was replaced at maintenance plus 7.5% dehydration, with correction over 48 h. Within 2 h, the boy developed signs and symptoms of cerebral edema and was treated with intravenous mannitol (5 mL/kg × 2), and fluids were decreased by one-third. A further fall in his Glasgow Coma Score was managed with hypertonic (2.7%) saline (5 mL/kg), intubation and ventilation, and transfer to the regional pediatric intensive care unit (PICU). At the PICU, a decision was made to give maintenance fluid plus 5% dehydration correction over 72 h as a neuroprotective strategy. Within an hour of the boy’s admission to the PICU, an elevated, corrected calcium of 2.96 mmol/L was noted (normal range [NR]: 2.10–2.56 mmol/L). Retrospective analysis of the district hospital’s sample taken 4 h earlier showed a corrected calcium of 2.57 mmol/L. Over the next 24 h, the boy gradually developed acute, severe hypercalcemia with corrected calcium levels reaching a maximum of 3.75 mmol/L 33 h after the initial presentation. Parathyroid hormone was 8.3 ng/L (NR: 11–35), urine calcium/creatinine ratio, 0.17 (NR: 0–0.7), and maximum alkaline phosphatase 423 units/L (NR: 76–308). He had significant hyperglycemia, requiring up to 0.2 units/kg/h of intravenous insulin. Severe metabolic acidosis persisted for 4 days. This was attributed to a combination of severe dehydration, combined ketoacidosis and lacticacidosis, and hyperchloremia (maximum chloride levels, 145 mmol/L). Other electrolyte imbalances included Continue reading >>

Restoring Electrolyte Balance

Restoring Electrolyte Balance

Looking for news and information on electrolyte balance? Here are a few more articles on the topic: Management of chronic kidney disease: An emphasis on delaying disease progression and treatment options Improving quality of life for patients with kidney failure Defenses gone awry: Inflammatory bowel disease Restoring electrolyte balance CE credit is no longer available for this article. (Expired May 2007) Originally posted May 2005 By Sonia M. Astle, RN, MS, CCRN Sonia Astle is a critical care clinical specialist at Inova Fairfax Hospital in Falls Church, VA, and a member of the RN editorial board. The author has no financial relationships to disclose. A shift up. A shift down. Either way, an imbalance in electrolytes spells trouble for your patients. Averting a crisis hinges on your clinical skills. This review will help you sharpen them. Electrolytes, or ions, are the charged particles in body fluids that help transmit electrical impulses for proper nerve, heart, and muscle function.1,2 The number of positive ions, called cations, and negative ions, called anions, is supposed to be equal. Anything that upsets this balance can have life-threatening consequences. There's a long list of conditions that lead to electrolyte imbalances, including dehydration, diabetic ketoacidosis, cancer, and even head injury. But renal disease is at the top of the list.1-3 It's the kidneys' job to control fluid, electrolyte, and acid-base balance. Because too much or too little of any one of the electrolytes quickly becomes a major problem of its own, doing everything possible to maintain the proper balance is a vital component of patient care. Therefore, monitoring electrolytes and checking for signs of an imbalance should be an integral part of your nursing assessment. Here, then, is a Continue reading >>

Hypernatraemia And Acidosis

Hypernatraemia And Acidosis

aka Metabolic Muddle 005 A 20 year old male presents with 3 days of lethargy and generalised malaise. He is confused and looks very unwell. The following blood tests are obtained: Questions Q1. Describe the acid base disturbance. Q2. What is the likely diagnosis? Q3. Describe the electrolyte abnormalities. Q4.Should the corrected sodium be used for calculating the anion gap? Q5. It emerges that the patient has recently been diagnosis with Schizophrenia and has commenced olanzepine. What is the significance of this additional history? Q6. An amylase is measured and is found to be 3 times the upper limit of normal. What is the significance of this finding? References and Links Beck, LH. Should the actual or the corrected serum sodium be used to calculate the anion gap in diabetic ketoacidosis? CLEVELAND CLINIC JOURNAL OF MEDICINE 2001; 68 (8) 673-674. (pdf) Continue reading >>

Cerebral Edema In Diabetic Ketoacidosis: A Look Beyond Rehydration

Cerebral Edema In Diabetic Ketoacidosis: A Look Beyond Rehydration

The Journal of Clinical Endocrinology & Metabolism Cerebral Edema in Diabetic Ketoacidosis: A Look Beyond Rehydration Department of Pediatrics University of Florida Gainesville, Florida 32610 Search for other works by this author on: The Journal of Clinical Endocrinology & Metabolism, Volume 85, Issue 2, 1 February 2000, Pages 509513, Andrew Muir; Cerebral Edema in Diabetic Ketoacidosis: A Look Beyond Rehydration, The Journal of Clinical Endocrinology & Metabolism, Volume 85, Issue 2, 1 February 2000, Pages 509513, INJUDICIOUS fluid resuscitation is frequently suggested as the cause of the cerebral edema that is the most common cause of mortality among pediatric patients with diabetic ketoacidosis (DKA) ( 1 ). The evidence, however, supports the hypothesis that neurological demise in DKA is a multifactorial process that cannot be reliably prevented by cautious rehydration protocols. Mortality and severe morbidity can, however, be reduced when healthcare providers watch vigilantly for and respond rapidly to the sentinel neurological signs and symptoms that precede, often by hours, the dramatic collapse that is typically described in these patients. Children being treated for DKA develop clinically important neurological compromise about 0.21.0% of the time ( 2 ). Subclinical neurological pathology, causing raised intracranial pressure, likely precedes the initiation of therapy in almost all cases of DKA ( 3 5 ). Intracranial hypertension has been considered to be aggravated by therapy of the DKA ( 4 , 6 , 7 ), but in keeping with the physicians perplexity about the problem, even this widely held tenet has recently been challenged ( 8 ). The pathogenic mechanism for this terrifying complication remains unknown. Hypothetical causes of cerebral edema in children with DKA m Continue reading >>

Hyponatremia In Diabetes Mellitus: Clues To Diagnosis And Treatment

Hyponatremia In Diabetes Mellitus: Clues To Diagnosis And Treatment

Department of Internal Medicine, School of Medicine, University of Ioannina, Ioannina, Greece Citation: Liamis G, Tsimihodimos V, Elisaf M (2015) Hyponatremia in Diabetes Mellitus: Clues to Diagnosis and Treatment. J Diabetes Metab 6: 560. doi: 10.4172/2155-6156.1000560 Copyright: © 2015 Liamis G, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Visit for more related articles at Journal of Diabetes & Metabolism Hyponatremia is the most common electrolyte abnormality in clinical practice and is associated with increased morbidity and mortality [1,2]. Even small decreases of serum sodium are associated with increased probability for adverse outcomes (cognitive impairment, falls, osteoporosis and fractures) [3]. Decreased serum sodium levels are occasionally observed in patients with diabetes mellitus and can be attributed to numerous underlying pathogenetic mechanisms (Table 1) [4,5]. A) Non hypotonic hyponatremia With increased Posm: Hyperglycemia - induced (dilutional) With normal Posm: Pseudohyponatremia (marked hypertriglyceridemia and hyperproteinemia) B) Hypotonic hyponatremia • Hypovolemia-induced • Drug –induced hyponatremia (mainly with thiazides and first generation sulphonylureas) • Diabetes mellitus - associated hyponatremia • Syndrome of inappropriate antidiuresis associated with coexisting disorders or administered drugs • Chronic renal failure (diabetic nephropathy) or associated with the syndrome of hyporeninemichypoaldosteronism Table 1: Causes of hyponatremia in diabetic patients. The direct measurement of serum osmolality (Posm) can differentiate be Continue reading >>

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