diabetestalk.net

Dka Hypernatremia

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 >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Practice Essentials Diabetic ketoacidosis (DKA) is an acute, major, life-threatening complication of diabetes that mainly occurs in patients with type 1 diabetes, but it is not uncommon in some patients with type 2 diabetes. This condition is a complex disordered metabolic state characterized by hyperglycemia, ketoacidosis, and ketonuria. Signs and symptoms The most common early symptoms of DKA are the insidious increase in polydipsia and polyuria. The following are other signs and symptoms of DKA: Nausea and vomiting; may be associated with diffuse abdominal pain, decreased appetite, and anorexia History of failure to comply with insulin therapy or missed insulin injections due to vomiting or psychological reasons or history of mechanical failure of insulin infusion pump Altered consciousness (eg, mild disorientation, confusion); frank coma is uncommon but may occur when the condition is neglected or with severe dehydration/acidosis Signs and symptoms of DKA associated with possible intercurrent infection are as follows: See Clinical Presentation for more detail. Diagnosis On examination, general findings of DKA may include the following: Characteristic acetone (ketotic) breath odor In addition, evaluate patients for signs of possible intercurrent illnesses such as MI, UTI, pneumonia, and perinephric abscess. Search for signs of infection is mandatory in all cases. Testing Initial and repeat laboratory studies for patients with DKA include the following: Serum electrolyte levels (eg, potassium, sodium, chloride, magnesium, calcium, phosphorus) Note that high serum glucose levels may lead to dilutional hyponatremia; high triglyceride levels may lead to factitious low glucose levels; and high levels of ketone bodies may lead to factitious elevation of creatinine levels. 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 >>

I’ll See Your Ketoacidosis And Raise You A Renal Failure

I’ll See Your Ketoacidosis And Raise You A Renal Failure

A while back I posted on a paper that appeared in The Lancet about an obese woman who came to the emergency room with gastroenteritis and was misdiagnosed as being in diabetic ketoacidosis (a life-threatening disorder). She was misdiagnosed because the pinheads covering the ER couldn’t get past the fact that she had been on a low-carb diet. At the time I posted on this travesty I noted that this Lancet paper would from here on out be waved in the face of anyone who was following or advocated a low-carb diet as proof that such a diet is dangerous and can cause diabetic ketoacidosis (DKA). Well, now we’ve got an answer. Next time someone tells you that it has been proven that low-carb diets are dangerous and can cause ketoacidosis, you can resort to poker terminology and reply that you’ll see their ketoacidosis and raise them a renal failure. A few days ago I got wind of a paper published a few years ago that can be used as a counterpoint to the above mentioned idiotic paper in The Lancet that has given low-carbers such a bad time. This paper, published in the journal Renal Failure in 1998, is, like the other paper, a case report. The short version is as follows: An obese young man arrived comatose in the emergency room. In an effort to lose weight he had been consuming a high-carbohydrate canned beverage as his sole source of nutrition for the two weeks prior. His blood sugar–at about 20 times normal–was extremely elevated and led to a diagnosis of diabetic ketoacidosis. The physicians on staff treated the patient appropriately, and he, over the next 20 hours or so, regained consciousness as his blood sugar levels and other lab parameters began to normalize. During a lab analysis 22 hours after admission the doctors found the patient to be breaking down and rel Continue reading >>

University Of Zagreb

University Of Zagreb

SCHOOL OF MEDICINE Mohammad Imran Khan Malik A review of the efficacy of the Milwaukee protocol in the treatment of ketoacidosis in pediatric Intensive Care Unit patients at Rebro hospital between 2009-2014. GRADUATE THESIS Zagreb, 2014 UNIVERSITY OF ZAGREB SCHOOL OF MEDICINE Mohammad Imran Khan Malik A review of the efficacy of the Milwaukee protocol in the treatment of ketoacidosis in pediatric Intensive Care Unit patients at Rebro hospital between 2009-2014. GRADUATE THESIS Zagreb, 2014 This graduation paper has been completed at the Department of Paediatrics at the University Hospital Centre Zagreb (Rebro hospital) under the supervision of Dr. sc. Mario Ćuk and was submitted for evaluation during the academic year 2013 /2014. LIST OF TABLES Table 1: DKA laboratory diagnosis criteria Table 2: Classification of DKA. Modified from Kliegman et al. Nelson Textbook of Pediatrics, 2011. Table 3: Table 3: Summary of key data of patients admitted to pediatric ICU at Rebro hospital. LIST OF FIGURES Figure 1: DKA pathogenesis. Figure 2: Ketone bodies: showing formation of negatively charged conjugate bases of the ketoacids. The conjugate bases cause the increased anion gap in DKA metabolic acidosis. Figure 3: Algorithm of key steps in DKA pathophysiology. Colour coded to highlight the two areas that treatment should target: metabolic acidosis and hyperglycemia. Figure 4: True sodium level calculations for glucose levels above 100mg/dL (5.6mmol/L). Figure 5: Goals of DKA management Figure 6: Diabetic ketoacidosis treatment: Milwaukee protocol. Modified from Kliegman et al. Nelson Textbook of Paediatrics. 2011 p.1979 Figure 7: DKA incidence between 1 st January 2009 – 30 th June 2014. LIST OF ABBREVIATIONS DKA ..............Diabetic Ketoacidosis CE...................C 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 >>

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 >>

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 >>

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 >>

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 >>

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 >>

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 >>

Understanding And Treating Diabetic Ketoacidosis

Understanding And Treating Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a serious metabolic disorder that can occur in animals with diabetes mellitus (DM).1,2 Veterinary technicians play an integral role in managing and treating patients with this life-threatening condition. In addition to recognizing the clinical signs of this disorder and evaluating the patient's response to therapy, technicians should understand how this disorder occurs. DM is caused by a relative or absolute lack of insulin production by the pancreatic b-cells or by inactivity or loss of insulin receptors, which are usually found on membranes of skeletal muscle, fat, and liver cells.1,3 In dogs and cats, DM is classified as either insulin-dependent (the body is unable to produce sufficient insulin) or non-insulin-dependent (the body produces insulin, but the tissues in the body are resistant to the insulin).4 Most dogs and cats that develop DKA have an insulin deficiency. Insulin has many functions, including the enhancement of glucose uptake by the cells for energy.1 Without insulin, the cells cannot access glucose, thereby causing them to undergo starvation.2 The unused glucose remains in the circulation, resulting in hyperglycemia. To provide cells with an alternative energy source, the body breaks down adipocytes, releasing free fatty acids (FFAs) into the bloodstream. The liver subsequently converts FFAs to triglycerides and ketone bodies. These ketone bodies (i.e., acetone, acetoacetic acid, b-hydroxybutyric acid) can be used as energy by the tissues when there is a lack of glucose or nutritional intake.1,2 The breakdown of fat, combined with the body's inability to use glucose, causes many pets with diabetes to present with weight loss, despite having a ravenous appetite. If diabetes is undiagnosed or uncontrolled, a series of metab 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 >>

Osmotic Demyelination Syndrome As The Initial Manifestation Of A Hyperosmolar Hyperglycemic State

Osmotic Demyelination Syndrome As The Initial Manifestation Of A Hyperosmolar Hyperglycemic State

Copyright © 2014 Karla Victoria Rodríguez-Velver et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Osmotic demyelination syndrome (ODS) is a life-threatening demyelinating syndrome. The association of ODS with hyperosmolar hyperglycemic state (HHS) has been seldom reported. The aim of this study was to present and discuss previous cases and the pathophysiological mechanisms involved in ODS secondary to HHS. A 47-year-old man arrived to the emergency room due to generalized tonic-clonic seizures and altered mental status. The patient was lethargic and had a Glasgow coma scale of 11/15, muscle strength was 4/5 in both lower extremities, and deep tendon reflexes were diminished. Glucose was 838 mg/dL; serum sodium and venous blood gas analyses were normal. Urinary and plasma ketones were negative. Brain magnetic resonance revealed increased signal intensity on T2-weighted FLAIR images with restricted diffusion on the medulla and central pons. Supportive therapy was started and during the next 3 weeks the patient progressively regained consciousness and muscle strength and was able to feed himself. At 6-month follow-up, the patient was asymptomatic and MRI showed no residual damage. In conclusion, the association of ODS with HHS is extremely rare. The exact mechanism by which HHS produces ODS still needs to be elucidated, but we favor a rapid hypertonic insult as the most plausible mechanism. 1. Background Osmotic demyelination syndrome (ODS) is a life-threatening demyelinating syndrome, which usually occurs in the setting of a rapid correction of severe chronic hyponatremia [1, 2]. Now rarely Continue reading >>

More in ketosis