diabetestalk.net

Alcoholic Ketoacidosis Uptodate

Emdocs.net Emergency Medicine Educationhow To Crush Abgs - Emdocs.net - Emergency Medicine Education

Emdocs.net Emergency Medicine Educationhow To Crush Abgs - Emdocs.net - Emergency Medicine Education

Stepwise Approach w/ interpretations found below. You wont need to look anywhere else unless you want to do the Stewart Acid Base Approach. Step 1: Is there alkalemia or acidemia present? Remember: an acidosis or alkalosis may be present even if the pH is in the normal range (7.35 7.45) You will need to check the PaCO2, HCO3-, anion gap, and Albumin Step 2: Is the disturbance respiratory or metabolic? What is the relationship between the direction of change in the pH and the direction of change in the PaCO2? In primary respiratory disorders, the pH and PaCO2 change in opposite directions; in metabolic disorders the pH and PaCO2 change in the same direction. Chronic => for every PaC02 increase of 10 mmhg, ph drops by .03 Acute => for every paC02 increase of 10 mmhg, ph drops by .08 Chronic => Decrease of PaC02 by 10 mmHg, pH increase by .03 Acute => Decrease of PaC02 by 10 mmHg, pH increase by .08 Step 3: Is there appropriate compensation for the primary disturbance? Usually, compensation does not return the pH to normal (7.35 7.45). If the observed compensation is not the expected compensation, it is likely that more than one acid-base disorder is present. Metabolic Acidosis: PaC02 = 1.5 (HC03) + 8 +/- 2 Acute Respiratory Acidosis: Increase in HC03 = Change in PaC02/10 +/- 3 Chronic Respiratory Acidosis (3-5 Days) Increase in HC03 = 3.5 (Change PaC02/10) Metabolic Alkalosis: Increase in PaC02 = .6 (Change in Bicarb) Acute Respiratory Alkalosis: Decease in Bicarb = 2 (Change PaC02/10) Chronic Respiratory Alkalosis: Decrease in Bicarb = 5(Change in PaC02/10) to 7(Change in PaC02/10) A normal anion gap is approximately 12 meq/L. Correct for albumin. Correct for Alb: (2.5) (4-pts Alb) + AG. Super important in the Unit. If the anion gap is elevated, consider calculating the Continue reading >>

Starvation-induced True Diabetic Euglycemic Ketoacidosis In Severe Depression

Starvation-induced True Diabetic Euglycemic Ketoacidosis In Severe Depression

Go to: A 34-year-old man with a 19-year history of type 1 diabetes presented as an emergency with a 4-day history of nausea, vomiting, and flu-like symptoms. He was on a basal bolus insulin regime comprising 8 units of bolus insulin lispro injected at mealtimes and 12 units of basal isophane insulin at bedtime, but did not monitor capillary blood glucose levels. He did however empirically increase his insulin doses during times of illness and had increased his isophane insulin to 15 units during the 3 days prior to presentation. He had only one prior hospital admission, which occurred 6 years previously and was due to an episode of DKA precipitated by gastroenteritis. He was single, unemployed, did not drink alcohol, had no previous psychiatric history, no family history of diabetes or other medical conditions, and lived in a hostel. He had a record of poor clinic attendances and a history of long-term cannabis use. He denied any salicylate consumption, but admitted to some weight loss; however, he was unable to quantify this. His body mass index (BMI) was 19 kg/m2, and he looked unkempt. Physical examination revealed a temperature of 36.4°C (97.5°F), heart rate of 106 beats per minute, supine blood pressure of 131/85 mmHg, and sitting blood pressure of 122/80 mmHg. He had a respiratory rate of 30 breaths per minute, and his oxygen saturation using a pulsoximeter was 99% on room air. He appeared clinically dehydrated with dry oral mucosa, but cardiovascular, respiratory, abdominal, and neurological examinations were otherwise normal. Diabetic ketoacidosis (DKA) was suspected; metabolic acidosis was confirmed with a pH of 7.3, bicarbonate concentration of 10 mEq/l, and an elevated anion gap of 29 mEq/l [sodium = 134 mEq/l, potassium = 5.7 mEq/l, chloride = 101 mEq/l, b Continue reading >>

Treatment Of Severe Alcohol Poisoning

Treatment Of Severe Alcohol Poisoning

Nefrologia (English Version) 2008;28:369-72 | doi: Tratamiento de las intoxicaciones graves por alcoholes a Servicio de Nefrolog??a, Hospital Universitario La Paz, Madrid, Madrid, Espa??a, b 2??rea de Tecnolog??a de la Informaci??n, SESCAM, Toledo, Toledo, Espa??a, La intoxicacin por alcoholes (metanol, etanol o etilenglicol) puede originar acidosis metablica severa con hiato aninico y/o osmolal elevados, alteraciones neurolgicas que van desde la obnubilacin al coma profundo, amaurosis, y muerte. Adems, algunos pacientes pueden desarrollar un cuadro de fracaso renal agudo [1-3]. A pesar de la terapia intensiva la morbilidad y la mortalidad de estas intoxicaciones siguen siendo muy elevadas, debido fundamentalmente al retraso en el diagnstico y en el inicio del tratamiento [4, 5]. En ausencia de una historia de ingesta de metanol, etanol o etilenglicol, el diagnstico inicial es difcil de realizar. La determinacin de los niveles sricos del alcohol txico es til, pero no siempre se encuentran disponibles inmediatamente al ingreso en el hospital. Poisoning induced by alcohols (methanol, ethanol, or ethylene glycol) may cause severe metabolic acidosis with high anion and/or osmolal gaps, neurological changes ranging from confusion to deep coma, amaurosis, and death. Some patients may also develop acute renal failure.1-3 Despite intensive treatment, morbidity and mortality of these poisonings continue to be very high, mainly because of the delay in diagnosis and start of treatment. Poisoning induced by alcohols (methanol, ethanol, or ethylene glycol) may cause severe metabolic acidosis with high anion and/or osmolal gaps, neurological changes ranging from confusion to deep coma, amaurosis, and death. Some patients may also develop acute renal failure.1-3 Despite intensive tre Continue reading >>

Emergency Medicine News

Emergency Medicine News

Thought you might appreciate this item(s) I saw at Emergency Medicine News. Your message has been successfully sent to your friend. Some error has occurred while processing your request. Please try after some time. A 44-year-old-man with a past medical history of alcohol abuse was brought to the emergency department by EMS. He was found sleeping on a bench and appeared intoxicated. His initial vital signs were temperature 90.9F, heart rate 62 bpm, blood pressure 130/84 mm Hg, respiratory rate 16 bpm, and pulse oximetry 98% on room air. He is disheveled patient, and has a depressed level of consciousness, slurred speech, and the distinct odor of mint and urine. Pertinent lab findings include an ethanol level of 340 mg/dL. The minty odor is tipoff in this case that he is inebriated from mouthwash. The ethanol concentration in mouthwashes commercially available in the United States varies widely. The highest ethanol concentration reported is 26.9 % . Alcohol-free products are also available. The risk of toxicity from the nonalcoholic ingredients is minimal in most ingestions of mouthwash: One standard drink is equivalent to 2.2 fluid ounces of 27% alcohol/volume mouthwash: National Institute on Alcohol Abuse and Alcoholism; . It is important to recognize the signs of ethanol intoxication in patients who have ingested any alcohol-containing mouthwash. Management strategies for ethanol-intoxicated patients are: n Supportive care is the mainstay of treatment. n Exclude other causes of altered mental status such as hypoglycemia, trauma, infection, co-ingestants, and stroke. n Evaluate and treat complications of ethanol intoxication such as hypothermia, hypoglycemia, and alcoholic ketoacidosis. n Nutritional support as needed: intravenous fluids with multivitamins, thiamine, a Continue reading >>

Metabolic Acidosis In A Patient With Isopropyl Alcohol Intoxication: A Case Report

Metabolic Acidosis In A Patient With Isopropyl Alcohol Intoxication: A Case Report

Metabolic Acidosis in a Patient With Isopropyl Alcohol Intoxication: A Case Report Xiaomei Meng, MD, PhD; Suman Paul, MBBS, PhD; Douglas J. Federman, MD From University of Toledo Medical Center, Toledo, Ohio; and University of Toledo College of Medicine, Toledo, Ohio. From University of Toledo Medical Center, Toledo, Ohio; and University of Toledo College of Medicine, Toledo, Ohio. From University of Toledo Medical Center, Toledo, Ohio; and University of Toledo College of Medicine, Toledo, Ohio. Author, Article, and Disclosure Information From University of Toledo Medical Center, Toledo, Ohio; and University of Toledo College of Medicine, Toledo, Ohio. Disclosures: Authors have disclosed no conflicts of interest. Forms can be viewed at www.acponline.org/authors/icmje/ConflictOfInterest Forms.do?msNum=L14-0336 . Background: An elevated plasma osmolal gap is common in all forms of alcohol intoxication. Methyl alcohol and ethylene glycol are metabolized to compounds that produce metabolic acidosis. Isopropyl alcohol, however, is metabolized to acetone, which does not cause metabolic acidosis and cannot be metabolized to compounds that do ( 1 ). Therefore, the presence of metabolic acidosis is used to rule out isopropyl alcohol intoxication. This distinction is important because fomepizole is used to treat methyl alcohol and ethylene glycol intoxication but is contraindicated in isopropyl alcohol intoxication because it reduces the clearance of isopropyl alcohol and thus prolongs its effects ( 2 ). Continue reading >>

Evaluation Of Delirium

Evaluation Of Delirium

Delirium is an acute, fluctuating change in mental status, with inattention, disorganized thinking, and altered levels of consciousness. [1] Inouye SK, Schlesinger MJ, Lydon TJ. Delirium: a symptom of how hospital care is failing older persons and a window to improve quality of hospital care. Am J Med. 1999;106:565-573. It is a potentially life-threatening disorder characterized by high morbidity and mortality. Guidelines address recognition, risk factors, and treatment for delirium. [2] Barr J, Fraser GL, Puntillo K, et al; American College of Critical Care Medicine. Clinical practice guidelines for the management of pain, agitation, and delirium in adult patients in the intensive care unit. Crit Care Med. 2013;41:263-306. [3] Neto AS, Nassar AP Jr, Cardoso SO, et al. Delirium screening in critically ill patients: a systematic review and meta-analysis. Crit Care Med. 2012;40:1946-1951. Mortality for those diagnosed with delirium in the hospital is twice that of patients with similar medical conditions without delirium and rises as high as 14% within 1 month of diagnosis. [4] Cole MG, Primeau FJ. Prognosis of delirium in elderly hospital patients. CMAJ. 1993;149:41-46. Delirium occurs in >20% of hospitalizations annually and is the most common hospital-related complication in the US. [5] US Department of Health and Human Services. 2004 CMS Statistics. Washington, DC: Centers for Medicare and Medicaid Services, 2004:34. (CMS Publication No 03445) Delirium is common in the intensive care unit especially among mechanically ventilated patients. In critically ill patients it is associated with an increased length of stay and increased mortality. [6] Cavallazzi R, Saad M, Marik PE. Delirium in the ICU: an overview. Ann Intensive Care. 2012;2:49. Studies have demonstrated a 1 Continue reading >>

Malignant Or Benign Leukocytosis

Malignant Or Benign Leukocytosis

1Department of Pathology, Stanford University School of Medicine, Stanford, CA Leukocytosis, or elevated WBC count, is a commonly encountered laboratory finding. Distinguishing malignant from benign leukocytosis is a critical step in the care of a patient, which initiates a vastly different decision tree. Confirmation of the complete blood cell count and the WBC differential is the first step. Examination of the PB smear is essential to confirming the automated blood cell differential or affirming the manual differential performed on the PB smear. Next is separation of the leukocytosis into a myeloid versus a lymphoid process. Distinguishing a reactive lymphoid proliferation from a lymphoproliferative disorder requires examination of lymphocyte morphology for pleomorphic lymphocytes versus a monomorphic population, with the latter favoring a lymphoproliferative neoplasm. Samples suspicious for lymphoproliferative disorders can be confirmed and characterized by flow cytometry, with molecular studies initiated in select cases; precursor lymphoid neoplasms (lymphoblasts) should trigger a BM examination. Myeloid leukocytosis triggers a differential diagnosis of myeloid leukemoid reactions versus myeloid malignancies. The manual differential is key, along with correct enumeration of blasts and blast equivalents, immature granulocytes, basophils, and eosinophils and identifying dysplasia to identify myeloid malignancies. Confirmation and characterization of myeloid malignancies should be performed with a BM examination and the appropriate ancillary studies. Myeloid leukemoid reactions commonly result from infections and show activated neutrophil changes on morphology; these should prompt evaluation for infection. Other causes of reactive myeloid leukocytoses are also discuss Continue reading >>

Harwood-nuss Reading For September 2016

Harwood-nuss Reading For September 2016

Spinal Trauma, Chest, Abdomen and GU Trauma: Chapters 27-35 General principles of Trauma, Trauma Airway Management, Traumatic Shock, Wound Management, Head Injuries: Chapters 18-22 Pelvic Fractures, Hip and Femur Fractures, Knee Injuries, Ankle and Foot Injuries: Chapters 42-45 Urolithiasis, Urinary Incontinence and Retention, GU stents and catheters : Chapters 126-128 Acid-Base Disturbances, Diabetes, Mellitus, Hyperglycemic Crises, Hypoglycemia, Alcoholic Ketoacidosis, Thyroid Emergencies : Chapters 203-208 Pediatrics: Diabetic Ketoacidosis and Metabolic and Endocrine Disorders : Chapter 274-275 Urinary Tract Infections in Children : Chapter 288 Hematuria, AKI, CKD/ESRD, Renal Transplant, Scrotal Pain, Penile disorders, UTI, Prostatitis, Fournier Gangrene : Chapters 117-125 Pelvic Pain, PID, Vaginal Bleeding, Vaginitis, Bartholin Gland Cyst/Abscess, Breast Masses, Sexual Assault : Chapters 129-135 Pediatrics: Hematuria and Dysuria : Chapter 243 Pediatrics: Genitourinary Disorders : Chapter 287 General Approach to Toxicology, Toxic Alcohols, Acetaminophen, Salicylates, NSAIDs, Opioids, Complications of IVDU : Chapters 295-306 Isoniazid, Organophosphates, Carbamates : Chapters 317-318 Antidysrhythmics, Local Anesthetics, Clonidine, Beta Blockers, Calcium Channel Blockers, Digoxin : Chapters 321-325 Tricyclics, Dystonia, Lithium, MAOI, SSRIs/Serotonin Syndrome, Anticholinergics, Cocaine : Chapters 339-345 PCP, Ketamine, Amphetamines : Chapter 347-348 Must be on YNHH campus or log in through Yale VPN to access links Must be on YNHH campus or log in through Yale VPN to access links Appendicitis, Bowel Obstruction, Hernias, Inflammatory Bowel Disease, Diarrhea, Diverticular Disease, Anorectal, GI Foreign Bodies, Feeding Tubes : Chapters 108-116 Bacteremia, Sepsis, and Sept Continue reading >>

Pulmcrit- Hypertriglyceridemic Pancreatitis: Can We Defuse The Bomb?

Pulmcrit- Hypertriglyceridemic Pancreatitis: Can We Defuse The Bomb?

Medications including propofol, valproic acid, protease inhibitors, thiazides, olanzapine, mirtazapine, estrogen-containing oral contraceptives, tamoxifen, clomiphene, and isotretinoin ( Scherer 2014 ) Identifying the cause of hypertriglyceridemia generally isn't critical for management. However, any potentially causative drugs should be discontinued. Other diagnostic issues in these patients Severe hypertriglyceridemia may cause the serum to appear milky (latescent). Although this may be a useful diagnostic sign, it can also interfere with certain laboratory tests. In particular, measurements of amylase and sodium may be artificially low (pseudohyponatremia; Melnick 2016 ). In extreme cases, the lab may be unable to run multiple tests. General treatment of hypertriglyceridemic pancreatitis The basics of treating hypertriglyceridemic pancreatitis are the same as for treating any patient with pancreatitis. Resuscitation should be performed using a judicious volume of fluid and vasopressors, similar to sepsis resuscitation(rather than blindly drowning patients with massive fluid resuscitation). Intubated patients benefit from early enteral nutrition . Overall, the treatment of pancreatitis largely centers on high-quality supportive care, similar to any other critically ill patient. Patients generally receive lipid lowering medications (e.g. gemfibrozil 600 mg BID). Dietary fat restriction is also sensible. Treatments directed at lowering triglyceride levels When is specific therapy needed to lower triglyceride levels? Triglyceride levels fall naturally over time, without any specific intervention (figure below). This may reflect reduced fat intake and fluid resuscitation. When are additional therapies beneficial to accelerate the fall in triglyceride levels? This questio Continue reading >>

Emedicine - Diabetic Ketoacidosis : Article By Donald W Rucker

Emedicine - Diabetic Ketoacidosis : Article By Donald W Rucker

<scriptlanguage="JavaScript1.2" type="text/javascript" charset="ISO-8859-1"src="<scriptlanguage="JavaScript1.2" type="text/javascript" charset="ISO-8859-1"src="Author:Donald W Rucker, MD, Clinical Assistant Professor of Emergency Medicine, Department of Emergency Medicine, University of Pennsylvania DonaldWRuckeris a member of the following medical societies: American College of Emergency Physicians Editors:Erik D Schraga, MD, Consulting Staff,Permanente Medical Group, Kaiser Permanente, Santa Clara MedicalCenter; Consulting Staff, Department of Emergency Medicine,Mills-Peninsula Emergency Medical Associates; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Howard A Bessen, MD,Professor of Medicine, Department of Emergency Medicine, UCLA School ofMedicine; Program Director, Harbor-UCLA Medical Center; John D Halamka, MD, MS,Associate Professor of Medicine, Harvard Medical School, Beth IsraelDeaconess Medical Center; Chief Information Officer, CareGroupHealthcare System and Harvard Medical School; Attending Physician,Division of Emergency Medicine, Beth Israel Deaconess Medical Center; Barry E Brenner, MD, PhD, FACEP, Program Director, Department of Emergency Medicine, University Hospitals, Case Medical Center Synonyms and related keywords: DKA , diabetes , diabetes mellitus , insulin deficiency , hyperglycemia , low bicarbonate, acidosis , ketonemia , ketonuria , type 1diabetes , type 1 diabetes mellitus , insulin-dependent diabetes , IDD , insulin-dependent diabetes mellitus , IDDM , childhood diabetes ,childhood diabetes mellitus, childhood-onset diabetes, childhood-onsetdiabetes mellitus, diabetes in childhood, diabetes mellitus inchildhood, juvenile-onset diabetes , juvenile-onset diabetes mellitus, ketosis-prone diabetes , autoimmune diabe Continue reading >>

The Mechanisms And Management Strategies For Diabetic Ketoacidosis

The Mechanisms And Management Strategies For Diabetic Ketoacidosis

are discussed elsewhere, as one of the scenarios in critical care endocrinology. Rather than get bogged down in thick endocrinology (thereby duplicating content from the Endocrinology section) I offer this brief summary, aimed at answering the short ABG interpretation questions rather than the long "how'd you manage this ketoacidosis" or "critically evaluate something" questions. Ketoacidosis-asociated ABG interpretation questions include the following: Question 7.1 from the second paper of 2013 Question 26.2 from the second paper of 2013 Question 8.3 from the first paper of 2012 Question 7.1 from the first paper of 2009 Question 6.1 from the first paper of 2008 Just like in real life, the ketoacidosis in these questions if often paired with some sort of hyperglycaemic hyperosmolar state. Calculation of corrected sodium is occasionally called for. A brief summary of different ketoacidosis subvarieties follows: The Varieties of Ketoacidosis Starvation ketoacidosis Alcoholic ketoacidosis Diabetic ketoacidosis Trigger Prolonged starvation: ~3 days Starvation following a binge Inadequate insulin supplementation in the face of increased requirements. eg. sepsis Mechanism Diminished intake of carbohydrates leads to decreased insulin levels, and thus ketogenesis Ketogenesis occurs in the absence of adequate hepatic glycogen stores Diminished intake of carbohydrates leads to decreased insulin levels, and thus ketogenesis Hepatic metabolism of ethanol depletes NAD+ and increases NADH levels, favouring conversion of acetoacetate into β-hydroxybutyrate In the absence of insulin, and the presence of stress hormones and glucagin, hepatic lipid metabolism switches to ketogenesis Characteristic features mild acidosis Low ketone levels Anion gap may be normal BSL is frequently low Pat Continue reading >>

Some Thoughts On The Keto Diet

Some Thoughts On The Keto Diet

10 America has a new (old) fad diet. Have you heard of it? The keto diet (short for ketogenic) is a high-fat, adequate-protein, low-carbohydrate diet. It is essentially the Atkins diet of the 2000s, but it dates back to the 1920s, when it was used to treat children with epilepsy. The goal of a keto diet is to get at least 70 percent of your calories from fat, no more than 25 percent of calories from protein and only 5 to 10 percent from carbohydrates. For most people, that means restricting your carbohydrate intake to below 50 grams a day. If you’re a breakfast taco fan like me, two tacos will put you at your daily carbohydrate limit, and don’t even think of putting potatoes in there! Half a cup of roasted potatoes will send you over the 50-gram limit. To further put that number of carbs into perspective, the following contain about 15 grams of carbohydrates: one slice of bread, 1/3 cup of rice, one cup of milk, 15 grapes, half of a large banana and a 12-ounce Bud Light (beers with higher alcohol will most certainly contain much more than 15 grams). The impetus for such a carbohydrate restrictive diet was therapeutic in nature. The diet first started nearly 100 years ago when doctors found that when epileptic children switched to a strict all-fat diet, the brain adapted its fuel source and the children had fewer seizures. The ketogenic diet is used to this day to help treat epilepsy, but over the past year or so, millions of everyday eaters have flocked to it for its purported health weight loss benefits. The goal of this diet is to force the body to burn fat instead of carbohydrates as fuel, which produces ketones. Our body and brain then use these ketones to fuel our cells. The increase in ketones puts the body in ketosis, a natural process the body initiates to h Continue reading >>

Phosphate Homeostasis In Critical Care

Phosphate Homeostasis In Critical Care

Advanced Trainee in Intensive Care Medicine Consultant in Anaesthesia and Intensive Care Medicine To whom correspondence should be addressed. Tel: +44 1226 432022; E-mail: [email protected] Search for other works by this author on: BJA Education, Volume 16, Issue 9, 1 September 2016, Pages 305309, RL Wadsworth, S Siddiqui; Phosphate homeostasis in critical care, BJA Education, Volume 16, Issue 9, 1 September 2016, Pages 305309, Serum phosphate is under tight physiological control. Hypophosphataemia is common in hospitalized patients, particularly in the critically ill. Hypophosphataemia causes multisystem effects if left untreated. Phosphate disturbances are often multifactorial. Treatment of hyperphosphataemia secondary to rhabdomyolysis or tumour lysis syndrome should be instituted promptly. Phosphorus plays a critical role in many biological processes, including energy metabolism, cellular signalling, nucleic acid metabolism, membrane integrity, and bone mineralization. 1 Phosphate is an inorganic molecule containing four oxygen atoms and a central phosphorus atom. In its ionic form, phosphate is negatively charged, leading it to be an ideal buffer and easily combining with positively charged calcium ions to contribute to hydroxyapatite, the main mineral component of bone, where up to 85% of the body's phosphate stores exist. Phosphorus in the diet is present in inorganic and organic forms. Organic phosphorus is absorbed less freely than inorganic phosphate. Phosphate absorption is highly efficient, with 6070% of an intestinal load absorbed from a typical diet, 2 occurring mostly in the duodenum and jejunum. Intestinal absorption occurs both by non-regulated passive transport through the paracellular pathway and regulated active mechanisms 3 via type IIb sodium phos Continue reading >>

Best Case Ever 58 Euglycemic Dka

Best Case Ever 58 Euglycemic Dka

This is EM Cases Best Case Ever 58 – Euglycemic DKA with Walter Himmel, the walking encyclopedia of emergency medicine. It’s not only run of the mill DKA, starvation and alcoholic ketoacidosis that can cause a metabolic acidosis with elevated ketones. Euglycemic DKA can be caused by the newer diabetes medications sodium-glucose co-transporter 2 inhibitors like Canagliflozin; and it’s important to recognize this tricky diagnosis early and initiate treatment for DKA despite a normal serum glucose level, because DKA can lead to serious complications like renal failure, cerebral edema, ARDS, shock, and death. Podcast production, sound design and editing by Anton Helman; Written by Anton Helman, June 2017 Euglycemic DKA can occur in any diabetic and has been reported in the literature since the 1970’s, but there has recently been a rise in incidence of euglycemic DKA associated with sodium-glucose co-transporter 2 inhibitors (SGLT-2 inhibitors, or the “zins”) such as Canagliflozin, Dapagliflozin and Empagliflozin. When to suspect euglycemic DKA Any patient with Type 1 or 2 diabetes taking SGLT-2 inhibitors who presents with nausea, vomiting, SOB or malaise or is found to have a metabolic acidosis should have blood drawn for serum ketones. Triggers of euglycemic DKA are similar to the triggers for any DKA: Alcohol use, infection and reduced oral intake. Distinguishing euglycemic DKA from alcoholic DKA Alcoholic ketoacidosis may also present with nausea, vomiting, malaise, ketones and anion gap metabolic acidosis. The key differentiating factor besides the obvious history of heavy alcohol use vs a diabetic taking an SGLT-2 inhibitor, is that patients with alcoholic ketoacidosis tend to have frankly low glucose. How is treatment of euglycemic DKA different? In addit Continue reading >>

Full Bibliography

Full Bibliography

Introduction: Core Knowledge for Medical DecisionMaking Finnell SM, Carroll AE, Downs SM, the Subcommittee on Urinary Tract I. Technical ReportDiagnosis and Management of an Initial UTI in Febrile Infants and Young Children. Pediatrics. 2011 Guide to Clinical Preventive Services, 2012: Recommendations of the U.S. Preventive Services Task Force. AHRQ Publication No. 1205154, October 2012. Agency for Healthcare Research and Quality, Rockville, MD. Hajjaj FM, Salek MS, Basra MK, Finlay AY. Nonclinical influences on clinical decisionmaking: a major challenge to evidencebased practice. Journal of the Royal Society of Medicine. 2010;103:178187 Harris RP, Helfand M, Woolf SH, et al. Current methods of the US Preventive Services Task Force. A review of the process. Am J Prev Med. 2001;20(3S):2135 Kianifar H, Akhondian J, NajafiSani M, SadeghiR. Evidence Based Medicine in Pediatric Practice: Brief Review. Iranian Journal of Pediatrics. 2010;20(3) : 261268 MacKinnon RJ. Evidence based medicine methods (part 1): the basics. Paediatric anaesthesia. 2007;17:918923 MacKinnon RJ. Evidence based medicine methods (part 2): extension into the clinical area. Paediatric anaesthesia. 2007;17:10211027 Onady GM. Evidencebased medicine: applying valid evidence. Pediatr Rev. 2009;30:317322 Papier A. Decision support in dermatology and medicine: history and recent developments. Seminars in cutaneous medicine and surgery. 2012;31:153159 PerryParrish C, Dodge R. Research and statistics: validity hierarchy for study design and study type. Pediatr Rev. 2010;31:2729 Raslich MA, Onady GM. Evidencebased medicine: critical appraisal of the literature (critical appraisal tools). Pediatr Rev. 2007;28:132138 Sandhu H, Carpenter C, Freeman K, Nabors SG, Olson A. Clinical decisionmaking: Opening the black b Continue reading >>

More in ketosis