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Alcoholic Ketoacidosis Uptodate

How Does Chronic Alcohol Use Affect Electrolyte Imbalance?

How Does Chronic Alcohol Use Affect Electrolyte Imbalance?

A review discusses the association between chronic alcohol use and electrolyte imbalance, and the therapies that could be adopted to address these issues. Chronic alcohol use, or alcoholism, affects roughly 4% of Canadians1 and roughly 12.5% of Americans.2 Alcohol consumption is known to increase the risk of several types of cancer, diabetes, cardiovascular disease, and liver disease in a dose-dependent manner.3Additionally, chronic alcohol use is associated with acid-base and electrolyte imbalance. A recent review published in The New England Journal of Medicine discusses these disorders, as well as the therapeutic approaches that can be adopted to treat these disorders.4 A variety of acid-base disturbances are observed in roughly 78% of the patients with chronic alcohol use. One of these is alcoholic ketoacidosis, which manifests as abdominal pain and vomiting. These symptoms are caused by gastritis and pancreatitis that follow chronic alcohol use. Clinically, alcoholic ketoacidosis is characterized by high ketone levels in the blood, a high anion gap (or an increased concentration of anions), and normal to slightly elevated glucose levels. Alcoholic ketoacidosis is a consequence of ethanol metabolism and prolonged starvation with the depletion of glycogen stores in the liver. The authors recommend that initial treatment in such patients should involve terminating the ketogenic process by intravenous administration of dextrose. Additionally, they recommend administering thiamine but not insulin or bicarbonate. Acute hypophosphatemia, or phosphorus deficiency, is seen in up to 50% of patients over the first 2-3 days after they are hospitalized for alcohol overuse. Hypophosphatemia is manifested as rhabdomyolysis (muscle breakdown) and weakness of the skeletal muscles. 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 >>

Pyramidal Tetraparesis & Fasting Ketosis: Causes & Diagnoses | Symptoma.com

Pyramidal Tetraparesis & Fasting Ketosis: Causes & Diagnoses | Symptoma.com

Patients typically present after age 40 years with a variable combination of cognitive impairment, pyramidal tetraparesis, peripheral neuropathy, and neurogenic bladder. [humpath.com] tetraparesis, sensory neuropathy in the lowerextremities, neurogenic bladder, and occasionally cognitiveimpairment. [medigoo.com] They presented clinically with late onset pyramidal tetraparesis, micturition difficulties, peripheral neuropathy, and mild cognitive impairment. [eurekamag.com] tetraparesis cognitive impairment white matter abnormalities (MRI) polyglucosan bodies (round intracellular inclusions) found in neuronal and astrocytic processes peripheral [humpath.com] Symptoms: The disorder is characterized bya gradual progression of involvement of both the central andperipheral nervous systems with a variable phenotype that oftenincludes pyramidal [medigoo.com] Glycogen Storage Disease due to Liver Phosphorylase Kinase Deficiency , or lactic acidosis; episodes provoked by fasting, febrile infection, or ingestion of fructose, sorbitol, or glycerol Treatment: Avoidance of fasting and fructose, sorbitol [merckmanuals.com] [] cornstarch, which prevents ketosis. [clinicaladvisor.com] Ketosis after relatively short fasts is a feature. [tp.amegroups.com] Frequency: Rare Onset: Early childhood Clinical features: Benign course with symptoms lessening with aging; growth retardation, hepatomegaly, hypoglycemia, hyperlipidemia, ketosis [merckmanuals.com] Uncooked (raw) cornstarch (1-1.5 grams per kg) administered at bedtime prevents morning hypoglycemia and ketosis. [clinicaladvisor.com] Some medical professionals confuse ketoacidosis , an extremely abnormal form of ketosis, with the normal benign ketosis associated with ketogenic diets and fasting states [ketogenic-diet-resource.com] See als Continue reading >>

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The main types of fats usually measured in the blood are: Triglycerides are a kind of fat normally found in the blood and one of the sources of energy usable by the cells, these come from fat absorption in foods. We could say that triglycerides are the bodys way to store energy. When an excess of calories is ingested, triglycerides deposits and its blood levels increase. To avoid these levels from increasing, fat, sugar, and alcohol ingestion should be reduced, in addition to maintaining a healthy weight. This is a type of fat that is present in almost every organ. It is involved in the production of hormones, vitamin D, cell membranes, and substances needed for fat absorption (salts and bile acids). Elevated cholesterol levels are directly related to the development of cardiovascular diseases, which is why they should be kept within proper limits. In order to achieve this, one should keep a healthy weight, do physical activity, and reduce the consumption of foods which are high in fat and cholesterol (pork, chicken skin, organ meats, fried foods, eggs, whole milk, butter, etc.). These are a type of fat found in the cell membranes. Their levels hardly ever vary with diet. Lipoproteins are a combination of lipids with proteins; this is the way in which lipids are transported in the bloodstream. There are several types of lipoproteins depending on the type and amount of fat. These carry triglycerides from the intestine and liver to the muscles and adipose tissue (stored fat) to be either used as energy or be accumulated, depending on what the body needs. These lipoproteins contain more triglycerides and less cholesterol. LDL carry cholesterol from the liver to other tissues and organs. They contain more cholesterol and less proteins and triglycerides. Because these deliv Continue reading >>

Ketoacidosis

Ketoacidosis

GENERAL ketoacidosis is a high anion gap metabolic acidosis due to an excessive blood concentration of ketone bodies (keto-anions). ketone bodies (acetoacetate, beta-hydroxybutyrate, acetone) are released into the blood from the liver when hepatic lipid metabolism has changed to a state of increased ketogenesis. a relative or absolute insulin deficiency is present in all cases. CAUSES The three major types of ketosis are: (i) Starvation ketosis (ii) Alcoholic ketoacidosis (iii) Diabetic ketoacidosis STARVATION KETOSIS when hepatic glycogen stores are exhausted (eg after 12-24 hours of total fasting), the liver produces ketones to provide an energy substrate for peripheral tissues. ketoacidosis can appear after an overnight fast but it typically requires 3 to 14 days of starvation to reach maximal severity. typical keto-anion levels are only 1 to 2 mmol/l and this will usually not alter the anion gap. the acidosis even with quite prolonged fasting is only ever of mild to moderate severity with keto-anion levels up to a maximum of 3 to 5 mmol/l and plasma pH down to 7.3. ketone bodies also stimulate some insulin release from the islets. patients are usually not diabetic. ALCOHOLIC KETOSIS Presentation a chronic alcoholic who has a binge, then stops drinking and has little or no oral food intake for a few days (ethanol and fasting) volume depletion is common and this can result in increased levels of counter regulatory hormones (eg glucagon) levels of free fatty acids (FFA) can be high (eg up to 3.5mM) providing plenty of substrate for the altered hepatic lipid metabolism to produce plenty of ketoanions GI symptoms are common (eg nausea, vomiting, abdominal pain, haematemesis, melaena) acidaemia may be severe (eg pH down to 7.0) plasma glucose may be depressed or normal or Continue reading >>

Ketone Body @ :: Xuite

Ketone Body @ :: Xuite

False-negative nitroprusside testingFalse-negative results can occur by the following mechanism. Nitroprusside reacts with acetoacetateand, to a lesser degree, acetone (which is not an acid)butnot with beta-hydroxybutyrate. This is an important limitation since alcohol metabolism causes a redox shift toward NADH which drives the reaction toward beta-hydroxybutyrate. As a result, the ratio of beta-hydroxybutyrate to acetoacetate, which is normally 1:1 and increases to 3:1 in diabetic ketoacidosis, may increase to 10:1 in alcoholic ketoacidosis [ 27 ]. Thus, in most patients with alcoholic ketoacidosis, nitroprusside testsunderestimatethe degree of ketone bodies in plasma, and some patients may have negative tests [ 7,9 ]. It has been suggested that the sensitivity of the urine nitroprusside test can be improved by adding a few drops of hydrogen peroxide to a urine specimen in an attempt to nonenzymatically convert beta-hydroxybutyrate into acetoacetate. However, several studies have shown that this approach isnotclinically useful [ 33,34 ]. Continue reading >>

Metformin And Lacticacidosis

Metformin And Lacticacidosis

The major toxic effect of metformin is lactic acidosis. It causes glucose to be converted to lactate in the small intestines, and decreases gluconeogenesis from lactate and pyruvate and alanine- increasing LA and substrates that can get converted to LA. its RARE: Only 5.1 cases per 100,000 patient yrs of lactic acidosis in non-comorbitiy (renal or liver disease) patients. However in patients that do develop LA, there is a mortality of 45%. These deaths were speculated to be related to comorbid conditions, rather than the levels of metformin in their blood. Most accurate predictor was liver function. Lactic acidosis likely to occur in patients with renal insufficiency (Cr above 1.4/1.5), liver or ETOH disease, HF, history of prior LA, hypoxic states, hemodynamic instability. consider bicarb if pH < 7.1, otherwise may cause electrolyte abnormalities. Patients with severe renal insufficiency or are simply very sick require emergent HD. References: Risk of fatal and nonfatal lactic acidosis with metformin use in type 2 diabetes mellitus. Salpeter S, Greyber E, Pasternak G, Salpeter E, Cochrane Database Syst Rev. 2006; uptodate.com: metformin poisoning; Metformin. AU Bailey CJ, Turner RC SO, N Engl J Med. 1996;334(9):574. picture 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 >>

Em Didactic: Alcohol Related Ketoacidosis (aka)

Em Didactic: Alcohol Related Ketoacidosis (aka)

This blog intends to create an educational platform for Emergency Physicians, sharing EM related basics and updates. Every week, I come up with a new post which can be in the form of written material with references/other FOAMed resources OR a 15-20 minute podcast with a written summary. My goal with this blog is to improve Resident education, Academic EM and Flipping the classroom. To get the maximum benefit from this blog, subscribe by your e-mail. Alcoholic ketoacidosis is often associated with acute cessation of alcohol consumption afterlong termconsumption. Few cases have been described in binge drinkers as well. It shows up asahigh anion gap metabolic acidosis (HAGMA)on blood gas and is typically associated with nausea, vomiting,and GI complaints.Metabolism ofalcoholcombined with poor glycogen reserves results in elevated ketoacid levels.Death can occur from excessive ketonemia and thus treatment is focused on fluid andelectrolytes management.HB is the pre-dominant ketone product formed in AKA. Classically presents with history of heavy drinking followed by vomitingand an acute decrease in alcohol consumption. Common symptoms are nausea, vomiting, and nonspecific abdominal pain. AKA can presentwith concomitantgastritis or pancreatitis, hypoglycemia, alcohol-withdrawal seizures, GI Bleed, Hepatitis, Sepsis or unrecognized head injury. Diagnosis (AKA is adiagnosis of exclusion) Low, normal, or slightly elevated serum glucose Binge drinking ending in nausea, vomiting, and decreased intake Wide anion gap metabolic acidosis without alternate explanation Normally, the ratio of Beta HB (beta hydroxybutyric acid) toacetoacetate to1:1 but in alcoholic ketoacidosis, the ratio can goup to 7:1.Ketone production can be further stimulated in malnourished, vomiting patients.The Continue reading >>

Postmortem Diagnosis Of Diabetes Mellitus And Its Complications

Postmortem Diagnosis Of Diabetes Mellitus And Its Complications

Diabetes mellitus has become a major cause of death worldwide and diabetic ketoacidosis is the most common cause of death in children and adolescents with type 1 diabetes. Acute complications of diabetes mellitus as causes of death may be difficult to diagnose due to missing characteristic macroscopic and microscopic findings. Biochemical analyses, including vitreous glucose, blood (or alternative specimen) beta-hydroxybutyrate, and blood glycated hemoglobin determination, may complement postmortem investigations and provide useful information for determining the cause of death even in corpses with advanced decompositional changes. In this article, we performed a review of the literature pertaining to the diagnostic performance of classical and novel biochemical parameters that may be used in the forensic casework to identify disorders in glucose metabolism. We also present a review focusing on the usefulness of traditional and alternative specimens that can be sampled and subsequently analyzed to diagnose acute complications of diabetes mellitus as causes of death. The snippet could not be located in the article text. This may be because the snippet appears in a figure legend, contains special characters or spans different sections of the article. Postmortem diagnosis of diabetes mellitus and its complications. CURML, Centre Universitaire Romand De Medecine Legale, Lausanne University Hospital, Lausanne, Switzerland CURML, Centre Universitaire Romand De Medecine Legale Received 2015 March 2; Accepted 2015 May 11. Copyright 2015 by the Croatian Medical Journal. All rights reserved. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provid 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 >>

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 >>

Compendium

Compendium

Acute MI 2 out of 3 criteria130 minutes retrosternal pain - must R/O MI, PE, Aortic dissection2Cardiac enzymes elevated3ECG changes Unstable Angina -Chest pain at rest - cardiac ischemia w/o ECG changes MI Causes See also: Abdominal pain DdxPathophysiology Premature activation of pancreatic enzymes causing autodigestion of the pancreas. Release of lipolytic enzymes from the pancreas causes significant inflammation o Source: Academic Life in Emergency Medicine Gaze-Evoked NystagmusFrom: the patient to gaze at a target placed 20 to 30 degrees to the left and right of center for Diagnostic action Abolishes conduction through the AV node E.g. PSVT Terminates some re-entrant type tachycardiasDose 3-12 mg rapid IV push Age-appropriate Pediatric Fever Without a Source workup See also: Pediatric fever Ddx Terms:Fever without a source FWS: No adequate explanation for fever after H&P.Fever of unknown origin FUO: No adequate explanation for fever lasting at least 8 days' duration, af Sx Poor nutritionLabs Low thiamine levels due to poor nutrition Low glucose due to suppression of gluconeogenesis by alcohol (give thiamine first to prevent precipitating Wernicke's encep A BDZ, the #1 prescribed mental health drugMechanism Binds GABA-alpha receptors Enhances the affinity of GABA for the receptor, allows increased opening of the GABA-alpha channelIndications See also: COPD ExacerbationEpidemiology More common in male children than female children More common in female adults than male adults Higher prevalence in African-Americans thanTriggers Ddx Coarctation BP in arm(s) greater than legs BP in R arm greater than L arm Subclavian artery atherosclerosis & What&rsquos your name? What happened?100% O2 non-rebreather, pulse ox, cardiac monitor, BP, two Continue reading >>

Alcoholic Ketoacidosis | Receiving.

Alcoholic Ketoacidosis | Receiving.

Medications: None (the patient does state she is supposed to be on both levothyroxine and coumadin). Social history: Significant for both tobacco and heavy alcohol abuse. No intravenous drug abuse. Vitals: BP 119/84, HR 126, RR 38, T 35.4, SaO2 99% (room air) General: Well developed African American female in respiratory distress. HEENT: Normocephalic, atraumatic. No conjunctival pallor. No scleral icterus. Dry mucous membranes. No pharyngeal erythema. The patients breath has a fruity odor. Cardiovascular: Tachycardic, regular rhythm. No murmurs. No jugular venous distention, no edema. Respiratory: Tachypnic. Lungs clear to auscultation bilaterally, no wheezes or crackles. No accessory muscle use, no retractions. Gastrointestinal: Abdomen soft, slightly tender to palpation in the epigastric area, and non-distended. No rebound tenderness, no guarding. Bowel sounds present. Neurologic: Alert and oriented x 3. Strength equal in all four extremities. Basic metabolic panel: Na 137, K 4, Cl 98, HCO3 5, BUN 13, Cr 1.06, glucose 122 Complete blood count: WBC 15.7, Hb 14.2, Hct 43.5, platelets 338 Coagulation studies: PT 10.9, PTT 29.2, INR 1.03 Arterial blood gas: pH 6.879, pCO2 22.1, pO2 95, HCO3 4 Beta-hydroxybutyrate 77.5 (normal 0.2 2.8) Liver function tests: amylase 97, lipase 888, total bilirubin 0.4, direct bilirubin 0.1, ALT 21, AST 68, alkaline phosphatase 98, albumin 2.9 Urinalysis: 2+ ketones, 2+ protein, specific gravity 1.010, otherwise unremarkable 1. The patients acid base status is best described as which of the following? A) anion gap metabolic acidosis (with complete respiratory compensation) B) non-anion gap metabolic acidosis (with complete respiratory compensation) C) anion gap metabolic acidosis (with incomplete respiratory compensation) D) non-anion gap Continue reading >>

Er Goldbook: Alcoholic Ketoacidosis

Er Goldbook: Alcoholic Ketoacidosis

ethanol metabolism nicotinamide adenine dinucleotide (NAD) alcohol dehydrogenase enzyme ethanol acetaldehyde, acetate acetyl coenzyme A acetyl coenzyme A Krebs cycle free fatty acid NAD ethanol metabolism aerobic metabolism Krebs cycle glycogen stores lipolysis ketone formation NAD ketone -hydroxybutyrate (HB) acetoacetic acid (AcAc) > 7 ( AcAc + NADH <-> HB + NAD) high NADH:NAD ratio lactate production ( shock sepsis) AcAc metabolites acetone osmolol gap ketone AKA malnourished, vomiting, hypophosphatemia gastritis pancreatitis Altered consciousness toxic, hypoglycemia, alcoholic-withdrawal seizure, postictal state,head injury serum glucose Wide AG metabolic acidosis () Positive serum ketone ( nitroprusside test AcAc) Ix: CBC, electrolytes, Ca,Mg, PO2, LFTs, lipase, ketones, lactate, serum osmolality; ethanol,methanol, isopropyl alcohol level AG 16-33 wide AG AG > 20 Osmolol gap (< 20 mmol/kg) acetone ethanol level ethanol 100 mg/dL ethanol osmolol gap 22 ( large osmolol gap MEDIE methanol,ethylene glycol, isopropyl alcohol) Ketone alcohol methanol ethylene glycol ketone; isopropylalcohol ketone; starvation ketosis fasting > 3 stress dehydration ketonuria ketonemia metabolicacidosis 5%D/NSS IV rehydration 5%D/N/2 IV MT glucose IVF insulin lipolysis NADH NAD ketone Thiamine 100 mg IV, folate 1 mg IV () Continue reading >>

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