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Alcoholic Ketoacidosis Uptodate

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis Damian Baalmann, 2nd year EM resident A 45-year-old male presents to your emergency department with abdominal pain. He is conscious, lucid and as the nurses are hooking up the monitors, he explains to you that he began experiencing abdominal pain, nausea, vomiting about 2 days ago. Exam reveals a poorly groomed male with dry mucous membranes, diffusely tender abdomen with voluntary guarding. He is tachycardic, tachypneic but normotensive. A quick review of the chart reveals a prolonged history of alcohol abuse and after some questioning, the patient admits to a recent binge. Pertinent labs reveal slightly elevated anion-gap metabolic acidosis, normal glucose, ethanol level of 0, normal lipase and no ketones in the urine. What are your next steps in management? Alcoholic Ketoacidosis (AKA): What is it? Ketones are a form of energy made by the liver by free fatty acids released by adipose tissues. Normally, ketones are in small quantity (<0.1 mmol/L), but sometimes the body is forced to increase its production of these ketones. Ketones are strong acids and when they accumulate in large numbers, their presence leads to an acidosis. In alcoholics, a combination or reduced nutrient intake, hepatic oxidation of ethanol, and dehydration can lead to ketoacidosis. Alcoholics tend to rely on ethanol for their nutrient intake and when the liver metabolizes ethanol it generates NADH. This NADH further promotes ketone formation in the liver. Furthermore, ethanol promotes diuresis which leads to dehydration and subsequently impairs ketone excretion in the urine. Alcoholic Ketoacidosis: How do I recognize it? Typical history involves a chronic alcohol abuser who went on a recent binge that was terminated by severe nausea, vomiting, and abdominal pain. These folk 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 >>

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 >>

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 >>

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 >>

Alcoholic Ketoacidosis - Medicine Bibliographies - In Harvard Style

Alcoholic Ketoacidosis - Medicine Bibliographies - In Harvard Style

Not logged in. Log in or create an account These are the sources and citations used to research Alcoholic Ketoacidosis. This bibliography was generated on Cite This For Me on Ngatchu, T., Sangwaiya, A., Dabiri, A., Dhar, A., McNeil, I. and Arnold, J. D. Alcoholic ketoacidosis with multiple complications: a case report Your Bibliography: Ngatchu, T., Sangwaiya, A., Dabiri, A., Dhar, A., McNeil, I. and Arnold, J. (2007). Alcoholic ketoacidosis with multiple complications: a case report. Emergency Medicine Journal, 24(11), pp.776-777. Your Bibliography: Carpenter, C. (2013). Alcoholic Ketoacidosis. In: J. Adams, ed., Emergency Medicine, 2nd ed. [online] Saunders. Available at: [Accessed 22 May 2016]. Fasting ketosis and alcoholic ketoacidosis Your Bibliography: Mehta, A. and Emmett, M. (2016). Fasting ketosis and alcoholic ketoacidosis. [online] UpToDate. Available at: [Accessed 22 May 2016]. 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 >>

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 >>

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 >>

My Wired Lyme Story - Lymenet Europe

My Wired Lyme Story - Lymenet Europe

Here you can introduce yourself and give an account of your medical history, visits to physicians, results of treatments, etc. MY CURRENT STATE DESCRIBED THE BEST I COULD: I have never felt so horrible in my entire life, there is nothing like it, the symptoms are like an objective thing but really feel like a part of me and agonazing most of the time. I don't feel like the same person, is difficult to even put the feelings or sypthoms into words almost like I would try to describe an emotion, feeling totaly out of it, headeach, brain pressure, dizzy, drunk like or drugged (this one is the worst), sound sensitive, light sensitive, brain fog, memory problems, lack of vitality and energy, food feels like alcoohol and sleeping pills, complete stress and anxiety that can trend to overweling pannic and sinking feelings, it feels like like half of my brain is totally missing, not even human conscience should feel like it should. Detached, unreal, sereal, with a symphony of ringging and woosing in my ears, emotions on total roller coster from the darkest depression to sinking, mood swings. Hours long, anxiety attacks to anger and rage, things look different, is hard to say what is off, depth, color, dimention, brigthness. Static over everything, sometimes feeling like I will lose my mind.I believe that at this point I am half insane and I have suicidal tendencies. I was diagnosed with chronic lyme and bartenella based on IIF and DFM test, by Dr. Bela P. Bozsik, a well know lyme specialist from Hungary and I will start treatment soon. I want to share my story for other to read because is an insane story and also ask any help and adices. Before I started to feel ill I was a person full of life, I was going to gym 4-5 times a week and tried to have a healthy diet, I owed a I.T. s 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 >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

Alcoholic ketoacidosis is a metabolic complication of alcohol use and starvation characterized by hyperketonemia and anion gap metabolic acidosis without significant hyperglycemia. Alcoholic ketoacidosis causes nausea, vomiting, and abdominal pain. Diagnosis is by history and findings of ketoacidosis without hyperglycemia. Treatment is IV saline solution and dextrose infusion. Alcoholic ketoacidosis is attributed to the combined effects of alcohol and starvation on glucose metabolism. Alcohol diminishes hepatic gluconeogenesis and leads to decreased insulin secretion, increased lipolysis, impaired fatty acid oxidation, and subsequent ketogenesis, causing an elevated anion gap metabolic acidosis. Counter-regulatory hormones are increased and may further inhibit insulin secretion. Plasma glucose levels are usually low or normal, but mild hyperglycemia sometimes occurs. Diagnosis requires a high index of suspicion; similar symptoms in an alcoholic patient may result from acute pancreatitis, methanol or ethylene glycol poisoning, or diabetic ketoacidosis (DKA). In patients suspected of having alcoholic ketoacidosis, serum electrolytes (including magnesium), BUN and creatinine, glucose, ketones, amylase, lipase, and plasma osmolality should be measured. Urine should be tested for ketones. Patients who appear significantly ill and those with positive ketones should have arterial blood gas and serum lactate measurement. The absence of hyperglycemia makes DKA improbable. Those with mild hyperglycemia may have underlying diabetes mellitus, which may be recognized by elevated levels of glycosylated Hb (HbA1c). Typical laboratory findings include a high anion gap metabolic acidosis, ketonemia, and low levels of potassium, magnesium, and phosphorus. Detection of acidosis may be com 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 >>

Diabetic Ketoacidosis Uptodate - New Videos

Diabetic Ketoacidosis Uptodate - New Videos

Channel: MedCram - Medical Lectures Explained CLEARLY & Total View: 156999 Add Date: January 13, 2013, 2:05 pm & Duration: 00:11:34 Understand the treatment of diabetic ketoacidosis (DKA) with this clear explanation from Dr. Seheult of This is video 2 of 2 on diabetic ketoacidosis (DKA). Board Certified in Internal Medicine, Pulmonary Disease, Critical Care, and Sleep Medicine. MedCram: Medical topics explained clearly including: Asthma, COPD, Acute Renal Failure, Mechanical Ventilation, Oxygen Hemoglobin Dissociation Curve, Hypertension, Shock, Diabetic Ketoacidosis (DKA), Medical Acid Base, VQ Mismatch, Hyponatremia, Liver Function Tests, Pulmonary Function Tests (PFTs), Adrenal Gland, Pneumonia Treatment, any many others. New topics are often added weekly- please subscribe to help support MedCram and become notified when new videos have been uploaded. Subscribe: Recommended Audience: Health care professionals and medical students: including physicians, nurse practitioners, physician assistants, nurses, respiratory therapists, EMT and paramedics, and many others. Review for USMLE, MCAT, PANCE, NCLEX, NAPLEX, NDBE, RN, RT, MD, DO, PA, NP school and board examinations. Channel: Diabetic diet chart & Total View: 15 Add Date: November 21, 2016, 10:58 pm & Duration: 00:03:19 best medicine for diabetes , type 1 diabetes treatments , type 2 diabetes treatments , prediabetes treatments , diabetes treatment at home , diabetes cure found , prevention for diabetes , permanent cure for diabetes , can diabetes be cured without medicine , diabetes cure naturally , is diabetes curable at early stage , can diabetes be cured naturally , new diabetes treatment , is there a cure for diabetes type 2 , is there a cure for diabetes type 1 , diabetes treatment naturally Get here @ - The wo 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 >>

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