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Alcoholic Ketoacidosis Uptodate

Emergent Treatment Of Alcoholic Ketoacidosis

Emergent Treatment Of Alcoholic Ketoacidosis

Exenatide extended-release causes an increased incidence in thyroid C-cell tumors at clinically relevant exposures in rats compared to controls. It is unknown whether BYDUREON BCise causes thyroid C-cell tumors, including medullary thyroid carcinoma (MTC), in humans, as the human relevance of exenatide extended-release-induced rodent thyroid C-cell tumors has not been determined BYDUREON BCise is contraindicated in patients with a personal or family history of MTC or in patients with Multiple Endocrine Neoplasia syndrome type 2 (MEN 2). Counsel patients regarding the potential risk of MTC with the use of BYDUREON BCise and inform them of symptoms of thyroid tumors (eg, mass in the neck, dysphagia, dyspnea, persistent hoarseness). Routine monitoring of serum calcitonin or using thyroid ultrasound is of uncertain value for detection of MTC in patients treated with BYDUREON BCise Acute Pancreatitis including fatal and non-fatal hemorrhagic or necrotizing pancreatitis has been reported. After initiation, observe patients carefully for symptoms of pancreatitis. If suspected, discontinue promptly and do not restart if confirmed. Consider other antidiabetic therapies in patients with a history of pancreatitis Acute Kidney Injury and Impairment of Renal Function Altered renal function, including increased serum creatinine, renal impairment, worsened chronic renal failure, and acute renal failure, sometimes requiring hemodialysis and kidney transplantation have been reported. Not recommended in patients with severe renal impairment or end-stage renal disease. Use caution in patients with renal transplantation or moderate renal impairment Gastrointestinal Disease Because exenatide is commonly associated with gastrointestinal adverse reactions, not recommended in patients with sev Continue reading >>

Effects Of Chronic Alcohol Exposure On Ischemiareperfusion-induced Acute Kidney Injury In Mice: The Role Of -arrestin 2 And Glycogen Synthase Kinase 3

Effects Of Chronic Alcohol Exposure On Ischemiareperfusion-induced Acute Kidney Injury In Mice: The Role Of -arrestin 2 And Glycogen Synthase Kinase 3

Original Article | Open Effects of chronic alcohol exposure on ischemiareperfusion-induced acute kidney injury in mice: the role of -arrestin 2 and glycogen synthase kinase 3 Experimental & Molecular Medicine volume 49, page e347 (2017) Little is known about the effects of chronic alcohol intake on the outcome of acute kidney injury (AKI). Hence, we examined the effects of chronic alcohol intake on the development of renal fibrosis following AKI in an animal model of bilateral renal ischemiareperfusion (IR) injury. We first found that chronic alcohol exposure exacerbated bilateral IR-induced renal fibrosis and renal function impairment. This phenomenon was associated with increased bilateral IR-induced extracellular matrix deposition and an increased myofibroblast population as well as increased bilateral IR-induced expression of fibrosis-related genes in the kidneys. To explore the mechanisms underlying this phenomenon, we showed that chronic alcohol exposure enhanced -arrestin 2 (Arrb2) expression and Akt and glycogen synthase kinase-3 (GSK3) activation in the kidneys. Importantly, pharmacological GSK3 inhibition alleviated bilateral IR-induced renal fibrosis and renal function impairment. Furthermore, we demonstrated that Arrb2/ mice exhibited resistance to IR-induced renal fibrosis and renal function impairment following chronic alcohol exposure, and these effects were associated with attenuated GSK3 activation in the kidneys. Taken together, our results suggest that chronic alcohol exposure may potentiate AKI via -arrestin 2/Akt/GSK3-mediated signaling in the kidney. Acute kidney injury (AKI) is a major clinical problem that can result in prolonged hospitalization, chronic renal failure and death. 1 , 2 , 3 , 4 , 5 One of the leading causes of AKI is renal ischemi Continue reading >>

Management Of Gastroparesis

Management Of Gastroparesis

Michael Camilleri, MD1, Henry P. Parkman, MD2, Mehnaz A. Shafi, MD3, Thomas L. Abell, MD4 and Lauren Gerson, MD, MSc5 1Department of Gastroenterology, Mayo Clinic, Rochester, Minnesota, USA; 2Temple University, Philadelphia, Pennsylvania, USA; 3University of Texas, MD Anderson Cancer Center, Houston, Texas, USA; 4University of Mississippi, Jackson, Mississippi, USA; 5Stanford University, Palo Alto, California, USA Am J Gastroenterol2013; 108:1837; doi:10.1038/ajg.2012.373; published online 13 November 2012 Received 24 May 2012; accepted 5 October 2012 Correspondence: Michael Camilleri, Department of Gastroenterology, Mayo Clinic, 200 First Street SW, Charlton 8-110, Rochester, Minnesota 55905, USA. E-mail: [email protected] This guideline presents recommendations for the evaluation and management of patients with gastroparesis. Gastroparesis is identified in clinical practice through the recognition of the clinical symptoms and documentation of delayed gastric emptying. Symptoms from gastroparesis include nausea, vomiting, early satiety, postprandial fullness, bloating, and upper abdominal pain. Management of gastroparesis should include assessment and correction of nutritional state, relief of symptoms, improvement of gastric emptying and, in diabetics, glycemic control. Patient nutritional state should be managed by oral dietary modifications. If oral intake is not adequate, then enteral nutrition via jejunostomy tube needs to be considered. Parenteral nutrition is rarely required when hydration and nutritional state cannot be maintained. Medical treatment entails use of prokinetic and antiemetic therapies. Current approved treatment options, including metoclopramide and gastric electrical stimulation (GES, approved on a humanitarian device exemption), do no Continue reading >>

Fasting Ketosis And Alcoholic Ketoacidosis

Fasting Ketosis And Alcoholic Ketoacidosis

INTRODUCTION Ketoacidosis is the term used for metabolic acidoses associated with an accumulation of ketone bodies. The most common cause of ketoacidosis is diabetic ketoacidosis. Two other causes are fasting ketosis and alcoholic ketoacidosis. Fasting ketosis and alcoholic ketoacidosis will be reviewed here. Issues related to diabetic ketoacidosis are discussed in detail elsewhere. (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Epidemiology and pathogenesis" and "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Clinical features, evaluation, and diagnosis" and "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Treatment".) PHYSIOLOGY OF KETONE BODIES There are three major ketone bodies, with the interrelationships shown in the figure (figure 1): Acetoacetic acid is the only true ketoacid. The more dominant acid in patients with ketoacidosis is beta-hydroxybutyric acid, which results from the reduction of acetoacetic acid by NADH. Beta-hydroxybutyric acid is a hydroxyacid, not a true ketoacid. 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 >>

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 >>

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 >>

Vitreous Humor: A Short Review On Post-mortem Applications

Vitreous Humor: A Short Review On Post-mortem Applications

Received Date: September 01, 2014; Accepted Date: November 12, 2014; Published Date: November 15, 2014 Citation: Baniak N, Campos-Baniak G, Mulla A, Kalra J (2015) Vitreous Humor: A Short Review on Post-mortem Applications. J Clin Exp Pathol 5:199. doi: 10.4172/2161-0681.1000199 Copyright: 2015 Baniak N, 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. Vitreous humor has been investigated since the 1960s, with many debates occurring over the years with regard to the usefulness of its specific applications. The composition of several electrolytes in post-mortem vitreous humour has been extensively studied. Using the fluid for determining the cause of death has also become commonplace, including testing glucose levels of diabetic related deaths, as well as alcohol and drug related fatalities. The debate regarding the composition between two eyes of the same individual has been an issue in the past, but has since been resolved. Vitreous humor; Post-mortem; Thanatochemistry Analysis of chemical changes within intraocular fluid , post-mortem, was introduced by Naumann [ 1 ] and has since generated great interest in the many applications of Vitreous Humor (VH) analysis [ 2 ]. VH is a colourless, jelly-like, hydrophilic gel within the vitreous body with approximately 45 mL in quantity [ 3 ]. It is composed of a complex network of cross-linked collagen fibers and hydrophilic glycosaminoglycan hyaluronan [ 4 ], which constitutes a hydrated gel containing few cells [ 5 , 6 ]. It contains 99% water and solids in the form of macromolecular and low molecular weight constituents, such as suga 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 >>

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 >>

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 >>

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 >>

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 >>

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 >>

Ketosis Vs. Ketoacidosis: What You Should Know

Ketosis Vs. Ketoacidosis: What You Should Know

Despite the similarity in name, ketosis and ketoacidosis are two different things. Ketoacidosis refers to diabetic ketoacidosis (DKA) and is a complication of type 1 diabetes mellitus. It’s a life-threatening condition resulting from dangerously high levels of ketones and blood sugar. This combination makes your blood too acidic, which can change the normal functioning of internal organs like your liver and kidneys. It’s critical that you get prompt treatment. DKA can occur very quickly. It may develop in less than 24 hours. It mostly occurs in people with type 1 diabetes whose bodies do not produce any insulin. Several things can lead to DKA, including illness, improper diet, or not taking an adequate dose of insulin. DKA can also occur in individuals with type 2 diabetes who have little or no insulin production. Ketosis is the presence of ketones. It’s not harmful. You can be in ketosis if you’re on a low-carbohydrate diet or fasting, or if you’ve consumed too much alcohol. If you have ketosis, you have a higher than usual level of ketones in your blood or urine, but not high enough to cause acidosis. Ketones are a chemical your body produces when it burns stored fat. Some people choose a low-carb diet to help with weight loss. While there is some controversy over their safety, low-carb diets are generally fine. Talk to your doctor before beginning any extreme diet plan. DKA is the leading cause of death in people under 24 years old who have diabetes. The overall death rate for ketoacidosis is 2 to 5 percent. People under the age of 30 make up 36 percent of DKA cases. Twenty-seven percent of people with DKA are between the ages of 30 and 50, 23 percent are between the ages of 51 and 70, and 14 percent are over the age of 70. Ketosis may cause bad breath. Ket Continue reading >>

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