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Alcoholic Ketoacidosis Uptodate

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 >>

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 >>

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 >>

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 >>

Hyperosmolar Hyperglycemic State

Hyperosmolar Hyperglycemic State

Acute hyperglycemia, or high blood glucose, may be either the initial presentation of diabetes mellitus or a complication during the course of a known disease. Inadequate insulin replacement (e.g., noncompliance with treatment) or increased insulin demand (e.g., during times of acute illness, surgery, or stress) may lead to acute hyperglycemia. There are two distinct forms: diabetic ketoacidosis (DKA), typically seen in type 1 diabetes, and hyperosmolar hyperglycemic state (HHS), occurring primarily in type 2 diabetes. In type 1 diabetes, no insulin is available to suppress fat breakdown, and the ketones resulting from subsequent ketogenesis manifest as DKA. This is in contrast to type 2 diabetes, in which patients can still secrete small amounts of insulin to suppress DKA, instead resulting in a hyperglycemic state predominated simply by glucose. The clinical presentation of both DKA and HHS is one of polyuria, polydipsia, nausea and vomiting, volume depletion (e.g., dry oral mucosa, decreased skin turgor), and eventually mental status changes and coma. In patients with altered mental status, fingerstick glucose should always be checked in order to exclude serum glucose abnormalities. Several clinical findings pertaining only to DKA include a fruity odor to the breath, hyperventilation, and abdominal pain. HHS patients, in contrast to those with DKA, will present with more extreme volume depletion. The treatment of both DKA and HHS is primarily IV electrolyte and fluid replacement. Insulin for hyperglycemia may be given with caution and under vigilant monitoring of serum glucose. Other treatment options depend on the severity of symptoms and include bicarbonate and potassium replacement. Osmotic diuresis and hypovolemia Hypovolemia resulting from DKA can lead to acute Continue reading >>

Apo-gliclazide Mr

Apo-gliclazide Mr

NOTICE: This Consumer Medicine Information (CMI) is intended for persons living in Australia. 30 mg Tablets What is in this leaflet This leaflet answers some common questions about gliclazide. It does not contain all the available information. It does not take the place of talking to your doctor, pharmacist or diabetes educator. The information in this leaflet was last updated on the date listed on the last page. More recent information on this medicine may be available. You can also download the most up to date leaflet from www.apotex.com.au. All medicines have risks and benefits. Your doctor has weighed the risks of you using this medicine against the benefits they expect it will have for you. Pharmaceutical companies cannot give you medical advice or an individual diagnosis. Keep this leaflet with your medicine. You may want to read it again. What this medicine is used for The name of your medicine is APO-Gliclazide MR. It contains the active ingredient gliclazide. The medicine is used to control, blood glucose in patients with Type II diabetes mellitus. This type of diabetes is also known as non-insulin-dependent diabetes mellitus (NIDDM) or maturity onset diabetes. Gliclazide is used when diet and exercise are not enough to control your blood glucose. Gliclazide can be used alone, or together with other medicines for treating diabetes Ask your doctor if you have any questions about why this medicine has been prescribed for you. Your doctor may have prescribed this medicine for another reason. This medicine is available only with a doctor's prescription. How it works Gliclazide lowers high blood glucose by increasing the amount of insulin produced by your pancreas. Glucose is used by the body as fuel, and all people have glucose circulating in their blood. In diabet 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 >>

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 >>

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 >>

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 >>

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 >>

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 >>

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 >>

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 >>

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 >>

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