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Alcoholic Ketoacidosis Lab Results

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

Go to: CHARACTERISATION In 1940, Dillon et al1 described a series of nine patients who had episodes of severe ketoacidosis in the absence of diabetes mellitus, all of whom had evidence of prolonged excessive alcohol consumption. It was not until 1970 that Jenkins et al2 described a further three non‐diabetic patients with a history of chronic heavy alcohol misuse and recurrent episodes of ketoacidosis. This group also proposed a possible underlying mechanism for this metabolic disturbance, naming it alcoholic ketoacidosis. Further case series by Levy et al, Cooperman et al, and Fulop et al were subsequently reported, with remarkably consistent features.3,4,5 All patients presented with a history of prolonged heavy alcohol misuse, preceding a bout of particularly excessive intake, which had been terminated several days earlier by nausea, severe vomiting, and abdominal pain. Clinical signs included tachypnoea, tachycardia, and hypotension. In 1974, Cooperman's series of seven ketoacidotic alcoholic patients all displayed diffuse epigastric tenderness on palpation.4 In contrast to patients with diabetic ketoacidosis, the patients were usually alert and lucid despite the severity of the acidosis and marked ketonaemia. When altered mental status occurred, this was clearly attributable to other causes. Laboratory results included absent blood alcohol with normal or low blood glucose level, no glycosuria, and a variably severe metabolic acidosis with a raised anion gap. This acidosis appeared to result from the accumulation in plasma of lactate and ketone bodies including beta‐hydroxybutyrate (BOHB) and acetoacetate (AcAc).3 Cooperman et al found that near patient testing for ketone bodies using nitroprusside test (Acetest, Ketostix) produced a low to moderate result in th Continue reading >>

A Primer On Arterial Blood Gas Analysis By Andrew M. Luks, Md(cont.)

A Primer On Arterial Blood Gas Analysis By Andrew M. Luks, Md(cont.)

Step 4: Identify the compensatory process (if one is present) In general, the primary process is followed by a compensatory process, as the body attempts to bring the pH back towards the normal range. If the patient has a primary respiratory acidosis (high PCO2 ) leading to acidemia: the compensatory process is a metabolic alkalosis (rise in the serum bicarbonate). If the patient has a primary respiratory alkalosis (low PCO2 ) leading to alkalemia: the compensatory process is a metabolic acidosis (decrease in the serum bicarbonate) If the patient has a primary metabolic acidosis (low bicarbonate) leading acidemia, the compensatory process is a respiratory alkalosis (low PCO2 ). If the patient has a primary metabolic alkalosis (high bicarbonate) leading to alkalemia, the compensatory process is a respiratory acidosis (high PCO2 ) The compensatory processes are summarized in Figure 2. (opens in a new window) Important Points Regarding Compensatory Processes There are several important points to be aware of regarding these compensatory processes: The body never overcompensates for the primary process. For example, if the patient develops acidemia due to a respiratory acidosis and then subsequently develops a compensatory metabolic alkalosis (a good example of this is the COPD patient with chronic carbon dioxide retention), the pH will move back towards the normal value of 7.4 but will not go to the alkalemic side of normal This might result in a pH of 7.36, for example but should not result in a pH such as 7.44 or another value on the alkalemic side of normal. If the pH appears to "over-compensate" then an additional process is at work and you will have to try and identify it. This can happen with mixed acid-base disorders, which are described further below. The pace of co Continue reading >>

The Ed Arterial Blood Gas (abg) Emergencypedia

The Ed Arterial Blood Gas (abg) Emergencypedia

Blood Gas Worksheet (Checklist) Download PDF You are a new staff member working in the Emergency Department (ED) During yourinduction you are introduced to the practical workings of the Point of Care Arterial Blood Gas (ABG) Machine in the ED: As you struggle to listen to the machine company representative talking about cleaning the machine youthink about lunch and briefly recall that you fell asleep in all those boringbasic science lectures Whatbasic science do you need to know to understand ABGs? pH is a measure of hydrogen ion concentration. In other words, a measure of the acidity or alkalinity of a solution. Aqueous solutions at room temperature with a pH less than 7.0 are acidic, while those with a pH greater than 7.0 are alkaline (basic). The Normal Physiological pH is around 7.4. (1) Carbon Dioxide (CO2) 15000 mmol/day Generates carbonic acidin combinationwith water Sulphuric acid derived from the metabolism amino acids The Anion Gap is the Gap between the MEASURED(not the total) Positive and NegativeIons The strong ions in the Body are Sodium (Na+) and Chloride (Cl-) and the Normal gap between these should be about 38mmol/L. (e.g. Na 140 Cl 102 = 38) Practically speaking if the Chloride goes up the Strong Ion Difference goes down and the body must compensate for the extra Anion (negatively charged chloride) with a positively charged ion. The freely available pool in the body of +ve charges is Protons (H+)! Therefore, when the chloride goes up we often see a Normal Anion Gap Metabolic Acidosis the clinical significance of this may be limited outside the ICU setting, but its worth thinking about this when prescribing Fluids (e.g. Normal Saline, Hartmanns andPlasmalyte). Why Take a Blood Gas in the Emergency Department? Helps guide management of sepsis, respirato Continue reading >>

Evaluation Of Delirium

Evaluation Of Delirium

Diagnostic Tests Common Differential 1st Tests Other Tests Dementia the diagnosis of dementia is based predominantly on historical factors: diagnosis is clinical Pain diagnosis is clinical: causes of underlying pain should be sought (e.g., hip fracture) Stroke/cerebrovascular accident and transient ischemic attack neuroimaging (CT and/or MRI): ischemic CVA: hyperdense vessels at the site of blood clot in middle cerebral artery (MCA), posterior cerebral artery (PCA), or anterior cerebral artery (ACA); loss of insular stripe located between Sylvian fissure and basal ganglia is frequently associated with early MCA stroke; subtle mass effect; [78] hemorrhagic CVA: hyperdense to grey matter lesion at the site of hemorrhage; mass effect may also be evident but frequently subtle in early stroke more Findings frequently absent for transient ischemic attacks and ischemic strokes. Findings frequently absent for transient ischemic attacks and ischemic strokes. Myocardial infarction ECG: ST segment elevation or depression, or T wave changes serum troponin: elevated CXR: evidence of pulmonary congestion/ pleural effusion if secondary heart failure, may show enlarged cardiac shadow coronary angiogram: presence of thrombus with occlusion of the artery Acute systemic infection basic test panel (CBC, serum electrolytes, blood glucose, serum liver function tests, coagulation profile): elevated WBC count or leukopenia with sepsis; may be elevated urea and creatinine with sepsis; may be low platelets with sepsis; blood glucose may be elevated or, more rarely, low with sepsis; serum transaminases and serum bilirubin may be elevated with sepsis; may be prolonged or elevated INR, PT, aPTT more If shock is present, urgent simultaneous treatment required. WBC count may be normal in early stages Continue reading >>

Urine Test Types: Ph, Ketones, Proteins, And Cells

Urine Test Types: Ph, Ketones, Proteins, And Cells

Urine as a Diagnostic Tool A long time ago, disgusting as it may be, people used to actually taste and drink urine in order to try and diagnose a patient's disease! I'm not even kidding you. Thankfully, modern-day doctors do not have to resort to such disgusting and even dangerous methods. One of the reasons the doctor barbers of yesteryear used to drink their patient's urine was to see if it had a sweet taste, often indicative of diabetes mellitus. Finding the sweet-tasting glucose in the urine was covered in detail in another lesson, so we'll focus on other important measurements here instead. Interpreting Urine pH One value that can be measured in the urine is known as urine pH. pH is a measure of the acidity or alkalinity of a substance. If the pH is low, then it is acidic. If the pH is high, then it is basic, or alkaline. To remember which is which, I'll give you a little trick that has worked for me. If you grew up watching cartoons, you probably saw some comical ones where cartoonish robbers poured acid on the roof of a bank vault and waited while the acid ate its way downward into the vault, so the robbers could get down there to steal all the cash. If you can recall that acid likes to eat its way downward into things, then you'll remember that acidic substances go down the pH scale. That is to say, their pH numbers are lower than basic substances. Normal urine pH is roughly 4.6-8, with an average of 6. Urine pH can increase, meaning it will become more basic, or alkaline, due to: A urinary tract infection Kidney failure The administration of certain drugs such as sodium bicarbonate Vegetarian diets On the flip side, causes for a decreased, or acidic, urine pH, include: Metabolic or respiratory acidosis Diabetic ketoacidosis, a complication of diabetes mellitus Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a serious problem that can occur in people with diabetes if their body starts to run out of insulin. This causes harmful substances called ketones to build up in the body, which can be life-threatening if not spotted and treated quickly. DKA mainly affects people with type 1 diabetes, but can sometimes occur in people with type 2 diabetes. If you have diabetes, it's important to be aware of the risk and know what to do if DKA occurs. Symptoms of diabetic ketoacidosis Signs of DKA include: needing to pee more than usual being sick breath that smells fruity (like pear drop sweets or nail varnish) deep or fast breathing feeling very tired or sleepy passing out DKA can also cause high blood sugar (hyperglycaemia) and a high level of ketones in your blood or urine, which you can check for using home-testing kits. Symptoms usually develop over 24 hours, but can come on faster. Check your blood sugar and ketone levels Check your blood sugar level if you have symptoms of DKA. If your blood sugar is 11mmol/L or over and you have a blood or urine ketone testing kit, check your ketone level. If you do a blood ketone test: lower than 0.6mmol/L is a normal reading 0.6 to 1.5mmol/L means you're at a slightly increased risk of DKA and should test again in a couple of hours 1.6 to 2.9mmol/L means you're at an increased risk of DKA and should contact your diabetes team or GP as soon as possible 3mmol/L or over means you have a very high risk of DKA and should get medical help immediately If you do a urine ketone test, a result of more than 2+ means there's a high chance you have DKA. When to get medical help Go to your nearest accident and emergency (A&E) department straight away if you think you have DKA, especially if you have a high level of ketones in Continue reading >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

Glucose or sugar is the preferred source of fuel for the body. If the body’s cells get insufficient glucose, fat is used as the alternative source of energy. When fat is used as a source of energy, it produces ketones, which are acidic chemicals. A buildup of ketones causes the blood to become too acidic. This leads to chemical derangements called ketoacidosis. Ketoacidosis comes in two different forms - diabetic ketoacidosis and alcoholic ketoacidosis. Here is more information about alcoholic ketoacidosis. What Is Alcoholic Ketoacidosis? Alcoholic Ketoacidosis (AKA) is a condition that develops in people who drink too much alcohol. This condition results in the increase of Ketones. AKA is common in adults who have a history with alcoholism. Any person showing signs of AKA needs to seek immediate medical attention because it is a potentially fatal condition. If you consume alcoholic beverages excessively without eating a balanced diet, the acidic levels of your blood might rise, causing health complications. Drinking alcoholic beverages in moderation or drinking as you eat can help reduce the likelihood of getting AKA. When the body’s fat cells breakdown after they have been consumed, ketones are formed. Consequently, the amount of acid in the blood dramatically increases and the blood’s pH (potenz Hydrogen) balance drops. While people who drink lots of alcoholic drinks and do not eat sufficient nutrients, or a balanced diet are likely to develop AKA, they are not the only ones. Inexperienced drinkers who binge drink can also develop this condition. What Are the Symptoms of Alcoholic Ketoacidosis? AKA symptoms vary based on the amount of alcohol you consume. Symptoms also depend on the amount of ketones you have in the bloodstream. If any of the following symptoms Continue reading >>

Alcoholic Ketoacidosis And Ketosis In The Emergency Room

Alcoholic Ketoacidosis And Ketosis In The Emergency Room

Alcoholic Ketoacidosis and Ketosis in the Emergency Room Department of Emergency & Critical Care Medicine, School of Medicine, Keio University Department of Emergency & Critical Care Medicine, School of Medicine, Keio University Department of Emergency & Critical Care Medicine, School of Medicine, Keio University Department of Emergency & Critical Care Medicine, School of Medicine, Keio University Department of Emergency & Critical Care Medicine, School of Medicine, Keio University Objective: We clarified the frequency and clinical features of alcoholic ketoacidosis (AKA) and alcoholic ketosis (AK) in the emergency room of a Japanese hospital. Subjects and Methods: 1) We prospectively evaluated blood gas analysis, serum ketones, and urine ketones by dipstick among alcohol-related disorders in 940 patients at the Department of Emer-gency and Critical Care Medicine at Keio University Hospital in 3 months. 2) We retrospectively evaluated AKA among alcohol-related disorders registered in a database of 27, 952 patients at the same Department in the last 11 years: AKA was defined as metabolic acidosis with either high serum ketones or positive dipstick of urine ketones in heavy drinkers. Results: 1) Alcohol-related disorders were found in 16 patients (1.7%). AKA was diagnosed in 2 of the 16 (13%). Seven of the 16 (43%) showed both ketosis and low ratio of serum acetoacetate/-hydroxybutyrate. 2) Alcohol-related disorders were found in 210 patients (0.8%), out of whom 9 (4%) met the criteria of AKA. All AKA patients were men. The most commonly complaint was consciousness disturbance. Some 73% had hypoglycemia and 36% hypothermia. Dipstick test of urine ketones showed high false-negative results (55%) due to low ratio of serum acetoacetate/-hydroxybutyrate. Conclusion: Intensiv Continue reading >>

Alcoholic Ketoacidosis – A Case Report

Alcoholic Ketoacidosis – A Case Report

Summarized from Noor N, Basavaraju K, Sharpstone D. Alcoholic ketoacidosis: a case report and review of the literature. Oxford Medical Case Reports 2016; 3: 31-33 Three parameters generated during blood gas analysis, pH, pCO2 and bicarbonate, provide the means for assessment of patient acid-base status, which is frequently disturbed in the acutely/critically ill. Four broad classes of acid-base disturbance are recognized: metabolic acidosis, respiratory acidosis, metabolic alkalosis and respiratory alkalosis. Metabolic acidosis, which is characterized by primary reduction in pH and bicarbonate, and secondary (compensatory) decrease in pCO2, has many possible causes including the abnormal accumulation of the keto-acids, β-hydroxybutyrate and acetoacetate. This particular form of metabolic acidosis, called ketoacidosis, has three etiologies giving rise to three quite separate conditions with common biochemical features: diabetes (diabetic ketoacidosis); excessive alcohol ingestion (alcoholic ketoacidosis) and severe starvation (starvation ketoacidosis). Diabetic ketoacidosis, which is the most common of the three, is the subject of a recent review (discussed below) whilst alcoholic ketoacidosis is the focus of this recent case study report. The case concerns a 64-year-old lady who presented to the emergency department of her local hospital with acute-onset abdominal pain, nausea, vomiting and shortness of breath. Blood gas results (pH 7.10, bicarbonate 2.9 mmol/L) confirmed metabolic acidosis, and the presence of raised ketones (serum ketones 5.5 mmol/L) allowed a diagnosis of ketoacidosis. Initially, doctors caring for the patient entertained the possibility that the lady was suffering diabetic ketoacidosis, but her normal blood glucose concentration (5.8 mmol/L) and pr Continue reading >>

Emdocs.net Emergency Medicine Educationtoxcards: Alcoholic Ketoacidosis - Emdocs.net - Emergency Medicine Education

Emdocs.net Emergency Medicine Educationtoxcards: Alcoholic Ketoacidosis - Emdocs.net - Emergency Medicine Education

Author: Cynthia Santos, MD (Senior Medical Toxicology Fellow, Emory University School of Medicine) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) and Brit Long, MD (@long_brit) A 45 year old male presents intoxicated, smelling of alcohol and appears disheveled with vomit on his clothes. He is sleepy but arousable to noxious stimuli. His serum ethanol level is 143 mg/dL. Na 135, K 3.9, Cl 97, CO2 20, BUN 33, Cr 1.1. Lactate 3.1. pH 7.35, CO2 28, HCO3 15. His urine is negative for ketones. His vitals are HR 103, RR 30, BP 115/65, O2 98% RA. Could these laboratory results be consistent with alcohol ketoacidosis (AKA)? The classic laboratory findings in patients with AKA include an elevated anion gap metabolic acidosis and an elevated lactate. Early in AKA patients may be negative for ketones when the nitroprusside test is used because it does not detect beta-hydroxybutyrate. As patients recover, the nitroprusside test will become positive as beta-hydroxybutyrate gets converted to acetone and acetate. Patients with AKA typically have elevated anion gap metabolic acidosis. However, vomiting may cause a primary metabolic alkalosis and a compensatory respiratory alkalosis which may result in a normal or even elevated pH. AKA patients, as compared to DKA patients, typically have higher pH, lower K and Cl, and higher HCO3 in their blood tests. As ethanol is metabolized by ADH and ALDH to acetaldehyde and acetate, respectively, an increased amount of NADH forms which causes a high redox state and excess of reducing potential (increased NADH:NAD+ ratio). Increased lactate due to pyruvate shunting: Reduced caloric intake, decreased glycogen stores, and thiamine depletion results in amino acids being c Continue reading >>

Exam Shows Diffuse Abdominal Tenderness With Guarding.

Exam Shows Diffuse Abdominal Tenderness With Guarding.

A 14 y/o female is brought to the emergency department by her mother after being found unresponsive at home. She had been ill the day before with nausea and vomiting, but was not running a fever. Her parents had kept her home from school that day. When her mother came home at lunchtime to check on her, she was very lethargic and not responding coherently. By the time she arrived at the hospital, she had to be brought in to the ED on a gurney. Initial evaluation showed O2 sat 100% on room air, pulse 126, respirations 30, BP 92/68, temperature 101.2 F. She appears pale, mucous membranes are dry and she only responds to painful stimuli. Exam shows diffuse abdominal tenderness with guarding. Differential diagnosis? What initial treatment would you suggest? What labs would you order? Any xrays or additional studies? CBC WBC 23,500 Hgb 14.2 g/dL Hct 45% Platelets 425,000 BMP Sodium 126 Potassium 5.2 Chloride 87 CO2 <5 BUN 32 Creatinine 1.5 Glucose 1,376 Arterial Blood Gases pH 7.19 Po2 100 mm Hg HCO3 7.5 mmo/L Pco2 20 mm Hg Sao2 98% (room air) Urine Specific gravity 1.015 Ketones 4+ Leukocytes few Glucose 4+ Nitrates 0 RBCs many Diabetic ketoacidosis (DKA) is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis. DKA occurs mostly in type 1 diabetics. It causes nausea, vomiting, and abdominal pain and can progress to cerebral edema, coma, and death. DKA is diagnosed by detection of hyperketonemia and anion gap metabolic acidosis in the presence of hyperglycemia. Treatment involves volume expansion, insulin replacement, and prevention of hypokalemia. Symptoms and signs of DKA Nausea & vomiting Abdominal pain--particularly in children Lethargy and somnolence Kussmaul respirations Hypotension Tachycardia Fruity breath Continue reading >>

Beta Hydroxybutyric Acidan Indicator For An Alcoholic Ketoacidosis As Cause Of Death In Deceased Alcohol Abusers

Beta Hydroxybutyric Acidan Indicator For An Alcoholic Ketoacidosis As Cause Of Death In Deceased Alcohol Abusers

We analyzed the postmortem blood of a total of 100 fatal cases for beta-hydroxybutyric acid (BHBA). In 25 cases of sudden and unexpected death of alcoholics we found pathologically increased levels of BHBA of 1260 to 47 200 (median 8000) mol/L. This led us to the diagnosis of an alcoholic ketoacidosis (AKA) as cause of death in these cases. The control group of 69 postmortem cases revealed that BHBA concentrations below 500 can be regarded as normal, and values up to 2500 mol/L as elevated. Our study shows that BHBA values over 2500 mol/L could lead to death, if no medical attention is sought. During storage we did not find any indication of postmortem formation or decomposition of BHBA in blood in vitro or in the corpses. In our opinion, BHBA should be considered the diagnostic marker of choice for the postmortem determination of alcoholic ketoacidosis (AKA) as the cause of death. The classical indications of such deaths are: unexpected death of a chronic alcoholic; none or only traces of ethanol in the blood; increased acetone blood concentration; and neither autopsy, histology, microbiology, nor toxicology reveal the cause of death. In six further cases a diabetic ketoacidosis (DKA) was diagnosed as the cause of death. Institute of Forensic Medicine, University of Zurich, Zurich, Institute of Forensic Medicine, University of Zurich, Zurich, Continue reading >>

Alcoholic Ketoacidosis: Case Report And Review

Alcoholic Ketoacidosis: Case Report And Review

A Patient with Alcoholic Ketoacidosis and Profound Lactemia. Gerrity RS et al. J Emerg Med 2016 Oct;51:447-449. This is a very good short case-based review of alcoholic ketoacidosis (AKA), and well-worth the 5 – 10 minutes reading time. Some key points: Development of AKA requires increased (binge) alcohol intake along with starvation (decreased food and water intake.) The characteristic high anion gap metabolic acidosis with elevated lactate and β-hydroxybutyrate levels are the result of dehydration, decreased glycogen stores, increased reducing potential (increased NADH) and release of stress hormones (catecholamines, glucagon, cortisol, and growth hormone.) The critical steps in treating AKA include fluid repletion along with administration of dextrose and parenteral thiamine, followed by feeding the patient as soon the clinical condition allows. Although the differential diagnosis includes most conditions on the metabolic acidosis mnemonic, the key alternative diagnosis is usually toxic alcohol poisoning. There are some parts of the discussion I wish the authors had expanded upon. The AKA patient in the case report remained hypotensive “despite fluid resuscitation,” was started on norepinephrine. The only fluids detailed in the report were 1 liter of D5NS bolus followed by 150 cc per hour. This is almost certainly grossly inadequate. AKA patients can be profoundly volume depleted from multiple factors such as prolonged decreased fluid intake, vomiting, and the diuretic effect of ethanol. This would be an excellent indication for the Toxicologic Ultrasound in Shock and Hypotension (TUSH) exam, using bedside sonography to visualize collapsibility of the inferior vena cava to help guide fluid resuscitation. Since AKA patients as a rule have increased catecholami Continue reading >>

Diabetic Ketoacidosis And Hyperglycemic Hyperosmolar Syndrome

Diabetic Ketoacidosis And Hyperglycemic Hyperosmolar Syndrome

In Brief Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic syndrome (HHS) are two acute complications of diabetes that can result in increased morbidity and mortality if not efficiently and effectively treated. Mortality rates are 2–5% for DKA and 15% for HHS, and mortality is usually a consequence of the underlying precipitating cause(s) rather than a result of the metabolic changes of hyperglycemia. Effective standardized treatment protocols, as well as prompt identification and treatment of the precipitating cause, are important factors affecting outcome. The two most common life-threatening complications of diabetes mellitus include diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar syndrome (HHS). Although there are important differences in their pathogenesis, the basic underlying mechanism for both disorders is a reduction in the net effective concentration of circulating insulin coupled with a concomitant elevation of counterregulatory hormones (glucagon, catecholamines, cortisol, and growth hormone). These hyperglycemic emergencies continue to be important causes of morbidity and mortality among patients with diabetes. DKA is reported to be responsible for more than 100,000 hospital admissions per year in the United States1 and accounts for 4–9% of all hospital discharge summaries among patients with diabetes.1 The incidence of HHS is lower than DKA and accounts for <1% of all primary diabetic admissions.1 Most patients with DKA have type 1 diabetes; however, patients with type 2 diabetes are also at risk during the catabolic stress of acute illness.2 Contrary to popular belief, DKA is more common in adults than in children.1 In community-based studies, more than 40% of African-American patients with DKA were >40 years of age and more than 2 Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a serious, life-threatening complication of diabetes mellitus. DKA is characterized by the triad of hyperglycemia, anion gap metabolic acidosis, and ketonemia. It is part of a spectrum of hyperglycemia on which lies hyperosmolar hyperglycemic state (HHS). Though the two are distinct entities, they do share some commonalities. DKA is caused by the reduced effect of insulin, either due to deficit or reduction of levels, with concomitant elevation of counter regulatory hormones (glucagon, catecholamines, cortisol, and growth hormones), generally due to a precipitating stress. Increased gluconeogenesis, glycogenolysis, and decreased glucose uptake by cells leads to hyperglycemia, while insulin deficiency leads to mobilization and oxidization of fatty acids leading to ketogenesis. Although DKA may be the initial manifestation of diabetes, it is typically precipitated by other factors. It is critical for a clinician to identify and treat these factors. Infection can be found in 40-50% of patients with hyperglycemic crisis, with urinary tract infection and pneumonia accounting for the majority of cases. DKA is a life-threatening medical emergency with a mortality rate just under 5% in individuals under 40 years of age, but with a more serious prognosis in the elderly, who have mortality rates over 20%. Deaths may also occur as a result of hypokalemia induced arrhythmias and cerebral edema (more common in children). II. Diagnostic confirmation: are you sure your patient has diabetic ketoacidosis? Although the diagnosis of DKA can be suspected on clinical grounds, confirmation is based on laboratory tests including potential hydrogen (pH) level, urinalysis, and basic metabolic profile. summarizes the biochemical criteria for the diagnosis and asse Continue reading >>

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