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Alcoholic Ketoacidosis Lab Results

Blood Gases | Lab Tests Online

Blood Gases | Lab Tests Online

For more information, please read the article Reference Ranges and What They Mean . Blood gases are a group of tests that are performed together to measure the pH and the amount of oxygen (O2) and carbon dioxide (CO2) present in a sample of blood, usually from an artery, in order to evaluate lung function and help detect an acid-base imbalance that could indicate a respiratory, metabolic or kidney disorder . A person's body carefully regulates blood pH, maintaining it within a narrow range of 7.35-7.45, not allowing blood to become too acidic ( acidosis ) nor too alkaline/basic ( alkalosis ). The body's regulation of acids and bases has two main components. The first component involves both metabolism and the kidneys: the cellular process of converting one substance to another for energy produces large amounts of acid that the kidneys help eliminate. The second component of regulating pH balance involves eliminating carbon dioxide (an acid when dissolved in blood) through exhalation of the lungs. This respiratory component is also the way that the body supplies oxygen to tissues . The lungs inhale oxygen, which is then dissolved in the blood and carried throughout the body to tissues. These processes of gas exchange and acid/base balance are also closely associated with the body's electrolyte balance. In a normal state of health, these processes are in a dynamic balance and the blood pH is stable. (For more on this, see Acidosis and Alkalosis ). There is a wide range of acute and chronic conditions that can affect kidney function, acid production, and lung function, and they have the potential to cause a pH, carbon dioxide/oxygen, or electrolyte imbalance. Examples include uncontrolled diabetes , which can lead to ketoacidosis and metabolic acidosis, and severe lung di 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 >>

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 >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

Also found in: Dictionary, Thesaurus, Acronyms, Encyclopedia. alcoholic ketoacidosis the fall in blood pH (acidosis) sometimes seen in alcoholics and associated with a rise in the levels of serum ketone bodies. alcoholic ketoacidosis Acute metabolic ketoacidosis classically seen 1–2 days after an alcohol binge coupled with a decrease in “real” food, resulting in a starvation response, which is exacerbated by vomiting, beta-hydroxybutyrate accumulation due to reduced fatty acid oxidation, and an excess of acetyl-co-A. Clinical findings Nausea, vomiting, abdominal pain; intact mental status. DiffDx Diabetic ketoacidosis, hypothermia. Lab No alcohol on board, high free fatty acids, increased ketones (acetone, acetoacetate, beta-hydroxybutyrate), no hyperglycaemia. alcoholic ketoacidosis Ketoacidosis 2º to alcohol abuse, in which ketone bodies–eg, acetone, accumulate in the circulation, which is evoked by conditions that encourage fat metabolism. See Diabetic ketoacidosis. alcoholic ketoacidosis Ketoacidosis that results from the hypercatecholaminergic effects of alcohol withdrawal, in addition to starvation, and dehydration. Continue reading >>

Acid-base (anesthesia Text)

Acid-base (anesthesia Text)

There are four native buffer systems – bicarbonate, hemoglobin, protein, and phosphate systems. Bicarbonate has a pKa of 6.1, which is not ideal. Hemoglobin has histidine residues with a pKa of 6.8. Chemoreceptors in the carotid bodies, aortic arch, and ventral medulla respond to changes in pH/pCO2 in a matter of minutes. The renal response takes much longer. Arterial vs. Venous Gases Venous blood from the dorsum of the hand is moderately arterialized by general anesthesia, and can be used as a substitute for an ABG. pCO2 will only be off by ~ 5 mm Hg, and pH by 0.03 or 0.04 units [Williamson et. al. Anesth Analg 61: 950, 1982]. Confounding variables include air bubbles, heparin (which is acidic), and leukocytes (aka “leukocyte larceny”). VGB/ABG samples should be cooled to minimize leukocyte activity, however when blood is cooled, CO2 solubility increases (less volatile), and thus pCO2 drops. As an example – a sample taken at 37°C and at 7.4 will actually read as a pH of 7.6 if measured at 25°C. Most VBG/ABGs are actually measured at 37°C. A-aDO2 increases with age, as well as with increased FiO2 and vasodilators (which impair hypoxic pulmonary vasoconstriction). In the setting of a shunt, pulse oximetry can be misleading, thus the A-aDO2 should be calculated. If PaO2 is > 150 mm Hg (i.e., Hg saturation is essentially 100%), every 20 mm Hg of A-aDO2 represents 1% shunting of cardiac output. A/a is even better than A-aDO2 because it is independent of FiO2. PaO2/FiO2 is a reasonable alternative, with hypoxia defined as PaO2/FiO2 < 300 (a PaO2/FiO2 < 200 suggests a shunt fraction of 20% or more). Mixed venous blood should have a pO2 of ~ 40 mm Hg. Values < 30 mm Hg suggest hypoxemia, although one must always keep in mind that peripheral shunting and cyanide tox Continue reading >>

Severe Metabolic Acidosis In The Alcoholic: Differential Diagnosis And Management

Severe Metabolic Acidosis In The Alcoholic: Differential Diagnosis And Management

1 A chronic alcoholic with severe metabolic acidosis presents a difficult diagnostic problem. The most common cause is alcoholic ketoacidosis, a syndrome with a typical history but often misleading laboratory findings. This paper will focus on this important and probably underdiagnosed syndrome. 2 The disorder occurs in alcoholics who have had a heavy drinking-bout culminating in severe vomiting, with resulting dehydration, starvation, and then a β- hydroxybutyrate dominated ketoacidosis. 3 Awareness of this syndrome, thorough history-taking, physical examination and routine laboratory analyses will usually lead to a correct diagnosis. 4 The treatment is simply replacement of fluid, glucose, electrolytes and thiamine. Insulin or alkali should be avoided. 5 The most important differential diagnoses are diabetic ketoacidosis, lactic acidosis and salicylate, methanol or ethylene glycol poisoning, conditions which require quite different treatment. 6 The diagnostic management of unclear cases should always include toxicological tests, urine microscopy for calcium oxalate crystals and calculation of the serum anion and osmolal gaps. 7 It is suggested here, however, that the value of the osmolal gap should be considered against a higher reference limit than has previously been recom mended. An osmolal gap above 25 mosm/kg, in a patient with an increased anion gap acidosis, is a strong indicator of methanol or ethylene glycol intoxication. Continue reading >>

Common Laboratory (lab) Values - Anion Gap

Common Laboratory (lab) Values - Anion Gap

Question: Please define the Anion Gap and its utility in diagnosis and how it relates to osmolality. The anion gap provides an estimation of the unmeasured anions in the plasma and is useful in the setting of arterial blood gas analysis. It is especially useful in helping to differentiate the cause of a metabolic acidosis, as well as following the response to therapy. Its basic premise is based on the fact that electroneutrality must exist in the body, or in other words the net charges of serum anions, which includes albumin, bicarbonate, chloride, organic acids and phosphate must equal the net charges of the serum cations, which includes calcium, magnesium, potassium and sodium. In clinical practice, the anion gap is calculated using three lab values (Na+, Cl-, and HCO3-). [Occasionally, you may see an alternative equation: Anion Gap = [Na+] + [K+] - [Cl-] - [HCO3-]. This equation is preferred by some nephrologists, because of the wide fluctuations that may occur with potassium in renal disease. ] Serum sodium represents over 90 percent of the extracellular cations, whereas chloride and bicarbonate represent approximately 85 percent of the extracellular anions. It follows then, that the anion gap in normal conditions will be a positive number since the sum of the serum anions used in the calculation represent a smaller value compared to the serum sodium concentration. The normal value for the anion gap is 12 +/-4. some newer references will list the normal anion gap as 7 +/- 4. This lower level may represent a more accurate reflection of the true anion gap based on changes that have occurred in contemporary medical labs. In the past, electrolyte analysis was performed using predominantly flame photometer measurement compared to the modern day use of ion-selective elec Continue reading >>

Alcoholic Ketoacidosis: Causes, Symptoms, Treatment, Prognosis

Alcoholic Ketoacidosis: Causes, Symptoms, Treatment, Prognosis

Ketoacidosis is a medical condition in which the food that is ingested by an individual is either metabolized or converted into acid. Alcoholic Ketoacidosis is a condition in which there is development of Ketoacidosis as a result of excessive alcohol intake for a long period of time and less ingestion of food resulting in malnutrition. Drinking excessive alcohol causes the individual to be able to eat less food. Additionally, if excess alcohol is ingested then it may lead to vomiting which further worsens the nutritional status of the individual which results in formation of excess acids resulting in Alcoholic Ketoacidosis. The symptoms caused by Alcoholic Ketoacidosis include abdominal pain, excessive fatigue, persistent vomiting, and the individual getting dehydrated due to frequent vomiting episodes and less fluid intake. If an individual has a history of alcohol abuse and experiences the above mentioned symptoms then it is advised that the individual goes to the nearest emergency room to get evaluated and if diagnosed treated for Alcoholic Ketoacidosis. As stated above, the root cause of Alcoholic Ketoacidosis is drinking excessive amounts of alcohol for a prolonged period of time. When an individual indulges in binge drinking he or she is not able to take in enough food that is required by the body to function. This eventually results in malnourishment. Additionally, vomiting caused by excessive drinking also results in loss of vital nutrients and electrolytes from the body such that the body is not able to function normally. This results in the insulin that is being produced by the body becoming less and less. All of these ultimately results in the development of Alcoholic Ketoacidosis. An individual may develop symptoms within a day after binge drinking, dependin Continue reading >>

You Don't Understand The Osm Gap - Guest Post By Rory Spiegel

You Don't Understand The Osm Gap - Guest Post By Rory Spiegel

Rory is just graduated EM Residency at Beth Israel Newark and is now pursuing advanced training in Resuscitation with Brian Wright and me at Stony Brook Hospital. He is the editor of the amazing EMNerd Blog and tweets at @EMNerd_ . This post will serve as a discussion of serum osmolarity*, its clinical utility, and the relationship between the Osm and anion gaps. The serum osmolarity has been relegated to the dark arts of medical science. Primarily, it is used to calculate the exact fluid status of patients presenting in various dysnatremic states by the physicians who happen to care for such physiological disruptions. Simply put the serum osmolarity is the number of particles present in the serum. The osmolarity does not discriminate based on a particles size or weight, but rather is concerned only with its concentration in the blood (1). As such, particles with low molecular weight that are capable of accumulating in large quantities in the serum, have the greatest potential to influence the osmolarity. In a healthy subject, the osmolarity is predominantly comprised of sodium ions and their counter anions, serum glucose, as well as blood urea nitrogen (BUN) (1). The serum osmolarity can be grossly estimated using the following formula: Briefly, this formula insures that each molecule is accounted for in its molar quantity (mmol/L) (1). The serum osmolality can also be directly measured by observing either the serums freezing point depression or boiling point elevation. If we compare this measured value to the calculated osmolarity, the difference between the two measurements is the Osm gap. Ideally this would equate to the amount of particles present in the serum that are not accounted for by the calculated formula. As such, the Osm gap should be positive in most phy Continue reading >>

Ketones Blood Test

Ketones Blood Test

Acetone bodies; Ketones - serum; Nitroprusside test; Ketone bodies - serum; Ketones - blood; Ketoacidosis - ketones blood test A ketone blood test measures the amount of ketones in the blood. How the Test is Performed How to Prepare for the Test No preparation is needed. How the Test will Feel When the needle is inserted to draw blood, some people feel slight pain. Others feel a prick or stinging. Afterward, there may be some throbbing or a slight bruise. This soon goes away. Why the Test is Performed Ketones are substances produced in the liver when fat cells break down in the blood. This test is used to diagnose ketoacidosis. This is a life-threatening problem that affects people who: Have diabetes. It occurs when the body cannot use sugar (glucose) as a fuel source because there is no insulin or not enough insulin. Fat is used for fuel instead. When fat breaks down, waste products called ketones build up in the body. Drink large amounts of alcohol. Normal Results A normal test result is negative. This means there are no ketones in the blood. Normal value ranges may vary slightly among different laboratories. Some labs use different measurements or test different samples. Talk to your health care provider about the meaning of your specific test results. What Abnormal Results Mean A test result is positive if ketones are found in the blood. This may indicate: Other reasons ketones are found in the blood include: A diet low in carbohydrates can increase ketones. After receiving anesthesia for surgery Glycogen storage disease (condition in which the body can't break down glycogen, a form of sugar that is stored in the liver and muscles) Being on a weight-loss diet Risks Veins and arteries vary in size from one person to another and from one side of the body to the other. Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Abbas E. Kitabchi, PhD., MD., FACP, FACE Professor of Medicine & Molecular Sciences and Maston K. Callison Professor in the Division of Endocrinology, Diabetes & Metabolism UT Health Science Center, 920 Madison Ave., 300A, Memphis, TN 38163 Aidar R. Gosmanov, M.D., Ph.D., D.M.Sc. Assistant Professor of Medicine, Division of Endocrinology, Diabetes & Metabolism, The University of Tennessee Health Science Center, 920 Madison Avenue, Suite 300A, Memphis, TN 38163 Clinical Recognition Omission of insulin and infection are the two most common precipitants of DKA. Non-compliance may account for up to 44% of DKA presentations; while infection is less frequently observed in DKA patients. Acute medical illnesses involving the cardiovascular system (myocardial infarction, stroke, acute thrombosis) and gastrointestinal tract (bleeding, pancreatitis), diseases of endocrine axis (acromegaly, Cushing`s syndrome, hyperthyroidism) and impaired thermo-regulation or recent surgical procedures can contribute to the development of DKA by causing dehydration, increase in insulin counter-regulatory hormones, and worsening of peripheral insulin resistance. Medications such as diuretics, beta-blockers, corticosteroids, second-generation anti-psychotics, and/or anti-convulsants may affect carbohydrate metabolism and volume status and, therefore, could precipitateDKA. Other factors: psychological problems, eating disorders, insulin pump malfunction, and drug abuse. It is now recognized that new onset T2DM can manifest with DKA. These patients are obese, mostly African Americans or Hispanics and have undiagnosed hyperglycemia, impaired insulin secretion, and insulin action. A recent report suggests that cocaine abuse is an independent risk factor associated with DKA recurrence. Pathophysiology 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 >>

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 >>

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 >>

Alcoholism: Facts On Alcoholic Symptoms & Treatment

Alcoholism: Facts On Alcoholic Symptoms & Treatment

For More Information About Alcoholism and Alcohol Use Disorder Alcohol problems vary in severity from mild to life threatening and affect the individual, the person's family, and society in numerous adverse ways. Despite the focus on illegal drugs of abuse such as cocaine , alcohol remains the number-one drug problem in the United States. Nearly 17 million adults in the U.S. are dependent on alcohol or have other alcohol-related problems, and about 88,000 people die from preventable alcohol-related causes. In teenagers, alcohol is the most commonly abused drug. Thirty-five percent of teens have had at least one drink by age 15. Even though it is illegal, about 8.7 million people 12 to 20 years of age have had a drink in the past month, and this age group accounted for 11% of all alcohol consumed in the U.S. Among underaged youth, alcohol is responsible for about 189,000 emergency-room visits and 4,300 deaths annually. Withdrawal, for those physically dependent on alcohol, is much more dangerous than withdrawal from heroin or other narcotic drugs. Alcohol abuse and alcohol dependence are now grouped together under the diagnosis of alcohol use disorder. What was formerly called alcohol abuse refers to excessive or problematic use with one or more of the following: Failure to fulfill major obligations at work, school, or home Recurrent use in situations where it is hazardous (such as driving a car or operating machinery) Continued use of alcohol despite having medical, social, family, or interpersonal problems caused by or worsened by drinking Despite negative outcomes resulting from drinking, the alcoholic continues to drink to try to attain the feeling of euphoria they first experienced when they started drinking. Previously called alcohol dependence, this aspect of alc Continue reading >>

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