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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 >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

• The characteristic example is an alcoholic person who abruptly abstains and has signs and symptoms such as vomiting, abdominal pain, malnutrition, and an anion gap metabolic acidosis, but no measurable alcohol levels. • A ratio of β-hydroxybutyrate to acetoacetate in excess of 10 : 1 is pathognomonic for alcoholic ketoacidosis, whereas a 3 : 1 ratio is more common in diabetic ketoacidosis. • Treatment emphasizes hydration with dextrose-containing solutions and thiamine; resolution of the acidosis usually occurs within 6 to 12 hours. The term alcoholic acidosis describes a syndrome of four types of metabolic acidosis that occur in alcoholics and vary in severity: ketoacidosis, lactic acidosis, acetic acidosis, and loss of bicarbonate in urine. AKA arises from a complicated interplay of the metabolic effects of alcohol in fasted, dehydrated alcoholics who abruptly stop their intake of ethanol.4 β-Hydroxybutyrate is the predominant ketoacid.5 Metabolism of ethanol to acetaldehyde is catalyzed by alcohol dehydrogenase in the liver and results in accumulation of the reduced form of nicotinamide adenine dinucleotide (NADH) relative to the oxidized form of nicotinamide adenine dinucleotide (NAD+). The altered ratio of NADH/NAD+ is the rate-limiting step in alcohol metabolism and favors the conversion of acetoacetate to β-hydroxybutyrate, as illustrated in Figure 161.1. Alcohol dehydrogenase in hepatocyte cytosol metabolizes ethanol to acetaldehyde, which is then transported into the mitochondria for metabolism to acetate. Acetate is activated by adenosine triphosphate (ATP), coenzyme A (CoA), and acetate thiokinase to form acetyl CoA, which can (1) be oxidized to carbon dioxide (CO2) by the citric acid cycle, (2) form ketone bodies, or (3) be converted to fat. Insul Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find one of our health articles more useful. See also separate Lactic Acidosis and Arterial Blood Gases - Indications and Interpretations articles. Description Metabolic acidosis is defined as an arterial blood pH <7.35 with plasma bicarbonate <22 mmol/L. Respiratory compensation occurs normally immediately, unless there is respiratory pathology. Pure metabolic acidosis is a term used to describe when there is not another primary acid-base derangement - ie there is not a mixed acid-base disorder. Compensation may be partial (very early in time course, limited by other acid-base derangements, or the acidosis exceeds the maximum compensation possible) or full. The Winter formula can be helpful here - the formula allows calculation of the expected compensating pCO2: If the measured pCO2 is >expected pCO2 then additional respiratory acidosis may also be present. It is important to remember that metabolic acidosis is not a diagnosis; rather, it is a metabolic derangement that indicates underlying disease(s) as a cause. Determination of the underlying cause is the key to correcting the acidosis and administering appropriate therapy[1]. Epidemiology It is relatively common, particularly among acutely unwell/critical care patients. There are no reliable figures for its overall incidence or prevalence in the population at large. Causes of metabolic acidosis There are many causes. They can be classified according to their pathophysiological origin, as below. The table is not exhaustive but lists those that are most common or clinically important to detect. Increased acid 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 >>

Ethylene Glycol And Propylene Glycol Toxicity What Laboratory Tests Can Help In Evaluating Patients Exposed To Ethylene Glycol?

Ethylene Glycol And Propylene Glycol Toxicity What Laboratory Tests Can Help In Evaluating Patients Exposed To Ethylene Glycol?

Ethylene Glycol and Propylene Glycol Toxicity What Laboratory Tests Can Help In Evaluating Patients Exposed to Ethylene Glycol? Upon completion of this section, you should be able to identify the abnormal laboratory findings associated with ethylene glycol poisoning and list three measurements that can assist with diagnosis of ethylene glycol poisoning. All patients with known or suspected ethylene glycol ingestion require the following tests Other helpful laboratory tests may include urinalysis (with special attention to crystalluria) A measured osmolality by the freezing point depression method is needed to detect an osmolal gap. Results of these laboratory tests will confirm the presence and degree of metabolic acidosis and allow calculation of the anion and osmolal gaps ( Figure 2 ). A blood ethanol level will establish whether initial CNS symptoms may be due to ethanol. The presence of ethanol will also have a substantial impact on metabolism and therapy. Patients who have both anion and osmolal gap should also have blood methanol tests. Serum lactate and betahydroxybutyrate levels may be indicated for an alcoholic patient, if alcoholic ketoacidosis is suspected (Meditext 2004). The presence of calcium oxalate or hippurate crystals in the urine, together with an elevated anion gap or osmolal gap, strongly suggests ethylene glycol poisoning (Albertson 1999). Urinary crystals result from the precipitation of calcium by the oxalic acid metabolite of ethylene glycol the reaction of the glycine metabolite with benzoic acid, which forms hippuric acid needles (most commonly) (Jacobsen, Hewlett et al. 1988) Absence of urinary crystals, however, does not rule out poisoning. Numerous studies have documented that renal damage occurs after ethylene glycol ingestion without de Continue reading >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

Seen in patients with recent history of binge drinking with little/no nutritional intake Anion gap metabolic acidosis associated with acute cessation of ETOH consumption after chronic abuse Characterized by high serum ketone levels and an elevated AG Consider other causes of elevated AG, as well as co-ingestants Concomitant metabolic alkalosis can occur from dehydration (volume depletion) and emesis Ethanol metabolism depletes NAD stores[1] Results in inhibition of Krebs cycle, depletion of glycogen stores, and ketone formation High NADH:NAD also results in increased lactate production Acetoacetate is metabolized to acetone so elevated osmolal gap may also be seen Differential Diagnosis Starvation Ketosis Binge drinking ending in nausea, vomiting, and decreased intake Positive serum ketones Wide anion gap metabolic acidosis without alternate explanation Urine ketones may be falsely negative or low Lab measured ketone is acetoacetate May miss beta-hydroxybutyrate Consider associated diseases (ie pancreatitis, rhabdomyolysis, hepatitis, infections) Oral nutrition if able to tolerate Consider bicarb if life-threatening acidosis (pH <7.1) unresponsive to fluid therapy Discharge home after treatment if able to tolerate POs and acidosis resolved Consider admission for those with severe volume depletion and/or acidosis Hypoglycemia is poor prognostic feature, indicating depleted glycogen stores See Also Continue reading >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

Workup When a chronic alcoholic presents with signs of AKA, the clinician should carefully evaluate the patient, obtain a history, perform a physical exam, and order the appropriate laboratory tests. Laboratory tests and results A comprehensive metabolic profile will allow the medical team to determine the overall clinical picture of the patient. This includes measurement of serum electrolytes, glucose, blood urea nitrogen (BUN), creatinine, lipase, amylase, and plasma osmolality. Also, urinalysis is helpful to detect ketones. Another useful tool is the blood alcohol level [8]. Finally, critically ill patients with positive ketones must have an analysis of their arterial blood gas (ABG) and serum lactate levels. With regards to expected findings, all patients demonstrate ketonuria and a majority display ketonemia. Also common are electrolyte imbalances such as hypokalemia, hyponatremia, hypophosphatemia, and hypomagnesemia. Additionally, the serum glucose may range from low to modest elevation while another abnormality is an increased osmolar gap (secondary to increased acetone and possibly ethanol). Most importantly, AKA is typically characterized by a high anion gap metabolic acidosis, which may be complicated by metabolic alkalosis secondary to concurrent vomiting. In cases where the pH is normal, the increased anion gap is an indicator of ketoacidosis. If there is a normal gap, this is the result of the excretion of ketoacid ions. Additionally, lactic acidosis is observed in more than 50% of cases due to hypoperfusion [9]. Differential diagnoses Differentials include diabetic ketoacidosis (DKA),however, the absence of hyperglycemia excludes this. Pancreatitis may also present similar to AKA and should be ruled out. If alcohol intoxication is not conclusive, serum me Continue reading >>

What Is Metabolic Acidosis?

What Is Metabolic Acidosis?

Metabolic acidosis happens when the chemical balance of acids and bases in your blood gets thrown off. Your body: Is making too much acid Isn't getting rid of enough acid Doesn't have enough base to offset a normal amount of acid When any of these happen, chemical reactions and processes in your body don't work right. Although severe episodes can be life-threatening, sometimes metabolic acidosis is a mild condition. You can treat it, but how depends on what's causing it. Causes of Metabolic Acidosis Different things can set up an acid-base imbalance in your blood. Ketoacidosis. When you have diabetes and don't get enough insulin and get dehydrated, your body burns fat instead of carbs as fuel, and that makes ketones. Lots of ketones in your blood turn it acidic. People who drink a lot of alcohol for a long time and don't eat enough also build up ketones. It can happen when you aren't eating at all, too. Lactic acidosis. The cells in your body make lactic acid when they don't have a lot of oxygen to use. This acid can build up, too. It might happen when you're exercising intensely. Big drops in blood pressure, heart failure, cardiac arrest, and an overwhelming infection can also cause it. Renal tubular acidosis. Healthy kidneys take acids out of your blood and get rid of them in your pee. Kidney diseases as well as some immune system and genetic disorders can damage kidneys so they leave too much acid in your blood. Hyperchloremic acidosis. Severe diarrhea, laxative abuse, and kidney problems can cause lower levels of bicarbonate, the base that helps neutralize acids in blood. Respiratory acidosis also results in blood that's too acidic. But it starts in a different way, when your body has too much carbon dioxide because of a problem with your lungs. Continue reading >>

Serum Ketone Level

Serum Ketone Level

This test measures the amount of ketones in blood. It is used to evaluate and manage ketone-producing disorders[1][2][3][4], such as uncontrolled diabetes[5][2][6][7] and alcoholic ketoacidosis[4][8][9][10]. Laboratory tests may be done for many reasons. Tests are performed for routine health screenings or if a disease or toxicity is suspected. Lab tests may be used to determine if a medical condition is improving or worsening. Lab tests may also be used to measure the success or failure of a medication or treatment plan. Lab tests may be ordered for professional or legal reasons. You may need this test if you have: When and how often should I have this test? When and how often laboratory tests are done may depend on many factors. The timing of laboratory tests may rely on the results or completion of other tests, procedures, or treatments. Lab tests may be performed immediately in an emergency, or tests may be delayed as a condition is treated or monitored. A test may be suggested or become necessary when certain signs or symptoms appear. Due to changes in the way your body naturally functions through the course of a day, lab tests may need to be performed at a certain time of day. If you have prepared for a test by changing your food or fluid intake, lab tests may be timed in accordance with those changes. Timing of tests may be based on increased and decreased levels of medications, drugs or other substances in the body. The age or gender of the person being tested may affect when and how often a lab test is required. Chronic or progressive conditions may need ongoing monitoring through the use of lab tests. Conditions that worsen and improve may also need frequent monitoring. Certain tests may be repeated to obtain a series of results, or tests may need to be repea Continue reading >>

Diagnosis And Treatment Of Ethylene Glycol (antifreeze) Ingestion

Diagnosis And Treatment Of Ethylene Glycol (antifreeze) Ingestion

Fast, free, expert help 247365 1-800-222-1222 Diagnosis and Treatment of Ethylene Glycol (Antifreeze) Ingestion Ethylene glycol is an odorless, colorless, sweet-tasting syrupy substance with a molecular weight of 62.07, freezing point of -13C and a boiling point of 197.6C. It is most commonly encountered as automotive antifreeze. Diethylene glycol behaves similarly to ethylene glycol in an overdose. The ethylene glycol molecule is incorporated into the structure of several ethers (e.g., ethylene glycol mono butyl ether and ethylene glycol mono ethyl ether), which may in very large amounts behave similarly to EG. A 27 year old male is found in a motel room, after telling an acquaintance that he was going to drink antifreeze. In the motel room is a glass with what looks like antifreeze. The patient says it is, and says that he drank one glass. He is brought to an ED in police custody. They are anxious to take him to jail. In the ED he is alert and cooperative, oriented to person, place and time. PMH reveals multiple prior suicide attempts. Physical examination is unremarkable. (He has multiple old scars from apparent self-harm efforts.) Initial labs at 20:33 hours are Na 149, Cl 108, CO2 25, K 4.1, BUN 9 and Cr 1.1. Ethyl alcohol is 197 mg/dl. Urine tox screen is negative for drugs of abuse. Urine shows no crystals. Blood ethylene glycol level measurement will not be available for more than 24 hours. The hospital cannot do a measured serum osmolality on site. An EG sample is sent out. In the absence of a stat EG level or a serum osmolality, the physician caring for the patient elects to follow the serum bicarbonate level as a possible marker of severity of ethylene glycol poisoning. His logic is that, since EG causes over time a profound metabolic acidosis, the absence o Continue reading >>

Alcoholic Ketoacidosis Workup

Alcoholic Ketoacidosis Workup

Approach Considerations Diagnosis of alcoholic ketoacidosis (AKA) requires arterial blood gas (ABG) measurement and serum chemistry assays. Usual laboratory findings include the following [19] : Continue reading >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

Ketoacidosis - alcoholic; Alcohol use - alcoholic ketoacidosis Alcoholic ketoacidosis is the buildup of ketones in the blood. Ketones are a type of acid that form when the body breaks down fat for energy. The condition is an acute form of metabolic acidosis , a condition in which there is too much acid in body fluids. Acute means sudden or severe. Acute symptoms appear, change, or worsen rapidly. It is the opposite of chronic. Metabolic acidosis is a condition in which there is too much acid in the body fluids. Alcoholic ketoacidosis is caused by very heavy alcohol use. It most often occurs in a malnourished person who drinks large amounts of alcohol every day. Malnutrition is the condition that occurs when your body does not get enough nutrients. Symptoms of alcoholic ketoacidosis include: Agitation is an unpleasant state of extreme arousal. An agitated person may feel stirred up, excited, tense, confused, or irritable. Confusion is the inability to think as clearly or quickly as you normally do. You may feel disoriented and have difficulty paying attention, remembe... Changed level of alertness, which may lead to coma Fatigue is a feeling of weariness, tiredness, or lack of energy. Hyperventilation is rapid and deep breathing. It is also called overbreathing, and it may leave you feeling breathless. Symptoms of dehydration , such as dizziness, lightheadedness, and thirst Dehydration occurs when your body does not have as much water and fluids as it should. Dehydration can be mild, moderate, or severe, based on how muc... Arterial blood gases (measures the acid/base balance and oxygen level in blood) Blood gasesare a measurement of how much oxygen and carbon dioxideare in your blood. They also determine the acidity (pH) of your blood. Blood chemistries, and liver func Continue reading >>

New Quantitative Test Ketone Beta-hydroxybutyrate

New Quantitative Test Ketone Beta-hydroxybutyrate

Effective December 13, 2016, TriCore changed to a new quantitative test to measure ketones in plasma or serum. The new test, Ketone Beta-hydroxybutyrate (KETBHB), measures Beta-hydroxybutyrate (BHB) and is not directly comparable to the previous test measuring acetoacetate. BHB shows different clearance during treatment of ketoacidosis. As diabetic ketoacidosis (DKA) is treated, serum BHB decreases more consistently than acetoacetate which is converted to BHB and does not change as rapidly. CLINICAL UTILITY BHB is the predominate ketone present during DKA and trends with a patient’s clinical status. Because KETBH is quantitative, it can be used for monitoring ketosis to resolution. Additionally, BHB can be used to clinically diagnose and monitor the disease status or severity of alcoholism, glycogen storage disease, high fat/low carbohydrate diets, pregnancy, alkalosis, ingestion of isopropyl alcohol, and salicylate poisoning. In these situations the levels are usually above the normal range which is up to 0.27 mml/L, but often do not reach the threshold for DKA diagnosis. RESULTS INTERPRETATION FOR BETA-HYDROXYBUTYRATE LEVELS Range mmol/dL Interpretation Sensitivity for DKA Specificity for DKA <0.27 no ketoacidosis, normal range 0.28-1.5 DKA not entirely excluded, other conditions should be considered 1.5-3.0 children DKA possible in diabetics with >250mg/dL glucose 98-100% 78-93% 1.5-3.8 adults DKA possible in diabetics with >250mg/dL glucose 98-100% 78-93% >3.0 children >3.8 adults Near diagnostic of DKA in diabetic patient near 100% 93-94% 1. A Beta-hyroxybutyrate level of more than 1.5 mmol/L had sensitivity ranging from 98-100% and specificity ranging from 78.6-93.3% for the diagnosis of diabetic ketoacidosis in diabetic patients presenting to the Emergency Continue reading >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

Alcoholic ketoacidosis is characterized by an anion gap acidosis due to high levels of ketoacids. It occurs exclusively in relation to alcohol abuse but not just in chronic alcoholics. It has been reported in first-time drinkers whose food intake is minimal. The true incidence is unknown, and the frequency is probably directly related to the incidence of alcoholism in a population. Several mechanisms have been postulated. In one explanation, ketosis results from increased mobilization of free fatty acids from adipose tissue coupled with simultaneous enhancement of the liver's capacity to convert these substrates into acetoacetate and $-hydroxybutyrate. During the metabolism of alcohol in the liver the rate of nicotinamide adenine dinucleotide (NAD) reduction exceeds the rate of mitochondrial NADH oxidation, causing a decrease in available NAD. This state persists for a few days in spite of no further alcohol consumption. An NAD-dependent step in the oxidation of fatty acids in the mitochondria of the hepatocyte is displaced in favor of ketone body formation. During alcoholic ketoacidosis insulin levels are low, whereas levels of cortisol, growth hormone, glucagon, and epinephrine are increased, possibly as a result of alcohol-induced hypoglycemia. This hormonal milieu promotes lipolysis, which increases the levels of free fatty acids available for conversion to ketones. Additional mechanisms that may contribute to ketosis include the conversion of acetate, an alcohol breakdown product, to ketones; alcohol-induced mitochondrial structural changes which enhance the rate of ketosis; and mitochondrial phosphorus depletion, which inhibits the utilization for NADH and increases ketone body formation. Finally, vomiting and starvation superimposed on chronic malnutrition also 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 >>

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