Diagnosis And Treatment Of Diabetic Ketoacidosis (dka) In Dogs And Cats
What is DKA in Dogs and Cats? Diabetic Ketoacidosis (DKA) is a serious and life-threatening complication of diabetes mellitus that can occur in dogs and cats. DKA is characterized by hyperglycemia, ketonemia, +/- ketonuria, and metabolic acidosis. Ketone bodies are formed by lipolysis (breakdown) of fat and beta-oxidation when the metabolic demands of the cells are not met by the limited intracellular glucose concentrations. This provides alternative energy sources for cells, which are most important for the brain. The three ketones that are formed include beta-hydroxybutyrate, acetoacetate and acetone. Beta-hydroxybutyrate (BHB) and acetoacetate are anions of moderately strong acids contributing most to the academia (low blood pH). Acetone is the ketone body that can be detected on breath. In a normal animal, glucose enters the cell (with help of insulin) – undergoes glycolysis to pyruvate within cytosol – pyruvate moves into mitochondria (energy generating organelle in the cell) to enter the TCA cycle and ATP is formed. ATP is the main energy source of the body. When glucose cannot enter the cell, free fatty acids are broken down (lipolysis) and move into the cell to undergo beta-oxidation (creation of pyruvate). The pyruvate then moves into the mitochondria to enter the TCA cycle (by conversion to Acetyl-CoA first). However, when the TCA cycle is overwhelmed, the Acetyl-CoA is used in ketogenesis to form ketone bodies. Summary Diabetic Ketoacidosis (DKA) in Dogs and Cats When there is no insulin the body cannot utilize glucose and there is no intracellular glucose. The body then uses ketone bodes as an alternate source. When there is decreased insulin and increased counterregulatory hormones fatty acids are converted to AcCoA and then ketones. In the non-diabetic Continue reading >>
Metabolic Acidosis
Metabolic acidosis is the most common acid–base disorder and can be life threatening. It results from excessive cellular acid production, reduced acid secretion, or loss of body alkali. The body has two buffering mechanisms to counteract an increase in acid. The initial response is to increase carbon dioxide excretion by increasing ventilation. The second response is increased renal excretion of acids and renal regeneration of bicarbonate. The adequacy of compensation can be assessed by the quick check method or the Winter formula (Table 2). Metabolic acidosis can be classified into two categories using the anion gap. Each category has a distinct differential diagnosis. Anion gap = [Sodium] – ([Chloride] + [Bicarbonate]) Normally, the anion gap is approximately 12 ± 2 meq/L (12 ± 2 mmol/L). Most unmeasured anions consist of albumin. Therefore, the presence of either a low albumin level or an unmeasured cationic light chain, which occurs in multiple myeloma, results in a low anion gap. Increased hydrogen ion concentration or decreased bicarbonate concentration will increase the gap. When the primary disturbance is a metabolic acidosis, the anion gap helps to narrow the diagnostic possibilities to an increased anion gap acidosis or a normal anion gap acidosis. Increased Anion Gap Metabolic Acidosis Common causes include ketoacidosis (diabetes mellitus, alcohol abuse, starvation), lactic acidosis, chronic kidney disease, salicylate toxicity, and ethylene glycol and methanol poisoning. Diabetic ketoacidosis is the most common cause of an increased anion gap acidosis, but a normal anion gap acidosis may be present early in the disease course when the extracellular fluid (ECF) volume is nearly normal. Ketoacidosis also may develop in patients with a histor Continue reading >>
The Difference Between Ketosis & Ketoacidosis - Can Anyone Explain?
The difference between Ketosis & Ketoacidosis - can anyone explain? The difference between Ketosis & Ketoacidosis - can anyone explain? I've read many posts about the desirability of ketosis when following a high protein diet with the aim of losing weight. As I have never had to every lose weight I have never given this much attention or really understood what this is all about. On the other hand, DKA is always something that I need to watch out when sick, so I understand that having ketones in the blood is always a worrying sign. I'm going through a mild cold right now & have exceptionally high BG levels upon waking (even in spite of bolusing a few hours before waking with fast acting insulin to prevent the DP spike!). I woke up this morning with a moderate blood ketone reading as well. My question is: do people experiencing ketosis have ketones? If so, what is considered normal & safe levels? I have drastically reduced my carb levels in my diet & so far - thankfully - I have not lost any weight. Does that mean I am not experiencing ketosis? I'd really appreciate knowing more about this. Ketosis = Metabolic process where the body is starved for quick and efficient sources of glucose such as carbs and thereby burns body fat and proteins for its energy needs. This produces low levels of ketones confirming that the low to no carb diet is working in burning fat for fuel. One downside is in the absence of enough fat stores, the body will burn muscle tissue instead. This is the basis for the Atkins diet. Ketones are an acid and when ketosis occurs the levels are usually low enough that the body can overcome the acidic effect of the ketones and keep the blood at a neutral PH while blood sugars are at a normal level. Ketoacidosis = A condition where the production of ketones, Continue reading >>
Fluid Management In Diabetic-acidosis—ringer's Lactate Versus Normal Saline: A Randomized Controlled Trial
Objective: To determine if Ringer's lactate is superior to 0.9% sodium chloride solution for resolution of acidosis in the management of diabetic ketoacidosis (DKA). Design: Parallel double blind randomized controlled trial. Methods: Patients presenting with DKA at Kalafong and Steve Biko Academic hospitals were recruited for inclusion in this study if they were >18 years of age, had a venous pH >6.9 and ≤7.2, a blood glucose of >13 mmol/l and had urine ketones of ≥2+. All patients had to be alert enough to give informed consent and should have received <1 l of resuscitation fluid prior to enrolment. Results: Fifty-seven patients were randomly allocated, 29 were allocated to receive 0.9% sodium chloride solution and 28 to receive Ringer's lactate (of which 27 were included in the analysis in each group). An adjusted Cox proportional hazards analysis was done to compare the time to normalization of pH between the 0.9% sodium chloride solution and Ringer's lactate groups. The hazard ratio (Ringer's compared with 0.9% sodium chloride solution) for time to venous pH normalization (pH = 7.32) was 1.863 (95% CI 0.937–3.705, P = 0.076). The median time to reach a pH of 7.32 for the 0.9% sodium chloride solution group was 683 min (95% CI 378–988) (IQR: 435–1095 min) and for Ringer's lactate solution 540 min (95% CI 184–896, P = 0.251). The unadjusted time to lower blood glucose to 14 mmol/l was significantly longer in the Ringer's lactate solution group (410 min, IQR: 240–540) than the 0.9% sodium chloride solution group (300 min, IQR: 235–420, P = 0.044). No difference could be demonstrated between the Ringer's lactate and 0.9% sodium chloride solution groups in the time to resolution of DKA (based on the ADA criteria) (unadjusted: P = 0.934, adjusted: P = 0.75 Continue reading >>
- A Website to Promote Physical Activity in People With Type 2 Diabetes Living in Remote or Rural Locations: Feasibility Pilot Randomized Controlled Trial
- Mobile App-Based Interventions to Support Diabetes Self-Management: A Systematic Review of Randomized Controlled Trials to Identify Functions Associated with Glycemic Efficacy
- Diabetes Care Management Teams Did Not Reduce Utilization When Compared With Traditional Care: A Randomized Cluster Trial
Metabolic Acidosis
Metabolic acidosis is primary reduction in bicarbonate (HCO3−), typically with compensatory reduction in carbon dioxide partial pressure (Pco2); pH may be markedly low or slightly subnormal. Metabolic acidoses are categorized as high or normal anion gap based on the presence or absence of unmeasured anions in serum. Causes include accumulation of ketones and lactic acid, renal failure, and drug or toxin ingestion (high anion gap) and GI or renal HCO3− loss (normal anion gap). Symptoms and signs in severe cases include nausea and vomiting, lethargy, and hyperpnea. Diagnosis is clinical and with ABG and serum electrolyte measurement. The cause is treated; IV sodium bicarbonate may be indicated when pH is very low. Acidemia (arterial pH < 7.35) results when acid load overwhelms respiratory compensation. Causes are classified by their effect on the anion gap (see The Anion Gap and see Table: Causes of Metabolic Acidosis). High anion gap acidosis Ketoacidosis is a common complication of type 1 diabetes mellitus (see diabetic ketoacidosis), but it also occurs with chronic alcoholism (see alcoholic ketoacidosis), undernutrition, and, to a lesser degree, fasting. In these conditions, the body converts from glucose to free fatty acid (FFA) metabolism; FFAs are converted by the liver into ketoacids, acetoacetic acid, and beta-hydroxybutyrate (all unmeasured anions). Ketoacidosis is also a rare manifestation of congenital isovaleric and methylmalonic acidemia. Lactic acidosis is the most common cause of metabolic acidosis in hospitalized patients. Lactate accumulation results from a combination of excess formation and decreased utilization of lactate. Excess lactate production occurs during states of anaerobic metabolism. The most serious form occurs during the various types o Continue reading >>
Lactic Acidosis, Hyperlactatemia And Sepsis | Montagnani | Italian Journal Of Medicine
Montagnani and Nardi: Lactic Acidosis, Hyperlactatemia and Sepsis Lactic Acidosis, Hyperlactatemia and Sepsis [1] Division of Internal Medicine, Misericordia Hospital, Grosseto [2] Division of Internal Medicine, Maggiore Hospital, Bologna, Italy Correspondence to: Ospedale Misericordia di Grosseto, via Senese, 58100 Grosseto, Italy. +39.0564.485330. [email protected] Among hospitalized patients, lactic acidosis represents the most common cause of metabolic acidosis. Lactate is not just a metabolic product of anaerobic glycolysis but is triggered by a variety of metabolites even before the onset of anaerobic metabolism as part of an adaptive response to a hypermetabolic state. On the basis of such considerations, lactic acidosis is divided into two classes: inadequate tissue oxygenation (type A) and absence of tissue hypoxia (type B). Lactic acidosis is characterized by non-specific symptoms but it should be suspected in all critical patients who show hypovolemic, hypoxic, in septic or cardiogenic shock or if in the presence of an unexplained high anion gap metabolic acidosis. Lactic acidosis in sepsis and septic shock has traditionally been explained as a result of tissue hypoxia when whole-body oxygen delivery fails to meet whole body oxygen requirements. In sepsis lactate levels correlate with increased mortality with a poor prognostic threshold of 4 mmol/L. In hemodynamically stable patients with sepsis, hyperlactatemia might be the result of impaired lactate clearance rather than overproduction. In critically ill patients the speed at which hyperlactatemia resolves with appropriate therapy may be considered a useful prognostic indicator. The measure of blood lactate should be performed within 3 h of presentation in acute care setting. The presence of lactic a Continue reading >>
Acid-base Disorders
Content currently under development Acid-base disorders are a group of conditions characterized by changes in the concentration of hydrogen ions (H+) or bicarbonate (HCO3-), which lead to changes in the arterial blood pH. These conditions can be categorized as acidoses or alkaloses and have a respiratory or metabolic origin, depending on the cause of the imbalance. Diagnosis is made by arterial blood gas (ABG) interpretation. In the setting of metabolic acidosis, calculation of the anion gap is an important resource to narrow down the possible causes and reach a precise diagnosis. Treatment is based on identifying the underlying cause. Continue reading >>
Metabolic Acidosis: Causes, Symptoms, And Treatment
The Terrible Effects of Acid Acid corrosion is a well-known fact. Acid rain can peel the paint off of a car. Acidifying ocean water bleaches and destroys coral reefs. Acid can burn a giant hole through metal. It can also burn holes, called cavities, into your teeth. I think I've made my point. Acid, regardless of where it's at, is going to hurt. And when your body is full of acid, then it's going to destroy your fragile, soft, internal organs even more quickly than it can destroy your bony teeth and chunks of thick metal. What Is Metabolic Acidosis? The condition that fills your body with proportionately too much acid is known as metabolic acidosis. Metabolic acidosis refers to a physiological state characterized by an increase in the amount of acid produced or ingested by the body, the decreased renal excretion of acid, or bicarbonate loss from the body. Metabolism is a word that refers to a set of biochemical processes within your body that produce energy and sustain life. If these processes go haywire, due to disease, then they can cause an excess production of hydrogen (H+) ions. These ions are acidic, and therefore the level of acidity in your body increases, leading to acidemia, an abnormally low pH of the blood, <7.35. The pH of the blood mimics the overall physiological state in the body. In short, a metabolic process is like a power plant producing energy. If a nuclear power plant goes haywire for any reason, then we know what the consequences will be: uncontrolled and excessive nuclear energetic reactions leading to the leakage of large amounts of radioactive material out into the environment. In our body, this radioactive material is acid (or hydrogen ions). Acidemia can also occur if the kidneys are sick and they do not excrete enough hydrogen ions out of th Continue reading >>
Glyburide And Metformin (oral Route)
Precautions Drug information provided by: Micromedex It is very important that your doctor check your progress at regular visits to make sure this medicine is working properly. Blood tests may be needed to check for unwanted effects. Under certain conditions, too much metformin can cause lactic acidosis. The symptoms of lactic acidosis are severe and quick to appear. They usually occur when other health problems not related to the medicine are present and very severe, such as a heart attack or kidney failure. The symptoms of lactic acidosis include abdominal or stomach discomfort; decreased appetite; diarrhea; fast, shallow breathing; a general feeling of discomfort; muscle pain or cramping; and unusual sleepiness, tiredness, or weakness. If you have any symptoms of lactic acidosis, get emergency medical help right away. It is very important to carefully follow any instructions from your health care team about: Alcohol—Drinking alcohol may cause severe low blood sugar. Discuss this with your health care team. Other medicines—Do not take other medicines unless they have been discussed with your doctor. This especially includes nonprescription medicines such as aspirin, and medicines for appetite control, asthma, colds, cough, hay fever, or sinus problems. Counseling—Other family members need to learn how to prevent side effects or help with side effects if they occur. Also, patients with diabetes may need special counseling about diabetes medicine dosing changes that might occur because of lifestyle changes, such as changes in exercise and diet. Furthermore, counseling on contraception and pregnancy may be needed because of the problems that can occur in patients with diabetes during pregnancy. Travel—Keep your recent prescription and your medical history with yo Continue reading >>
Alcoholic Ketoacidosis
By Erika F. Brutsaert, MD, Assistant Professor, Albert Einstein College of Medicine; Attending Physician, Montefiore Medical Center 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. Typically, an alcohol binge leads to vomiting and the cessation of alcohol or food intake for 24 h. During this period of starvation, vomiting continues and abdominal pain develops, leading the patient to seek medical attention. Pancreatitis may occur. 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 seru Continue reading >>
Metabolic Acidosis; Gap Positive
Metabolic acidosis is defined by low serum pH (less than 7.35-7.45) and low serum bicarbonate. It occurs by one of three major mechanisms: 1. Increased endogenous acid (i.e., lactic acidosis, diabetic ketoacidosis). 2. Decreased renal acid excretion (i.e., renal failure). In determining the underlying etiology for a metabolic acidosis, the serum anion gap must be calculated by subtracting the major measured anions (chloride and bicarbonate) from the major measured cation (sodium). If the result is greater than 12 meq/L (which is the normal value for most laboratories), the acidosis is said to be an anion gap acidosis. The expected anion gap should is lower in hypoalbuminemia and should be corrected - for each decrease of 1gm/dl in albumin, the normal anion gap should be decreased by approximately 2.5 meq/L. A. What is the differential diagnosis for this problem? Anion gap acidosis can be the result from: 1. A fall in unmeasured cations (as seen in hypomagnesemia or hypocalcemia). The most common reasons for a rise in anions are ingestions, lactic acidosis, ketoacidosis and renal failure. Ingestions of multiple different toxins can result in unmeasured anions causing a metabolic gap acidosis. Most commonly salicylate and the alcohols (methanol and ethylene glycol) can lead to severe acidosis. The inhalant toluene may also be a culprit. Lactic acidosis is the most common cause of an elevated anion gap acidosis in hospitalized patients, occurring with decreased perfusion causing relative tissue ischemia. This leads to increased lactic acid production and impaired renal excretion with resultant acid accumulation (Type A lactic acidosis). Type B lactic acidosis occurs in patients without overt tissue and can be seen in diabetics on metformin, patients with hematologic and s Continue reading >>
Starvation Ketoacidosis: A Cause Of Severe Anion Gap Metabolic Acidosis In Pregnancy
Copyright © 2014 Nupur Sinha et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Pregnancy is a diabetogenic state characterized by relative insulin resistance, enhanced lipolysis, elevated free fatty acids and increased ketogenesis. In this setting, short period of starvation can precipitate ketoacidosis. This sequence of events is recognized as “accelerated starvation.” Metabolic acidosis during pregnancy may have adverse impact on fetal neural development including impaired intelligence and fetal demise. Short periods of starvation during pregnancy may present as severe anion gap metabolic acidosis (AGMA). We present a 41-year-old female in her 32nd week of pregnancy, admitted with severe AGMA with pH 7.16, anion gap 31, and bicarbonate of 5 mg/dL with normal lactate levels. She was intubated and accepted to medical intensive care unit. Urine and serum acetone were positive. Evaluation for all causes of AGMA was negative. The diagnosis of starvation ketoacidosis was established in absence of other causes of AGMA. Intravenous fluids, dextrose, thiamine, and folic acid were administered with resolution of acidosis, early extubation, and subsequent normal delivery of a healthy baby at full term. Rapid reversal of acidosis and favorable outcome are achieved with early administration of dextrose containing fluids. 1. Introduction A relative insulin deficient state has been well described in pregnancy. This is due to placentally derived hormones including glucagon, cortisol, and human placental lactogen which are increased in periods of stress [1]. The insulin resistance increases with gestational age Continue reading >>
Acid-base Imbalance, Abnormal Blood Ph
Metabolic acidosis, metabolic alkalosis, respiratory acidosis, respiratory alkalosis, mixed acid-base disorders Derangements in blood pH result from increased intake, altered production or impaired/excessive excretion of acid or base. With time, respiratory and renal adjustments correct the pH towards normal by altering the plasma levels of pCO2 or strong ions (Na+,Cl- ), and result in predictable changes in bicarbonate concentration that can also be used to characterize the disorder (see = [(pCO2 -40)/10] +24= [(pCO2 -40)/3] +24 Acidosis: A physiologic process leading to acidemia Alkalosis: A physiologic process leading to alkalemi. Respiratory: The primary disorder results from an abnormal pCO2 --increased = acidosis; decreased = alkalosis Metabolic: The primary disorder does not result from abnormal pCO2 Mixed (Complex): More than one disorder is present Compensation: Changes in pCO2 or strong ions (Na+,Cl- ) resulting from normal physiologic mechanisms to restore acid-base balance Standard base excess (SBE): Quantity of metabolic acid-base disturbance where a positive value indicates alkalosis and a negative value (also referred to as a base deficit) indicates an acidosis Strong ion difference: The difference in charge between "strong" (completely dissociated) cations (positive) and anions (negative). (See pathophysiology section.) Anion gap: The difference in charge between commonly measured electrolytes (See laboratory findings section.) Acidosis: chloride administration (e.g. saline), aspirin overdose Alkalosis: NaHCO3 administration, antacid abuse, buffered replacement fluid (hemofiltration) Increased acid production: lactic acidosis, diabetic ketoacidosis Hypercapnic respiratory failure, permissive hypercapnia Alkalosis: vomiting, large gastric aspirates, diur Continue reading >>
Measure Electrolyte And Ketone Levels And Determine Anion Gap In Patients With Diabetes And Normal Sugar Levels
DIABETIC KETOACIDOSIS DX: Diabetic Ketoacidosis (DKA) when the blood glucose is >=250 mg/dL, arterial pH <=7.30, serum bicarbonate <=15 mEq/L, and positive serum ketones. (Hyperglycemia, ketonemia, ketonuria, metabolic acidosis) Screening for Diabetic Ketoacidosis - Consider DKA if hyperglycemia, acidosis, or ketonemia are present. Screen all patients with moderate to severely elevated blood sugars (glucose >350 mg/dL). Measure electrolytes, glucose, ketones, and blood gases to determine whether anion gap metabolic acidosis is present in patients with positive ketones, constitutional symptoms, or suspicion of DKA. in patients with an anion gap metabolic acidosis. Measure serum glucose in patients with metabolic acidosis. in diabetes patients with infection, CVA, MI, or other illness. Measure serum glucose and if glucose >250 mg/dL, check the patient's electrolyte and ketone levels and anion gap. in diabetic patients with symptoms of nausea and vomiting (with polyuria, polydipsia), even if blood glucose is <250 mg/dL. if symptoms suggest DKA despite normal blood sugar levels. in patients on atypical antipsychotics who present with hyperglycemia. Measure anion gap and ketones in patients on atypical antipsychotics who present with moderate to severe hyperglycemia. SX: Dehydration with hypotension, hyperventilation with fruity "acetone" odor, polyphagia, polydipsia, polyuria, altered mental status, N&V. History and Physical Examination Elements for Diabetic Ketoacidosis History Type 1 diabetes - DKA is a frequent complication of type 1 diabetes Constitutional symptoms - DKA may show vague symptoms of lethargy, diminished appetite, and headache Polyuria, polydipsia - May precede the development of DKA by 1 or 2 days, especially if intercurrent illness (infection) is present Continue reading >>
Diabetic Ketoacidosis: Evaluation And Treatment
Diabetic ketoacidosis is characterized by a serum glucose level greater than 250 mg per dL, a pH less than 7.3, a serum bicarbonate level less than 18 mEq per L, an elevated serum ketone level, and dehydration. Insulin deficiency is the main precipitating factor. Diabetic ketoacidosis can occur in persons of all ages, with 14 percent of cases occurring in persons older than 70 years, 23 percent in persons 51 to 70 years of age, 27 percent in persons 30 to 50 years of age, and 36 percent in persons younger than 30 years. The case fatality rate is 1 to 5 percent. About one-third of all cases are in persons without a history of diabetes mellitus. Common symptoms include polyuria with polydipsia (98 percent), weight loss (81 percent), fatigue (62 percent), dyspnea (57 percent), vomiting (46 percent), preceding febrile illness (40 percent), abdominal pain (32 percent), and polyphagia (23 percent). Measurement of A1C, blood urea nitrogen, creatinine, serum glucose, electrolytes, pH, and serum ketones; complete blood count; urinalysis; electrocardiography; and calculation of anion gap and osmolar gap can differentiate diabetic ketoacidosis from hyperosmolar hyperglycemic state, gastroenteritis, starvation ketosis, and other metabolic syndromes, and can assist in diagnosing comorbid conditions. Appropriate treatment includes administering intravenous fluids and insulin, and monitoring glucose and electrolyte levels. Cerebral edema is a rare but severe complication that occurs predominantly in children. Physicians should recognize the signs of diabetic ketoacidosis for prompt diagnosis, and identify early symptoms to prevent it. Patient education should include information on how to adjust insulin during times of illness and how to monitor glucose and ketone levels, as well as i Continue reading >>
