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Emergency Management Of Diabetic Ketoacidosis In Adults

Emergency Management Of Diabetic Ketoacidosis In Adults

Diabetic ketoacidosis (DKA) is a potentially fatal metabolic disorder presenting most weeks in most accident and emergency (A&E) departments.1 The disorder can have significant mortality if misdiagnosed or mistreated. Numerous management strategies have been described. Our aim is to describe a regimen that is based, as far as possible, on available evidence but also on our experience in managing patients with DKA in the A&E department and on inpatient wards. A literature search was carried out on Medline and the Cochrane Databases using “diabetic ketoacidosis” as a MeSH heading and as textword. High yield journals were hand searched. Papers identified were appraised in the ways described in the Users’ guide series published in JAMA. We will not be discussing the derangements in intermediary metabolism involved, nor would we suggest extrapolating the proposed regimen to children. Although some of the issues discussed may be considered by some to be outwith the remit of A&E medicine it would seem prudent to ensure that A&E staff were aware of the probable management of such patients in the hours after they leave the A&E department. AETIOLOGY AND DEFINITION DKA may be the first presentation of diabetes. Insulin error (with or without intercurrent illness) is the most common precipitating factor, accounting for nearly two thirds of cases (excluding those where DKA was the first presentation of diabetes mellitus).2 The main features of DKA are hyperglycaemia, metabolic acidosis with a high anion gap and heavy ketonuria (box 1). This contrasts with the other hyperglycaemic diabetic emergency of hyperosmolar non-ketotic hyperglycaemia where there is no acidosis, absent or minimal ketonuria but often very high glucose levels (>33 mM) and very high serum sodium levels (>15 Continue reading >>

Diabetic Emergencies-diagnosis And Clinical Management: Diabetic Ketoacidosis In Adults, Part 2

Diabetic Emergencies-diagnosis And Clinical Management: Diabetic Ketoacidosis In Adults, Part 2

Hyperglycemia Hyperglycemia in DKA is the result of reduced glucose uptake and utilization from the liver, muscle, and fat tissue and increased gluconeogenesis as well as glycogenolysis. The lack of insulin results in an increase in gluconeogenesis, primarily in the liver but also in the kidney, and increased glycogenolysis in liver and muscle.8,9 In addition, the inhibitory effect of insulin on glucagon secretion is abolished and plasma glucagon levels increase. The increase of glucagon aggravates hyperglycemia by enhancing gluconeogenesis and glycogenolysis. In parallel, the increased concentrations of the other counter-regulatory hormones enhance further gluconeogenesis. In addition to increased gluconeogenesis, in DKA there is excess production of substances which are used as a substrate for endogenous glucose production. Thus, the amino acids glutamine and alanine increase because of enhanced proteolysis and reduced protein synthesis.8,9 Hyperglycemia-induced osmotic diuresis leads to dehydration, hyperosmolality, electrolyte loss (Na+, K +, Mg 2 +, PO 4 3+, Cl−, and Ca+), and eventually decline in glomerular filtration rate. With decline in renal function, glucosuria diminishes and hyperglycemia worsens. Dehydration results in augmentation of plasma osmolality, which results in water movement out of the cells to the extracellular space. Osmotic diuresis caused by hyperglycemia results in loss of sodium in urine; in addition, the excess of glucagon aggravates hyponatremia because it inhibits reabsorption of sodium in the kidneys. With impaired insulin action and hyperosmolality, utilization of potassium by skeletal muscles is markedly decreased leading to intracellular potassium deficiency. Potassium is also lost due to osmotic diuresis. In addition, metabolic ac Continue reading >>

* Diabetic Ketoacidosis

* Diabetic Ketoacidosis

* Diabetic Ketoacidosis #155767 malak - 01/24/07 22:35 Diabetic Ketoacidosis In children under 10 years of age, diabetic ketoacidosis causes 70% of diabetes-related deaths. Diabetic ketoacidosis is defined by the triad of hyperglycemia, acidosis, and ketosis. Clinical Presentation Diabetes is newly diagnosed in 20% of cases of diabetic ketoacidosis. The remainder of cases occur in known diabetics in whom ketosis develops because of a precipitating factor, such as infection or noncompliance with insulin. Symptoms of DKA include polyuria, polydipsia, fatigue, nausea, and vomiting, developing over 1 to 2 days. Abdominal pain is prominent in 25%. Physical Exam Patients are typically flushed, tachycardic, and tachypneic. Kussmaul's respiration, with deep breathing and air hunger, occurs when the serum pH is between 7.0 and 7.24. A fruity odor on the breath indicates the presence of acetone, a by-product of diabetic ketoacidosis. Fever is seldom present even though infection is common. Hypothermia and hypotension may also occur. Eighty percent of patients with diabetic ketoacidosis have altered mental status. Most are awake but confused; 10% are comatose. Laboratory Findings Serum glucose level >250 mg/dL pH <7.35 Bicarbonate level below normal with an elevated anion gap Presence of ketones in the serum Indications for Hospital Admission of Patients with Diabetic Ketoacidosis Hyperglycemia (glucose >250 mg/dL) Arterial pH <7.35, or venous pH <7.30, or serum bicarbonate <15 mEq/L Ketonuria, ketonemia, or both Differential Diagnosis Differential Diagnosis of Ketosis-Causing Conditions Alcoholic ketoacidosis does not cause an elevated serum glucose. Alcoholic ketoacidosis occurs with heavy drinking and vomiting. Starvation ketosis occurs after 24 hours without food and is not us Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetes mellitus is the name given to a group of conditions whose common hallmark is a raised blood glucose concentration (hyperglycemia) due to an absolute or relative deficiency of the pancreatic hormone insulin. In the UK there are 1.4 million registered diabetic patients, approximately 3 % of the population. In addition, an estimated 1 million remain undiagnosed. It is a growing health problem: In 1998, the World Health Organization (WHO) predicted a doubling of the worldwide prevalence of diabetes from 150 million to 300 million by 2025. For a very tiny minority, diabetes is a secondary feature of primary endocrine disease such as acromegaly (growth hormone excess) or Cushing’s syndrome (excess corticosteroid), and for these patients successful treatment of the primary disease cures diabetes. Most diabetic patients, however, are classified as suffering either type 1 or type 2 diabetes. Type 1 diabetes Type 1 diabetes, which accounts for around 15 % of the total diabetic population, is an autoimmune disease of the pancreas in which the insulin-producing β-cells of the pancreas are selectively destroyed, resulting in an absolute insulin deficiency. The condition arises in genetically susceptible individuals exposed to undefined environmental insult(s) (possibly viral infection) early in life. It usually becomes clinically evident and therefore diagnosed during late childhood, with peak incidence between 11 and 13 years of age, although the autoimmune-mediated β-cell destruction begins many years earlier. There is currently no cure and type 1 diabetics have an absolute life-long requirement for daily insulin injections to survive. Type 2 diabetes This is the most common form of diabetes: around 85 % of the diabetic population has type 2 diabetes. The primary prob Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic Ketoacidosis Definition Diabetic ketoacidosis is a dangerous complication of diabetes mellitus in which the chemical balance of the body becomes far too acidic. Description Diabetic ketoacidosis (DKA) always results from a severe insulin deficiency. Insulin is the hormone secreted by the body to lower the blood sugar levels when they become too high. Diabetes mellitus is the disease resulting from the inability of the body to produce or respond properly to insulin, required by the body to convert glucose to energy. In childhood diabetes, DKA complications represent the leading cause of death, mostly due to the accumulation of abnormally large amounts of fluid in the brain (cerebral edema). DKA combines three major features: hyperglycemia, meaning excessively high blood sugar kevels; hyperketonemia, meaning an overproduction of ketones by the body; and acidosis, meaning that the blood has become too acidic. Insulin deficiency is responsible for all three conditions: the body glucose goes largely unused since most cells are unable to transport glucose into the cell without the presence of insulin; this condition makes the body use stored fat as an alternative source instead of the unavailable glucose for energy, a process that produces acidic ketones, which build up because they require insulin to be broken down. The presence of excess ketones in the bloodstream in turn causes the blood to become more acidic than the body tissues, which creates a toxic condition. Causes and symptoms DKA is most commonly seen in individuals with type I diabetes, under 19 years of age and is usually caused by the interruption of their insulin treatment or by acute infection or trauma. A small number of people with type II diabetes also experience ketoacidosis, but this is rare give Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

© 1996–2017 themedicalbiochemistrypage.org, LLC | info @ themedicalbiochemistrypage.org Definition of Diabetic Ketoacidosis The most severe and life threatening complication of poorly controlled type 1 diabetes is diabetic ketoacidosis (DKA). DKA is characterized by metabolic acidosis, hyperglycemia and hyperketonemia. Diagnosis of DKA is accomplished by detection of hyperketonemia and metabolic acidosis (as measured by the anion gap) in the presence of hyperglycemia. The anion gap refers to the difference between the concentration of cations other than sodium and the concentration of anions other than chloride and bicarbonate. The anion gap therefore, represents an artificial assessment of the unmeasured ions in plasma. Calculation of the anion gap involves sodium (Na+), chloride (Cl–) and bicarbonate (HCO3–) measurements and it is defined as [Na+ – (Cl– + HCO3–)] where the sodium and chloride concentrations are measured as mEq/L and the bicarbonate concentration is mmol/L. The anion gap will increase when the concentration of plasma K+, Ca2+, or Mg2+ is decreased, when organic ions such as lactate are increased (or foreign anions accumulate), or when the concentration or charge of plasma proteins increases. Normal anion gap is between 8mEq/L and 12mEq/L and a higher number is diagnostic of metabolic acidosis. Rapid and aggressive treatment is necessary as the metabolic acidosis will result in cerebral edema and coma eventually leading to death. The hyperketonemia in DKA is the result of insulin deficiency and unregulated glucagon secretion from α-cells of the pancreas. Circulating glucagon stimulates the adipose tissue to release fatty acids stored in triglycerides. The free fatty acids enter the circulation and are taken up primarily by the liver where Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

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 the Pre-diabetes (Impaired Glucose Tolerance) article more useful, or one of our other health articles. See also the separate Childhood Ketoacidosis article. Diabetic ketoacidosis (DKA) is a medical emergency with a significant morbidity and mortality. It should be diagnosed promptly and managed intensively. DKA is characterised by hyperglycaemia, acidosis and ketonaemia:[1] Ketonaemia (3 mmol/L and over), or significant ketonuria (more than 2+ on standard urine sticks). Blood glucose over 11 mmol/L or known diabetes mellitus (the degree of hyperglycaemia is not a reliable indicator of DKA and the blood glucose may rarely be normal or only slightly elevated in DKA). Bicarbonate below 15 mmol/L and/or venous pH less than 7.3. However, hyperglycaemia may not always be present and low blood ketone levels (<3 mmol/L) do not always exclude DKA.[2] Epidemiology DKA is normally seen in people with type 1 diabetes. Data from the UK National Diabetes Audit show a crude one-year incidence of 3.6% among people with type 1 diabetes. In the UK nearly 4% of people with type 1 diabetes experience DKA each year. About 6% of cases of DKA occur in adults newly presenting with type 1 diabetes. About 8% of episodes occur in hospital patients who did not primarily present with DKA.[2] However, DKA may also occur in people with type 2 diabetes, although people with type 2 diabetes are much more likely to have a hyperosmolar hyperglycaemic state. Ketosis-prone type 2 diabetes tends to be more common in older, overweight, non-white people with type 2 diabetes, and DKA may be their Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Practice Essentials Diabetic ketoacidosis (DKA) is an acute, major, life-threatening complication of diabetes that mainly occurs in patients with type 1 diabetes, but it is not uncommon in some patients with type 2 diabetes. This condition is a complex disordered metabolic state characterized by hyperglycemia, ketoacidosis, and ketonuria. Signs and symptoms The most common early symptoms of DKA are the insidious increase in polydipsia and polyuria. The following are other signs and symptoms of DKA: Nausea and vomiting; may be associated with diffuse abdominal pain, decreased appetite, and anorexia History of failure to comply with insulin therapy or missed insulin injections due to vomiting or psychological reasons or history of mechanical failure of insulin infusion pump Altered consciousness (eg, mild disorientation, confusion); frank coma is uncommon but may occur when the condition is neglected or with severe dehydration/acidosis Signs and symptoms of DKA associated with possible intercurrent infection are as follows: See Clinical Presentation for more detail. Diagnosis On examination, general findings of DKA may include the following: Characteristic acetone (ketotic) breath odor In addition, evaluate patients for signs of possible intercurrent illnesses such as MI, UTI, pneumonia, and perinephric abscess. Search for signs of infection is mandatory in all cases. Testing Initial and repeat laboratory studies for patients with DKA include the following: Serum electrolyte levels (eg, potassium, sodium, chloride, magnesium, calcium, phosphorus) Note that high serum glucose levels may lead to dilutional hyponatremia; high triglyceride levels may lead to factitious low glucose levels; and high levels of ketone bodies may lead to factitious elevation of creatinine levels. Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

I. Review of normal lipid metabolism Triglycerides in adipose ==lipolysis==> Long-chain FAs Long-chain FAs==hepatic beta-oxidation==>Acetyl CoA Acetyl CoA==hepatic ketogenesis==>ketone bodies Ketone bodies are Beta-hydroxybutyrate and Acetoacetate Beta-OHB is oxidized to AcAc-; their relative concentrations depend on redox state of cell; Beta-OHB predominates in situation favoring reductive metabolism (e.g. decreased tissue perfusion, met. acidosis, catabolic states--like DKA!) Typical ratio Beta-OHB:AcAc- is 3:1; us. increases in DKA II. Hormonal influences on glucose and lipid metabolism Insulin In liver, increases glu uptake from portal blood; stimulates glycogenesis, inhibits glycogenolysis and gluconeogenesis In skeletal muscle, increases glu uptake from blood, stimulates protein synth, inhibits proteolysis In adipose tissue, required for glu and lipoprotein uptake from blood; stimulates lipogenesis, inhibits lipolysis Tissues which don't require insulin to transport glucose into cells: brain, renal medulla, formed blood elements Counterregulatory hormones: glucagon (major player in DKA), epi/norepi, cortisol, growth hormone (no acute effects, only over days-weeks) Glucagon: increases hepatic beta-oxidation, ketogenesis, gluconeogenesis and glycogenolysis; decreases hepatic FA synth. Epi/Norepi: increase hepatic gluconeogenesis & glycogenolysis; increases adipose lipolysis; decreases peripheral glu utilization Cortisol: major effect is decreased peripheral glu utiliz; little effect on production Growth hormone: increases hepatic gluconeogenesis and glycogenolysis; increases adipose lipolysis In high counterreg. hormone states (see above), require high levels of insulin to avoid progressive hyperglycemia and ketoacidosis--glucagon levels in DKA are 5-6 x nl* III. Pa Continue reading >>

Bicarbonate Therapy In Severe Diabetic Ketoacidosis

Bicarbonate Therapy In Severe Diabetic Ketoacidosis

Twenty-one adult patients with severe diabetic ketoacidosis entered a randomized prospective protocol in which variable doses of sodium bicarbonate, based on initial arterial pH (6.9 to 7.14), were administered to 10 patients (treatment group) and were withheld from 11 patients (control group). During treatment, there were no significant differences in the rate of decline of glucose or ketone levels or in the rate of increase in pH or bicarbonate levels in the blood or cerebrospinal fluid in either group. Similarly, there were no significant differences in the time required for the plasma glucose level to reach 250 mg/dL, blood pH to reach 7.3, or bicarbonate level to reach 15 meq/L. We conclude that in severe diabetic ketoacidosis (arterial pH 6.9 to 7.14), the administration of bicarbonate does not affect recovery outcome variables as compared with those in a control group. Continue reading >>

Diabetic Ketoacidosis Guidelines

Diabetic Ketoacidosis Guidelines

Diabetic ketoacidosis is a complication of diabetes mellitus that results in blood glucose levels of more than 250 mg/dL, a serum bicarb level of less than 18 mEq/l, a blood pH level of less than 7.3, increased serum ketone levels, and clinical hydration. The main cause of diabetic ketoacidosis (DKA) is a lack of insulin in the body. Diabetic ketoacidosis can happen in any type of diabetic and in diabetics of all ages; however, it is most commonly seen in type 1 diabetics. Statistically, 14 percent of DKA occurs in people who are 70 years of age or older, 23 percent of DKA is seen in people between 51 and 70, 27 percent is seen in those 30 to 50 years of age, while 36 percent occur in people who are under 30 years of age. About one to five percent of people with DKA ultimately die from their condition. About a third of all people with DKA do not know they have diabetes before having their first bout of ketoacidosis. Typical symptoms seen in the disease include weight loss, increased thirst, increased frequency of urination, abdominal pain, shortness of breath, nausea and vomiting, and a history of a recent fever. Even though there have been many advances in the treatment of DKA, the rate of morbidity and mortality remain high. In one study involving almost 29,000 individuals with diabetes who were under the age of 20 years, the vast majority (94 percent) of individuals had no DKA episodes, 5 percent had only a single episode of DKA, while 1 percent had at least 2 episodes of DKA. The most common cause of death in DKA patients is cerebral edema. Although most people with DKA have a preexisting case of diabetes, up to 37 percent of people did not know they had diabetes when they had their first episode of the disorder. This is especially the case in young children with a Continue reading >>

Electrolyte Imbalance In Diabetic Ketoacidosis

Electrolyte Imbalance In Diabetic Ketoacidosis

If you have diabetes, it's important to be familiar with diabetic ketoacidosis (DKA). DKA is a serious complication of diabetes that occurs when lack of insulin and high blood sugar lead to potentially life-threatening chemical imbalances. The good news is DKA is largely preventable. Although DKA is more common with type 1 diabetes, it can also occur with type 2 diabetes. High blood sugar causes excessive urination and spillage of sugar into the urine. This leads to loss of body water and dehydration as well as loss of important electrolytes, including sodium and potassium. The level of another electrolyte, bicarbonate, also falls as the body tries to compensate for excessively acidic blood. Video of the Day Insulin helps blood sugar move into cells, where it is used for energy production. When insulin is lacking, cells must harness alternative energy by breaking down fat. Byproducts of this alternative process are called ketones. High concentrations of ketones acidify the blood, hence the term "ketoacidosis." Acidosis causes unpleasant symptoms like nausea, vomiting and rapid breathing. Bicarbonate is an electrolyte that normally counteracts blood acidity. In DKA, the bicarbonate level falls as ketone production increases and acidosis progresses. Treatment of DKA includes prompt insulin supplementation to lower blood sugar, which leads to gradual restoration of the bicarbonate level. Potassium may be low in DKA because this electrolyte is lost due to excessive urination or vomiting. When insulin is used to treat DKA, it can further lower the blood potassium by pushing it into cells. Symptoms associated with low potassium include fatigue, muscle weakness, muscle cramps and an irregular heart rhythm. Severely low potassium can lead to life-threatening heart rhythm abnorm Continue reading >>

Pseudo Dka Secondary To Severe Hypertriglyceridemia

Pseudo Dka Secondary To Severe Hypertriglyceridemia

Abstract: Case presentation : A 44 year old female presented with a 24 hour history of abdominal pain radiating to the back,lethargy, nausea, vomiting, and a fever of 103.7. Past medical history is significant for lipodystrophiy, diabetes mellitus, hypertriglyceridemia, previous episode of pancreatitis, psoriatic arthritis. The patient does not smoke,drink, or use any non-prescription drugs. The patient was noncompliant in taking fenofibrate, methotrexate, andlevemir. The physical exam was significant for abdominal distension in the epigastric region. Vital signsshowed a blood pressure of 143/74, pulse 101. Respirations 16, pulse ox of 99, and a temperature of 38.1. Laboratory findings revealed Hgb of 15.5, platelet count of 246, and WBC of 11.3. Sodium was 131, chloride97, potassium 3.6, bicarbonate 5 mEq/L , Cr 0.73, glucose level of 321, and . Lipase was 1,228U/L and amylase was 90 U/L. Lipid panel showed cholesterol at 632 mg/dL, triglycerides at 4,502 mg/dL, patient received fluids,intravenous insulin , and IV antibiotics. The day after, serum glucose was 167 mg/dL, lipase decreased to 769, sodium was down to 127, triglycerides were still 4,500 mg/dL, and the bicarbonate dropped to 3 mEq/L . Patient was kept on DKA protocol for extra day because of persistant Anion gap acidosis The endocrinology consult was obtained for hard to treat DKA , ABG was ordered and showed normal PH 7.39 with Bicarb of 20 while concomitant serum Bicarb 3 mEq/L . and it was concluded that hyponatremia and low bicarbonate were due to dilutionional effect of severe hypertriglyceredimia. plasmapheresis was intitated with normalization of serum bicarbonate after significant improvement in tryiglyceride level . Discussion: Insulin deficiency in DKA enables the increase release of free fatty aci Continue reading >>

Pulmcrit – Four Dka Pearls

Pulmcrit – Four Dka Pearls

Introduction I have a confession to make: I love treating DKA. It’s satisfying to take a patient from severe acidosis, electrolytic disarray, and hypovolemia to normal physiology during an ICU shift. Although it's usually straightforward, there are some pitfalls and a few tricks that may help your patients improve faster.0 Pearl #1: Avoid normal saline A common phenomenon observed when starting a DKA resuscitation with normal saline (NS) is worseningof the patient’s acidosis with decreasing bicarbonate levels (example below). This occurs despite an improvement in the anion gap, and is explained by a hyperchloremic metabolic acidosis caused by bolusing with NS. This could be a real problem for a patient whose initial bicarbonate level is extremely low.1 A while ago I made the switch from NS to lactated ringers (LR) for resuscitation of DKA patients, and have not observed this phenomenon when using LR. Example of the effect of normal saline resuscitation during the initial phase of DKA resuscitation. This patient received approximately 3 liters normal saline between admission labs and the next set of labs as well as an insulin infusion, all textbook management per American Diabetes Association guidelines. The anion gap decreased from 33 mEq/L to 30 mEq/L, indicating improvement of ketoacidosis. However, the bicarbonate decreased from 8 mEq/L to 5 mEq/L due to a hyperchloremic metabolic acidosis caused by the normal saline. Note the increase in chloride over four hours. Failure of the potassium to decrease significantly despite insulin infusion may reflect potassium shifting out of the cells in response to the hyperchloremic metabolic acidosis. There is only one randomized controlled trial comparing NS to LR for resuscitation in DKA (Zyl et al, 2011). These authors fou 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 >>

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