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Paradoxical Hyperkalemia In Dka

Drug Treatment For Diabetic Ketoacidosis

Drug Treatment For Diabetic Ketoacidosis

Insulin (regular insulin; insulin aspart; insulin lispro; insulin glulisine; isophane insulin [NPH]; lente insulin; ultralente insulin; insulin glargine; insulin detemir; insulin lispro, insulin lispro protamine; insulin aspart, insulin aspart protamine; regular insulin, isophane insulin [NPH]; semilente insulin; protamine zinc insulin [PZI]) Corrects insulin deficiency and overcomes insulin resistance. Allows shift of glucose into cells and suppresses hepatic glucose production Initial bolus of 0.15 U/kg, then 0.1 U/kg·h iv. Hold insulin until K is >3.3 mEq/L Correct hyperglycemia and stop ketogenesis Hypoglycemia, hypokalemia. Low-dose insulin less likely to cause hypoglycemia or hypokalemia Once blood glucose level is ~200 mg/dL, switch fluids to include dextrose 5%-10%. Target blood glucose to 150-200 mg/dL. Once DKA is resolved (blood glucose 200 mg/dL, bicarbonate 18 mEq/L, pH >7.30) subcutaneous insulin therapy with multiple dose insulin can begin at 0.5-0.8 U/kg·d. Overlap therapy for 1-2 h before stopping iv regular insulin. If patient is unable to eat, continue iv insulin therapy Potassium Replace potassium deficit Replace at rate of 20-30 mEq/h if K is <3.3 mEq/L. Use 20 mEq/h if >3.3 and <5.0-5.5 mEq/L Reverse hypokalemia and associated complications Risk of over treatment leading to hyperkalemia. Use cautiously in anuric patients and only if K+ is <3.3 mEq/L Monitor potassium at least every 2 hours until normal. KCl is most common form of potassium replacement. Can use 2/3 KCl and 1/3 KPO4 to prevent excessive Cl levels Sodium bicarbonate Corrects metabolic acidosis If pH is <6.9 give 100 mmol NaHCO3 in 400 mL water at 200 mL/h. If pH is 6.9 to 7.0, give 50 mmol of NaHCO3 in 200 mL sterile water at 200 mL/h, repeat every 2 hours until pH is >7 By correcti Continue reading >>

Dynamic Changes In Serum Phosphorus Levels In Diabetic Ketoacidosis

Dynamic Changes In Serum Phosphorus Levels In Diabetic Ketoacidosis

Volume 79, Issue 5 , November 1985, Pages 571-576 Dynamic changes in serum phosphorus levels in diabetic ketoacidosis Author links open overlay panel R.KeblerM.D. F.D.McDonaldM.D. P.CadnapaphornchaiM.D. Get rights and content The dynamic changes in serum phosphorus levels in 69 episodes of ketoacidosis in 48 diabetic patients were retrospectively evaluated. The mean age was 41 2 years (mean SEM), and the duration of diabetes mellitus was 7 1 years. The serum phosphorus levels determined within the first six hours of admission were analyzed. Before initiation of therapy, the incidence of hyperphosphatemia was 94.7 percent. At the end of 12 hours, the mean serum phosphorus level fell from 9.2 0.6 to 2.8 0.3 mg/dl. Before therapy, the serum phosphorus level correlated positively with the serum glucose level, the effective plasma osmolality, and anion gaps, and correlated negatively with the serum chloride level. It is concluded that hyperphosphatemia is common in diabetic ketoacidosis before therapy. The increase in serum phosphorus is likely to be due to a transcellular shift. Potential factors responsible for the shift are serum glucose, through its osmotic effect, and the organic anions. Continue reading >>

Diabetic Emergencies: Diabetic Ketoacidosis In Childhood And Adolescence, Part 3 Of 3

Diabetic Emergencies: Diabetic Ketoacidosis In Childhood And Adolescence, Part 3 Of 3

Severe acidosis is reversible by fluid and insulin replacement. Insulin stops lipolysis and further ketone production and allows ketoacids to be metabolized, generating bicarbonate.4 Moreover, treatment of hypovolemia improves tissue perfusion and renal function, thereby increasing the excretion of organic acids. Controlled trials have shown no clinical benefit from bicarbonate administration 3,4 and there are well-recognized serious adverse effects, including paradoxical CNS acidosis 28,29 and hypokalemia from rapid acidosis correction. 30,31 Nevertheless, there may be selected patients who may profit from cautious alkali administration, such as patients with severe acidemia (arterial pH < 6.9) in whom decreased cardiac contractility and peripheral vasodilatation can further impair tissue perfusion, and patients with life-threatening hyperkalemia. 4,32…. If bicarbonate is considered necessary, cautiously give 1-2 mmol/kg over 60 minutes. 3,4 Follow-up management — transition to per os fluid intake and SC insulin injections Oral fluids should be introduced only when substantial clinical improvement has occurred and when oral fluids are well tolerated; IV fluid administration should then be reduced. The most convenient time to change to SC insulin is just before a mealtime, provided that ketoacidosis has resolved (venous pH > 7.3 and serum bicarbonate > 18 mmol/L), plasma glucose is < 200 mg/dl (11.1 mmol/L), and oral fluid intake is well tolerated. To prevent rebound hyperglycemia, the first SC insulin injection should be given 15-30 minutes (with rapid-acting insulin analog) or 1-2 hours (with regular insulin) before stopping the insulin infusion to allow sufficient time for the insulin to be absorbed. With intermediate or long-acting insulin the overlap should be Continue reading >>

Paradoxical Glucose-induced Hyperkalemia. Combined Aldosterone-insulin Deficiency.

Paradoxical Glucose-induced Hyperkalemia. Combined Aldosterone-insulin Deficiency.

Paradoxical glucose-induced hyperkalemia. Combined aldosterone-insulin deficiency. Goldfarb S , Strunk B , Singer I , Goldberg M . Severe hyperkalemia associated with spontaneous hyperglycemia as well as with the intravenous infusions of glucose occurred in an insulin-requiring diabetic patient in the absence of potassium administration, the use of diuretics which inhibit urinary potassium excretion or acidemia. Metabolic balance studies revealed, in addition to diabets, the presence of isolated aldosterone deficiency of the hyporeninemic type. Intravenous glucose infusions (0.5 g/kg body weight) produced significant hyperkalemia but desoxycortisone acetate (DOCA) therapy (10 mg/day) prevented the glucose-induced hyperkalemia. In this patient, the serum potassium concentration increases after the intravenous infusions of glucose because there is insufficient aldosterone and insulin to reverse the transfer of potassium to the extracellular fluid which normally occurs after hypertonic infusions of glucose. Although DOCA replacement modifies the distribution of potassium in the extracellular fluid and blunts the hyperkalemic effect of intravenous infusions of glucose, a rise in the insulin level is required for the usual hypokalemic response to intravenously administered glucose. These studies illustrate the risk of raising blood glucose levels in patients with combined aldosterone and insulin deficiency and the tendency towards hyperkalemia in diabetic patients under certain clinical conditions. Continue reading >>

Usmle Endocrine I

Usmle Endocrine I

Home > Preview Clinical Features: coarse facial features, arthralgias, uncontrolled hypertension, enlargement of the digits·, carpal tunnel syndrome. This condition is caused by excessive secretion of growth hormone (GH), usually due to a pituitary somatotroph adenoma. Other common features include malocclusion of the jaw, hyperhidrosis, heart failure, macroglossia, and local mass-effect symptoms (eg, headache, visual field defects). GH stimulates hepatic insulin-like growth factor 1 (IGF-1) secretion, which is responsible for most of the clinical manifestations of acromegaly. IGF-1 levels in acromegaly are consistently elevated throughout the day. In contrast, GH levels can fluctuate widely and cannot be used alone to diagnose acromegaly. As a result, IGF-1 is the preferred initial test. Patients with elevated IGF-1 should undergo confirmatory testing with an oral glucose suppression test Once acromegaly is confirmed with a glucose suppression test, patients should have an MRI of the brain to identify a pituitary mass. Acromegaly causes concentric myocardial hypertrophy leading to diastolic dysfunction, along with left ventricular dilation and global hypokinesis. This cardiomyopathy is worsened by concurrent hypertension, obstructive sleep apnea , and valvular heart disease, which are common in acromegaly. Complications include heart failure (eg, dyspnea, crackles at bases) and arrhythmias. Cardiovascular disease is the leading cause of death in patients with acromegaly, but normalization of growth hormone levels following successful treatment markedly reduces cardiovascular mortality. a congenital cardiomyopathy that should be distinguished from myocardial hypertrophy due to other cardiovascular diseases (eg, hypertensive, valvular, ischemic) - is characterized by as Continue reading >>

Management Of Adult Diabetic Ketoacidosis

Management Of Adult Diabetic Ketoacidosis

Go to: Abstract Diabetic ketoacidosis (DKA) is a rare yet potentially fatal hyperglycemic crisis that can occur in patients with both type 1 and 2 diabetes mellitus. Due to its increasing incidence and economic impact related to the treatment and associated morbidity, effective management and prevention is key. Elements of management include making the appropriate diagnosis using current laboratory tools and clinical criteria and coordinating fluid resuscitation, insulin therapy, and electrolyte replacement through feedback obtained from timely patient monitoring and knowledge of resolution criteria. In addition, awareness of special populations such as patients with renal disease presenting with DKA is important. During the DKA therapy, complications may arise and appropriate strategies to prevent these complications are required. DKA prevention strategies including patient and provider education are important. This review aims to provide a brief overview of DKA from its pathophysiology to clinical presentation with in depth focus on up-to-date therapeutic management. Keywords: DKA treatment, insulin, prevention, ESKD Go to: Introduction In 2009, there were 140,000 hospitalizations for diabetic ketoacidosis (DKA) with an average length of stay of 3.4 days.1 The direct and indirect annual cost of DKA hospitalizations is 2.4 billion US dollars. Omission of insulin is the most common precipitant of DKA.2,3 Infections, acute medical illnesses involving the cardiovascular system (myocardial infarction, stroke) and gastrointestinal tract (bleeding, pancreatitis), diseases of the endocrine axis (acromegaly, Cushing’s syndrome), and stress of recent surgical procedures can contribute to the development of DKA by causing dehydration, increase in insulin counter-regulatory hor Continue reading >>

Hypokalemia

Hypokalemia

Hypokalemia, also spelled hypokalaemia, is a low level of potassium (K+) in the blood serum.[1] Normal potassium levels are between 3.5 and 5.0 mmol/L (3.5 and 5.0 mEq/L) with levels below 3.5 mmol/L defined as hypokalemia.[1][2] Mildly low levels do not typically cause symptoms.[3] Symptoms may include feeling tired, leg cramps, weakness, and constipation.[1] It increases the risk of an abnormal heart rhythm, which are often too slow, and can cause cardiac arrest.[1][3] Causes of hypokalemia include diarrhea, medications like furosemide and steroids, dialysis, diabetes insipidus, hyperaldosteronism, hypomagnesemia, and not enough intake in the diet.[1] It is classified as severe when levels are less than 2.5 mmol/L.[1] Low levels can also be detected on an electrocardiogram (ECG).[1] Hyperkalemia refers to a high level of potassium in the blood serum.[1] The speed at which potassium should be replaced depends on whether or not there are symptoms or ECG changes.[1] Mildly low levels can be managed with changes in the diet.[3] Potassium supplements can be either taken by mouth or intravenously.[3] If given by intravenous, generally less than 20 mmol are given over an hour.[1] High concentration solutions (>40 mmol/L) should be given in a central line if possible.[3] Magnesium replacement may also be required.[1] Hypokalemia is one of the most common water–electrolyte imbalances.[4] It affects about 20% of people admitted to hospital.[4] The word "hypokalemia" is from hypo- means "under"; kalium meaning potassium, and -emia means "condition of the blood".[5] Play media Video explanation Signs and symptoms[edit] Mild hypokalemia is often without symptoms, although it may cause elevation of blood pressure,[6] and can provoke the development of an abnormal heart rhythm. Se 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: Malaise, generalized weakness, and fatigability Nausea and vomiting; may be associated with diffuse abdominal pain, decreased appetite, and anorexia Rapid weight loss in patients newly diagnosed with type 1 diabetes 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) Serum or capillary beta-hydroxybutyrate levels Urine and blood cultures if intercurrent infection is suspected ECG Continue reading >>

3,518 Possible Causes For Hyperkalemia + Ketonuria + Ketosis + Bicarbonate Increased + Metabolic Acidosis In Usa

3,518 Possible Causes For Hyperkalemia + Ketonuria + Ketosis + Bicarbonate Increased + Metabolic Acidosis In Usa

Acidosis Hyperkalemia Bicarbonate Increased Ketonuria Ketosis It is due to the accumulation of ketoacids (via excessive ketosis) and reflects a severe shift from glycolysis to lipolysis for energy needs.[en.wikipedia.org] Causes: Metabolic Acidosis and Elevated Anion Gap (Mnemonic: "MUD PILERS") Methanol , Metformin Uremia Diabetic Ketoacidosis (DKA), Alcohol ic ketoacidosis or starvation ketosis[fpnotebook.com] An increase in the production of other acids may also produce metabolic acidosis.[en.wikipedia.org] Hyperkalemia (hyperpotassemia) is the presence of an abnormally high concentration of potassium in the blood. Ketosis is a condition characterized by elevated levels of ketone bodies (β-hydroxybutyric acid, acetoacetic acid, acetone) in the body. Acidosis Bicarbonate Decreased Bicarbonate Wasting Renal Tubular Acidosis Chronic Lactic Acidosis Distal Renal Tubular Acidosis Episodic Lactic Acidosis Episodic Metabolic Acidosis Hyperchloremic Metabolic Acidosis Hyperchloremic Metabolic Acidosis - HCO3 15.5 +- 2.0 mM Hyperkalemic Metabolic Acidosis Incomplete Distal Renal Tubular Acidosis Increased Basal Metabolic Rate Ketosis Is Exacerbated by Protein Ingestion Lactic Acidosis Lactic Acidosis May Be Mild Lactic Acidosis during Infection Lactic Acidosis in E3 Deficiency Metabolic Acidosis due to Renal Bicarbonate Loss Metabolic Acidosis in Infancy Mild Hyperchloremic Metabolic Acidosis Mild Metabolic Acidosis No Lactic Acidosis Persistent Lactic Acidosis Proximal Renal Tubular Acidosis Renal Tubular Acidosis Respiratory Acidosis Severe Lactic Acidosis Severe Metabolic Acidosis Transient Metabolic Acidosis that Resolves in Infancy List represents a sample of symptoms, diseases, and other queries. Updated weekly. Hungry Bones Syndrome Altitude Sickness Cavernous Sinus T Continue reading >>

Hyperkalemia (high Blood Potassium)

Hyperkalemia (high Blood Potassium)

How does hyperkalemia affect the body? Potassium is critical for the normal functioning of the muscles, heart, and nerves. It plays an important role in controlling activity of smooth muscle (such as the muscle found in the digestive tract) and skeletal muscle (muscles of the extremities and torso), as well as the muscles of the heart. It is also important for normal transmission of electrical signals throughout the nervous system within the body. Normal blood levels of potassium are critical for maintaining normal heart electrical rhythm. Both low blood potassium levels (hypokalemia) and high blood potassium levels (hyperkalemia) can lead to abnormal heart rhythms. The most important clinical effect of hyperkalemia is related to electrical rhythm of the heart. While mild hyperkalemia probably has a limited effect on the heart, moderate hyperkalemia can produce EKG changes (EKG is a reading of theelectrical activity of the heart muscles), and severe hyperkalemia can cause suppression of electrical activity of the heart and can cause the heart to stop beating. Another important effect of hyperkalemia is interference with functioning of the skeletal muscles. Hyperkalemic periodic paralysis is a rare inherited disorder in which patients can develop sudden onset of hyperkalemia which in turn causes muscle paralysis. The reason for the muscle paralysis is not clearly understood, but it is probably due to hyperkalemia suppressing the electrical activity of the muscle. Common electrolytes that are measured by doctors with blood testing include sodium, potassium, chloride, and bicarbonate. The functions and normal range values for these electrolytes are described below. Hypokalemia, or decreased potassium, can arise due to kidney diseases; excessive losses due to heavy sweating Continue reading >>

Treatment And Prevention Of Hyperkalemia In Adults

Treatment And Prevention Of Hyperkalemia In Adults

INTRODUCTION Hyperkalemia is a common clinical problem that is most often a result of impaired urinary potassium excretion due to acute or chronic kidney disease (CKD) and/or disorders or drugs that inhibit the renin-angiotensin-aldosterone system (RAAS). Therapy for hyperkalemia due to potassium retention is ultimately aimed at inducing potassium loss [1,2]. In some cases, the primary problem is movement of potassium out of the cells, even though the total body potassium may be reduced. Redistributive hyperkalemia most commonly occurs in uncontrolled hyperglycemia (eg, diabetic ketoacidosis or hyperosmolar hyperglycemic state). In these disorders, hyperosmolality and insulin deficiency are primarily responsible for the transcellular shift of potassium from the cells into the extracellular fluid, which can be reversed by the administration of fluids and insulin. Many of these patients have a significant deficit in whole body potassium and must be monitored carefully for the development of hypokalemia during therapy. (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Treatment", section on 'Potassium replacement'.) The treatment and prevention of hyperkalemia will be reviewed here. The causes, diagnosis, and clinical manifestations of hyperkalemia are discussed separately. (See "Causes and evaluation of hyperkalemia in adults" and "Clinical manifestations of hyperkalemia in adults".) DETERMINING THE URGENCY OF THERAPY The urgency of treatment of hyperkalemia varies with the presence or absence of the symptoms and signs associated with hyperkalemia, the severity of the potassium elevation, and the cause of hyperkalemia. Our approach to therapeutic urgency is as follows (algorithm 1): Continue reading >>

Diabetic Ketoacidosis | Tintinallis Emergency Medicine: A Comprehensive Study Guide, 8e | Accessmedicine | Mcgraw-hill Medical

Diabetic Ketoacidosis | Tintinallis Emergency Medicine: A Comprehensive Study Guide, 8e | Accessmedicine | Mcgraw-hill Medical

Diabetic ketoacidosis (DKA) is an acute, life-threatening complication of diabetes mellitus. DKA occurs predominantly in patients with type 1 (insulin-dependent) diabetes mellitus, but 10% to 30% of cases occur in newly diagnosed type 2 (noninsulin-dependent) diabetes mellitus, especially in African Americans and Hispanics. 1 , 2 Between 1993 and 2003, the yearly rate of U.S. ED visits for DKA was 64 per 10,000 with a trend toward an increased rate of visits among the African American population compared with the Caucasian population. 3 Europe has a comparable incidence. A better understanding of the pathophysiology of DKA and an aggressive, uniform approach to its diagnosis and management have reduced mortality to <5% of reported episodes in experienced centers. 4 However, mortality is higher in the elderly due to underlying renal disease or coexisting infection and in the presence of coma or hypotension. Figure 225-1 illustrates the complex relationships between insulin and counterregulatory hormones. DKA is a response to cellular starvation brought on by relative insulin deficiency and counterregulatory or catabolic hormone excess ( Figure 225-1 ). Insulin is the only anabolic hormone produced by the endocrine pancreas and is responsible for the metabolism and storage of carbohydrates, fat, and protein. Counterregulatory hormones include glucagon, catecholamines, cortisol, and growth hormone. Complete or relative absence of insulin and the excess counterregulatory hormones result in hyperglycemia (due to excess production and underutilization of glucose), osmotic diuresis, prerenal azotemia, worsening hyperglycemia, ketone formation, and a wide-anion-gap metabolic acidosis. 4 Insulin deficiency. Pathogenesis of diabetic ketoacidosis secondary to relative insulin def Continue reading >>

Hyperosmolar Hyperglycemic State

Hyperosmolar Hyperglycemic State

Acute hyperglycemia, or high blood glucose, may be either the initial presentation of diabetes mellitus or a complication during the course of a known disease. Inadequate insulin replacement (e.g., noncompliance with treatment) or increased insulin demand (e.g., during times of acute illness, surgery, or stress) may lead to acute hyperglycemia. There are two distinct forms: diabetic ketoacidosis (DKA), typically seen in type 1 diabetes, and hyperosmolar hyperglycemic state (HHS), occurring primarily in type 2 diabetes. In type 1 diabetes, no insulin is available to suppress fat breakdown, and the ketones resulting from subsequent ketogenesis manifest as DKA. This is in contrast to type 2 diabetes, in which patients can still secrete small amounts of insulin to suppress DKA, instead resulting in a hyperglycemic state predominated simply by glucose. The clinical presentation of both DKA and HHS is one of polyuria, polydipsia, nausea and vomiting, volume depletion (e.g., dry oral mucosa, decreased skin turgor), and eventually mental status changes and coma. In patients with altered mental status, fingerstick glucose should always be checked in order to exclude serum glucose abnormalities. Several clinical findings pertaining only to DKA include a fruity odor to the breath, hyperventilation, and abdominal pain. HHS patients, in contrast to those with DKA, will present with more extreme volume depletion. The treatment of both DKA and HHS is primarily IV electrolyte and fluid replacement. Insulin for hyperglycemia may be given with caution and under vigilant monitoring of serum glucose. Other treatment options depend on the severity of symptoms and include bicarbonate and potassium replacement. Osmotic diuresis and hypovolemia Hypovolemia resulting from DKA can lead to acute Continue reading >>

Chapter 225: Diabetic Ketoacidosis

Chapter 225: Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is an acute, life-threatening complication of diabetes mellitus. DKA occurs predominantly in patients with type 1 (insulin-dependent) diabetes mellitus, but 10% to 30% of cases occur in newly diagnosed type 2 (non–insulin-dependent) diabetes mellitus, especially in African Americans and Hispanics.1,2 Between 1993 and 2003, the yearly rate of U.S. ED visits for DKA was 64 per 10,000 with a trend toward an increased rate of visits among the African American population compared with the Caucasian population.3 Europe has a comparable incidence. A better understanding of the pathophysiology of DKA and an aggressive, uniform approach to its diagnosis and management have reduced mortality to <5% of reported episodes in experienced centers.4 However, mortality is higher in the elderly due to underlying renal disease or coexisting infection and in the presence of coma or hypotension. Figure 225-1 illustrates the complex relationships between insulin and counterregulatory hormones. DKA is a response to cellular starvation brought on by relative insulin deficiency and counterregulatory or catabolic hormone excess (Figure 225-1). Insulin is the only anabolic hormone produced by the endocrine pancreas and is responsible for the metabolism and storage of carbohydrates, fat, and protein. Counterregulatory hormones include glucagon, catecholamines, cortisol, and growth hormone. Complete or relative absence of insulin and the excess counterregulatory hormones result in hyperglycemia (due to excess production and underutilization of glucose), osmotic diuresis, prerenal azotemia, worsening hyperglycemia, ketone formation, and a wide-anion-gap metabolic acidosis.4 Insulin deficiency. Pathogenesis of diabetic ketoacidosis secondary to relative insulin deficienc Continue reading >>

Management Of Adult Diabetic Ketoacidosis

Management Of Adult Diabetic Ketoacidosis

Authors Gosmanov AR, Gosmanova E, Dillard-Cannon E Accepted for publication 13 May 2014 Checked for plagiarism Yes Peer reviewer comments 2 Aidar R Gosmanov,1 Elvira O Gosmanova,2 Erika Dillard-Cannon3 1Division of Endocrinology, Diabetes and Metabolism, 2Division of Nephrology, Department of Medicine, 3Department of Microbiology, Immunology, and Biochemistry, University of Tennessee Health Science Center, Memphis, TN, USA Abstract: Diabetic ketoacidosis (DKA) is a rare yet potentially fatal hyperglycemic crisis that can occur in patients with both type 1 and 2 diabetes mellitus. Due to its increasing incidence and economic impact related to the treatment and associated morbidity, effective management and prevention is key. Elements of management include making the appropriate diagnosis using current laboratory tools and clinical criteria and coordinating fluid resuscitation, insulin therapy, and electrolyte replacement through feedback obtained from timely patient monitoring and knowledge of resolution criteria. In addition, awareness of special populations such as patients with renal disease presenting with DKA is important. During the DKA therapy, complications may arise and appropriate strategies to prevent these complications are required. DKA prevention strategies including patient and provider education are important. This review aims to provide a brief overview of DKA from its pathophysiology to clinical presentation with in depth focus on up-to-date therapeutic management. Keywords: DKA treatment, insulin, prevention, ESKD Letter about this article has been published In 2009, there were 140,000 hospitalizations for diabetic ketoacidosis (DKA) with an average length of stay of 3.4 days.1 The direct and indirect annual cost of DKA hospitalizations is 2.4 billion Continue reading >>

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