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Dka Hypokalemia Or Hyperkalemia

Esrd And Dka

Esrd And Dka

1. Thomas Lanning MD. Abdul Hamid Alraiyes MD. 2. 47 years old AAM Chief Complaints Nausea Vomiting Abdominal Pain CP 3. Past surgical Hx: Lt AKA (1 year ago) Rt AVF (radial artery) Rt Big toe amputation Lt IJ Dialysis catheter (3/10/2007) 4. Allergies: Penicillin “rash” Social History: Resident at Cleveland Rehab Denies any Hx of:  ETOH  Drug abuse  Ex- SMOKER Family History: DM HTN 5. Medications: Insulin aspart 5 units S.Q. Q AC Lantus 20 units S.Q. QHS Hydralazine 100mg P.O. Q8hr Lisinopril 20mg P.O. QD Lopressor 50mg P.O. BID Norvasc 10mg P.O. QD Renagel 800mg P.O. TID Nephrocap 1 tab P.O. QD Neurontin 300mg P.O. Q 8hr Fluoxetine 20mg P.O. QD Vancomycin 600mg I.V. with HD 6. Physical Exam:  V/S : 36- 120/56 - 62 – 17 - SPO2= 86% on RA  Pt is drowsy, dehydrated, not in distress  Skin: dry  Chest: Bil crackles, no wheezing + decreased air entry.  CVS: S1 + S2 + no M  ABD: soft, distended epigastric, tenderness, no rebound, BS+.  EXT: no edema , Lt AKA, Rt Big toe amputation, AVF on the Lt arm 7. Labs:  WBC = 10.9 , Hb= 12.6, Ht= 39.2, Plt= 184  Na= 119, K= 8, Cl= 86, CO2= 12 BUN= 103, Cr= 9.9 , Glucose=1140 8. Labs:  AG= 21 Serum Osmolality= 348 (275-290)  ABG= 7.048 / 41.8 / 75.1 / 11 A-a= 32 SAT= 86 FiO2 = 21% 9. 119 – (86 + 12) = 21 10. Expected AG = 21 + [ 2.5 X (4.5 – 3.8] = 22.75 11. PCO2 = (1.5 X 12 ) + 8 +/_ 2 = 28 - 24 12. PCO2 = (1.5 X 12 ) + 8 +/_ 2 = 28 – 24 ABG= 7.048 / 41.8 / 75.1 / 11 Metabolic Acidosis + Respiratory Acidosis 13. AG Excess / HCO3 deficit = 22 – 12 / 24 – 12 =~ 1 14. Labs:  Amylase= 102 Lipase=1082 LFT WNL ALP=242 CPP = 94 / 3 / 0.14 UA not done “Pt is anuric Continue reading >>

Why Is There Hyperkalemia In Diabetic Ketoacidosis?

Why Is There Hyperkalemia In Diabetic Ketoacidosis?

Diabetic ketoacidosis is a complicated condition which can be caused if you are unable to effectively treat and manage your diabetes. In this condition, ketones are accumulated in the blood which can adversely affect your health. It can be a fatal condition and may cause a lot of complications. One such complication in diabetic ketoacidosis is the onset of hyperkalemia or the high levels of potassium in the blood. In this article, we shall try to understand as to why hyperkalemia is caused in diabetic ketoacidosis? So, read on “Why is There Hyperkalemia in Diabetic Ketoacidosis?” What is Diabetic Ketoacidosis and Hyperkalemia? Diabetic ketoacidosis is a serious complication that is faced by many patients suffering from diabetes. In this condition, excess blood acids called ketones are produced by the body. The above condition should not be taken lightly and should be immediately treated as the same can cause diabetic coma, and eventually the death of the patient. Hyperkalemia refers to abnormally high levels of potassium in the blood of an individual. For a healthy individual, the level of potassium is around 3.5 to 5 milliequivalents per liter. If you have potassium levels higher than that, that is somewhere in between 5.1 to 6 milliequivalents per liter, then you have a mild level of hyperkalemia. Similarly, if the level of potassium in your blood is somewhere between 6.1 to 7 milliequivalents per liter, you have moderate hyperkalemia. Anything above that, you may be suffering from what is known as severe hyperkalemia. Relation Between Diabetic Ketoacidosis and Hyperkalemia There appears to be a strong relationship between hyperkalemia and diabetic ketoacidosis. In the paragraph that follows, we shall try to analyze and understand the same: If you have diabetes an Continue reading >>

Management Of Diabetic Ketoacidosis

Management Of Diabetic Ketoacidosis

Diabetic ketoacidosis is an emergency medical condition that can be life-threatening if not treated properly. The incidence of this condition may be increasing, and a 1 to 2 percent mortality rate has stubbornly persisted since the 1970s. Diabetic ketoacidosis occurs most often in patients with type 1 diabetes (formerly called insulin-dependent diabetes mellitus); however, its occurrence in patients with type 2 diabetes (formerly called non–insulin-dependent diabetes mellitus), particularly obese black patients, is not as rare as was once thought. The management of patients with diabetic ketoacidosis includes obtaining a thorough but rapid history and performing a physical examination in an attempt to identify possible precipitating factors. The major treatment of this condition is initial rehydration (using isotonic saline) with subsequent potassium replacement and low-dose insulin therapy. The use of bicarbonate is not recommended in most patients. Cerebral edema, one of the most dire complications of diabetic ketoacidosis, occurs more commonly in children and adolescents than in adults. Continuous follow-up of patients using treatment algorithms and flow sheets can help to minimize adverse outcomes. Preventive measures include patient education and instructions for the patient to contact the physician early during an illness. Diabetic ketoacidosis is a triad of hyperglycemia, ketonemia and acidemia, each of which may be caused by other conditions (Figure 1).1 Although diabetic ketoacidosis most often occurs in patients with type 1 diabetes (formerly called insulin-dependent diabetes mellitus), more recent studies suggest that it can sometimes be the presenting condition in obese black patients with newly diagnosed type 2 diabetes (formerly called non–insulin-depe Continue reading >>

Disorders Of Potassium: Hypokalemia And Hyperkalemia

Disorders Of Potassium: Hypokalemia And Hyperkalemia

Are you sure your patient has hypokalemia or hyperkalemia? What are the typical findings for this disease? Potassium is the predominant intracellular cation. Normal serum potassium levels are between 3.5 and 5.5 mEq/L. This is much less than intracellular levels that range between 140 and 150 mEq/L. The distribution of potassium levels across cellular membranes helps determine the resting membrane potential as well as the timing of membrane depolarization. Therefore, organ systems largely dependent on membrane depolarization for function are most affected by changes in serum potassium levels. In hypokalemia, the resting membrane potential is increased. Both action potentials and refractory periods are prolonged. Symptoms do not generally develop unless potassium levels are less than 3.0 mEq/L. The following signs and symptoms should raise the concern for hypokalemia: Cardiac manifestations: Skeletal and smooth muscle manifestations: In hyperkalemia, the resting membrane potential is decreased, and the membrane becomes partially depolarized. Initially, this increases membrane excitability. However, with prolonged depolarization, the cell membrane will become more refractory and less likely to fully depolarize. The following signs and symptoms should raise the concern for hyperkalemia: Cardiac manifestations: Skeletal muscle manifestations: What caused this disease to develop at this time? The causes of both hypokalemia and hyperkalemia can be classified into causes related to changes in intake, changes in excretion, and shifts between the intracellular and extracellular spaces. Decreased Intake: Daily potassium intake is 2 to 4 mEq/Kg/day up to 40-120 mEq/day in adults. Because the kidneys are able to significantly limit the excretion of potassium, hypokalemia rarely dev Continue reading >>

Diagnosis And Treatment Of Diabetic Ketoacidosis (dka) In Dogs And Cats

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 >>

Hyperkalemia In Diabetic Ketoacidosis.

Hyperkalemia In Diabetic Ketoacidosis.

Abstract Patients with diabetic ketoacidosis tend to have somewhat elevated serum K+ concentrations despite decreased body K+ content. The hyperkalemia was previously attributed mainly to acidemia. However, recent studies have suggested that "organic acidemias" (such as that produced by infusing beta-hydroxybutyric acid) may not cause hyperkalemia. To learn which, if any, routinely measured biochemical indices might correlate with the finding of hyperkalemia in diabetic ketoacidosis, we analyzed the initial pre-treatment values in 131 episodes in 91 patients. Serum K+ correlated independently and significantly (p less than 0.001) with blood pH (r = -0.39), serum urea N (r = 0.38) and the anion gap (r = 0.41). The mean serum K+ among the men was 5.55 mmol/l, significantly higher than among the women, 5.09 mmol/l (p less than 0.005). Twelve of the 16 patients with serum K+ greater than or equal to 6.5 mmol/l were men, as were all eight patients with serum K+ greater than or equal to 7.0 mmol/l. Those differences paralleled a significantly higher mean serum urea N concentration among the men (15.1 mmol/l) than the women (11.2 mmol/l, p less than 0.01). The greater tendency to hyperkalemia among the men in this series may have been due partly to their greater renal dysfunction during the acute illness. However, other factors that were not assessed, such as cell K+ release associated with protein catabolism, and insulin deficiency per se, may also have affected serum K+ in these patients. Continue reading >>

Myths In Dka Management

Myths In Dka Management

Anand Swaminathan, MD, MPH (@EMSwami) is an assistant professor and assistant program director at the NYU/Bellevue Department of Emergency Medicine in New York City. Review questions are available at the end of this post. Background Each year, roughly 10,000 patients present to the Emergency Department in diabetic ketoacidosis (DKA). Prior to the advent of insulin, the mortality rate of DKA was 100% although in recent years, that rate has dropped to approximately 2-5%.1 Despite clinical advances, the mortality rate has remained constant over the last 10 years. With aggressive resuscitative measures and appropriate continued management this trend may change. DKA is defined as: Hyperglycemia (glucose > 250 mg/dl) Acidosis (pH < 7.3) Ketosis In the absence of insulin, serum glucose rises leading to osmotic diuresis. This diuresis leads to loss of electrolytes including sodium, magnesium, calcium and phosphorous. The resultant volume depletion leads to impaired glomerular filtration rate (GFR) and acute renal failure. In patients with DKA, fatty acid breakdown produces 2 different ketone bodies, first acetoacetate, which then further converts to beta-hydroxybutyrate, the latter being the ketone body largely produced in DKA patients. With this background in mind, let’s take a look at four urban legends in the management of DKA and the evidence that dispels these legends. Here’s our case: Although this presentation likely represents DKA, a blood gas is typically obtained to confirm the diagnosis. Often, the question arises as to whether an arterial or venous blood gas is adequate. Urban Legend #1 – An ABG is necessary for the diagnosis and treatment of DKA ABG gets you pH, PaO2, PaCO2, HCO3, Lactate, electrolytes and O2Sat VBG gets all this except for PaO2 (but we have Continue reading >>

Management Of Diabetic Ketoacidosis In Children And Adolescents

Management Of Diabetic Ketoacidosis In Children And Adolescents

Objectives After completing this article, readers should be able to: Describe the typical presentation of diabetic ketoacidosis in children. Discuss the treatment of diabetic ketoacidosis. Explain the potential complications of diabetic ketoacidosis that can occur during treatment. Introduction Diabetic ketoacidosis (DKA) represents a profound insulin-deficient state characterized by hyperglycemia (>200 mg/dL [11.1 mmol/L]) and acidosis (serum pH <7.3, bicarbonate <15 mEq/L [15 mmol/L]), along with evidence of an accumulation of ketoacids in the blood (measurable serum or urine ketones, increased anion gap). Dehydration, electrolyte loss, and hyperosmolarity contribute to the presentation and potential complications. DKA is the most common cause of death in children who have type 1 diabetes. Therefore, the best treatment of DKA is prevention through early recognition and diagnosis of diabetes in a child who has polydipsia and polyuria and through careful attention to the treatment of children who have known diabetes, particularly during illnesses. Presentation Patients who have DKA generally present with nausea and vomiting. In individuals who have no previous diagnosis of diabetes mellitus, a preceding history of polyuria, polydipsia, and weight loss usually can be elicited. With significant ketosis, patients may have a fruity breath. As the DKA becomes more severe, patients develop lethargy due to the acidosis and hyperosmolarity; in severe DKA, they may present with coma. Acidosis and ketosis cause an ileus that can lead to abdominal pain severe enough to raise concern for an acutely inflamed abdomen, and the elevation of the stress hormones epinephrine and cortisol in DKA can lead to an elevation in the white blood cell count, suggesting infection. Thus, leukocytosi Continue reading >>

Understanding And Treating Diabetic Ketoacidosis

Understanding And Treating Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a serious metabolic disorder that can occur in animals with diabetes mellitus (DM).1,2 Veterinary technicians play an integral role in managing and treating patients with this life-threatening condition. In addition to recognizing the clinical signs of this disorder and evaluating the patient's response to therapy, technicians should understand how this disorder occurs. DM is caused by a relative or absolute lack of insulin production by the pancreatic b-cells or by inactivity or loss of insulin receptors, which are usually found on membranes of skeletal muscle, fat, and liver cells.1,3 In dogs and cats, DM is classified as either insulin-dependent (the body is unable to produce sufficient insulin) or non-insulin-dependent (the body produces insulin, but the tissues in the body are resistant to the insulin).4 Most dogs and cats that develop DKA have an insulin deficiency. Insulin has many functions, including the enhancement of glucose uptake by the cells for energy.1 Without insulin, the cells cannot access glucose, thereby causing them to undergo starvation.2 The unused glucose remains in the circulation, resulting in hyperglycemia. To provide cells with an alternative energy source, the body breaks down adipocytes, releasing free fatty acids (FFAs) into the bloodstream. The liver subsequently converts FFAs to triglycerides and ketone bodies. These ketone bodies (i.e., acetone, acetoacetic acid, b-hydroxybutyric acid) can be used as energy by the tissues when there is a lack of glucose or nutritional intake.1,2 The breakdown of fat, combined with the body's inability to use glucose, causes many pets with diabetes to present with weight loss, despite having a ravenous appetite. If diabetes is undiagnosed or uncontrolled, a series of metab Continue reading >>

Potassium Balance In Acid-base Disorders

Potassium Balance In Acid-base Disorders

INTRODUCTION There are important interactions between potassium and acid-base balance that involve both transcellular cation exchanges and alterations in renal function [1]. These changes are most pronounced with metabolic acidosis but can also occur with metabolic alkalosis and, to a lesser degree, respiratory acid-base disorders. INTERNAL POTASSIUM BALANCE Acid-base disturbances cause potassium to shift into and out of cells, a phenomenon called "internal potassium balance" [2]. An often-quoted study found that the plasma potassium concentration will rise by 0.6 mEq/L for every 0.1 unit reduction of the extracellular pH [3]. However, this estimate was based upon only five patients with a variety of disturbances, and the range was very broad (0.2 to 1.7 mEq/L). This variability in the rise or fall of the plasma potassium in response to changes in extracellular pH was confirmed in subsequent studies [2,4]. Metabolic acidosis — In metabolic acidosis, more than one-half of the excess hydrogen ions are buffered in the cells. In this setting, electroneutrality is maintained in part by the movement of intracellular potassium into the extracellular fluid (figure 1). Thus, metabolic acidosis results in a plasma potassium concentration that is elevated in relation to total body stores. The net effect in some cases is overt hyperkalemia; in other patients who are potassium depleted due to urinary or gastrointestinal losses, the plasma potassium concentration is normal or even reduced [5,6]. There is still a relative increase in the plasma potassium concentration, however, as evidenced by a further fall in the plasma potassium concentration if the acidemia is corrected. A fall in pH is much less likely to raise the plasma potassium concentration in patients with lactic acidosis Continue reading >>

Diabetic Ketoacidosis Producing Extreme Hyperkalemia In A Patient With Type 1 Diabetes On Hemodialysis

Diabetic Ketoacidosis Producing Extreme Hyperkalemia In A Patient With Type 1 Diabetes On Hemodialysis

Hodaka Yamada1, Shunsuke Funazaki1, Masafumi Kakei1, Kazuo Hara1 and San-e Ishikawa2[1] Division of Endocrinology and Metabolism, Jichi Medical University Saitama Medical Center, Saitama, Japan [2] Division of Endocrinology and Metabolism, International University of Health and Welfare Hospital, Nasushiobara, Japan Summary Diabetic ketoacidosis (DKA) is a critical complication of type 1 diabetes associated with water and electrolyte disorders. Here, we report a case of DKA with extreme hyperkalemia (9.0 mEq/L) in a patient with type 1 diabetes on hemodialysis. He had a left frontal cerebral infarction resulting in inability to manage his continuous subcutaneous insulin infusion pump. Electrocardiography showed typical changes of hyperkalemia, including absent P waves, prolonged QRS interval and tented T waves. There was no evidence of total body water deficit. After starting insulin and rapid hemodialysis, the serum potassium level was normalized. Although DKA may present with hypokalemia, rapid hemodialysis may be necessary to resolve severe hyperkalemia in a patient with renal failure. Patients with type 1 diabetes on hemodialysis may develop ketoacidosis because of discontinuation of insulin treatment. Patients on hemodialysis who develop ketoacidosis may have hyperkalemia because of anuria. Absolute insulin deficit alters potassium distribution between the intracellular and extracellular space, and anuria abolishes urinary excretion of potassium. Rapid hemodialysis along with intensive insulin therapy can improve hyperkalemia, while fluid infusions may worsen heart failure in patients with ketoacidosis who routinely require hemodialysis. Background Diabetic ketoacidosis (DKA) is a very common endocrinology emergency. It is usually associated with severe circulatory Continue reading >>

Potassium Phosphate

Potassium Phosphate

Phosphorus Supplementation Similar to potassium, phosphate is deficient in animals with DKA regardless of the serum phosphorus concentration. Phosphorus is lost in patients with DKA because of a shift from the intracellular to the extracellular compartment secondary to hyperosmolality that is followed by urinary loss, decreased cellular uptake caused by insulin deficiency, inhibition of renal tubular phosphate absorption caused by acidosis, and osmotic diuresis.33,43 During treatment of DKA, the reduction in osmolality and insulin administration result in translocation of phosphate into the cell from the extracellular compartment. This translocation frequently causes a marked decrease in the plasma phosphorus concentration. However, clinically important consequences of hypophosphatemia are noted only when the serum phosphorus concentration is less than 1.0 to 1.5 mg/dL, and these signs are observed inconsistently. Hemolysis, muscle weakness, seizures, depression, and decreased leukocyte and platelet function leading to infection and bleeding can result from hypophosphatemia. The only abnormalities documented as caused by hypophosphatemia in veterinary DKA patients are hemolytic anemia in cats and possibly stupor and seizures in a dog.1,15,77 Hemolysis can occur despite phosphate supplementation and may have causes other than hypophosphatemia including oxidative injury.15,19 Hypophosphatemia is present at initial evaluation in 13% to 48% of cats and in 29% of dogs with DKA.15,20,37 Careful monitoring of serum phosphorus concentration during the initial 24 to 48 hours of management is important to identify severe hypophosphatemia necessitating phosphorus supplementation. Treatment of hypophosphatemia is indicated when the serum phosphorus concentration before treatment is Continue reading >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Definition: A hyperglycemic, acidotic state caused by insulin deficiency. The disease state consists of 3 parameters: Hyperglycemia (glucose > 250 mg/dl) Acidosis Ketosis Epidemiology Incidence of ~ 10,000 cases/year in US Mortality rate: 2-5% (prior to insulin was 100%) (Lebovitz 1995) Pathophysiology Insulin deficiency leads to serum glucose rise Increased glucose load in kidney leads to increased glucose in urine and osmotic diuresis Osmotic diuresis is accompanied by loss of electrolytes including sodium, magnesium, calcium and potassium Volume depletion leads to impaired glomerular filtration rate (GFR) Inability to properly metabolize glucose results in fatty acid breakdown with resultant ketone bodies (acetoacetate + beta-hydroxybutyrate) Causes: An acute insult leads to decompensation of a chronic disease. Can also be first manifestation of new onset diabetes (particularly in children). Below are common triggers Infection (particularly sepsis) Myocardial ischemia or infarction Medication non-compliance Clinical Presentation History Polydipsia, polyuria, polyphagia Weakness Weight loss Nausea/Vomiting Abdominal Pain Physical Examination Acetone odor on breath (“fruity” smell) Kussmaul’s respirations – deep fast breathing (tachypnea and hyperpnea) Tachycardia Hypotension Altered mental status Abdominal tenderness Diagnostic Testing Definitive diagnosis is established by laboratory criteria as detailed above (hyperglycemia, ketosis and acidosis) Essential Diagnostic Tests Serum glucose Typically > 350 mg/dL Euglycemic DKA (< 300 mg/dL) reported in up to 18% of patients Blood gas Patients will exhibit an anion gap metabolic Electrolytes: hypo/hyper/normokalemia, hyponatremia Arterial or venous blood gas can be used (Savage 2011) Urinalysis Glucosuria Ketonur Continue reading >>

Part 10.1: Life-threatening Electrolyte Abnormalities

Part 10.1: Life-threatening Electrolyte Abnormalities

Electrolyte abnormalities are commonly associated withcardiovascular emergencies. These abnormalities may cause or contribute to cardiac arrest and may hinder resusci- tative efforts. In some cases therapy for life-threatening electrolyte disorders should be initiated before laboratory results become available. Potassium (K�) The magnitude of the potassium gradient across cell membranes determines excitability of nerve and muscle cells, including the myocardium. Rapid or significant changes in the serum potas- sium concentration can have life-threatening consequences. Evaluation of serum potassium must consider the effects of changes in serum pH. When serum pH falls, serum potassium rises because potassium shifts from the cellular to the vascular space. When serum pH rises, serum potassium falls because potassium shifts from the vascular space into the cells. Effects of pH changes on serum potassium should be anticipated during therapy for hyperkalemia or hypokalemia and during any therapy that may cause changes in serum pH (eg, treatment of diabetic ketoacidosis). Hyperkalemia Although hyperkalemia is defined as a serum potassium concentration �5 mEq/L, it is moderate (6 to 7 mEq/L) and severe (�7 mEq/L) hyperkalemia that are life-threatening and require immediate therapy. Hyperkalemia is most com- monly seen in patients with end-stage renal disease. Other causes are listed in the Table. Many medications can contrib- ute to the development of hyperkalemia. Identification of potential causes of hyperkalemia will contribute to rapid identification and treatment.1–3 Signs and symptoms of hyperkalemia include weakness, ascending paralysis, and respiratory failure. A variety of electrocardiographic (ECG) changes suggest hyperkalemia. Early findings inc Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes mellitus.[1] Signs and symptoms may include vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion, and occasionally loss of consciousness.[1] A person's breath may develop a specific smell.[1] Onset of symptoms is usually rapid.[1] In some cases people may not realize they previously had diabetes.[1] DKA happens most often in those with type 1 diabetes, but can also occur in those with other types of diabetes under certain circumstances.[1] Triggers may include infection, not taking insulin correctly, stroke, and certain medications such as steroids.[1] DKA results from a shortage of insulin; in response the body switches to burning fatty acids which produces acidic ketone bodies.[3] DKA is typically diagnosed when testing finds high blood sugar, low blood pH, and ketoacids in either the blood or urine.[1] The primary treatment of DKA is with intravenous fluids and insulin.[1] Depending on the severity, insulin may be given intravenously or by injection under the skin.[3] Usually potassium is also needed to prevent the development of low blood potassium.[1] Throughout treatment blood sugar and potassium levels should be regularly checked.[1] Antibiotics may be required in those with an underlying infection.[6] In those with severely low blood pH, sodium bicarbonate may be given; however, its use is of unclear benefit and typically not recommended.[1][6] Rates of DKA vary around the world.[5] In the United Kingdom, about 4% of people with type 1 diabetes develop DKA each year, while in Malaysia the condition affects about 25% a year.[1][5] DKA was first described in 1886 and, until the introduction of insulin therapy in the 1920s, it was almost univ Continue reading >>

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