Diabetic Emergencies, Diabetic Ketoacidosis In Adults, Part 3
Clinical Management Treatment consists of rehydration with intravenous fluids, the administration of insulin, and replacement of electrolytes. General medical care and close supervision by trained medical and nursing staff is of paramount importance in the management of patients with DKA. A treatment flowchart (Table 1.3) should be used and updated meticulously. A urine catheter is necessary if the patient is in coma or if no urine is passed in the first 4 hours…. Replacement of water deficit Patients with DKA have severe dehydration. The amount of fluid needing to be administered depends on the degree of dehydration (Table 1.4). Fluid replacement aims at correction of the volume deficit and not to restore serum osmolality to normal. Isotonic solution NaCl (0.9%) (normal saline; osmolality 308 mOsm/kg) should be administered even in patients with high serum osmolality since this solution is hypotonic compared to the extracellular fluid of the patient. 10 The initial rate of fluid administration depends on the degree of volume depletion and underlying cardiac and renal function. In a young adult with normal cardiac and/or renal function 1 L of normal saline is administered intravenously within the first half- to one hour. In the second hour administer another 1 L, and between the third and the fifth hours administer 0.5–1 L per hour. Thus, the total volume in the first 5 hours should be 3.5–5 L [1]. If the patient is in shock or blood pressure does not respond to normal saline infusion, colloid solutions together with normal saline may be used.1,6 Some authors suggest replacement of normal saline with hypotonic (0.45%) saline solution after stabilization of the hemodynamic status of the patient and when corrected serum sodium levels are normal.8 However, this appro Continue reading >>
Diabetic Ketoacidosis
A Preventable Crisis People who have had diabetic ketoacidosis, or DKA, will tell you it’s worse than any flu they’ve ever had, describing an overwhelming feeling of lethargy, unquenchable thirst, and unrelenting vomiting. “It’s sort of like having molasses for blood,” says George. “Everything moves so slow, the mouth can feel so dry, and there is a cloud over your head. Just before diagnosis, when I was in high school, I would get out of a class and go to the bathroom to pee for about 10–12 minutes. Then I would head to the water fountain and begin drinking water for minutes at a time, usually until well after the next class had begun.” George, generally an upbeat person, said that while he has experienced varying degrees of DKA in his 40 years or so of having diabetes, “…at its worst, there is one reprieve from its ill feeling: Unfortunately, that is a coma.” But DKA can be more than a feeling of extreme discomfort, and it can result in more than a coma. “It has the potential to kill,” says Richard Hellman, MD, past president of the American Association of Clinical Endocrinologists. “DKA is a medical emergency. It’s the biggest medical emergency related to diabetes. It’s also the most likely time for a child with diabetes to die.” DKA occurs when there is not enough insulin in the body, resulting in high blood glucose; the person is dehydrated; and too many ketones are present in the bloodstream, making it acidic. The initial insulin deficit is most often caused by the onset of diabetes, by an illness or infection, or by not taking insulin when it is needed. Ketones are your brain’s “second-best fuel,” Hellman says, with glucose being number one. If you don’t have enough glucose in your cells to supply energy to your brain, yo Continue reading >>
Fluid Management In Diabetic Ketoacidosis
Young people with insulin dependent diabetes mellitus are three times more likely to die in childhood than the general population.1 Despite advances in management over the past 20 years, the incidence of mortality associated with diabetic ketoacidosis (DKA) remains unchanged. Cerebral oedema is the predominant cause of this mortality; young children are particularly at risk, with an incidence of 0.7–1% of episodes of DKA.2,3 The mortality appears to be greatest among patients at first presentation,1,3,4 if there has been a long history of symptoms prior to admission,3 and during the first 24 hours of treatment.4 In a recently published retrospective multicentre analysis of children with DKA, low pco2 levels and high serum sodium concentration at presentation were identified as particular risk factors for the development of cerebral oedema, together with bicarbonate therapy.5 However, in the accompanying editorial, Dunger and Edge point out that this may simply be revealing an association between severe DKA and dehydration and the risk of cerebral oedema.6 The pathogenesis of cerebral oedema remains poorly understood but there may be many contributing factors.7 The aim of management of DKA is to restore metabolic homoeostasis while minimising the risks of complications including hypoglycaemia, hypokalaemia, cardiac failure, and in children the development of cerebral oedema. How best to achieve this remains contentious, with particular controversy centred on optimal fluid management. The most appropriate volume, type, and rate of fluid to be given have all been the subject of debate. A survey in 1994 of UK paediatricians found a threefold variation in the amount of fluid recommended within the first 12 hours.8 Since then national guidelines have been developed by the B Continue reading >>
Management Of Diabetic Ketoacidosis And Other Hyperglycemic Emergencies
Understand the management of patients with diabetic ketoacidosis and other hyperglycemic emergencies. The acute onset of hyperglycemia with attendant metabolic derangements is a common presentation in all forms of diabetes mellitus. The most current data from the National Diabetes Surveillance Program of the Centers for Disease Control and Prevention estimate that during 2005-2006, at least 120,000 hospital discharges for diabetic ketoacidosis (DKA) occurred in the United States,(1) with an unknown number of discharges related to hyperosmolar hyperglycemic state (HHS). The clinical presentations of DKA and HHS can overlap, but they are usually separately characterized by the presence of ketoacidosis and the degree of hyperglycemia and hyperosmolarity, though HHS will occasionally have some mild degree of ketosis. DKA is defined by a plasma glucose level >250 mg/dL, arterial pH <7.3, the presence of serum ketones, a serum bicarbonate measure <18 mEq/L, and a high anion gap metabolic acidosis. The level of normal anion gap may vary slightly by individual institutional standards. The anion gap also needs to be corrected in the presence of hypoalbuminemia, a common condition in the critically ill. Adjusted anion gap = observed anion gap + 0.25 * ([normal albumin]-[observed albumin]), where the given albumin concentrations are in g/L; if given in g/dL, the correction factor is 2.5.(3) HHS is defined by a plasma glucose level >600 mg/dL, with an effective serum osmolality >320 mOsm/kg. HHS was originally named hyperosmolar hyperglycemic nonketotic coma; however, this name was changed because relatively few patients exhibit coma-like symptoms. Effective serum osmolality = 2*([Na] + [K]) + glucose (mg/dL)/18.(2) Urea is freely diffusible across cell membranes, thus it will Continue reading >>
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 >>
Ask An Expert: Is It Really Ok To Treat Hyperglycemia With Glucose?
Article Content Q: Why would I give I.V. glucose to a patient being treated for hyperglycemia?-D.L., Conn. Figure. No caption available. A: Although this seems like a contradiction, it can be appropriate. The primary reason is to prevent hypoglycemia once the blood glucose level begins to return to normal. Patients suffering from diabetic ketoacidosis (DKA), for example, can benefit from intravenous (I.V.) glucose. We'll explain why later, but first let's talk more about DKA. On admission, patients with DKA usually have blood glucose levels between 250 mg/dl and 800 mg/dl. Because normal blood glucose is 70 to 120 mg/dl premeal, the blood glucose level is way too high. To accurately diagnose a patient with DKA, we need to consider more than his blood glucose level. As the term DKA indicates, plasma or urine ketones must also be present. Ketones are weak acids, and when they accumulate, the blood pH drops to an average of 7.15. The normal blood pH range is from 7.35 to 7.45. As the pH falls, the plasma bicarbonate level drops as it tries to buffer the acids and restore a normal blood pH. An absence of ketosis or acidosis usually excludes a DKA diagnosis. Put simply, the diagnostic parameters for DKA are: arterial pH of less than 7.2, plasma bicarbonate level less than 15 mg/dl, blood glucose level of greater than 250 mg/dl, and presence of serum and urine ketones. Because patients with DKA have an absence of insulin, their cells can't use glucose properly. These patients usually have Type 1 diabetes. Treatment goals include fluids (fluids alone will help decrease the glucose concentrations), adequate insulin to restore normal glucose metabolism, and correction of the precipitating factor. The most effective way to deliver the required insulin is through a continuous I.V. Continue reading >>
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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 >>
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 >>
Too Much Of A Good Thing
A healthy 19-year-old man presents to your emergency department complaining of weakness and lethargy for the past 2 weeks. He sleeps 10 hours a day, yet remains tired. His appetite has been poor and he constantly feels thirsty. He voids frequently with no dysuria or hematuria. For the past 24 hours, he has been experiencing moderately severe and diffuse abdominal pain; he vomited 4 times in the past 2 hours. He has lost 10 kg over the past 2 weeks. He denies other symptoms or using drugs or medications, and he drinks alcohol only socially. His personal and family medical histories are not relevant. An examination reveals blood pressure of 115/60 mm Hg, heart rate of 135 beats per minute, temperature of 36.9°C, respiration rate of 24 breaths per minute, and oxygen saturation of 100% on room air. The patient is alert and appears uncomfortable, retching repeatedly. The mucosae are dry and the abdomen soft but diffusely tender, with normal bowel sounds and no peritoneal signs. There is no costovertebral angle tenderness. Findings from the remainder of the examination are noncontributory. A bedside glucometer displays “High-High-High.” Laboratory investigations reveal a white blood cell count of 14.2 × 109/L, a hemoglobin level of 143 g/L, a platelet count of 365 × 109/L, a sodium level of 133 mmol/L, a potassium level of 2.9 mmol/L, a chloride level of 103 mmol/L, a blood urea nitrogen level of 17 mmol/L, a creatinine level of 144 μmol/L, a glucose level of 29.7 mmol/L, an arterial pH of 7.10, a Pco2 of 23 mm Hg, a Po2 of 95 mm Hg, a bicarbonate level of 11 mmol/L, and an oxygen saturation of 95%. Urinalysis results are positive for high levels of ketones and glucose. How would you approach this patient? Diabetic ketoacidosis (DKA) occurs in 4.6 to 8 of 1000 diabeti Continue reading >>
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 >>
My Site - Chapter 15: Hyperglycemic Emergencies In Adults
Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) should be suspected in ill patients with diabetes. If either DKA or HHS is diagnosed, precipitating factors must be sought and treated. DKA and HHS are medical emergencies that require treatment and monitoring for multiple metabolic abnormalities and vigilance for complications. A normal blood glucose does not rule out DKA in pregnancy. Ketoacidosis requires insulin administration (0.1 U/kg/h) for resolution; bicarbonate therapy should be considered only for extreme acidosis (pH7.0). Note to readers: Although the diagnosis and treatment of diabetic ketoacidosis (DKA) in adults and in children share general principles, there are significant differences in their application, largely related to the increased risk of life-threatening cerebral edema with DKA in children and adolescents. The specific issues related to treatment of DKA in children and adolescents are addressed in the Type 1 Diabetes in Children and Adolescents chapter, p. S153. Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are diabetes emergencies with overlapping features. With insulin deficiency, hyperglycemia causes urinary losses of water and electrolytes (sodium, potassium, chloride) and the resultant extracellular fluid volume (ECFV) depletion. Potassium is shifted out of cells, and ketoacidosis occurs as a result of elevated glucagon levels and absolute insulin deficiency (in the case of type 1 diabetes) or high catecholamine levels suppressing insulin release (in the case of type 2 diabetes). In DKA, ketoacidosis is prominent, while in HHS, the main features are ECFV depletion and hyperosmolarity. Risk factors for DKA include new diagnosis of diabetes mellitus, insulin omission, infection, myocardial infarc Continue reading >>
Diabetic Ketoacidosis In Adults
Pathophysiology Relative insulin deficiency = ↑Glu, ↓pH and ketonaemia. ↑glucagon, cortisol, catecholamines⇒ ↑ gluconeogenesis ⇒ ↑↑ glucose. ↑ lipolysis ⇒ ↑ FFA - ketogenesis - metab acidosis (3-β-hydroxybutyrate). Dehydration 2°: osmotic diuresis & vomiting = electrolyte (K+⇑ or K+⇓) shifts. Mortality from Children: Cerebral oedema Adults: ⇓K+, ARDS, co-existing sepsis/ AMI etc Aims and principles 1. Replace lost fluid & electrolytes 2. Correction of ketoacidosis Insulin suppression of ketogenesis Insulin stimulated entry of glucose into cells (correct ketonaemia) To achieve this you need to give enough insulin to correct the acidosis. Once the blood glucose falls you will often need to support the insulin with infused dextrose 3. Slow correct hyperglycaemia aim for glucose fall 3-5 mmol/l/hr only allow acidosis to correct as above No bicarb. unless pH < 6.9 If necessary use IL 1.26% solution + 20 mmol KCl 4. Treat cause Resuscitate A, B, C 1L over 1hr 1L over 2hr 1L over 4hr 1L over 8hr When Glu. <12mmol/L change to 5% dextrose When Glu. >12mmol/L change to normal saline If hypoglycaemia consider 10% dextrose Start infusion at 0.1U/Kg/hour Later move to sliding IV infusion rate Cap Glu. (mmol/L) Units / hr (=ml / hr) 0 - 4 0 4.1 - 6 0.5 6.1 - 8 1 8.1 - 10 2 10.1 - 12 3 12.1 - 16 4 16.1 - 20 6 > 20 Call doctor For patients on basal bolus insulin (e.g. Glargine, Detemir) it should be continued where possible. Additional Mx Monitor intake/output Hourly glucose monitoring. Aim for drop 4-5mmol/L/hr. Avoid rapid reduction. Check ketones every 1-2 hour Check K+ every 2-4 hrs (need ECG monitor?) Inform endocrine team of patient Do not use bicarbonate without prior discussion with EM senior/endocrine agreement Common DKA precipitants include infe Continue reading >>
> Hyperglycemia And Diabetic Ketoacidosis
When blood glucose levels (also called blood sugar levels) are too high, it's called hyperglycemia. Glucose is a sugar that comes from foods, and is formed and stored inside the body. It's the main source of energy for the body's cells and is carried to each through the bloodstream. But even though we need glucose for energy, too much glucose in the blood can be unhealthy. Hyperglycemia is the hallmark of diabetes — it happens when the body either can't make insulin (type 1 diabetes) or can't respond to insulin properly (type 2 diabetes). The body needs insulin so glucose in the blood can enter the cells to be used for energy. In people who have developed diabetes, glucose builds up in the blood, resulting in hyperglycemia. If it's not treated, hyperglycemia can cause serious health problems. Too much sugar in the bloodstream for long periods of time can damage the vessels that supply blood to vital organs. And, too much sugar in the bloodstream can cause other types of damage to body tissues, which can increase the risk of heart disease and stroke, kidney disease, vision problems, and nerve problems in people with diabetes. These problems don't usually show up in kids or teens with diabetes who have had the disease for only a few years. However, they can happen in adulthood in some people, particularly if they haven't managed or controlled their diabetes properly. Blood sugar levels are considered high when they're above someone's target range. The diabetes health care team will let you know what your child's target blood sugar levels are, which will vary based on factors like your child's age. A major goal in controlling diabetes is to keep blood sugar levels as close to the desired range as possible. It's a three-way balancing act of: diabetes medicines (such as in Continue reading >>
Diabetic Ketoacidosis Treatment & Management
Approach Considerations Managing diabetic ketoacidosis (DKA) in an intensive care unit during the first 24-48 hours always is advisable. When treating patients with DKA, the following points must be considered and closely monitored: It is essential to maintain extreme vigilance for any concomitant process, such as infection, cerebrovascular accident, myocardial infarction, sepsis, or deep venous thrombosis. It is important to pay close attention to the correction of fluid and electrolyte loss during the first hour of treatment. This always should be followed by gradual correction of hyperglycemia and acidosis. Correction of fluid loss makes the clinical picture clearer and may be sufficient to correct acidosis. The presence of even mild signs of dehydration indicates that at least 3 L of fluid has already been lost. Patients usually are not discharged from the hospital unless they have been able to switch back to their daily insulin regimen without a recurrence of ketosis. When the condition is stable, pH exceeds 7.3, and bicarbonate is greater than 18 mEq/L, the patient is allowed to eat a meal preceded by a subcutaneous (SC) dose of regular insulin. Insulin infusion can be discontinued 30 minutes later. If the patient is still nauseated and cannot eat, dextrose infusion should be continued and regular or ultra–short-acting insulin should be administered SC every 4 hours, according to blood glucose level, while trying to maintain blood glucose values at 100-180 mg/dL. The 2011 JBDS guideline recommends the intravenous infusion of insulin at a weight-based fixed rate until ketosis has subsided. Should blood glucose fall below 14 mmol/L (250 mg/dL), 10% glucose should be added to allow for the continuation of fixed-rate insulin infusion. [19, 20] In established patient Continue reading >>
Pem Pearls: Treatment Of Pediatric Diabetic Ketoacidosis And The Two-bag Method
Insulin does MANY things in the body, but the role we care about in the Emergency Department is glucose regulation. Insulin allows cells to take up glucose from the blood stream, inhibits liver glucose production, increases glycogen storage, and increases lipid production. When insulin is not present, such as in patients with Type 1 diabetes mellitus (DM), all of the opposite effects occur. A lack of insulin causes the following downstream effects: Prevents glucose from being used as an energy source – Free fatty acids are used instead and produce ketoacids during metabolism. Causes a surge of stress hormones and induces gluconeogenesis – When blood glucose levels are elevated, the kidneys cannot absorb all of the glucose from the urine, and the extra glucose in the urine causes polyuria, even in the setting of dehydration. In addition, acidosis causes potassium to shift out of cells into the blood, and the combination of this with dehydration causes the body to preferentially retain sodium at the expense of potassium.1,2 When insulin homeostasis is disrupted and decompensates, patients are at risk for developing diabetic ketoacidosis (DKA). All of the following criteria are required for a diagnosis of DKA: Hyperglycemia (glucose >200 mg/dL) Acidosis (pH <7.3 or bicarb <15 mmol/L) Ketosis (by urine or blood test) Treatment is based on a simple principle: return the body’s glucose regulation to its normal state and replace all of the things the body consumed while insulin-deficient. While bolus insulin is common in the treatment of DKA in adults, it is relatively contraindicated in the pediatric patient. Dehydration and secondary sympathetic activation can interfere with local tissue perfusion and may cause irregular and unpredictable absorption. Step 1: Correction Continue reading >>
