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Why Are Dka Patients Dehydrated

Diabetic Ketoacidosis: Evaluation And Treatment

Diabetic Ketoacidosis: Evaluation And Treatment

Diabetic ketoacidosis is characterized by a serum glucose level greater than 250 mg per dL, a pH less than 7.3, a serum bicarbonate level less than 18 mEq per L, an elevated serum ketone level, and dehydration. Insulin deficiency is the main precipitating factor. Diabetic ketoacidosis can occur in persons of all ages, with 14 percent of cases occurring in persons older than 70 years, 23 percent in persons 51 to 70 years of age, 27 percent in persons 30 to 50 years of age, and 36 percent in persons younger than 30 years. The case fatality rate is 1 to 5 percent. About one-third of all cases are in persons without a history of diabetes mellitus. Common symptoms include polyuria with polydipsia (98 percent), weight loss (81 percent), fatigue (62 percent), dyspnea (57 percent), vomiting (46 percent), preceding febrile illness (40 percent), abdominal pain (32 percent), and polyphagia (23 percent). Measurement of A1C, blood urea nitrogen, creatinine, serum glucose, electrolytes, pH, and serum ketones; complete blood count; urinalysis; electrocardiography; and calculation of anion gap and osmolar gap can differentiate diabetic ketoacidosis from hyperosmolar hyperglycemic state, gastroenteritis, starvation ketosis, and other metabolic syndromes, and can assist in diagnosing comorbid conditions. Appropriate treatment includes administering intravenous fluids and insulin, and monitoring glucose and electrolyte levels. Cerebral edema is a rare but severe complication that occurs predominantly in children. Physicians should recognize the signs of diabetic ketoacidosis for prompt diagnosis, and identify early symptoms to prevent it. Patient education should include information on how to adjust insulin during times of illness and how to monitor glucose and ketone levels, as well as i Continue reading >>

The Accuracy Of Clinical Assessment Of Dehydration During Diabetic Ketoacidosis In Childhood

The Accuracy Of Clinical Assessment Of Dehydration During Diabetic Ketoacidosis In Childhood

The objective of this study was to examine the accuracy of the assessment of clinical dehydration in children with type 1 diabetes and diabetic ketoacidosis (DKA). DKA remains the single most common cause of diabetes-related death in childhood (1). Accurate assessment and management of dehydration is the cornerstone of DKA treatment (1,2). The assessment of the degree of dehydration has traditionally been according to clinical criteria including peripheral tissue perfusion and indicators of hemodynamic status (3). The clinical assessment of dehydration in children in common nonacidotic states (e.g., gastroenteritis) has been previously shown (4) to overestimate the degree of dehydration by ∼3.2%. There have been no comparable studies in either DKA or any other form of metabolic acidosis. RESEARCH DESIGN AND METHODS We studied a random convenience sample of 37 children with type 1 diabetes, newly or previously diagnosed, who presented to the Royal Children’s Hospital, Melbourne, with DKA. The patients were all <18 years of age and presented to the emergency department at Royal Children’s Hospital between 1996 and 2000. The study entry criteria were pH <7.30 (capillary, venous, or arterial) and/or bicarbonate <15 mmol/l and ketones in the urine on dipstick testing. The following information was recorded by the primary assessing doctor: newly diagnosed or established diabetes, age, sex, date and time seen, heart rate, respiratory rate, blood pressure, pale and/or cool hands and feet, peripheral capillary refill time, reduced skin turgor, level of consciousness (on a rating scale of one to eight), sunken eyes, sunken fontanelle, dry tongue, Kussmaul breathing, blood glucose level, and estimated degree of dehydration (clinical assessment). A second emergency department Continue reading >>

Two Cases Of Diabetic Ketoacidosis In Hnf1a-mody Linked To Severe Dehydration: Is It Time To Change The Diagnostic Criteria For Mody?

Two Cases Of Diabetic Ketoacidosis In Hnf1a-mody Linked To Severe Dehydration: Is It Time To Change The Diagnostic Criteria For Mody?

Pruhova S, Dusatkova P, Neumann D, Hollay E, Cinek O, Lebl J, Sumnik Z. Diabetes Care. 2013 Sep;36(9):2573-4. doi: 10.2337/dc13-0058. Epub 2013 Apr 22. IF: 7.735 Department of Paediatrics Abstract OBJECTIVE: Hepatocyte nuclear factor-1A maturity-onset diabetes of the young (HNF1A-MODY) is a monogenic form of diabetes caused by heterozygous mutations in HNF1A. Currently, a history of diabetic ketoacidosis (DKA) is an exclusion criterion for genetic testing for MODY. HISTORY AND EXAMINATION: In this article, we describe two unrelated patients aged 17 and 24 years with severe DKA developed several years after the diagnosis of HNF1A-MODY. INVESTIGATION: Both patients were treated with insulin, but their metabolic control was poor (HbA1c 15%, 140 mmol/mol and 13%, 119 mmol/mol, respectively) due to noncompliance and missed insulin injections. In both patients, DKA followed a course of recurrent vomiting with dehydration and prerenal acute kidney injury. Their glycemia, blood pH, and base excess at admission were 97 mmol/L [1,748 mg/dL], 6.80, and -33 mmol/L (patient 1) and 34 mmol/L [613 mg/dL], 7.03, and -14 mmol/L (patient 2). CONCLUSIONS: This anecdotal observation supports the notion that a history of DKA does not exclude MODY. Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

List Clinicopathologic features that might be present with DKA? Elevation in liver enzymes (hepatic lipidosis, pancreatitis) Hyperlipidemia Hyperlipasemia Hyperamylasemia Metabolic Acidosis Serum Hyperosmolality Azotemia (usually pre-renal) Hemeturia, pyuria, bactiuria (always submit cysto for culture an dsensitivity) Ketonuria Continue reading >>

Ketoacidosis

Ketoacidosis

Ketoacidosis is a metabolic state associated with high concentrations of ketone bodies, formed by the breakdown of fatty acids and the deamination of amino acids. The two common ketones produced in humans are acetoacetic acid and β-hydroxybutyrate. Ketoacidosis is a pathological metabolic state marked by extreme and uncontrolled ketosis. In ketoacidosis, the body fails to adequately regulate ketone production causing such a severe accumulation of keto acids that the pH of the blood is substantially decreased. In extreme cases ketoacidosis can be fatal.[1] Ketoacidosis is most common in untreated type 1 diabetes mellitus, when the liver breaks down fat and proteins in response to a perceived need for respiratory substrate. Prolonged alcoholism may lead to alcoholic ketoacidosis. Ketoacidosis can be smelled on a person's breath. This is due to acetone, a direct by-product of the spontaneous decomposition of acetoacetic acid. It is often described as smelling like fruit or nail polish remover.[2] Ketosis may also give off an odor, but the odor is usually more subtle due to lower concentrations of acetone. Treatment consists most simply of correcting blood sugar and insulin levels, which will halt ketone production. If the severity of the case warrants more aggressive measures, intravenous sodium bicarbonate infusion can be given to raise blood pH back to an acceptable range. However, serious caution must be exercised with IV sodium bicarbonate to avoid the risk of equally life-threatening hypernatremia. Cause[edit] Three common causes of ketoacidosis are alcohol, starvation, and diabetes, resulting in alcoholic ketoacidosis, starvation ketoacidosis, and diabetic ketoacidosis respectively.[3] In diabetic ketoacidosis, a high concentration of ketone bodies is usually accomp Continue reading >>

> Hyperglycemia And Diabetic Ketoacidosis

> 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 And Hyperglycaemic Hyperosmolar State

Diabetic Ketoacidosis And Hyperglycaemic Hyperosmolar State

The hallmark of diabetes is a raised plasma glucose resulting from an absolute or relative lack of insulin action. Untreated, this can lead to two distinct yet overlapping life-threatening emergencies. Near-complete lack of insulin will result in diabetic ketoacidosis, which is therefore more characteristic of type 1 diabetes, whereas partial insulin deficiency will suppress hepatic ketogenesis but not hepatic glucose output, resulting in hyperglycaemia and dehydration, and culminating in the hyperglycaemic hyperosmolar state. Hyperglycaemia is characteristic of diabetic ketoacidosis, particularly in the previously undiagnosed, but it is the acidosis and the associated electrolyte disorders that make this a life-threatening condition. Hyperglycaemia is the dominant feature of the hyperglycaemic hyperosmolar state, causing severe polyuria and fluid loss and leading to cellular dehydration. Progression from uncontrolled diabetes to a metabolic emergency may result from unrecognised diabetes, sometimes aggravated by glucose containing drinks, or metabolic stress due to infection or intercurrent illness and associated with increased levels of counter-regulatory hormones. Since diabetic ketoacidosis and the hyperglycaemic hyperosmolar state have a similar underlying pathophysiology the principles of treatment are similar (but not identical), and the conditions may be considered two extremes of a spectrum of disease, with individual patients often showing aspects of both. Pathogenesis of DKA and HHS Insulin is a powerful anabolic hormone which helps nutrients to enter the cells, where these nutrients can be used either as fuel or as building blocks for cell growth and expansion. The complementary action of insulin is to antagonise the breakdown of fuel stores. Thus, the relea Continue reading >>

Fluid Management In Diabetic Ketoacidosis

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 >>

Symptoms Of Diabetic Ketoacidosis

Symptoms Of Diabetic Ketoacidosis

Diabetic ketoacidosis, or simply DKA, is one of the complications of diabetes mellitus. It occurs suddenly, is severe and can be life-threatening if neglected. The diabetic ketoacidosis is a complex metabolic state comprising of increased blood glucose levels (hyperglycemia), increased production and presence of ketone acids in the blood (ketonemia) and acidic changes in the internal environment of the body (acidosis). These changes together constitute the diabetic ketoacidosis. Diabetic ketoacidosis is more common in persons with type – 1 as compared to type – 2 diabetes mellitus. Sometimes, it may be the first sign of diabetes mellitus in patients with no previous diagnosis of diabetes. In normal individuals, insulin hormone is produced and secreted by an organ called pancreas. Insulin is necessary for the entry of blood glucose into our cells. Insulin works like a key and unlocks the cellular gates to help glucose enter the cells. The cells use entered glucose to produce energy. In type – 1 diabetes mellitus, the pancreatic cells producing insulin are destroyed. This lack of insulin prevents the entry of blood glucose into our cells as the cellular gates are closed, increasing the blood glucose levels (hyperglycemia). Our body cells starve and cannot utilize glucose for energy despite increased amounts of glucose in our blood. In this starving state, our body burns fats and produces ketones for energy purposes. Ketones have an advantage that they do not need insulin to enter into cells but the ketones also have a disadvantage that they are acidic in nature and when produced in excessive amounts, they change our body environment and make it acidic, which can be life-threatening. The patients often develop ketoacidosis when: They have missed their insulin doses T Continue reading >>

Diabetic Ketoacidosis And Cerebral Edema

Diabetic Ketoacidosis And Cerebral Edema

Elliot J. Krane, M.D. Departments of Pediatrics and Anesthesiology Stanford University Medical Center Introduction In 1922 Banting and Best introduced insulin into clinical practice. A decade later the first reported case of cerebral edema complicating diabetic ketoacidosis (DKA) was reported by Dillon, Riggs and Dyer writing in the pathology literature. While the syndrome of cerebral edema complicating DKA was either not seen, ignored, or was unrecognized by the medical community until 3 decades later when the complication was again reported by Young and Bradley at the Joslin Clinic, there has since been a flurry of case reports in the 1960's and 1970's and basic and clinical research from the 1970's to the 1990's leading to our present day acceptance of this as a known complication of DKA, or of the management of DKA. In fact, we now recognize that the cerebral complications of DKA (including much less frequent cerebral arterial infarctions, venous sinus thrombosis, and central nervous system infections) are the most common cause of diabetic-related death of young diabetic patients (1), accounting for 31% of deaths associated with DKA and 20% of all diabetic deaths, having surpassed aspiration, electrolyte imbalance, myocardial infarction, etc. Furthermore, diabetes mellitus remains an important cause of hospitalization of young children. The prevalence rate of diabetes continues to grow in all Western developed nations, nearly doubling every decade, resulting in 22,000 hospital admissions in children under 15 years of age for diabetes in the United States in 1994, the majority of which were due to ketoacidosis. With approximately 4 hospital admissions of children for DKA per 100,000 population per year (2), every PICU located in a major metropolitan center will conti Continue reading >>

Hypertension Despite Dehydration During Severe Pediatric Diabetic Ketoacidosis

Hypertension Despite Dehydration During Severe Pediatric Diabetic Ketoacidosis

Go to: Abstract Diabetic ketoacidosis (DKA) may result in both dehydration and cerebral edema but these processes may have opposing effects on blood pressure. We examined the relationship between dehydration and blood pressure in pediatric DKA. DKA (venous pH < 7.3, glucose > 300 mg/dL, HCO3 < 15 meq/l and urinary ketosis). Dehydration was calculated as percent body weight lost at admission compared to discharge. Hypertension (systolic and/or diastolic blood pressure percentile ≥ 95%ile) was defined based on 2004 National Heart, Lung, and Blood Institute nomograms and hypotension was defined as systolic blood pressure < 70 + 2 [age] Thirty-three patients (median 10.9 years; range 10 months - 17 years) were included. Fifty-eight percent of patients (19/33) had hypertension on admission prior to treatment and 82% had hypertension during the first 6 hours of admission. None had admission hypotension. Hypertension forty-eight hours after treatment and weeks after discharge was common (28% and 19%, respectively). Based on weight gained by discharge, 27% of patients had mild, 61% had moderate, and 12% presented with severe dehydration. Keywords: blood pressure, diabetes, pediatric, hypertension Go to: INTRODUCTION Dehydration from fluid loss secondary to glycosuria is a central feature of diabetic ketoacidosis (DKA) (1-3). Dehydration can theoretically lead to hypovolemia and systemic hypotension. However, there is a paucity of information on blood pressure in DKA. Many patients (15-67%) evaluated for new onset type 1 diabetes mellitus present with the constellation of dehydration, hyperglycemia and acidosis consistent with DKA (1-3). Dehydration, coupled with systemic hypotension may result in decreased cerebral perfusion and cerebral ischemia (4). Thus, in DKA, both dehyd Continue reading >>

How The Treatment Of Diabetic Ketoacidosis Has Improved

How The Treatment Of Diabetic Ketoacidosis Has Improved

For patients with type 1 diabetes, one of the most serious medical emergencies is diabetic ketoacidosis (DKA). It can be life-threatening and, in most cases, is caused by a shortage of insulin. Glucose is the “fuel” which feeds human cells. Without it, these cells are forced to “burn” fatty acids in order to survive. This process leads to the production of acidic ketone bodies which can cause serious symptoms and complications such as passing out, confusion, vomiting, dehydration, coma, and, if not corrected in a timely manner, even death. High levels of ketones poison the body. DKA can be diagnosed with blood and urine tests and is distinguished from other ketoacidosis by the presence of high blood sugar levels. Typical treatment for DKA consists of using intravenous fluids to correct the dehydration, insulin dosing to suppress the production of ketones, and treatment for any underlying causes such as infections. Medical history notes that DKA was first diagnosed and described in 1886 and until insulin therapy was introduced in the 1920’s, this condition was almost universally fatal. However, with availability and advances in insulin therapy, the mortality rate is less than one percent when timely treatment is applied. A Clinical Pharmacist Examines DKA Ron Fila (RPh) is a clinical pharmacist at McLaren Northern Michigan in Petoskey, MI. He has first-hand experience in treating patients with DKA and, as one of the early adaptors of EndoTool he has seen how this algorithmically-based glucose management software can help physicians save lives and improve patient outcomes. “We started using EndoTool in 2013, for treating patients in the ICU,” he noted in a recent interview. “Later, we expanded our use of this software for DKA and pediatrics. “Since DKA i Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic Ketoacidosis This is a life threatening, medical emergency. This is the most common way for new type 1 diabetics to present. Ketogenesis Ketogenesis occurs when there is insufficient glucose supply and glycogen stores are exhausted (such as prolonged fasting): The liver takes fatty acids and converts them to ketones. Ketones are water soluble fatty acids that can be used as fuel. They can cross the blood brain barrier and be used by the brain as fuel. Producing ketones is normal and not harmful in healthy patients when under fasting conditions or low carbohydrate, high fat diets. Ketones levels can be measured in the urine (dip stick) and blood (by ketone meter). People in ketosis (producing ketones) have a characteristic acetone smell to their breath. Ketone acids (ketones) are buffered in normal patients, so the blood does not become acidotic. When underlying pathology (i.e. Type 1 Diabetes) causes extreme hyperglycaemic ketosis, this results in a metabolic acidosis that is life threatening (see below). Diabetic Ketoacidosis Pathophysiology When there is no insulin, the cells of the body cannot take glucose from the blood and use it for fuel Therefore, the cells think the body is being fasted and has no glucose supply Meanwhile, the level of glucose in the blood keeps rising (hyperglycaemia) Ketoacidosis Because the cells in the body have no fuel and think they are starving, they initiate the process of ketogenesis, so that they have a usable fuel Over time, the patient gets higher and higher glucose and ketones levels Initially, the kidney produces bicarbonate to counteract the acidic blood and maintain a normal pH Over time, the ketone acids uses up the bicarbonate and the blood starts to become acidic (ketoacidosis) Dehydration The hyperglycaemia overwhelm Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

What Is It? Diabetic ketoacidosis is a potentially fatal complication of diabetes that occurs when you have much less insulin than your body needs. This problem causes the blood to become acidic and the body to become dangerously dehydrated. Diabetic ketoacidosis can occur when diabetes is not treated adequately, or it can occur during times of serious sickness. To understand this illness, you need to understand the way your body powers itself with sugar and other fuels. Foods we eat are broken down by the body, and much of what we eat becomes glucose (a type of sugar), which enters the bloodstream. Insulin helps glucose to pass from the bloodstream into body cells, where it is used for energy. Insulin normally is made by the pancreas, but people with type 1 diabetes (insulin-dependent diabetes) don't produce enough insulin and must inject it daily. Your body needs a constant source of energy. When you have plenty of insulin, your body cells can get all the energy they need from glucose. If you don't have enough insulin in your blood, your liver is programmed to manufacture emergency fuels. These fuels, made from fat, are called ketones (or keto acids). In a pinch, ketones can give you energy. However, if your body stays dependent on ketones for energy for too long, you soon will become ill. Ketones are acidic chemicals that are toxic at high concentrations. In diabetic ketoacidosis, ketones build up in the blood, seriously altering the normal chemistry of the blood and interfering with the function of multiple organs. They make the blood acidic, which causes vomiting and abdominal pain. If the acid level of the blood becomes extreme, ketoacidosis can cause falling blood pressure, coma and death. Ketoacidosis is always accompanied by dehydration, which is caused by high Continue reading >>

Understanding The Presentation Of Diabetic Ketoacidosis

Understanding The Presentation Of Diabetic Ketoacidosis

Hypoglycemia, diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar nonketotic syndrome (HHNS) must be considered while forming a differential diagnosis when assessing and managing a patient with an altered mental status. This is especially true if the patient has a history of diabetes mellitus (DM). However, be aware that the onset of DKA or HHNS may be the first sign of DM in a patient with no known history. Thus, it is imperative to obtain a blood glucose reading on any patient with an altered mental status, especially if the patient appears to be dehydrated, regardless of a positive or negative history of DM. In addition to the blood glucose reading, the history — particularly onset — and physical assessment findings will contribute to the formulation of a differential diagnosis and the appropriate emergency management of the patient. Pathophysiology of DKA The patient experiencing DKA presents significantly different from one who is hypoglycemic. This is due to the variation in the pathology of the condition. Like hypoglycemia, by understanding the basic pathophysiology of DKA, there is no need to memorize signs and symptoms in order to recognize and differentiate between hypoglycemia and DKA. Unlike hypoglycemia, where the insulin level is in excess and the blood glucose level is extremely low, DKA is associated with a relative or absolute insulin deficiency and a severely elevated blood glucose level, typically greater than 300 mg/dL. Due to the lack of insulin, tissue such as muscle, fat and the liver are unable to take up glucose. Even though the blood has an extremely elevated amount of circulating glucose, the cells are basically starving. Because the blood brain barrier does not require insulin for glucose to diffuse across, the brain cells are rece Continue reading >>

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