diabetestalk.net

Dka Pathophysiology Diagram

Living With Diabetes

Living With Diabetes

Managing diabetes is a daily challenge. There are so many variables to keep in mind -- food, exercise, stress, general health, etc. -- that keeping blood sugar levels in the desired range is a constant balancing act. We want to make managing diabetes easier. So, the DRI's Education Team hasdeveloped short brochures about the topics listed below -- offering useful tips on many of the day-to-day issues facing people living with diabetes. And, most of the materials are offered in English and Spanish. If you can benefit by learning about one or more of these subjects, just click on the title to expand. Do you know what foods have the greatest impact on your blood sugars? If you answered CARBOHYDRATE FOODS...youre right! Carbohydrates -- "carbs" -- are broken down into glucose. So if you eat too much of them, your blood sugar level may rise. For this reason, people with diabetes find it helpful to keep track of the carbs they eat in order to manage their blood sugars. Carb counting is easy. It just takes some practice at first. Caring for older people with diabetes requires special thought and consideration. The older individual is more likely to have other health problems and may be taking a variety of different medications. Many people are frightened to check their blood sugar -- or "blood glucose" -- levels because they do not want to see levels that are higher or lower than their target range. But, checking blood sugar at home, in school, and in the workplace is key to managing diabetes. It puts you in control of your diabetes. Remember, your blood sugar levels remain the same whether you know about them or not. Checking blood sugar levels is the most accurate way to see if your lifestyle changes and medications are helping you to better manage your diabetes. If levels Continue reading >>

Dka Vs Hhs (hhns) Nclex Review

Dka Vs Hhs (hhns) Nclex Review

Diabetic ketoacidosis vs hyperglycemic hyperosmolar nonketotic syndrome (HHNS or HHS): What are the differences between these two complications of diabetes mellitus? This NCLEX review will simplify the differences between DKA and HHNS and give you a video lecture that easily explains their differences. Many students get these two complications confused due to their similarities, but there are major differences between these two complications. After reviewing this NCLEX review, don’t forget to take the quiz on DKA vs HHNS. Lecture on DKA and HHS DKA vs HHNS Diabetic Ketoacidosis Affects mainly Type 1 diabetics Ketones and Acidosis present Hyperglycemia presents >300 mg/dL Variable osmolality Happens Suddenly Causes: no insulin present in the body or illness/infection Seen in young or undiagnosed diabetics Main problems are hyperglycemia, ketones, and acidosis (blood pH <7.35) Clinical signs/symptoms: Kussmaul breathing, fruity breath, abdominal pain Treatment is the same as in HHNS (fluids, electrolyte replacement, and insulin) Watch potassium levels closely when giving insulin and make sure the level is at least 3.3 before administrating. Hyperglycemic Hyperosmolar Nonketotic Syndrome Affects mainly Type 2 diabetics No ketones or acidosis present EXTREME Hyperglycemia (remember heavy-duty hyperglycemia) >600 mg/dL sometimes four digits High Osmolality (more of an issue in HHNS than DKA) Happens Gradually Causes: mainly illness or infection and there is some insulin present which prevents the breakdown of ketones Seen in older adults due to illness or infection Main problems are dehydration & heavy-duty hyperglycemia and hyperosmolarity (because the glucose is so high it makes the blood very concentrated) More likely to have mental status changes due to severe dehydrat Continue reading >>

Improving Care For Pediatric Diabetic Ketoacidosis

Improving Care For Pediatric Diabetic Ketoacidosis

Abstract OBJECTIVE: We sought to create and implement recommendations from an evidence-based pathway for hospital management of pediatric diabetic ketoacidosis (DKA) and to sustain improvement. We hypothesized that development and utilization of standard work for inpatient care of DKA would lead to reduction in hypokalemia and improvement in outcome measures. METHODS: Development involved systematic review of published literature by a multidisciplinary team. Implementation included multidisciplinary feedback, hospital-wide education, daily team huddles, and development of computer decision support and electronic order sets. RESULTS: Pathway-based order sets forced clinical pathway adherence; yet, variations in care persisted, requiring ongoing iterative review and pathway tool adjustment. Quality improvement measures have identified barriers and informed subsequent adjustments to interventions. We compared 281 patients treated postimplementation with 172 treated preimplementation. Our most notable findings included the following: (1) monitoring of serum potassium concentrations identified unanticipated hypokalemia episodes, not recognized before standard work implementation, and earlier addition of potassium to fluids resulted in a notable reduction in hypokalemia; (2) improvements in insulin infusion management were associated with reduced duration of ICU stay; and (3) with overall improved DKA management and education, cerebral edema occurrence and bicarbonate use were reduced. We continue to convene quarterly meetings, review cases, and process ongoing issues with system-based elements of implementing the recommendations. CONCLUSIONS: Our multidisciplinary development and implementation of an evidence-based pathway for DKA have led to overall improvements in care. We Continue reading >>

Diabetic Ketoacidosis And Hyperosmolar Hyperglycemic State In Adults: Treatment

Diabetic Ketoacidosis And Hyperosmolar Hyperglycemic State In Adults: Treatment

INTRODUCTION Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS, also known as hyperosmotic hyperglycemic nonketotic state [HHNK]) are two of the most serious acute complications of diabetes. They are part of the spectrum of hyperglycemia, and each represents an extreme in the spectrum. The treatment of DKA and HHS in adults will be reviewed here. The epidemiology, pathogenesis, clinical features, evaluation, and diagnosis of these disorders are discussed separately. DKA in children is also reviewed separately. (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Epidemiology and pathogenesis".) (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Clinical features, evaluation, and diagnosis".) Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Professor of Pediatric Endocrinology University of Khartoum, Sudan Introduction DKA is a serious acute complications of Diabetes Mellitus. It carries significant risk of death and/or morbidity especially with delayed treatment. The prognosis of DKA is worse in the extremes of age, with a mortality rates of 5-10%. With the new advances of therapy, DKA mortality decreases to > 2%. Before discovery and use of Insulin (1922) the mortality was 100%. Epidemiology DKA is reported in 2-5% of known type 1 diabetic patients in industrialized countries, while it occurs in 35-40% of such patients in Africa. DKA at the time of first diagnosis of diabetes mellitus is reported in only 2-3% in western Europe, but is seen in 95% of diabetic children in Sudan. Similar results were reported from other African countries . Consequences The latter observation is annoying because it implies the following: The late diagnosis of type 1 diabetes in many developing countries particularly in Africa. The late presentation of DKA, which is associated with risk of morbidity & mortality Death of young children with DKA undiagnosed or wrongly diagnosed as malaria or meningitis. Pathophysiology Secondary to insulin deficiency, and the action of counter-regulatory hormones, blood glucose increases leading to hyperglycemia and glucosuria. Glucosuria causes an osmotic diuresis, leading to water & Na loss. In the absence of insulin activity the body fails to utilize glucose as fuel and uses fats instead. This leads to ketosis. Pathophysiology/2 The excess of ketone bodies will cause metabolic acidosis, the later is also aggravated by Lactic acidosis caused by dehydration & poor tissue perfusion. Vomiting due to an ileus, plus increased insensible water losses due to tachypnea will worsen the state of dehydr Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

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

Pathophysiology Of Diabetic Ketoacidosis

Pathophysiology Of Diabetic Ketoacidosis

Diabetic Ketoacidosis is a serious complication of Diabetes Mellitus Type 1. The problem in Diabetes Mellitus Type 1 is the absolute lack of insulin. Without insulin, glucose will not be transported to the cells. Consequently, a person feels hungry despite of eating adequately and the level of glucose in the body is increasing because cell transportation is impossible. Consequently, as a response to cell hunger, the body will begin to breakdown proteins. If not managed promptly, the break down will continue and this time, it’s the fats. These will give rise to a high level of ketones in the blood. Ketones are blood acids and will result to Diabetic Ketoacidosis. If left untreated, this is fatal. Causes Decreased or missed dose of insulin – deficient insulin supply Illness or infection – causes resistance to insulin Undiagnosed and untreated diabetes Error in drawing up or injecting insulin – common in patients with visual impairment Intentional skipping of insulin doses – common in adolescents and those who have difficulty coping with the disease Equipment problems – example is occlusion of insulin pump tubing Clinical Manifestations Hyperglycemia – leads to polyuria, polydipsia, blurred vision, weakness, and headache Orthostatic hypotension – a decrease of 20 mmHg or more in systolic blood pressure caused by marked intravascular volume depletion; weak, rapid pulse is noted Ketosis and acidosis – lead to gastrointestinal symptoms such as anorexia, nausea, vomiting, and abdominal pain, acetone (a fruity odor) breath Kussmaul respirations – hyperventilation with very deep, but not labored, respirations Mental status varies widely. Patient may be alert, lethargic, or comatose Assessment and Diagnostic Findings Blood glucose level is between 300-800 mg/d Continue reading >>

Hyperosmolar Hyperglycemic State

Hyperosmolar Hyperglycemic State

Hyperosmolar hyperglycemic state (HHS) is a complication of diabetes mellitus in which high blood sugar results in high osmolarity without significant ketoacidosis.[4] Symptoms include signs of dehydration, weakness, legs cramps, trouble seeing, and an altered level of consciousness.[2] Onset is typically over days to weeks.[3] Complications may include seizures, disseminated intravascular coagulopathy, mesenteric artery occlusion, or rhabdomyolysis.[2] The main risk factor is a history of diabetes mellitus type 2.[4] Occasionally it may occur in those without a prior history of diabetes or those with diabetes mellitus type 1.[3][4] Triggers include infections, stroke, trauma, certain medications, and heart attacks.[4] Diagnosis is based on blood tests finding a blood sugar greater than 30 mmol/L (600 mg/dL), osmolarity greater than 320 mOsm/kg, and a pH above 7.3.[2][3] Initial treatment generally consists of intravenous fluids to manage dehydration, intravenous insulin in those with significant ketones, low molecular weight heparin to decrease the risk of blood clotting, and antibiotics among those in whom there is concerns of infection.[3] The goal is a slow decline in blood sugar levels.[3] Potassium replacement is often required as the metabolic problems are corrected.[3] Efforts to prevent diabetic foot ulcers are also important.[3] It typically takes a few days for the person to return to baseline.[3] While the exact frequency of the condition is unknown, it is relatively common.[2][4] Older people are most commonly affected.[4] The risk of death among those affected is about 15%.[4] It was first described in the 1880s.[4] Signs and symptoms[edit] Symptoms of high blood sugar including increased thirst (polydipsia), increased volume of urination (polyurea), and i Continue reading >>

Respiratory Failure In Diabetic Ketoacidosis

Respiratory Failure In Diabetic Ketoacidosis

Go to: INTRODUCTION Ketoacidosis in subjects with type 1, or less frequently, type 2 diabetes mellitus remains a potentially life-threatening diabetic manifestation. The subject has justifiably attracted attention in the literature. Sequential reviews[1-9] have documented important changes in the clinical concepts that are related to diabetic ketoacidosis (DKA) and its management. A large number of case series of DKA have addressed various aspects of its clinical presentation and management. For this review, we selected representative studies focused on management, outcome, age differences, gender differences, associated morbid conditions, ethnicity and prominent clinical and laboratory features[10-35]. In recognition of the complexity of treatment, the recommendation to provide this care in intensive care units was made more than 50 years ago[36]. Severe DKA is treated in intensive care units today[31]. Evidence-based guidelines for the diagnosis and management of DKA have been published and frequently revised in North America[37,38] and Europe[39]. Losses of fluids and electrolytes, which are important causes of morbidity and mortality in DKA, vary greatly between patients. Quantitative methods estimating individual losses and guiding their replacement have also been reported[40,41]. The outcomes of DKA have improved with new methods of insulin administration[42] and adherence to guidelines[43-46]. The aim of treatment is to minimize mortality and prevent sequelae. One study documented that the target of zero mortality is feasible[42]. However, mortality from DKA, although reduced progressively in the early decades after the employment of insulin treatment[1], remains high. Up to fifty plus years ago, mortality from DKA was between 3% and 10%[1,16]. A recent review re Continue reading >>

Diabetic Ketoacidosis - Symptoms

Diabetic Ketoacidosis - Symptoms

A A A Diabetic Ketoacidosis Diabetic ketoacidosis (DKA) results from dehydration during a state of relative insulin deficiency, associated with high blood levels of sugar level and organic acids called ketones. Diabetic ketoacidosis is associated with significant disturbances of the body's chemistry, which resolve with proper therapy. Diabetic ketoacidosis usually occurs in people with type 1 (juvenile) diabetes mellitus (T1DM), but diabetic ketoacidosis can develop in any person with diabetes. Since type 1 diabetes typically starts before age 25 years, diabetic ketoacidosis is most common in this age group, but it may occur at any age. Males and females are equally affected. Diabetic ketoacidosis occurs when a person with diabetes becomes dehydrated. As the body produces a stress response, hormones (unopposed by insulin due to the insulin deficiency) begin to break down muscle, fat, and liver cells into glucose (sugar) and fatty acids for use as fuel. These hormones include glucagon, growth hormone, and adrenaline. These fatty acids are converted to ketones by a process called oxidation. The body consumes its own muscle, fat, and liver cells for fuel. In diabetic ketoacidosis, the body shifts from its normal fed metabolism (using carbohydrates for fuel) to a fasting state (using fat for fuel). The resulting increase in blood sugar occurs, because insulin is unavailable to transport sugar into cells for future use. As blood sugar levels rise, the kidneys cannot retain the extra sugar, which is dumped into the urine, thereby increasing urination and causing dehydration. Commonly, about 10% of total body fluids are lost as the patient slips into diabetic ketoacidosis. Significant loss of potassium and other salts in the excessive urination is also common. The most common Continue reading >>

Sickly Sweet: Understanding Diabetic Ketoacidosis

Sickly Sweet: Understanding Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a potentially life threatening condition that can occur to people with diabetes. It is observed primarily in people with type 1 diabetes (insulin dependent), but it can occur in type 2 diabetes (non-insulin dependent) under certain circumstances. The reason for why it is not often seen in people with type 2 diabetes is because their body is still able to produce insulin, so the pathophysiology explained in the flowchart below is not as dramatic as compared to people with type 1 diabetes who do not make any insulin at all. There are various symptoms associated with DKA including: Hyperglycaemia Polyphagia (increased appetite and hunger) Polydipsia (increased thirst) Polyuria (increased urination) Glycosuria (glucose in the urine) Ketonuria (ketones in urine) Ketones in blood Sweet, fruity breath Tachypnoea leading to Kussmaul breathing (deep and laboured breathing pattern) The body tries to compensate for the ketone bodies (acid) by eliminating carbon dioxide (also an acid) thereby attempting to make the body more alkalotic to normalise the pH The compensation between the metabolic and respiratory system can be read about in this article Decreased bicarbonate The body tries to use the available bicarbonate (base) to buffer the ketone bodies (acid) in order to improve the metabolic ketoacidosis This actually worsens the situation the lower the bicarbonate becomes with a continual production of ketones Increased drowsiness/decreased level of consciousness As the pH decreases and becomes more acidotic, it has a direct effect on decreasing the level of consciousness in a person Increased urea Electrolyte disturbances Tachycardia and other cardiac arrhythmias Tachycardia is often a compensatory mechanism for the hypotension Cardiac arrhythmias a Continue reading >>

Incidence Of Diabetic Ketoacidosis Among Patients With Type 2 Diabetes Mellitus Treated With Sglt2 Inhibitors And Other Antihyperglycemic Agents

Incidence Of Diabetic Ketoacidosis Among Patients With Type 2 Diabetes Mellitus Treated With Sglt2 Inhibitors And Other Antihyperglycemic Agents

Jump to Section 1. Introduction Diabetic ketoacidosis (DKA) is a serious, acute metabolic complication of diabetes characterized by absolute or relative insulin deficiency [[1], [2]], with an overall mortality rate of up to 5% in experienced healthcare centers [3]. Insulin deficiency, increased insulin counter-regulatory hormones (cortisol, glucagon, growth hormone, and catecholamines) and peripheral insulin resistance lead to hyperglycemia, dehydration, ketosis, and electrolyte imbalance, which underlie the pathophysiology of DKA [2]. While DKA is a commonly recognized vulnerability in autoimmune diabetes, stressful conditions such as trauma, surgery, or infection also increase DKA risk in patients with type 2 diabetes mellitus [4]. In fact, studies have reported that patients with type 2 diabetes accounted for 12–56% of the DKA cases, had longer hospital stays, and higher mortality (which possibly was due to advanced age and comorbidities) than patients with type 1 diabetes [[3], [5]]. Sodium glucose co-transporter 2 inhibitors (SGLT2i’s) are a new class of oral antihyperglycemic agents (AHA) that lower blood glucose through an insulin-independent mechanism, by suppressing renal glucose reabsorption and increasing urinary glucose excretion [6]. Currently, 3 SGLT2i’s have been approved in the US and Europe for the treatment of type 2diabetes: canagliflozin, dapagliflozin, and empagliflozin (initial approval March 29, 2013, January 8, 2014, August 1, 2014 in the US, November 15, 2013, November 12, 2012, May 22, 2014 in Europe, respectively). By mid-2015, based on spontaneous adverse event reports, the US Food and Drug Administration and the European Medicines Agency [7] had both issued statements that medicines in the SGLT2i class of drugs may be associated with a 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 >>

Diabetes Pathophysiology

Diabetes Pathophysiology

Diabetes occurs when there is a dis-balance between the demand and production of the hormone insulin. Control of blood sugar When food is taken, it is broken down into smaller components. Sugars and carbohydrates are thus broken down into glucose for the body to utilize them as an energy source. The liver is also able to manufacture glucose. In normal persons the hormone insulin, which is made by the beta cells of the pancreas, regulates how much glucose is in the blood. When there is excess of glucose in blood, insulin stimulates cells to absorb enough glucose from the blood for the energy that they need. Insulin also stimulates the liver to absorb and store any excess glucose that is in the blood. Insulin release is triggered after a meal when there is a rise in blood glucose. When blood glucose levels fall, during exercise for example, insulin levels fall too. High insulin will promote glucose uptake, glycolysis (break down of glucose), and glycogenesis (formation of storage form of glucose called glycogen), as well as uptake and synthesis of amino acids, proteins, and fat. Low insulin will promote gluconeogenesis (breakdown of various substrates to release glucose), glycogenolysis (breakdown of glycogen to release gluose), lipolysis (breakdown of lipids to release glucose), and proteolysis (breakdown of proteins to release glucose). Insulin acts via insulin receptors. Liver Adipose or fat Tissue Muscle High insulin Glycolysis Glycogenesis Triglyceride synthesis Amino acid uptake Protein synthesis Low insulin Gluconeogenesis Glycogenolysis Lipolysis Proteolysis Normal Responses to Eating and Fasting In a fed state: there is increased insulin secretion, causing glycolysis, glycogen storage, fatty acid synthesis/storage, and protein synthesis. After an overnight fast: Continue reading >>

Diabetic Ketoacidosis Explained

Diabetic Ketoacidosis Explained

Twitter Summary: DKA - a major complication of #diabetes – we describe what it is, symptoms, who’s at risk, prevention + treatment! One of the most notorious complications of diabetes is diabetic ketoacidosis, or DKA. First described in the late 19th century, DKA represented something close to the ultimate diabetes emergency: In just 24 hours, people can experience an onset of severe symptoms, all leading to coma or death. But DKA also represents one of the great triumphs of the revolution in diabetes care over the last century. Before the discovery of insulin in 1920, DKA was almost invariably fatal, but the mortality rate for DKA dropped to below 30 percent within 10 years, and now fewer than 1 percent of those who develop DKA die from it, provided they get adequate care in time. Don’t skip over that last phrase, because it’s crucial: DKA is very treatable, but only as long as it’s diagnosed promptly and patients understand the risk. Table of Contents: What are the symptoms of DKA? Does DKA occur in both type 1 and type 2 diabetes? What Can Patients do to Prevent DKA? What is DKA? Insulin plays a critical role in the body’s functioning: it tells cells to absorb the glucose in the blood so that the body can use it for energy. When there’s no insulin to take that glucose out of the blood, high blood sugar (hyperglycemia) results. The body will also start burning fatty acids for energy, since it can’t get that energy from glucose. To make fatty acids usable for energy, the liver has to convert them into compounds known as ketones, and these ketones make the blood more acidic. DKA results when acid levels get too high in the blood. There are other issues too, as DKA also often leads to the overproduction and release of hormones like glucagon and adrenaline Continue reading >>

More in ketosis