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Infection Dka Pathophysiology

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 >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find the Pre-diabetes (Impaired Glucose Tolerance) article more useful, or one of our other health articles. See also the separate Childhood Ketoacidosis article. Diabetic ketoacidosis (DKA) is a medical emergency with a significant morbidity and mortality. It should be diagnosed promptly and managed intensively. DKA is characterised by hyperglycaemia, acidosis and ketonaemia:[1] Ketonaemia (3 mmol/L and over), or significant ketonuria (more than 2+ on standard urine sticks). Blood glucose over 11 mmol/L or known diabetes mellitus (the degree of hyperglycaemia is not a reliable indicator of DKA and the blood glucose may rarely be normal or only slightly elevated in DKA). Bicarbonate below 15 mmol/L and/or venous pH less than 7.3. However, hyperglycaemia may not always be present and low blood ketone levels (<3 mmol/L) do not always exclude DKA.[2] Epidemiology DKA is normally seen in people with type 1 diabetes. Data from the UK National Diabetes Audit show a crude one-year incidence of 3.6% among people with type 1 diabetes. In the UK nearly 4% of people with type 1 diabetes experience DKA each year. About 6% of cases of DKA occur in adults newly presenting with type 1 diabetes. About 8% of episodes occur in hospital patients who did not primarily present with DKA.[2] However, DKA may also occur in people with type 2 diabetes, although people with type 2 diabetes are much more likely to have a hyperosmolar hyperglycaemic state. Ketosis-prone type 2 diabetes tends to be more common in older, overweight, non-white people with type 2 diabetes, and DKA may be their 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

As fat is broken down, acids called ketones build up in the blood and urine. In high levels, ketones are poisonous. This condition is known as ketoacidosis. Diabetic ketoacidosis (DKA) is sometimes the first sign of type 1 diabetes in people who have not yet been diagnosed. It can also occur in someone who has already been diagnosed with type 1 diabetes. Infection, injury, a serious illness, missing doses of insulin shots, or surgery can lead to DKA in people with type 1 diabetes. People with type 2 diabetes can also develop DKA, but it is less common. It is usually triggered by uncontrolled blood sugar, missing doses of medicines, or a severe illness. Continue reading >>

Diabetic Ketoacidosis And Hyperglycemic Hyperosmolar Syndrome

Diabetic Ketoacidosis And Hyperglycemic Hyperosmolar Syndrome

In Brief Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic syndrome (HHS) are two acute complications of diabetes that can result in increased morbidity and mortality if not efficiently and effectively treated. Mortality rates are 2–5% for DKA and 15% for HHS, and mortality is usually a consequence of the underlying precipitating cause(s) rather than a result of the metabolic changes of hyperglycemia. Effective standardized treatment protocols, as well as prompt identification and treatment of the precipitating cause, are important factors affecting outcome. The two most common life-threatening complications of diabetes mellitus include diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar syndrome (HHS). Although there are important differences in their pathogenesis, the basic underlying mechanism for both disorders is a reduction in the net effective concentration of circulating insulin coupled with a concomitant elevation of counterregulatory hormones (glucagon, catecholamines, cortisol, and growth hormone). These hyperglycemic emergencies continue to be important causes of morbidity and mortality among patients with diabetes. DKA is reported to be responsible for more than 100,000 hospital admissions per year in the United States1 and accounts for 4–9% of all hospital discharge summaries among patients with diabetes.1 The incidence of HHS is lower than DKA and accounts for <1% of all primary diabetic admissions.1 Most patients with DKA have type 1 diabetes; however, patients with type 2 diabetes are also at risk during the catabolic stress of acute illness.2 Contrary to popular belief, DKA is more common in adults than in children.1 In community-based studies, more than 40% of African-American patients with DKA were >40 years of age and more than 2 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 >>

Diabetic Ketoacidosis And Hypersmolar Non-ketotic Coma

Diabetic Ketoacidosis And Hypersmolar Non-ketotic Coma

Diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS) are the most serious acute metabolic complications of diabetes. Recent data indicate there are more than 144,000 hospital admissions per year for DKA in the United States and the number of cases show an upward trend, with a 30% increase in the annual number of cases between 1995 and 2009. Treatment of DKA utilizes a large number of resources with an annual medical expense of $2.4 billion. The rate of hospital admissions for HHS is lower than for DKA, accounting for less than 1% of all diabetes-related admissions. Although DKA and HHS are often discussed as separate entities, they represent points along a spectrum of hyperglycemic emergencies due to poorly controlled diabetes. Both DKA and HHS are characterized by insulinopenia and severe hyperglycemia. Clinically, they differ only by the degree of dehydration and the severity of metabolic acidosis. DKA has long been considered a key clinical feature of type 1 diabetes (T1D), but in contrast to popular belief, DKA is more common in patients with type 2 diabetes (T2D). T2D now accounts for up to one half of all newly diagnosed diabetes in children ages 10-21 years. In the U.S., the SEARCH for Diabetes in Youth Study found that 29.4% of participants under 20 years of age with T1D presented with DKA, compared with 9.7% of youth with T2D. In community-based studies more than 40% of patients with DKA are older than 40 and more than 20% are older than 55. Patients with T2D may develop DKA under stressful conditions such as trauma, surgery or infections. In addition, in recent years an increasing number of unprovoked ketoacidosis cases without precipitating cause have been reported in children, adolescents and adult subjects with T2D. HHS occurs most commonl Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Print Overview Diabetic ketoacidosis is a serious complication of diabetes that occurs when your body produces high levels of blood acids called ketones. The condition develops when your body can't produce enough insulin. Insulin normally plays a key role in helping sugar (glucose) — a major source of energy for your muscles and other tissues — enter your cells. Without enough insulin, your body begins to break down fat as fuel. This process produces a buildup of acids in the bloodstream called ketones, eventually leading to diabetic ketoacidosis if untreated. If you have diabetes or you're at risk of diabetes, learn the warning signs of diabetic ketoacidosis — and know when to seek emergency care. Symptoms Diabetic ketoacidosis signs and symptoms often develop quickly, sometimes within 24 hours. For some, these signs and symptoms may be the first indication of having diabetes. You may notice: Excessive thirst Frequent urination Nausea and vomiting Abdominal pain Weakness or fatigue Shortness of breath Fruity-scented breath Confusion More-specific signs of diabetic ketoacidosis — which can be detected through home blood and urine testing kits — include: High blood sugar level (hyperglycemia) High ketone levels in your urine When to see a doctor If you feel ill or stressed or you've had a recent illness or injury, check your blood sugar level often. You might also try an over-the-counter urine ketones testing kit. Contact your doctor immediately if: You're vomiting and unable to tolerate food or liquid Your blood sugar level is higher than your target range and doesn't respond to home treatment Your urine ketone level is moderate or high Seek emergency care if: Your blood sugar level is consistently higher than 300 milligrams per deciliter (mg/dL), or 16.7 mill Continue reading >>

Diabetic Ketoacidosis In Type 1 And Type 2 Diabetes Mellitusclinical And Biochemical Differences

Diabetic Ketoacidosis In Type 1 And Type 2 Diabetes Mellitusclinical And Biochemical Differences

Background Diabetic ketoacidosis (DKA), once thought to typify type 1 diabetes mellitus, has been reported to affect individuals with type 2 diabetes mellitus. An analysis and overview of the different clinical and biochemical characteristics of DKA that might be predicted between patients with type 1 and type 2 diabetes is needed. Methods We reviewed 176 admissions of patients with moderate-to-severe DKA. Patients were classified as having type 1 or type 2 diabetes based on treatment history and/or autoantibody status. Groups were compared for differences in symptoms, precipitants, vital statistics, biochemical profiles at presentation, and response to therapy. Results Of 138 patients admitted for moderate-to-severe DKA, 30 had type 2 diabetes. A greater proportion of the type 2 diabetes group was Latino American or African American (P<.001). Thirty-five admissions (19.9%) were for newly diagnosed diabetes. A total of 85% of all admissions involved discontinuation of medication use, 69.2% in the type 2 group. Infections were present in 21.6% of the type 1 and 48.4% of the type 2 diabetes admissions. A total of 21% of patients with type 1 diabetes and 70% with type 2 diabetes had a body mass index greater than 27. Although the type 1 diabetes group was more acidotic (arterial pH, 7.21 ± 0.12 vs 7.27 ± 0.08; P<.001), type 2 diabetes patients required longer treatment periods (36.0 ± 11.6 vs 28.9 ± 8.9 hours, P = .01) to achieve ketone-free urine. Complications from therapy were uncommon. Conclusions A significant proportion of DKA occurs in patients with type 2 diabetes. The time-tested therapy for DKA of intravenous insulin with concomitant glucose as the plasma level decreases, sufficient fluid and electrolyte replacement, and attention to associated problems remai 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 one of the potentially life-threatening acute complications of diabetes mellitus. In the past, diabetic ketoacidosis was considered as the hallmark of Type I diabetes, but current data show that it can be also diagnosed in patients with type II diabetes mellitus. It is often seen among patients who are poorly compliant to insulin administration during an acute illness. It is commonly precipitated by an acute stressful event such as the development of infection leading to overt sepsis, organ infarction such as stroke and heart attack, burns, pregnancy or intake of drugs that affect carbohydrate metabolism such as corticosteroids, anti-hypertensives, loop diuretics, alcohol, cocaine, and ecstasy. The presence of these stressful conditions incite the release of counter-regulatory hormones such as glucagon, catecholamines and growth hormone. These hormones induce the mobilization of energy stores of fat, glycogen and protein. The net effect of which is the production of glucose. As a result of absent or deficient insulin release, diabetic ketoacidosis present with the following metabolic derangements: profound hyperglycemia, hyperketonemiaand metabolic acidosis. The production of ketones outweighs its excretion by the kidneys. This results in further reduction of systemic insulin, elevated concentrations of glucagon, cortisol, growth hormone and catecholamine. In peripheral tissues, such as the liver, lipolysis occurs to free fatty acids, resulting in further production of excess ketones. Thereby, causing ketosis and metabolic acidosis. Symptoms of diabetic ketoacidosis usually develop within 24 hours. Gastrointestinal symptoms such as nausea and vomiting are very prominent. If these symptoms are present in diabetics, investigation for diabetic keto Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Abbas E. Kitabchi, PhD., MD., FACP, FACE Professor of Medicine & Molecular Sciences and Maston K. Callison Professor in the Division of Endocrinology, Diabetes & Metabolism UT Health Science Center, 920 Madison Ave., 300A, Memphis, TN 38163 Aidar R. Gosmanov, M.D., Ph.D., D.M.Sc. Assistant Professor of Medicine, Division of Endocrinology, Diabetes & Metabolism, The University of Tennessee Health Science Center, 920 Madison Avenue, Suite 300A, Memphis, TN 38163 Clinical Recognition Omission of insulin and infection are the two most common precipitants of DKA. Non-compliance may account for up to 44% of DKA presentations; while infection is less frequently observed in DKA patients. Acute medical illnesses involving the cardiovascular system (myocardial infarction, stroke, acute thrombosis) and gastrointestinal tract (bleeding, pancreatitis), diseases of endocrine axis (acromegaly, Cushing`s syndrome, hyperthyroidism) and impaired thermo-regulation or recent surgical procedures can contribute to the development of DKA by causing dehydration, increase in insulin counter-regulatory hormones, and worsening of peripheral insulin resistance. Medications such as diuretics, beta-blockers, corticosteroids, second-generation anti-psychotics, and/or anti-convulsants may affect carbohydrate metabolism and volume status and, therefore, could precipitateDKA. Other factors: psychological problems, eating disorders, insulin pump malfunction, and drug abuse. It is now recognized that new onset T2DM can manifest with DKA. These patients are obese, mostly African Americans or Hispanics and have undiagnosed hyperglycemia, impaired insulin secretion, and insulin action. A recent report suggests that cocaine abuse is an independent risk factor associated with DKA recurrence. Pathophysiology 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 >>

Infections In Patients With Diabetes Mellitus: A Review Of Pathogenesis

Infections In Patients With Diabetes Mellitus: A Review Of Pathogenesis

Go to: Diabetes mellitus (DM) is a clinical syndrome associated with deficiency of insulin secretion or action. It is considered one of the largest emerging threats to health in the 21st century. It is estimated that there will be 380 million persons with DM in 2025.[1] Besides the classical complications of the disease, DM has been associated with reduced response of T cells, neutrophil function, and disorders of humoral immunity.[2–4] Consequently, DM increases the susceptibility to infections, both the most common ones as well as those that almost always affect only people with DM (e.g. rhinocerebral mucormycosis).[4] Such infections, in addition to the repercussions associated with its infectivity, may trigger DM complications such as hypoglycemia and ketoacidosis. This article aims to critically review the current knowledge on the mechanisms associated with the greater susceptibility of DM for developing infectious diseases and to describe the main infectious diseases associated with this metabolic disorder. Continue reading >>

Diabetic Ketoacidosis: Maintaining Glucose Control

Diabetic Ketoacidosis: Maintaining Glucose Control

The metabolic chain reaction that precedes diabetic ketoacidosis can occur rapidly, and this potentially life-threatening condition requires swift recognition and treatment. Two critical words in a diabetic’s vocabulary are “management” and “control.” When a patient with diabetes fails to manage food intake and loses control of blood sugar levels, hyperglycemia follows. In most cases, blood sugar levels elevate slightly, which prompts the individual with diabetes to take action to lower those levels. Under some conditions, blood sugar rises precipitously, which is usually caused by 1 or more of the following1-3 : • Developing or fulminant infection (especially Klebsiella pneumonia) or illness • Serious disruption of insulin treatment • New onset of diabetes • Physical or emotional stress • Adverse drug reaction (especially to corticosteroids, pentamidine, thiazides, sympathomimetics, or secondgeneration antipsychotics4 ) Acute, life-threatening diabetic ketoacidosis (DKA) can develop rapidly. Table 11,2 describes criteria usually used to define DKA. We typically associate this metabolic abnormality with type 1 diabetes, but it also occurs in some patients with type 2 diabetes, with infection or an adverse drug reaction as the primary causes. As blood sugar rises in DKA, the patient becomes dehydrated and metabolic changes produce acidosis.1,2,4,5 Pathophysiology DKA usually occurs when absolute or relative insulin deficiency leads to increased counter-regulatory hormones (ie, glucagon, cortisol, growth hormone, epinephrine). These hormones enhance hepatic glucose production (gluconeogenesis), glycogenolysis, and lipolysis, all of which increase free fatty acids (FFAs) in circulation. With insulin unavailable, the liver turns to FFAs as an alternative Continue reading >>

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