diabetestalk.net

Dka Vs Hhs Labs

Hyperosmolar Hyperglycemic State

Hyperosmolar Hyperglycemic State

Background Hyperosmolar hyperglycemic state (HHS) is one of two serious metabolic derangements that occurs in patients with diabetes mellitus (DM). [1] It is a life-threatening emergency that, although less common than its counterpart, diabetic ketoacidosis (DKA), has a much higher mortality rate, reaching up to 5-10%. (See Epidemiology.) HHS was previously termed hyperosmolar hyperglycemic nonketotic coma (HHNC); however, the terminology was changed because coma is found in fewer than 20% of patients with HHS. [2] HHS is most commonly seen in patients with type 2 DM who have some concomitant illness that leads to reduced fluid intake, as seen, for example, in elderly institutionalized persons with decreased thirst perception and reduced ability to drink water. [3] Infection is the most common preceding illness, but many other conditions, such as stroke or myocardial infarction, can cause this state. [3] Once HHS has developed, it may be difficult to identify or differentiate it from the antecedent illness. (See Etiology.) HHS is characterized by hyperglycemia, hyperosmolarity, and dehydration without significant ketoacidosis. Most patients present with severe dehydration and focal or global neurologic deficits. [2, 4, 5] The clinical features of HHS and DKA overlap and are observed simultaneously (overlap cases) in up to one third of cases. According to the consensus statement published by the American Diabetes Association, diagnostic features of HHS may include the following (see Workup) [4, 6] : Effective serum osmolality of 320 mOsm/kg or greater Profound dehydration, up to an average of 9L Detection and treatment of an underlying illness are critical. Standard care for dehydration and altered mental status is appropriate, including airway management, intravenous (I 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 >>

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 >>

Diagnosis And Treatment Of Diabetic Ketoacidosis And The Hyperglycemic Hyperosmolar State

Diagnosis And Treatment Of Diabetic Ketoacidosis And The Hyperglycemic Hyperosmolar State

Go to: Pathogenesis In both DKA and HHS, the underlying metabolic abnormality results from the combination of absolute or relative insulin deficiency and increased amounts of counterregulatory hormones. Glucose and lipid metabolism When insulin is deficient, the elevated levels of glucagon, catecholamines and cortisol will stimulate hepatic glucose production through increased glycogenolysis and enhanced gluconeogenesis4 (Fig. 1). Hypercortisolemia will result in increased proteolysis, thus providing amino acid precursors for gluconeogenesis. Low insulin and high catecholamine concentrations will reduce glucose uptake by peripheral tissues. The combination of elevated hepatic glucose production and decreased peripheral glucose use is the main pathogenic disturbance responsible for hyperglycemia in DKA and HHS. The hyperglycemia will lead to glycosuria, osmotic diuresis and dehydration. This will be associated with decreased kidney perfusion, particularly in HHS, that will result in decreased glucose clearance by the kidney and thus further exacerbation of the hyperglycemia. In DKA, the low insulin levels combined with increased levels of catecholamines, cortisol and growth hormone will activate hormone-sensitive lipase, which will cause the breakdown of triglycerides and release of free fatty acids. The free fatty acids are taken up by the liver and converted to ketone bodies that are released into the circulation. The process of ketogenesis is stimulated by the increase in glucagon levels.5 This hormone will activate carnitine palmitoyltransferase I, an enzyme that allows free fatty acids in the form of coenzyme A to cross mitochondrial membranes after their esterification into carnitine. On the other side, esterification is reversed by carnitine palmitoyltransferase I Continue reading >>

Hyperosmolar Hyperglycemic State (hhs)

Hyperosmolar Hyperglycemic State (hhs)

By Erika F. Brutsaert, MD, Assistant Professor, Albert Einstein College of Medicine; Attending Physician, Montefiore Medical Center Hyperosmolar hyperglycemic state is a metabolic complication of diabetes mellitus (DM) characterized by severe hyperglycemia, extreme dehydration, hyperosmolar plasma, and altered consciousness. It most often occurs in type 2 DM, often in the setting of physiologic stress. HHS is diagnosed by severe hyperglycemia and plasma hyperosmolality and absence of significant ketosis. Treatment is IV saline solution and insulin. Complications include coma, seizures, and death. Hyperosmolar hyperglycemic state (HHSpreviously referred to as hyperglycemic hyperosmolar nonketotic coma [HHNK] and nonketotic hyperosmolar syndrome) is a complication of type 2 diabetes mellitus and has an estimated mortality rate of up to20%, which is significantly higher than the mortality for diabetic ketoacidosis (currently < 1%). It usually develops after a period of symptomatic hyperglycemia in which fluid intake is inadequate to prevent extreme dehydration due to the hyperglycemia-induced osmotic diuresis. Acute infections and other medical conditions Drugs that impair glucose tolerance (glucocorticoids) or increase fluid loss (diuretics) Serum ketones are not present because the amounts of insulin present in most patients with type 2 DM are adequate to suppress ketogenesis. Because symptoms of acidosis are not present, most patients endure a significantly longer period of osmotic dehydration before presentation, and thus plasma glucose (> 600 mg/dL [> 33.3 mmol/L]) and osmolality (> 320 mOsm/L) are typically much higher than in diabetic ketoacidosis (DKA). The primary symptom of HHS is altered consciousness varying from confusion or disorientation to coma, usually as Continue reading >>

Hyperglycemic Crises: Diabetic Ketoacidosis (dka), And Hyperglycemic Hyperosmolar State (hhs)

Hyperglycemic Crises: Diabetic Ketoacidosis (dka), And Hyperglycemic Hyperosmolar State (hhs)

Go to: Diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS) are acute metabolic complications of diabetes mellitus that can occur in patients with both type 1 and 2 diabetes mellitus. Timely diagnosis, comprehensive clinical and biochemical evaluation, and effective management is key to the successful resolution of DKA and HHS. Critical components of the hyperglycemic crises management include coordinating fluid resuscitation, insulin therapy, and electrolyte replacement along with the continuous patient monitoring using available laboratory tools to predict the resolution of the hyperglycemic crisis. Understanding and prompt awareness of potential of special situations such as DKA or HHS presentation in comatose state, possibility of mixed acid-base disorders obscuring the diagnosis of DKA, and risk of brain edema during the therapy are important to reduce the risks of complications without affecting recovery from hyperglycemic crisis. Identification of factors that precipitated DKA or HHS during the index hospitalization should help prevent subsequent episode of hyperglycemic crisis. For extensive review of all related areas of Endocrinology, visit WWW.ENDOTEXT.ORG. Go to: INTRODUCTION Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) represent two extremes in the spectrum of decompensated diabetes. DKA and HHS remain important causes of morbidity and mortality among diabetic patients despite well developed diagnostic criteria and treatment protocols (1). The annual incidence of DKA from population-based studies is estimated to range from 4 to 8 episodes per 1,000 patient admissions with diabetes (2). The incidence of DKA continues to increase and it accounts for about 140,000 hospitalizations in the US in 2009 (Figure 1 a) (3). 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 And Hyperosmolar Hyperglycemic State In Adults: Clinical Features, Evaluation, And Diagnosis

Diabetic Ketoacidosis And Hyperosmolar Hyperglycemic State In Adults: Clinical Features, Evaluation, And Diagnosis

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. DKA is characterized by ketoacidosis and hyperglycemia, while HHS usually has more severe hyperglycemia but no ketoacidosis (table 1). Each represents an extreme in the spectrum of hyperglycemia. The precipitating factors, clinical features, evaluation, and diagnosis of DKA and HHS in adults will be reviewed here. The epidemiology, pathogenesis, and treatment 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".) Continue reading >>

Diabetic Ketoacidosis (dka) &

Diabetic Ketoacidosis (dka) &

DKA/HHS Presenting Signs Tachycardia Hypotension Dehydration Hypothermia Warm dry Skin Kussmaul Respiration Lethargy or Coma Fruity Odor DKA/HHS Precipitating Factors Infection Pneumonia Gastroenteritis UTI Sepsis Meningitis Influenza Mucormycosis Emotional Problems Trauma Acute Pancreatitis Myocardial Infarction Stroke Endocrine Acromegaly Thyrotoxicosis Cushing’s S. Omission of Antidiabetic Mx’s Drugs Any major Stress/Acute Illness DKA/HHS Drugs that can Precipitate Psychotropic Drugs Chlorpromazine Clozapine Risperidone Loxapine Steroids Immunosuppressants Beta Blockers Calcium Channel Blockers Diuretics Anticonvulsants Diazoxide DKA/HHS Pathogenesis Precipitating Factors Glucagon Catecholamines Cortisol Growth Hormone Absolute Insulin Deficiency Relative Insulin Deficiency Lipolysis FFAs Proteolysis Gluconeogenesis Ketogenesis Glycogenolysis Minimal Lipolysis Gluconeogenic Substrates Ketoacidosis Hyperglycemia Hyperosmolality Glucosuria (Osmotic Diuresis) Loss of Water & Electrolytes Triglycerides Hyperlipidemia Dehydration Decreased GFR DKA/HHS Enhanced Glucose Production G-6-P cAMP Glycogen F-6-P F-1,6-P2 PYR PFK-2 Fat CO2 Glucose Alanine F-2,6P2 Glycerol DKA/HHS Ketone Body Formation in Liver Fatty Acids Fatty Acyl-CoA Triglycerides Glucose Fatty Acyl-CoA Acetyl-CoA Acetoacetyl-CoA b-Hydroxy-b-methylglutaryl CoA Acetoacetate b -Hydroxybutyrate Acetone NADH NAD DKA/HHS Glucagon-induced Catabolic Cascade in Liver Glycogenolysis Glycogen Formation Gluconeogenesis Glycolysis Fatty acyl CoA Ketones Fatty Acids Malonyl-CoA Acetyl-CoA Glucose Glucose ACC DKA/HHS Ketone Body Utilization in Muscle b -Hydroxybutyrate Acetoacetate Acetoacetyl-CoA Acetyl-CoA Citric Acid Cycle Succinyl-CoA Succinate CoA EXTACELLULAR MITOCHONDRION b -Hydroxybutyrate Acetoacetate Continue reading >>

My Site - Chapter 15: Hyperglycemic Emergencies In Adults

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 >>

Hyperglycemic Crises In Adult Patients With Diabetes

Hyperglycemic Crises In Adult Patients With Diabetes

Go to: PATHOGENESIS The events leading to hyperglycemia and ketoacidosis are depicted in Fig. 1 (13). In DKA, reduced effective insulin concentrations and increased concentrations of counterregulatory hormones (catecholamines, cortisol, glucagon, and growth hormone) lead to hyperglycemia and ketosis. Hyperglycemia develops as a result of three processes: increased gluconeogenesis, accelerated glycogenolysis, and impaired glucose utilization by peripheral tissues (12–17). This is magnified by transient insulin resistance due to the hormone imbalance itself as well as the elevated free fatty acid concentrations (4,18). The combination of insulin deficiency and increased counterregulatory hormones in DKA also leads to the release of free fatty acids into the circulation from adipose tissue (lipolysis) and to unrestrained hepatic fatty acid oxidation in the liver to ketone bodies (β-hydroxybutyrate and acetoacetate) (19), with resulting ketonemia and metabolic acidosis. Increasing evidence indicates that the hyperglycemia in patients with hyperglycemic crises is associated with a severe inflammatory state characterized by an elevation of proinflammatory cytokines (tumor necrosis factor-α and interleukin-β, -6, and -8), C-reactive protein, reactive oxygen species, and lipid peroxidation, as well as cardiovascular risk factors, plasminogen activator inhibitor-1 and free fatty acids in the absence of obvious infection or cardiovascular pathology (20). All of these parameters return to near-normal values with insulin therapy and hydration within 24 h. The procoagulant and inflammatory states may be due to nonspecific phenomena of stress and may partially explain the association of hyperglycemic crises with a hypercoagulable state (21). The pathogenesis of HHS is not as wel 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 >>

Hyperglycemic Crises: Managing Acute Complications Of Diabetes

Hyperglycemic Crises: Managing Acute Complications Of Diabetes

Authors: Kim Cathcart, MS, RN, RRT | Cheryl Duksta, RN, ADN, M.Ed | Kate Biggs, RN, MSN Hyperglycemia occurs from time to time in all people with diabetes. However, at times, hyperglycemia can lead to acute, life-threatening complications known as Hyperglycemic Crises. This course is designed to educate healthcare professionals about the emergencies associated with hyperglycemic crises, including causes, diagnosis, treatment, and prevention of Hyperosmolar Hyperglycemic State (HHS) and Diabetic Ketoacidosis (DKA). Course objectives include: Paraphrase the pathophysiology of diabetic ketoacidosis (DKA) Interpret diagnostic findings related to DKA Relate the nurse’s role in caring for patients with diabetic complications About the Authors Kim Cathcart, MS, RN, RRT, started working in the field of inhalation therapy in 1976 and by 1979 had completed her first test to become a registered respiratory therapist. She earned a bachelor's degree in general studies and a master's degree in educational administration from the University of Dayton, and later she received her bachelor's degree in nursing from Wright State University. She has taught clinicals and labs in respiratory therapy and has served as a respiratory nurse liaison. Her nursing career includes work in skilled nursing, orthopedics, and med-surg/chemical detox. She has also worked as a diabetic resource nurse and in an infectious disease/HIV clinic. Her publishing credentials include articles on respiratory care, contributions to hospital publications, and a tribute in a nursing magazine. Cheryl Duksta, RN, ADN, M.Ed, is currently a critical care nurse in an intermediate care unit in Austin, Texas. She is an active member of the American Association of Critical-Care Nurses (AACN) Greater Austin chapter. A master' Continue reading >>

Difference Between Dka And Hhs

Difference Between Dka And Hhs

DKA vs HHS “DKA” means “diabetic ketoacidosis” and “HHS” means “Hyperosmolar Hyperglycemic Syndrome.” Both DKA and HHS are the two complications of diabetes mellitus. Though there are many differences between DKA and HHS, the basic problem is associated with insulin deficiency. When comparing the two, HHS has a higher mortality rate. When DKA has a mortality rate of 2 to 5 per cent, HHS has a 15 per cent mortality rate. Diabetic ketoacidosis is seen mainly in type 1 diabetic patients but is also seen in some type 2 diabetic patients. Hyperosmolar Hyperglycemic Syndrome is mainly seen in older patients having type 2 diabetes. DKA is mainly characterized by hyperglycemia, acidosis-producing derangements, and dehydration. Infection, disruption of insulin, and onset of diabetes are some of the common causes of DKA. Hyperglycemia, dehydration and hyperosmolarity are some of the common characteristics of Hyperosmolar Hyperglycemic Syndrome. But HHS does not have ketoacidosis. Some of the early symptoms of diabetic ketoacidosis include increased thirst and increased urination. Other symptoms include malaise, weakness, and fatigue. Bacterial infection, illness, insulin deficiency, stress, and insulin infusion catheter blockage are some of the causes that lead to DKA. When compared to diabetic ketoacidosis, the Hyperosmolar Hyperglycemic Syndrome develops only over the course of a week. Diabetic ketoacidosis develops rapidly. Increased dehydration, acute illness, vomiting, dementia, pneumonia, immobility, and urinary tract infections are some of the common causes of Hyperosmolar Hyperglycemic Syndrome. One of the main goals of treatment of DKA involves correcting high blood glucose levels by injecting insulin as well as replacing fluid lost because of vomiting an Continue reading >>

Diabetic Hyperglycemic Hyperosmolar Syndrome

Diabetic Hyperglycemic Hyperosmolar Syndrome

HHS is a condition of: Extremely high blood sugar (glucose) level Decreased alertness or consciousness (in many cases) Buildup of ketones in the body (ketoacidosis) may also occur. But it is unusual and is often mild compared with diabetic ketoacidosis. HHS is more often seen in people with type 2 diabetes who don't have their diabetes under control. It may also occur in those who have not been diagnosed with diabetes. The condition may be brought on by: Infection Other illness, such as heart attack or stroke Medicines that decrease the effect of insulin in the body Medicines or conditions that increase fluid loss Normally, the kidneys try to make up for a high glucose level in the blood by allowing the extra glucose to leave the body in the urine. But this also causes the body to lose water. If you do not drink enough water, or you drink fluids that contain sugar and keep eating foods with carbohydrates, the kidneys may become overwhelmed. When this occurs, they are no longer able to get rid of the extra glucose. As a result, the glucose level in your blood can become very high. The loss of water also makes the blood more concentrated than normal. This is called hyperosmolarity. It is a condition in which the blood has a high concentration of salt (sodium), glucose, and other substances. This draws the water out of the body's other organs, including the brain. Risk factors include: Impaired thirst Limited access to water (especially in people with dementia or who are bedbound) Older age Poor kidney function Poor management of diabetes, not following the treatment plan as directed Stopping insulin or other medicines that lower glucose level Continue reading >>

More in ketosis