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Dka Vs Hhs Chart

Hyperosmolar Hyperglycemic State

Hyperosmolar Hyperglycemic State

Dr. Richard Hellman, past president of the American Association of Clinical Endocrinologists, remembers once seeing a man whose blood glucose level was 2,400 mg/dl. “Basically,” he said, “his blood looked like syrup.” However, the man was not experiencing diabetic ketoacidosis (DKA). Instead, he had a condition called hyperosmolar hyperglycemic state, or HHS. Like DKA, HHS is characterized by very high blood glucose levels, but unlike in DKA, people with HHS do not generally have ketones in their blood or urine. Nonetheless, HHS can be deadly. According to the American Diabetes Association (ADA), while DKA has a death rate of less than 5%, that figure can reach around 15% for HHS. Luckily, HHS is rare. The ADA says the annual rate for DKA ranges from 4.6 to 8 episodes per 1,000 people admitted to the hospital. HHS accounts for less than 1% of hospital admissions related primarily to diabetes. HHS is most common in elderly people with new-onset Type 2 diabetes, particularly those who live in nursing homes, or in older people who have been diagnosed with Type 2 diabetes but who are unaware that their blood glucose is high or who haven’t had enough fluid intake. Compounding the problem is that the thirst mechanism can be impaired in older people, and they’re more apt to have kidney problems, Dr. Hellman says. When a person’s thirst mechanism is impaired, the kidneys — which normally work to remove excess glucose from the blood — begin to conserve water. That leads to a higher glucose concentration in the bloodstream. In many people, HHS begins with an infection, such as a urinary tract infection or pneumonia. Unlike DKA, which develops relatively quickly, HHS develops over several days, or even weeks. “Diagnosis is sometimes a problem,” Dr. Hellman sa 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 >>

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 Hypersmolar Non-ketotic Coma

Diabetic Ketoacidosis And Hypersmolar Non-ketotic Coma

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 preci Continue reading >>

W3l Para204 Dka, Hhs, Aka

W3l Para204 Dka, Hhs, Aka

Poorly managed/undiagnosed diabetes (Type I Diabetes is first presentation of SKA fast or slow how can a DKA patient technically be hypoglycaemic A decrease in the circulating insulin level forces the body to source glucose from the break down of fat/protein at an how does a DKA patient become dehydrated and hypovolaemic (A decrease in the circulating insulin level forces the body to source glucose from the break down of fat/protein at an increased rate to fuel the body > Lysis (break down) of protein and lipids produces ketones as a by product ) The increased ketone production and hyperglycaemia produces osmotic diuresis and as a result a concentration gradient occurs. Fluid moves out of cells into the blood resulting in cellular how does a DKA patient become hyperkalaemic Metabolic acidosis occurs due to the increase in acid The hyperosmolality and acidic state cause potassium to what does hyperkalaemic patient present as on ECG what is the risk of moving a DKA patient which has been lying down for an extended period of time and how should this be managed If a Pt has been lying down for an extended period, K will have been accumulating in blood stream. Once you stand them up the heart will be flooded with K and has high risk of arrhythmias or even arrest. before you move a DKA pt you should have a large bore IVC in situ and a bag of fluid ready to go. This will dilute K in blood stream and will increase vascular resistance and force fluid back into cells Respiratory compensation for metabolic acidosis Pts presenting with this have been shown to present with: Low partial pressure of CO2 (+low bicarbonate) Pt feels urge to breathe (appears involuntary) High BGL increases blood osmolarity drawing water out of cells resulting in cellular dehydration, polydipsia and fatig Continue reading >>

Hyperosmolar Hyperglycemic State

Hyperosmolar Hyperglycemic State

Acute hyperglycemia, or high blood glucose, may be either the initial presentation of diabetes mellitus or a complication during the course of a known disease. Inadequate insulin replacement (e.g., noncompliance with treatment) or increased insulin demand (e.g., during times of acute illness, surgery, or stress) may lead to acute hyperglycemia. There are two distinct forms: diabetic ketoacidosis (DKA), typically seen in type 1 diabetes, and hyperosmolar hyperglycemic state (HHS), occurring primarily in type 2 diabetes. In type 1 diabetes, no insulin is available to suppress fat breakdown, and the ketones resulting from subsequent ketogenesis manifest as DKA. This is in contrast to type 2 diabetes, in which patients can still secrete small amounts of insulin to suppress DKA, instead resulting in a hyperglycemic state predominated simply by glucose. The clinical presentation of both DKA and HHS is one of polyuria, polydipsia, nausea and vomiting, volume depletion (e.g., dry oral mucosa, decreased skin turgor), and eventually mental status changes and coma. In patients with altered mental status, fingerstick glucose should always be checked in order to exclude serum glucose abnormalities. Several clinical findings pertaining only to DKA include a fruity odor to the breath, hyperventilation, and abdominal pain. HHS patients, in contrast to those with DKA, will present with more extreme volume depletion. The treatment of both DKA and HHS is primarily IV electrolyte and fluid replacement. Insulin for hyperglycemia may be given with caution and under vigilant monitoring of serum glucose. Other treatment options depend on the severity of symptoms and include bicarbonate and potassium replacement. Osmotic diuresis and hypovolemia Hypovolemia resulting from DKA can lead to acute Continue reading >>

Diabetic Ketoacidosis And Hyperosmolar Hyperglycemic State.

Diabetic Ketoacidosis And Hyperosmolar Hyperglycemic State.

Med Klin (Munich). 2006 Mar 22;101 Suppl 1:100-5. Diabetic ketoacidosis and hyperosmolar hyperglycemic state. Clinic II and Polyclinic for Internal Medicine, University of Cologne, Germany. Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are the two most serious metabolic complications of diabetes mellitus (DM). These disorders can occur in both type 1 and type 2 DM. DKA is characterized by hyperglycemia, ketone body formation and metabolic acidosis. Precipitating causes are usually infection or insulin omission. Over the past 20 years, there has been no reduction in the DKA mortality rates, which remain between 3.4% and 4.6%. HHS is manifested by marked elevation of blood glucose, hyperosmolality and little or no ketosis. Precipitating causes of HHS are infection, undiagnosed diabetes and substance abuse. The mortality rates of the HHS remain high at approximately 15%. Basic common pathophysiological mechanisms in both conditions, which differ only in the magnitude of dehydration and degree of ketoacidosis, are the reduction in the effective insulin action combined with increased counterregulatory hormones (glucagon, catecholamines, cortisol, and growth hormone). While in DKA the lack of insulin combined with increased catecholamines results in accelerated lipolysis and thus production of excess fatty acids, leading to beta-oxidation and ketogenesis, in HHS residual beta-cell function is adequate to prevent lipolysis but not hyperglycemia. The prognosis of both conditions is substantially worsened in patients > 65 years of age and in the presence of coma and hypotension. Mainstays of therapy are intravenous insulin and fluid replacement as well as the concomitant treatment of the precipitating factors. Improved patient education and implementati Continue reading >>

A Nurse Managed Computerized Program For Continuous Iv Insulin Infusion:jiip(jefferson Insulin Infusion Protocol) And Non Jiip.

A Nurse Managed Computerized Program For Continuous Iv Insulin Infusion:jiip(jefferson Insulin Infusion Protocol) And Non Jiip.

Requirements: RN will review the PowerPoint presentation. RN will practice titration guidelines on practice pathway on computer. RN will complete program quiz with a grade of 100%. Unit CNS will review quiz results with staff member. Introduction Uncontrolled hyperglycemia in hospitalized patients results in poor clinical outcomes. IV insulin is the drug of choice for optimal glycemic management in many patients. Safe administration of IV insulin is a complex task. The Jefferson Hospital Insulin Infusion Protocol(JIIP) applies to all adult patients requiring IV insulin but ONLY if the JIIP is ordered. General Guidelines Physicians who do not order the JIIP but want continuous IV insulin infusion (NON-JIIP) for their patients, are responsible for the hourly titration of the infusion and specific fluid orders. The RN may titrate a non –JIIP infusion based on previous infusion guidelines online but only if the glucose and piggyback protocol is followed. JIIP Candidates ICU patients with BG>180mg/dl x 2 consecutive measurements. NOTE: Check Blood glucose (BG) on admission to ICU and q4 hours thereafter. If BG <140mg/dl for first 24 hours, measure BG daily or as clinically indicated. JIIP Candidates Type 1 DM requiring surgery/general anesthesia. Type 2 DM with uncontrolled hyperglycemia or insulin requiring type 2 DM needing surgery/general anesthesia. Note: It is best to start an IV insulin infusion the night before surgery. (Suggest Endo Consult for insulin orders.) Never discontinue insulin on patients with type 1 diabetes. If BG 70 or less,follow hypoglycemia protocol and restart insulin when BG normal. Physician enters order for JIIP and orders the bolus dose and the initial infusion rate as follows: Non DKA/HHS ex: (Pre-surgery, uncontrolled hyperglycemia,NPO p 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 >>

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 >>

Dka And Hhs Flashcards | Quizlet

Dka And Hhs Flashcards | Quizlet

Hyperglycemic Hyperosmolar Nonketotic Syndrome: Gradual onset of hyperglycemia and What are the expected BG levels for DKA and HHS? HHS because the super high BG levels increase risk for CVA, infection, MI One of the means by which the liver regulates BG by synthesizing glucose. Breakdown of glycogen for glucose formation in the liver Synthesis of glucose from amino acids in the liver. How much energy is provided per gram from: Where is insulin produced? What does it do? In the beta cells of the pancreas. Moves glucose from the blood into the cell, lowering BG Where is glucagon produced? What does it do? In the alpha cells of the pancreas. Increases BG by releasing more glucose from the liver. Inhibits insulin during times of stress to keep the BG levels high, and promotes release of glucose from the liver As GH increases, so does BG. When BG is low, the GH is also low. Critical during fasting and starvation, stimulates gluconeogenesis. (production of glucose from amino acids in the liver) pH = <7.3 (7.35-7.45 is norm). Metabolic acidosis 3 main electrolyte imbalances associated with DKA DKA vs HHS clinical manifestations chart: What kind of fluid therapy would you expect to see for DKA and HHS? D5W once BG hits 300 (so the BG doesn't drop too quickly) What do you expect to see re: potassium in DKA and HHS Because insulin pulls potassium into the cells, and it needs to be replaced. How do you go about transitioning from IV insulin to SQ insulin? Hyperkalemia leading to cardiac dysrhythmias and MI Take insulin or oral antidiabetic agents as usual BG assessed every 3-4 hours Vomiting, diarrhea, or fever - take liquids with sugar Continue reading >>

Diabetic Ketoacidosis (dka) Myths

Diabetic Ketoacidosis (dka) Myths

Recently, I was asked to give a lecture to both my residents and nurses at the University of Texas Health Science Center at San Antonio (UTHSCSA) on some common DKA myths. Now this topic was originally covered by my good friend Anand Swaminathan on multiple platforms and I did ask his permission to create this blogpost with the idea of improving patient care and wanted to express full disclosure of that fact. I specifically covered four common myths that I still see people doing in regards to DKA management: We should get ABGs instead of VBGs After Intravenous Fluids (IVF), Insulin is the Next Step Once pH <7.1, Patients Need Bicarbonate Therapy We Should Bolus Insulin before starting the infusion DKA Myths Case: 25 y/o female with PMH of Type I DM who presents via EMS with AMS. Per EMS report, the patient ran out of her insulin 3 days ago….. Vital Signs: BP 86/52 HR 136 RR 30 O2Sat 97% on room air Temp 99.1 Accucheck: CRITICAL HIGH EMS was not able to establish IV access, so decided to just bring her to the ED due to how sick she looks. Your nurses are on point today and get you two large bore 18G IVs and start to draw blood work to send to the lab. You state I need a blood gas, and the nurse turns to you and asks do you need an ABG or VBG? Myth #1: We should get ABGs instead of VBGs in DKA So you do a literature review and come across two studies that specifically look at ABG vs VBG in an ED population: Study #1: Kelly AM et al. Review Article – Can Venous Blood Gas Analysis Replace Arterial in Emergency Medical Care. Emery Med Australas 2010; 22: 493 – 498. PMID: 21143397 For pH, 3 studies of patients with DKA (265 patients) were reviewed showing a weighted mean difference of 0.02 pH units. Only one study, which was the largest study (200 patients) reported 95% 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 >>

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 >>

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 >>

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