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Hhs Vs Dka

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 >>

Hyperglycemic Emergencies: Diabetic Ketoacidosis And Hyperosmolar Hyperglycemia State

Hyperglycemic Emergencies: Diabetic Ketoacidosis And Hyperosmolar Hyperglycemia State

Hyperglycemic emergencies: diabetic ketoacidosis and hyperosmolar hyperglycemia state Diabetes Spectrum. January 2002 vol. 15 no. 1 28-36 Diabetic ketoacidosis (DKA), the hallmark of type 1 diabetes mellitus (T1DM), and hyperglycemic hyperosmolar state (HHS), primarily seen in type 2 diabetes (T2DM), are hyperglycemic emergencies that may lead to death if untreated. They are both associated with: Insulin deficiency (absolute in T1DM and relative in T2DM) and hyperglycemia Diabetes Care. 2015 Sep; 38(9): 16871693. DKA can very rarely occur with normal glucose levels, particularly in the setting of prior insulin use or pregnancy. This has been a known complication with the rise in the usage of SGLT2i (sodium glucose transporter type 2 inhibitors) class of medications. Renal wasting of glucose does not allow for serum glucose to rise to the levels seen in DKA and HHS. Curr Diabetes Rev. 2013 Jan 1; 9(1): 2553. Clin Biochem Rev. 2005 May; 26(2): 1939. Insulin, a peptide hormone, is produced by the beta-islet cells in the pancreas. Major functions of insulin include increased glucose uptake by the peripheral tissues (liver, skeletal muscle and adipose tissue), enhancing glycogenesis, adipogenesis and inhibition of lipolysis and glycogenolysis. These functions are summarized in the flowchart below. Please see the Diabetes chapter (in preparation) for further details. Endocrinol Metab Clin North Am. 2013 Dec;42(4):677-95 DKA is a result of an absolute or relative insulin deficiency, leading to ketoacidosis, volume depletion and hyperglycemia. Insulin is the primary anabolic hormone that allows peripheral tissues to uptake glucose. In the absence of insulin, the other counterregulatory hormones act together to break down triglycerides and stimulate gluconeogenesis. In DKA, the Continue reading >>

66: Diabetic Ketoacidosis (dka) And Hyperosmolar Hyperglycemic State (hhs)

66: Diabetic Ketoacidosis (dka) And Hyperosmolar Hyperglycemic State (hhs)

In this episode I’ll discuss diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS). Subscribe on iTunes, Android, or Stitcher Definition Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are the most serious acute complications of diabetes. These diabetic crises cause thousands of deaths annually in the US. DKA and HHS differ clinically according to the presence of ketoacidosis and the degree of hyperglycemia. In DKA metabolic acidosis is often the major finding. The serum glucose is below 800 mg/dL and usually in the 350-500 mg/dL range. DKA usually evolves rapidly. In HHS, there is little or no ketoacidosis and the serum glucose concentration frequently exceeds 1000 mg/dL. HHS usually evolves over a period of several days. Overlap between DKA and HHS occurs in more than one-third of patients. Pathogenesis Insulin deficiency/resistance and glucagon excess are responsible for the development of DKA and HHS. The deficiency in insulin (either absolute or relative deficiency) is more severe in DKA compared with HHS. In HHS the residual insulin secretion and its systemic activity minimizes the development of ketoacidosis but is not adequate to control hyperglycemia. In patients with absolute or relative insulin deficiency, DKA and HHS are usually precipitated by a stressor such as infection or discontinuation of / inadequate insulin therapy. Treatment The treatment of DKA and HHS involves the correction of fluid and electrolyte abnormalities, followed by the administration of insulin. Specific treatment protocols include: ADA guidelines, Joslin protocol, and Yale New Haven. The order of treatment is essential. A patient in DKA or HHS is already volume-depleted. Insulin forces glucose as well as potassium and water into cells. Therefor 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 >>

Hyperosmolar Hyperglycemic State

Hyperosmolar Hyperglycemic State

GREGG D. STONER, MD, University of Illinois College of Medicine, Peoria, Illinois Am Fam Physician.2017Dec1;96(11):729-736. Hyperosmolar hyperglycemic state is a life-threatening emergency manifested by marked elevation of blood glucose and hyperosmolarity with little or no ketosis. Although there are multiple precipitating causes, underlying infections are the most common. Other causes include certain medications, nonadherence to therapy, undiagnosed diabetes mellitus, substance abuse, and coexisting disease. In children and adolescents, hyperosmolar hyperglycemic state is often present when type 2 diabetes is diagnosed. Physical findings include profound dehydration and neurologic symptoms ranging from lethargy to coma. Treatment begins with intensive monitoring of the patient and laboratory values, especially glucose, sodium, and potassium levels. Vigorous correction of dehydration is critical, requiring an average of 9 L of 0.9% saline over 48 hours in adults. After urine output is established, potassium replacement should begin. Once dehydration is partially corrected, adults should receive an initial bolus of 0.1 units of intravenous insulin per kg of body weight, followed by a continuous infusion of 0.1 units per kg per hour (or a continuous infusion of 0.14 units per kg per hour without an initial bolus) until the blood glucose level decreases below 300 mg per dL. In children and adolescents, dehydration should be corrected at a rate of no more than 3 mOsm per hour to avoid cerebral edema. Identification and treatment of underlying and precipitating causes are necessary. Hyperosmolar hyperglycemic state (HHS) is a life-threatening endocrine emergency that most commonly affects adults with type 2 diabetes mellitus. 1 , 2 However, the incidence increased by 52.4% 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 >>

Dka Vs Hyperosmolar Hyperglycemic State (hhs)

Dka Vs Hyperosmolar Hyperglycemic State (hhs)

Don't miss your chance to win free admissions prep materials! Click here to see a list of raffles . DKA vs Hyperosmolar hyperglycemic state (HHS) why is plasma osmolarity (Posm) always high in HHS, whereas DKA Posm is variable? Pathogenesis of DKA and HHS are discussed in the same article in uptodate but the Posm difference between the 2 is not clearly explained (at least to my feeble mind). The increase in plasma osmolality created by hyperglycemia pulls water out of the cells, expands the ECF, and thereby reduces the plasma sodium (Na) concentration. If a patient with normal serum electrolytes (Na = 140 mEq/L) rapidly developed a glucose concentration of 1000 mg/100 mL, and no urine was made, then that patients serum Na would fall to value between 119 and 126 mEq/L and the osmolality would increase to a level between 294 and 308 mosm/L. However, the osmolality usually increases to a greater degree because a large volume of relatively electrolyte-deficient urine is excreted during the evolution of the hyperglycemic state. The loss of this electrolyte-free water further raises the osmolality . In patients with ketoacidosis, high plasma acetone levels also contribute to the elevated osmolality." according to the pathogenesis flowchart (see figure 1) in this article ( Hyperglycemic Crises in Adult Patients With Diabetes ), there is no real difference in the pathogenesis to HHS first aid does mention than HHS is classically seen in elderly T2DM w/ limited ability to drink. is that the sole reason than HHS has hyperosmolarity? is the sugar way higher in HHS b/c T2DM patients have so much insulin resistance? whereas T1DM patients don't have insulin resistance T1DM is insulin dependent because they dont produce insulin at all, whereras T2DM has insulin resistance but produce Continue reading >>

Treatment Of Diabetic Ketoacidosis (dka)/hyperglycemic Hyperosmolar State (hhs): Novel Advances In The Management Of Hyperglycemic Crises (uk Versus Usa)

Treatment Of Diabetic Ketoacidosis (dka)/hyperglycemic Hyperosmolar State (hhs): Novel Advances In The Management Of Hyperglycemic Crises (uk Versus Usa)

Go to: Diabetic Ketoacidosis Prior to the discovery and isolation of insulin in 1922 by Banting and Best, type 1 diabetes was universally fatal within a few months of initial diagnosis. Once mass production was started, the challenge to those early pioneers of insulin treatment was learning how to use this new wonder drug, e.g., how much to give and how often to give it, in order to treat the hyperglycemia without raising the inherent risk of hypoglycemia. In 1945, Howard Root in Boston described how they had improved the outcomes for people with diabetic ketoacidosis (DKA), reducing mortality to 12% by 1940 and to 1.6% by 1945 using high doses of insulin—giving an average of 83 units within the first 3 h of treatment in 1940 and 216 units by 1945 [3]. They described how in 1945, they used an average of 287 units in the first 24 h, but this ranged from 50 to 1770 units [3]. In Birmingham, UK, high-dose insulin was also being used with similar success—doses varying depending on the degree of consciousness, with those unarousable on admission given doses between 500 and 1400 units per 24 h [4]. DKA remains a medical emergency; over time, mortality has continued to fall but remains a significant risk, especially amongst the young, socially isolated and when care provision is fragmented [5•, 6•]. Overall, the diagnosis and treatment of DKA are very similar in the UK and USA with a few differences. The UK has separate guidelines on the management of DKA [7], while the USA has a position statement on DKA and HHS that was updated in 2009 [8]. The UK guideline differs in several ways from the US position statement. The concept of low-dose intravenous insulin was established in the late 1960s and early 1970s by teams on both sides of the Atlantic. The UK championed the u 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 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 >>

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 >>

Hyperosmolar Hyperglycemic State

Hyperosmolar Hyperglycemic State

Author: Dipa Avichal, DO; Chief Editor: George T Griffing, MD more... Hyperosmolar hyperglycemic state (HHS) isone of two serious metabolic derangements that occurs in patients with diabetes mellitus (DM). [ 1 ] It is alife-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 2DM who have some concomitant illness that leads to reduced fluid intake, as seen, for example, in elderly institutionalizedpersons with decreased thirst perception andreduced 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 toone thirdof cases. According to the consensus statement published by the American Diabetes Association, diagnostic features of HHS may include the following (see Workup) [ 4 , 6 ] : Plasma glucose level of 600 mg/dL or greater Effective serum osmolality of 320 mOsm/kg or greater Profound dehydration, up to an average of 9L Bicarbonate concentration greater than 15 mEq/L Small ketonuria a Continue reading >>

Treatment Of Diabetic Ketoacidosis (dka)/hyperglycemic Hyperosmolar State (hhs): Novel Advances In The Management Of Hyperglycemic Crises (uk Versus Usa)

Treatment Of Diabetic Ketoacidosis (dka)/hyperglycemic Hyperosmolar State (hhs): Novel Advances In The Management Of Hyperglycemic Crises (uk Versus Usa)

Go to: Diabetic Ketoacidosis Prior to the discovery and isolation of insulin in 1922 by Banting and Best, type 1 diabetes was universally fatal within a few months of initial diagnosis. Once mass production was started, the challenge to those early pioneers of insulin treatment was learning how to use this new wonder drug, e.g., how much to give and how often to give it, in order to treat the hyperglycemia without raising the inherent risk of hypoglycemia. In 1945, Howard Root in Boston described how they had improved the outcomes for people with diabetic ketoacidosis (DKA), reducing mortality to 12% by 1940 and to 1.6% by 1945 using high doses of insulin—giving an average of 83 units within the first 3 h of treatment in 1940 and 216 units by 1945 [3]. They described how in 1945, they used an average of 287 units in the first 24 h, but this ranged from 50 to 1770 units [3]. In Birmingham, UK, high-dose insulin was also being used with similar success—doses varying depending on the degree of consciousness, with those unarousable on admission given doses between 500 and 1400 units per 24 h [4]. DKA remains a medical emergency; over time, mortality has continued to fall but remains a significant risk, especially amongst the young, socially isolated and when care provision is fragmented [5•, 6•]. Overall, the diagnosis and treatment of DKA are very similar in the UK and USA with a few differences. The UK has separate guidelines on the management of DKA [7], while the USA has a position statement on DKA and HHS that was updated in 2009 [8]. The UK guideline differs in several ways from the US position statement. The concept of low-dose intravenous insulin was established in the late 1960s and early 1970s by teams on both sides of the Atlantic. The UK championed the u 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 >>

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