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Treatment For Dka And Hhs

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 >>

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 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 >>

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 >>

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 >>

Hyperglycemic Crises In Diabetes

Hyperglycemic Crises In Diabetes

Ketoacidosis and hyperosmolar hyperglycemia are the two most serious acute metabolic complications of diabetes, even if managed properly. These disorders can occur in both type 1 and type 2 diabetes. The mortality rate in patients with diabetic ketoacidosis (DKA) is <5% in experienced centers, whereas the mortality rate of patients with hyperosmolar hyperglycemic state (HHS) still remains high at ∼15%. The prognosis of both conditions is substantially worsened at the extremes of age and in the presence of coma and hypotension (1–10). This position statement will outline precipitating factors and recommendations for the diagnosis, treatment, and prevention of DKA and HHS. It is based on a previous technical review (11), which should be consulted for further information. PATHOGENESIS Although the pathogenesis of DKA is better understood than that of HHS, the basic underlying mechanism for both disorders is a reduction in the net effective action of circulating insulin coupled with a concomitant elevation of counterregulatory hormones, such as glucagon, catecholamines, cortisol, and growth hormone. These hormonal alterations in DKA and HHS lead to increased hepatic and renal glucose production and impaired glucose utilization in peripheral tissues, which result in hyperglycemia and parallel changes in osmolality of the extracellular space (12,13). 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 to ketone bodies (β-hydroxybutyrate [β-OHB] and acetoacetate), with resulting ketonemia and metabolic acidosis. On the other hand, HHS may be caused by plasma insulin concentrations that are in Continue reading >>

Hyperosmolar Hyperglycemic State Treatment & Management

Hyperosmolar Hyperglycemic State Treatment & Management

Approach Considerations Diagnosis and management guidelines for hyperglycemic crises are available from the American Diabetes Association. [6, 10, 24] The main goals in the treatment of hyperosmolar hyperglycemic state (HHS) are as follows: In an emergency situation, whenever possible, contact the receiving facility while en route to ensure preparation for a comatose, dehydrated, or hyperglycemic patient. When appropriate, notify the facility of a possible cerebrovascular accident or myocardial infarction (MI). Initiation of insulin therapy in the emergency department (ED) through a subcutaneous insulin pump may be an alternative to intravenous (IV) insulin infusion. [25] Airway management is the top priority. In comatose patients in whom airway protection is of concern, endotracheal intubation may be indicated. Rapid and aggressive intravascular volume replacement is always indicated as the first line of therapy for patients with HHS. Isotonic sodium chloride solution is the fluid of choice for initial treatment because sodium and water must be replaced in these severely dehydrated patients. Although many patients with HHS respond to fluids alone, IV insulin in dosages similar to those used in diabetic ketoacidosis (DKA) can facilitate correction of hyperglycemia. [26] Insulin used without concomitant vigorous fluid replacement increases the risk of shock. Adjust insulin or oral hypoglycemic therapy on the basis of the patient’s insulin requirement once serum glucose level has been relatively stabilized. All patients diagnosed with HHS require hospitalization; virtually all need admission to a monitored unit managed by medicine, pediatrics, or the intensive care unit (ICU) for close monitoring. When available, an endocrinologist should direct the care of these patien 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 >>

Management Of Diabetic Ketoacidosis And Other Hyperglycemic Emergencies

Management Of Diabetic Ketoacidosis And Other Hyperglycemic Emergencies

Understand the management of patients with diabetic ketoacidosis and other hyperglycemic emergencies. ​ The acute onset of hyperglycemia with attendant metabolic derangements is a common presentation in all forms of diabetes mellitus. The most current data from the National Diabetes Surveillance Program of the Centers for Disease Control and Prevention estimate that during 2005-2006, at least 120,000 hospital discharges for diabetic ketoacidosis (DKA) occurred in the United States,(1) with an unknown number of discharges related to hyperosmolar hyperglycemic state (HHS). The clinical presentations of DKA and HHS can overlap, but they are usually separately characterized by the presence of ketoacidosis and the degree of hyperglycemia and hyperosmolarity, though HHS will occasionally have some mild degree of ketosis. DKA is defined by a plasma glucose level >250 mg/dL, arterial pH <7.3, the presence of serum ketones, a serum bicarbonate measure <18 mEq/L, and a high anion gap metabolic acidosis. The level of normal anion gap may vary slightly by individual institutional standards. The anion gap also needs to be corrected in the presence of hypoalbuminemia, a common condition in the critically ill. Adjusted anion gap = observed anion gap + 0.25 * ([normal albumin]-[observed albumin]), where the given albumin concentrations are in g/L; if given in g/dL, the correction factor is 2.5.(3) HHS is defined by a plasma glucose level >600 mg/dL, with an effective serum osmolality >320 mOsm/kg. HHS was originally named hyperosmolar hyperglycemic nonketotic coma; however, this name was changed because relatively few patients exhibit coma-like symptoms. Effective serum osmolality = 2*([Na] + [K]) + glucose (mg/dL)/18.(2) Urea is freely diffusible across cell membranes, thus it will Continue reading >>

Hyperosmolar Hyperglycemic Statetreatment & Management

Hyperosmolar Hyperglycemic Statetreatment & Management

Standard Care for Dehydration and Altered Mental Status Diagnosis and management guidelines for hyperglycemic crises are available from the American Diabetes Association. [ 6 , 10 , 24 ] The main goals in the treatment of hyperosmolar hyperglycemic state (HHS) are as follows: To vigorously rehydrate the patient while maintaining electrolyte homeostasis To monitor and assist cardiovascular, pulmonary, renal, and central nervous system (CNS) function In an emergency situation, whenever possible, contact the receiving facility while en route to ensure preparation for a comatose, dehydrated, or hyperglycemic patient. When appropriate, notify the facility of a possible cerebrovascular accident or myocardial infarction (MI). Initiation of insulin therapy in the emergency department (ED) through a subcutaneous insulin pump may be an alternative to intravenous (IV) insulin infusion. [ 25 ] Airway management is the top priority. In comatose patients in whom airway protection is of concern, endotracheal intubation may be indicated. Rapid and aggressive intravascular volume replacement is always indicated as the first line of therapy for patients with HHS. Isotonic sodium chloride solution is the fluid of choice for initial treatment because sodium and water must be replaced in these severely dehydrated patients. Although many patients with HHS respond to fluids alone, IV insulin in dosages similar to those used in diabetic ketoacidosis (DKA) can facilitate correction of hyperglycemia. [ 26 ] Insulin used without concomitant vigorous fluid replacement increases the risk of shock. Adjust insulin or oral hypoglycemic therapy on the basis of the patients insulin requirement once serum glucose level has been relatively stabilized. All patients diagnosed with HHS require hospitalizati 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 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 >>

Diagnosis And Management Of Hyperglycemic Crises: Diabetic Ketoacidosis And The Hyperglycemic Hyperosmolar State

Diagnosis And Management Of Hyperglycemic Crises: Diabetic Ketoacidosis And The Hyperglycemic Hyperosmolar State

Download Slide Library Key Points DKA and HHS are life-threatening emergencies. Management involves Attention to precipitating cause Fluid and electrolyte management Insulin therapy Patient monitoring Prevention of metabolic complications during recovery Transition to long-term therapy Patient education and discharge planning should aim at prevention of recurrence. Suggested Reading Burghen GA, Etteldorf JN, Fisher JN, Kitabchi AQ. Comparison of high-dose and low-dose insulin by continuous intravenous infusion in the treatment of diabetic ketoacidosis in children. Diabetes Care. 1980;3:15-20. Devi R, Selvakumar G, Clark L, Downer C, Braithwaite SS. A dose-defining insulin algorithm for attainment and maintenance of glycemic targets during therapy of hyperglycemic crises. Diabetes Manage. 2011;1:397-412. Glaser N, Barnett P, McCaslin I, et al. Risk factors for cerebral edema in children with diabetic ketoacidosis. The Pediatric Emergency Medicine Collaborative Research Committee of the American Academy of Pediatrics. N Engl J Med. 2001;344:264-269. Mudaliar S, Mohideen P, Deutsch R, et al. Intravenous glargine and regular insulin have similar effects on endogenous glucose output and peripheral activation/deactivation kinetic profiles. Diabetes Care. 2002;25:1597-1602. Muir AB, Quisling RG, Yang MC, Rosenbloom AL. Cerebral edema in childhood diabetic ketoacidosis: natural history, radiographic findings, and early identification. Diabetes Care. 2004;27:1541-1546. 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 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 >>

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