Dka Vs Hhs Table

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 >>

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 >>

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

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 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 >>

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 >>

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 >>

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 >>

Hyperglycaemic Crises And Lactic Acidosis In Diabetes Mellitus

Hyperglycaemic crises are discussed together followed by a separate section on lactic acidosis. DIABETIC KETOACIDOSIS (DKA) AND HYPERGLYCAEMIC HYPEROSMOLAR STATE (HHS) Definitions DKA has no universally agreed definition. Alberti proposed the working definition of “severe uncontrolled diabetes requiring emergency treatment with insulin and intravenous fluids and with a blood ketone body concentration of >5 mmol/l”.1 Given the limited availability of blood ketone body assays, a more pragmatic definition comprising a metabolic acidosis (pH <7.3), plasma bicarbonate <15 mmol/l, plasma glucose >13.9 mmol/l, and urine ketostix reaction ++ or plasma ketostix ⩾ + may be more workable in clinical practice.2 Classifying the severity of diabetic ketoacidosis is desirable, since it may assist in determining the management and monitoring of the patient. Such a classification is based on the severity of acidosis (table 1). A caveat to this approach is that the presence of an intercurrent illness, that may not necessarily affect the level of acidosis, may markedly affect outcome: a recent study showed that the two most important factors predicting mortality in DKA were severe intercurrent illness and pH <7.0.3 HHS replaces the older terms, “hyperglycaemic hyperosmolar non-ketotic coma” and “hyperglycaemic hyperosmolar non-ketotic state”, because alterations of sensoria may be present without coma, and mild to moderate ketosis is commonly present in this state.4,5 Definitions vary according to the degree of hyperglycaemia and elevation of osmolality required. Table 1 summarises the definition of Kitabchi et al.5 Epidemiology The annual incidence of DKA among subjects with type 1 diabetes is between 1% and 5% in European and American series6–10 and this incidence appear Continue reading >>

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 And Hyperosmolar Coma | Harrison's Manual Of Medicine, 18e | Accessmedicine | Mcgraw-hill Medical

DKA results from insulin deficiency with a relative or absolute increase in glucagon and may be caused by inadequate insulin administration, infection (pneumonia, urinary tract infection, gastroenteritis, sepsis), infarction (cerebral, coronary, mesenteric, peripheral), surgery, trauma, drugs (cocaine), or pregnancy. A common precipitating scenario is the pt with type 1 DM who erroneously stops administering insulin because of anorexia/lack of food intake caused by a minor illness, followed by lipolysis and progressive ketosis leading to DKA. The initial symptoms of DKA include anorexia, nausea, vomiting, polyuria, and thirst. Abdominal pain, altered mental function, or frank coma may ensue. Classic signs of DKA include Kussmaul respirations and an acetone odor on the pt's breath. Volume depletion can lead to dry mucous membranes, tachycardia, and hypotension. Fever and abdominal tenderness may also be present. Laboratory evaluation reveals hyperglycemia, ketosis (-hydroxybutyrate > acetoacetate), and metabolic acidosis (arterial pH 6.87.3) with an increased anion gap ( Table 24-1 ). The fluid deficit is often 35 L and can be greater. Despite a total-body potassium deficit, the serum potassium at presentation may be normal or mildly high as a result of acidosis. Similarly, phosphate may be normal at presentation despite total body phosphate depletion. Leukocytosis, hypertriglyceridemia, and hyperlipoproteinemia are common. Hyperamylasemia is usually of salivary origin but may suggest a diagnosis of pancreatitis. The measured serum sodium is reduced as a consequence of osmotic fluid shifts due to hyperglycemia [1.6-meq reduction ... Continue reading >>

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 (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 >>

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 >>

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 >>