Diabetic Emergencies, Diagnosis And Clinical Management: Hyperosmolar Non-ketotic Hyperglycemia, Part 2
Home / Resources / Clinical Gems / Diabetic Emergencies, Diagnosis and Clinical Management: Hyperosmolar non-ketotic hyperglycemia, Part 2 Diabetic Emergencies, Diagnosis and Clinical Management: Hyperosmolar non-ketotic hyperglycemia, Part 2 The earliest symptoms of marked hyperglycemia are polyuria, polydipsia, and weight loss. Unlike DKA, which usually evolves rapidly over a 24-hour period, symptoms in HHS develop more insidiously, often persisting for several days or even weeks before people seek medical attention and require hospital admission. As the degree or duration of hyperglycemia progresses, neurological symptoms, including lethargy, focal signs, and obtundation, which can progress to coma in later stages, can be seen. Neurological symptoms are most common in HHS (because of higher degrees of dehydration and hyperosmolality or because of a cerebrovascular accident that precipitated the hyperglycemic crisis), while hyperventilation and abdominal pain are primarily limited to patients with DKA.1 Decreased mental state is the commonest reason why people withHHS are brought to the hospital. The clinical picture is related to the degree of dehydration and hypovolemia, the degree of hyperosmolality, and the precipitating factor that led to HHS. Polyuria, polydipsia, and weight loss are the usual prodromal symptoms. Due to hypovolemia, patients exhibit impaired peripheral circulation, tachycardia, hypotension, and cold extremities. Mental status may vary from slight confusion/ obtundation to coma. Serum osmolality has been shown to correlate significantly with mental status, both in DKA and HHS, and is the most important determinant of mental status. 7 The severity of hyperosmolality can be evaluated by calculating effective serum osmolality (normal values: 285 5) Continue reading >>
Management Of Diabetic Ketoacidosis In Adults
Management of diabetic ketoacidosis in adults Management of diabetic ketoacidosis in adults Insulin (blue dots) promotes glucose uptake in the liver and muscles, controlling blood sugar. Despite these losses, the increased delivery of potassium to the ECF from the intracellular space usually causes the serum concentration of potassium to be normal and, in some cases, high. This regular concentration of the ECF potassium creates the illusion of normalcy, despite the fact that total body potassium stores are almost always low. This concept becomes important in understanding the risk of potentially devastating hypokalemia in treating DKA. Insulin administration causes a rapid shift of potassium out of the ECF and into the cells. In addition, fluid resuscitation can be expected to cause a dilutional decrease in serum potassium concentration. For this reason, the ADA recommendations encompass a three-tiered approach to potassium regulation during fluid and insulin therapy for DKA: Patients with a serum potassium concentration >5.2 mEq/L should receive insulin and IV fluid without potassium, but the level should be checked every two hours.3 Patients with a serum potassium concentration between 3.3 and 5.2 mEq/L should have 20-30 mEq of potassium added to each liter of IV fluid with a goal to maintain a level of 4.0-5.0 mEq/L.3 The addition of potassium to the infusion should be delayed until urine output has been established. Patients with a serum potassium concentration <3.3 mEq/L should receive 20.0-30.0 mEq/hr of potassium until the concentration exceeds 3.3 mEq/L. These patients should not receive IV insulin until the serum potassium concentration is >3.3.3 Other electrolytes. Sodium: Sodium concentration may vary. Both sodium and water are lost during osmotic diuresis; Continue reading >>
Diabetic Ketoacidosis
Abbas E. Kitabchi, PhD., MD., FACP, FACE Professor of Medicine & Molecular Sciences and Maston K. Callison Professor in the Division of Endocrinology, Diabetes & Metabolism UT Health Science Center, 920 Madison Ave., 300A, Memphis, TN 38163 Aidar R. Gosmanov, M.D., Ph.D., D.M.Sc. Assistant Professor of Medicine, Division of Endocrinology, Diabetes & Metabolism, The University of Tennessee Health Science Center, 920 Madison Avenue, Suite 300A, Memphis, TN 38163 Clinical Recognition Omission of insulin and infection are the two most common precipitants of DKA. Non-compliance may account for up to 44% of DKA presentations; while infection is less frequently observed in DKA patients. Acute medical illnesses involving the cardiovascular system (myocardial infarction, stroke, acute thrombosis) and gastrointestinal tract (bleeding, pancreatitis), diseases of endocrine axis (acromegaly, Cushing`s syndrome, hyperthyroidism) and impaired thermo-regulation or recent surgical procedures can contribute to the development of DKA by causing dehydration, increase in insulin counter-regulatory hormones, and worsening of peripheral insulin resistance. Medications such as diuretics, beta-blockers, corticosteroids, second-generation anti-psychotics, and/or anti-convulsants may affect carbohydrate metabolism and volume status and, therefore, could precipitateDKA. Other factors: psychological problems, eating disorders, insulin pump malfunction, and drug abuse. It is now recognized that new onset T2DM can manifest with DKA. These patients are obese, mostly African Americans or Hispanics and have undiagnosed hyperglycemia, impaired insulin secretion, and insulin action. A recent report suggests that cocaine abuse is an independent risk factor associated with DKA recurrence. Pathophysiology In 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 >>
Serum Osmolality Blood Test: Purpose, Procedure, And Results
Your blood is a little like a liquid chemistry set. Along with oxygen, it contains proteins, minerals, hormones, and a long list of chemicals. Your body usually does a good job balancing all these things. But sometimes you can have too much of a mineral or chemical -- or too little. This can trigger reactions in your body, some of which can cause serious health problems. If your doctor thinks you have such a chemical imbalance in your blood , she may recommend that you get a serum osmolality test. Osmolality refers to the concentration of dissolved particles of chemicals and minerals -- such as sodium and other electrolytes -- in your blood. Higher osmolality means certain particles are more concentrated. Lower osmolality means theyre more diluted. A serum osmolality test is a way to check the fluid balance in your body. It can help your doctor diagnose several possible conditions. You may also hear it called an osmolality serum test. Serum is the fluid in your veins and arteries minus the blood cells. So you will have blood taken anytime you get a serum test. The main reason to get this test is if youre showing signs of dehydration or other problems related to your fluid levels. The main one is hyponatremia. This condition happens when your sodium levels are too low and your body starts retaining fluid. Sodium is one of the major electrolytes in your bloodstream. (Others include magnesium and potassium .) Electrolytes are chemicals that help cells absorb nutrients and get rid of waste products, among other important functions. One of sodiums other main jobs is to balance water levels inside cells and throughout your body. You may also have a serum osmolality test if you have a problem with antidiuretic hormone (ADH). ADH helps your body retain water rather than losing Continue reading >>
Hyperosmolar Hyperglycemic State
Hyperosmolar hyperglycemic state (HHS) is a complication of diabetes mellitus in which high blood sugar results in high osmolarity without significant ketoacidosis.[4] Symptoms include signs of dehydration, weakness, legs cramps, trouble seeing, and an altered level of consciousness.[2] Onset is typically over days to weeks.[3] Complications may include seizures, disseminated intravascular coagulopathy, mesenteric artery occlusion, or rhabdomyolysis.[2] The main risk factor is a history of diabetes mellitus type 2.[4] Occasionally it may occur in those without a prior history of diabetes or those with diabetes mellitus type 1.[3][4] Triggers include infections, stroke, trauma, certain medications, and heart attacks.[4] Diagnosis is based on blood tests finding a blood sugar greater than 30 mmol/L (600 mg/dL), osmolarity greater than 320 mOsm/kg, and a pH above 7.3.[2][3] Initial treatment generally consists of intravenous fluids to manage dehydration, intravenous insulin in those with significant ketones, low molecular weight heparin to decrease the risk of blood clotting, and antibiotics among those in whom there is concerns of infection.[3] The goal is a slow decline in blood sugar levels.[3] Potassium replacement is often required as the metabolic problems are corrected.[3] Efforts to prevent diabetic foot ulcers are also important.[3] It typically takes a few days for the person to return to baseline.[3] While the exact frequency of the condition is unknown, it is relatively common.[2][4] Older people are most commonly affected.[4] The risk of death among those affected is about 15%.[4] It was first described in the 1880s.[4] Signs and symptoms[edit] Symptoms of high blood sugar including increased thirst (polydipsia), increased volume of urination (polyurea), and i Continue reading >>
Diabetic Ketoacidosis And 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 >>
You Don't Understand The Osm Gap - Guest Post By Rory Spiegel
Rory is just graduated EM Residency at Beth Israel Newark and is now pursuing advanced training in Resuscitation with Brian Wright and me at Stony Brook Hospital. He is the editor of the amazing EMNerd Blog and tweets at @EMNerd_ . This post will serve as a discussion of serum osmolarity*, its clinical utility, and the relationship between the Osm and anion gaps. The serum osmolarity has been relegated to the dark arts of medical science. Primarily, it is used to calculate the exact fluid status of patients presenting in various dysnatremic states by the physicians who happen to care for such physiological disruptions. Simply put the serum osmolarity is the number of particles present in the serum. The osmolarity does not discriminate based on a particles size or weight, but rather is concerned only with its concentration in the blood (1). As such, particles with low molecular weight that are capable of accumulating in large quantities in the serum, have the greatest potential to influence the osmolarity. In a healthy subject, the osmolarity is predominantly comprised of sodium ions and their counter anions, serum glucose, as well as blood urea nitrogen (BUN) (1). The serum osmolarity can be grossly estimated using the following formula: Briefly, this formula insures that each molecule is accounted for in its molar quantity (mmol/L) (1). The serum osmolality can also be directly measured by observing either the serums freezing point depression or boiling point elevation. If we compare this measured value to the calculated osmolarity, the difference between the two measurements is the Osm gap. Ideally this would equate to the amount of particles present in the serum that are not accounted for by the calculated formula. As such, the Osm gap should be positive in most phy Continue reading >>
Diabetic Ketoacidosis Workup
Approach Considerations Diabetic ketoacidosis is typically characterized by hyperglycemia over 250 mg/dL, a bicarbonate level less than 18 mEq/L, and a pH less than 7.30, with ketonemia and ketonuria. While definitions vary, mild DKA can be categorized by a pH level of 7.25-7.3 and a serum bicarbonate level between 15-18 mEq/L; moderate DKA can be categorized by a pH between 7.0-7.24 and a serum bicarbonate level of 10 to less than 15 mEq/L; and severe DKA has a pH less than 7.0 and bicarbonate less than 10 mEq/L. [17] In mild DKA, anion gap is greater than 10 and in moderate or severe DKA the anion gap is greater than 12. These figures differentiate DKA from HHS where blood glucose is greater than 600 mg/dL but pH is greater than 7.3 and serum bicarbonate greater than 15 mEq/L. Laboratory studies for diabetic ketoacidosis (DKA) should be scheduled as follows: Repeat laboratory tests are critical, including potassium, glucose, electrolytes, and, if necessary, phosphorus. Initial workup should include aggressive volume, glucose, and electrolyte management. It is important to be aware that high serum glucose levels may lead to dilutional hyponatremia; high triglyceride levels may lead to factitious low glucose levels; and high levels of ketone bodies may lead to factitious elevation of creatinine levels. 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 >>
Acid–base Problems In Diabetic Ketoacidosis
Disorders of Fluids and Electrolytes The case description below highlights issues raised in an upcoming article about acid–base disturbance and its clinical implications in patients with diabetic ketoacidosis in the series “Disorders of Fluids and Electrolytes.” A 15-year-old boy with nephrotic syndrome presented with abdominal pain and vomiting. Lab data include: blood glucose 849 mg/dL, blood pH 7.19, PCO2 18 mm Hg, PO2 40 mm Hg, bicarbonate 7 mmol/L, sodium 125 mmol/L, potassium 6.2 mmol/L, chloride 81 mmol/L, and total carbon dioxide 8 mmol/L. What is the best strategy to support this patient? Polling and commenting are now closed. The editor’s recommendations appear below. The next challenge appears on March 5. Share: A 15-year-old boy with a history of glucocorticoid-dependent nephrotic syndrome since 5 years of age arrives in a community emergency department because of chest pain and nausea that has progressed to abdominal pain over the preceding 16 hours. The nephrotic syndrome was in remission while the patient was receiving glucocorticoids and cyclosporine. The patient and his mother stated that he had become very thirsty and had been drinking huge amounts of water over the past week. On the day of admission, he had several episodes of vomiting. There was no fever, cough, rhinorrhea, or diarrhea, and no family member, friend, or associate had been ill. The patient’s usual medications at the time of presentation included prednisone (at a dose of 50 mg daily), cyclosporine (125 mg twice daily), enalapril (10 mg daily), and ranitidine (75 mg daily). In addition, treatment with recombinant human growth hormone had been initiated for glucocorticoid-induced short stature. The patient and his family said that the urinary albumin level had been negative on a Continue reading >>
Diagnosis And Treatment Of Diabetic Ketoacidosis And The Hyperglycemic Hyperosmolar State
Go to: Pathogenesis In both DKA and HHS, the underlying metabolic abnormality results from the combination of absolute or relative insulin deficiency and increased amounts of counterregulatory hormones. Glucose and lipid metabolism When insulin is deficient, the elevated levels of glucagon, catecholamines and cortisol will stimulate hepatic glucose production through increased glycogenolysis and enhanced gluconeogenesis4 (Fig. 1). Hypercortisolemia will result in increased proteolysis, thus providing amino acid precursors for gluconeogenesis. Low insulin and high catecholamine concentrations will reduce glucose uptake by peripheral tissues. The combination of elevated hepatic glucose production and decreased peripheral glucose use is the main pathogenic disturbance responsible for hyperglycemia in DKA and HHS. The hyperglycemia will lead to glycosuria, osmotic diuresis and dehydration. This will be associated with decreased kidney perfusion, particularly in HHS, that will result in decreased glucose clearance by the kidney and thus further exacerbation of the hyperglycemia. In DKA, the low insulin levels combined with increased levels of catecholamines, cortisol and growth hormone will activate hormone-sensitive lipase, which will cause the breakdown of triglycerides and release of free fatty acids. The free fatty acids are taken up by the liver and converted to ketone bodies that are released into the circulation. The process of ketogenesis is stimulated by the increase in glucagon levels.5 This hormone will activate carnitine palmitoyltransferase I, an enzyme that allows free fatty acids in the form of coenzyme A to cross mitochondrial membranes after their esterification into carnitine. On the other side, esterification is reversed by carnitine palmitoyltransferase I Continue reading >>
Diabetic Ketoacidosis
Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes mellitus.[1] Signs and symptoms may include vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion, and occasionally loss of consciousness.[1] A person's breath may develop a specific smell.[1] Onset of symptoms is usually rapid.[1] In some cases people may not realize they previously had diabetes.[1] DKA happens most often in those with type 1 diabetes, but can also occur in those with other types of diabetes under certain circumstances.[1] Triggers may include infection, not taking insulin correctly, stroke, and certain medications such as steroids.[1] DKA results from a shortage of insulin; in response the body switches to burning fatty acids which produces acidic ketone bodies.[3] DKA is typically diagnosed when testing finds high blood sugar, low blood pH, and ketoacids in either the blood or urine.[1] The primary treatment of DKA is with intravenous fluids and insulin.[1] Depending on the severity, insulin may be given intravenously or by injection under the skin.[3] Usually potassium is also needed to prevent the development of low blood potassium.[1] Throughout treatment blood sugar and potassium levels should be regularly checked.[1] Antibiotics may be required in those with an underlying infection.[6] In those with severely low blood pH, sodium bicarbonate may be given; however, its use is of unclear benefit and typically not recommended.[1][6] Rates of DKA vary around the world.[5] In the United Kingdom, about 4% of people with type 1 diabetes develop DKA each year, while in Malaysia the condition affects about 25% a year.[1][5] DKA was first described in 1886 and, until the introduction of insulin therapy in the 1920s, it was almost univ Continue reading >>
Diabetic Ketoacidosis
Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find the Pre-diabetes (Impaired Glucose Tolerance) article more useful, or one of our other health articles. See also the separate Childhood Ketoacidosis article. Diabetic ketoacidosis (DKA) is a medical emergency with a significant morbidity and mortality. It should be diagnosed promptly and managed intensively. DKA is characterised by hyperglycaemia, acidosis and ketonaemia:[1] Ketonaemia (3 mmol/L and over), or significant ketonuria (more than 2+ on standard urine sticks). Blood glucose over 11 mmol/L or known diabetes mellitus (the degree of hyperglycaemia is not a reliable indicator of DKA and the blood glucose may rarely be normal or only slightly elevated in DKA). Bicarbonate below 15 mmol/L and/or venous pH less than 7.3. However, hyperglycaemia may not always be present and low blood ketone levels (<3 mmol/L) do not always exclude DKA.[2] Epidemiology DKA is normally seen in people with type 1 diabetes. Data from the UK National Diabetes Audit show a crude one-year incidence of 3.6% among people with type 1 diabetes. In the UK nearly 4% of people with type 1 diabetes experience DKA each year. About 6% of cases of DKA occur in adults newly presenting with type 1 diabetes. About 8% of episodes occur in hospital patients who did not primarily present with DKA.[2] However, DKA may also occur in people with type 2 diabetes, although people with type 2 diabetes are much more likely to have a hyperosmolar hyperglycaemic state. Ketosis-prone type 2 diabetes tends to be more common in older, overweight, non-white people with type 2 diabetes, and DKA may be their Continue reading >>
Common Laboratory (lab) Values - Anion Gap
Question: Please define the Anion Gap and its utility in diagnosis and how it relates to osmolality. The anion gap provides an estimation of the unmeasured anions in the plasma and is useful in the setting of arterial blood gas analysis. It is especially useful in helping to differentiate the cause of a metabolic acidosis, as well as following the response to therapy. Its basic premise is based on the fact that electroneutrality must exist in the body, or in other words the net charges of serum anions, which includes albumin, bicarbonate, chloride, organic acids and phosphate must equal the net charges of the serum cations, which includes calcium, magnesium, potassium and sodium. In clinical practice, the anion gap is calculated using three lab values (Na+, Cl-, and HCO3-). [Occasionally, you may see an alternative equation: Anion Gap = [Na+] + [K+] - [Cl-] - [HCO3-]. This equation is preferred by some nephrologists, because of the wide fluctuations that may occur with potassium in renal disease. ] Serum sodium represents over 90 percent of the extracellular cations, whereas chloride and bicarbonate represent approximately 85 percent of the extracellular anions. It follows then, that the anion gap in normal conditions will be a positive number since the sum of the serum anions used in the calculation represent a smaller value compared to the serum sodium concentration. The normal value for the anion gap is 12 +/-4. some newer references will list the normal anion gap as 7 +/- 4. This lower level may represent a more accurate reflection of the true anion gap based on changes that have occurred in contemporary medical labs. In the past, electrolyte analysis was performed using predominantly flame photometer measurement compared to the modern day use of ion-selective elec Continue reading >>
