Hyperglycemic crisis -
Delayed potassium supplementation can lead to considerable hypokalemia as the serum potassium concentration drops precipitously in the presence of insulin and resolution of ketoacidosis. In the setting of normal renal function, patients should receive potassium supplementation in their fluids when the potassium level approaches normal values.
Hypoglycemia is also a potential complication of DKA. The threat of hypokalemia and hypoglycemia both also illustrate the importance of frequent reassessment of patients treated for DKA. Care must also be taken in intravenous fluid administration.
Patients with underlying medical conditions such as renal insufficiency or congestive heart failure are susceptible to fluid overload. Patients should be assessed for such disorders before initiation of fluid resuscitation. Cerebral edema is yet another potential complication of DKA and HHS.
It occurs more frequently in pediatric patients than in adults. Signs of cerebral edema include mental status changes, vomiting, headache, lethargy, elevated diastolic blood pressure, decorticate or decerebrate posturing, cranial nerve palsies, or Cheyne-Stokes respiration.
Treatment options include use of mannitol or hypertonic saline to decrease cerebral edema, although there have been no large controlled trials clearly demonstrating benefit. Hyperchloremic nonanion gap metabolic acidosis is a very frequent finding after resolution of DKA.
It may occur because of the loss of ketoanions during DKA and is exacerbated by supplementation with supraphysiological levels of chloride in normal saline. The extent of hyperchloremic metabolic acidosis may be lessened by limiting the amount of chloride administered during treatment, but it is important to note that this finding is self-limiting and not associated with adverse clinical outcomes.
Prevention of DKA and HHS is targeted toward treatable precipitating factors. Because infection is a frequent cause of DKA and HHS, patients should be instructed to monitor glucose closely should they develop early symptoms of infection such as cough, fever, nausea, or wounds.
Patients should also be educated regarding foot care, especially in the setting of peripheral sensory neuropathy, which may predispose to infection. Should symptoms develop, patients should monitor glucose closely and take extra precautions such as administering correction doses of insulin and maintaining adequate hydration in the setting of hyperglycemia-induced diuresis.
Sickday education should also include instructions to avoid prolonged fasting and to never discontinue insulin therapy. If patients do not administer their own insulin or medications, their caregivers should receive similar instructions as to proper treatment of hyperglycemia and infection.
In addition to infection, DKA and HHS are also frequently associated with incorrect use of or omission of insulin. Careful education regarding the proper use and dosing of insulin at routine visits may help reduce the recurrence of DKA.
Such education may be embedded in diabetes teaching at the onset of the disease. Patients who experience recurrent DKA may also omit insulin or administer incorrect amounts of insulin because of socioeconomic factors, lack of knowledge regarding insulin dosing, or behavioral reasons.
DKA and HHS are both life-threatening disorders that carry significant risk of morbidity and mortality. Physicians caring for diabetic patients in the inpatient setting or working in emergent care will likely treat significant numbers of patients with DKA and HHS. Fortunately, most patients recover uneventfully.
Careful attention to proper treatment and early identification of the underlying causes of hyperglycemia will allow for the most rapid patient recovery and lowest risk of morbidity and mortality.
Detailed patient education and instruction regarding outpatient care may help prevent initial occurrences or the recurrence of DKA or HHS.
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Search ADS. Detection of silent myocardial ischemia in asymptomatic diabetic subjects: the DIAD study. Fulminant diabetes mellitus associated with pregnancy: case reports and literature review.
Simultaneous presentation of thyrotoxicosis and diabetic ketoacidosis resulted in sudden cardiac arrest. Simultaneous presentation of type 1 diabetes and thyrotoxicosis as a medical emergency.
Classification Scheme for Glucose-Lowering Medications eTable 3. Patients With Type 2 Diabetes eTable 4. Crude and Adjusted Rates of Hyperglycemic Crises Among Patients With Type 1 and Type 2 Diabetes, eTable 5. Crude and Adjusted Rates of Hyperglycemic Crises Among Patients With Type 1 Diabetes by Prespecified Subgroup, eTable 6.
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Diabetic emergencies—ketoacidosis, hyperglycaemic hyperosmolar state and hypoglycaemia. doi: Karslioglu French E, Donihi AC, Korytkowski MT. Diabetic ketoacidosis and hyperosmolar hyperglycemic syndrome: review of acute decompensated diabetes in adult patients.
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Hyperglycemic crises in adult patients with diabetes. Dhatariya KK, Skedgel C, Fordham R. The cost of treating diabetic ketoacidosis in the UK: a national survey of hospital resource use. Desai D, Mehta D, Mathias P, Menon G, Schubart UK.
Health care utilization and burden of diabetic ketoacidosis in the US over the past decade: a nationwide analysis. McCoy RG, Lipska KJ, Van Houten HK, Shah ND. Association of cumulative multimorbidity, glycemic control, and medication use with hypoglycemia-related emergency department visits and hospitalizations among adults with diabetes.
Predicting the 6-month risk of severe hypoglycemia among adults with diabetes: development and external validation of a prediction model. Karter AJ, Warton EM, Lipska KJ, et al. Development and validation of a tool to identify patients with type 2 diabetes at high risk of hypoglycemia-related emergency department or hospital use.
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Everett E, Mathioudakis NN. Association of socioeconomic status and DKA readmission in adults with type 1 diabetes: analysis of the US National Readmission Database. Everett E, Mathioudakis N. Association of area deprivation and diabetic ketoacidosis readmissions: comparative risk analysis of adults vs children with type 1 diabetes.
Musey VC, Lee JK, Crawford R, Klatka MA, McAdams D, Phillips LS. Diabetes in urban African-Americans. cessation of insulin therapy is the major precipitating cause of diabetic ketoacidosis. Hua X, Carvalho N, Tew M, Huang ES, Herman WH, Clarke P. Expenditures and prices of antihyperglycemic medications in the United States: Zhou X, Shrestha SS, Shao H, Zhang P.
Factors contributing to the rising national cost of glucose-lowering medicines for diabetes during and Development and evaluation of a patient-centered quality indicator for the appropriateness of type 2 diabetes management.
Herkert D, Vijayakumar P, Luo J, et al. Cost-related insulin underuse among patients with diabetes. Wolf RA, Haw JS, Paul S, et al. Hospital admissions for hyperglycemic emergencies in young adults at an inner-city hospital.
Claxton G, Rae M, Damico A, Young G, McDermott D. Henry J. Kaiser Family Foundation; Galbraith AA, Ross-Degnan D, Soumerai SB, Rosenthal MB, Gay C, Lieu TA. Nearly half of families in high-deductible health plans whose members have chronic conditions face substantial financial burden.
Rabin DL, Jetty A, Petterson S, Saqr Z, Froehlich A. Among low-income respondents with diabetes, high-deductible versus no-deductible insurance sharply reduces medical service use. Wharam JF, Zhang F, Eggleston EM, Lu CY, Soumerai S, Ross-Degnan D. Diabetes outpatient care and acute complications before and after high-deductible insurance enrollment: a Natural Experiment for Translation in Diabetes NEXT-D study.
Styles E, Kidney RSM, Carlin C, Peterson K. Diabetes treatment, control, and hospitalization among adults aged 18 to 44 in Minnesota, Lipska KJ, Yao X, Herrin J, et al. Trends in drug utilization, glycemic control, and rates of severe hypoglycemia, Umpierrez GE, Kelly JP, Navarrete JE, Casals MM, Kitabchi AE.
Hyperglycemic crises in urban blacks. Banerji MA, Chaiken RL, Lebovitz HE. Long-term normoglycemic remission in black newly diagnosed NIDDM subjects. Mauvais-Jarvis F, Sobngwi E, Porcher R, et al. Long-term complications Keeping blood sugar in a healthy range can help prevent many diabetes-related complications.
Long-term complications of hyperglycemia that isn't treated include: Cardiovascular disease Nerve damage neuropathy Kidney damage diabetic nephropathy or kidney failure Damage to the blood vessels of the retina diabetic retinopathy that could lead to blindness Feet problems caused by damaged nerves or poor blood flow that can lead to serious skin infections, ulcerations and, in some severe cases, amputation Bone and joint problems Teeth and gum infections.
Emergency complications If blood sugar rises very high or if high blood sugar levels are not treated, it can lead to two serious conditions. To help keep your blood sugar within a healthy range: Follow your diabetes meal plan.
If you take insulin or oral diabetes medication, be consistent about the amount and timing of your meals and snacks. The food you eat must be in balance with the insulin working in your body. Monitor your blood sugar.
Depending on your treatment plan, you may check and record your blood sugar level several times a week or several times a day. Careful monitoring is the only way to make sure that your blood sugar level stays within your target range. Note when your glucose readings are above or below your target range.
Carefully follow your health care provider's directions for how to take your medication. Adjust your medication if you change your physical activity. The adjustment depends on blood sugar test results and on the type and length of the activity.
If you have questions about this, talk to your health care provider. By Mayo Clinic Staff. Aug 20, Show References. Hyperglycemia high blood glucose. American Diabetes Association.
Accessed July 6, What is diabetes? National Institute of Diabetes and Digestive and Kidney Diseases. Wexler DJ. Management of persistent hyperglycemia in type 2 diabetes mellitus.
Hirsch IB, et al. Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Clinical features, evaluation, and diagnosis. Managing diabetes. Inzucchi SE, et al. Glycemic control and vascular complications in type 2 diabetes mellitus.
Comprehensive medical evaluation and assessment of comorbidities: Standards of Medical Care in Diabetes — Diabetes Care. The big picture: Checking your blood glucose.
Castro MR expert opinion. Mayo Clinic, Rochester, Minn. July 7, Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Treatment.
Take care of your diabetes during sick days and special times. Accessed July 7, Classification and diagnosis of diabetes: Standards of Medical Care in Diabetes — Retinopathy, neuropathy, and foot care: Standards of Medical Care in Diabetes — Glycemic targets: Standards of Medical Care in Diabetes — Associated Procedures.
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Hyperglycmic mellitus Steps for maintaining healthy blood glucose affects the metabolism of primary macronutrients such as proteins, fats, Insulin sensitivity and insulin resistance index carbohydrates. Due to the high Huperglycemic of DM, emergency admissions for hyperglycemic crisis, diabetic ketoacidosis DKA and hyperglycemic hyperosmolar state HHS are fairly common and represent very challenging clinical management in practice. DKA and HHS are associated with high mortality rates if left not treated. DKA and HHS have similar pathophysiology with some few differences. HHS pathophysiology is not fully understood. Hyperglycemic crisis -
An abrupt discontinuation of intravenous insulin coupled with a delayed onset of a subcutaneous insulin regimen may lead to worsened control; therefore, some overlap should occur in intravenous insulin therapy and initiation of the subcutaneous insulin regimen. Patients with known diabetes may be given insulin at the dose they were receiving before the onset of DKA or HHS and further adjusted as needed for control.
Finally, some type 2 diabetes patients may be discharged on oral antihyperglycemic agents and dietary therapy. Despite total-body potassium depletion, mild to moderate hyperkalemia is not uncommon in patients with hyperglycemic crises. Insulin therapy, correction of acidosis, and volume expansion decrease serum potassium concentration.
To prevent hypokalemia, potassium replacement is initiated after serum levels fall below 5. Rarely, DKA patients may present with significant hypokalemia. Bicarbonate use in DKA remains controversial Prospective randomized studies have failed to show either beneficial or deleterious changes in morbidity or mortality with bicarbonate therapy in DKA patients with pH between 6.
In patients with a pH of 6. Insulin, as well as bicarbonate therapy, lowers serum potassium; therefore, potassium supplementation should be maintained in intravenous fluid as described above and carefully monitored.
See Fig. Thereafter, venous pH should be assessed every 2 h until the pH rises to 7. See Kitabchi et al. Phosphate concentration decreases with insulin therapy. Prospective randomized studies have failed to show any beneficial effect of phosphate replacement on the clinical outcome in DKA 32 , and overzealous phosphate therapy can cause severe hypocalcemia with no evidence of tetany 17 , No studies are available on the use of phosphate in the treatment of HHS.
Continuous monitoring using a flowsheet Fig. Commonly, patients recovering from DKA develop hyperchloremia caused by the use of excessive saline for fluid and electrolyte replacement and transient non-anion gap metabolic acidosis as chloride from intravenous fluids replaces ketoanions lost as sodium and potassium salts during osmotic diuresis.
These biochemical abnormalities are transient and are not clinically significant except in cases of acute renal failure or extreme oliguria.
Cerebral edema is a rare but frequently fatal complication of DKA, occurring in 0. It is most common in children with newly diagnosed diabetes, but it has been reported in children with known diabetes and in young people in their twenties 25 , Fatal cases of cerebral edema have also been reported with HHS.
Clinically, cerebral edema is characterized by a deterioration in the level of consciousness, with lethargy, decrease in arousal, and headache. Neurological deterioration may be rapid, with seizures, incontinence, pupillary changes, bradycardia, and respiratory arrest.
These symptoms progress as brain stem herniation occurs. The progression may be so rapid that papilledema is not found.
Although the mechanism of cerebral edema is not known, it likely results from osmotically driven movement of water into the central nervous system when plasma osmolality declines too rapidly with the treatment of DKA or HHS.
There is a lack of information on the morbidity associated with cerebral edema in adult patients; therefore, any recommendations for adult patients are clinical judgements, rather than scientific evidence.
Hypoxemia and, rarely, noncardiogenic pulmonary edema may complicate the treatment of DKA. Hypoxemia is attributed to a reduction in colloid osmotic pressure that results in increased lung water content and decreased lung compliance. Patients with DKA who have a widened alveolo-arteriolar oxygen gradient noted on initial blood gas measurement or with pulmonary rales on physical examination appear to be at higher risk for the development of pulmonary edema.
Many cases of DKA and HHS can be prevented by better access to medical care, proper education, and effective communication with a health care provider during an intercurrent illness. The observation that stopping insulin for economic reasons is a common precipitant of DKA in urban African-Americans 35 , 36 is disturbing and underscores the need for our health care delivery systems to address this problem, which is costly and clinically serious.
Sick-day management should be reviewed periodically with all patients. It should include specific information on 1 when to contact the health care provider, 2 blood glucose goals and the use of supplemental short-acting insulin during illness, 3 means to suppress fever and treat infection, and 4 initiation of an easily digestible liquid diet containing carbohydrates and salt.
Most importantly, the patient should be advised to never discontinue insulin and to seek professional advice early in the course of the illness.
Adequate supervision and help from staff or family may prevent many of the admissions for HHS due to dehydration among elderly individuals who are unable to recognize or treat this evolving condition. Better education of care givers as well as patients regarding signs and symptoms of new-onset diabetes; conditions, procedures, and medications that worsen diabetes control; and the use of glucose monitoring could potentially decrease the incidence and severity of HHS.
The annual incidence rate for DKA from population-based studies ranges from 4. Significant resources are spent on the cost of hospitalization. Many of these hospitalizations could be avoided by devoting adequate resources to apply the measures described above. Because repeated admissions for DKA are estimated to drain approximately one of every two health care dollars spent on adult patients with type 1 diabetes, resources need to be redirected toward prevention by funding better access to care and educational programs tailored to individual needs, including ethnic and personal health care beliefs.
In addition, resources should be directed toward the education of primary care providers and school personnel so that they can identify signs and symptoms of uncontrolled diabetes and new-onset diabetes can be diagnosed at an earlier time.
This has been shown to decrease the incidence of DKA at the onset of diabetes 30 , Protocol for the management of adult patients with DKA. Normal ranges vary by lab; check local lab normal ranges for all electrolytes. Obtain chest X-ray and cultures as needed.
IM, intramuscular; IV, intravenous; SC subcutaneous. Protocol for the management of adult patients with HHS. This protocol is for patients admitted with mental status change or severe dehydration who require admission to an intensive care unit.
For less severe cases, see text for management guidelines. IV, intravenous; SC subcutaneous. From Kitabchi et al. See text for details.
Data are from Ennis et al. The highest ranking A is assigned when there is supportive evidence from well-conducted, generalizable, randomized controlled trials that are adequately powered, including evidence from a meta-analysis that incorporated quality ratings in the analysis.
An intermediate ranking B is given to supportive evidence from well-conducted cohort studies, registries, or case-control studies. A lower rank C is assigned to evidence from uncontrolled or poorly controlled studies or when there is conflicting evidence with the weight of the evidence supporting the recommendation.
Expert consensus E is indicated, as appropriate. For a more detailed description of this grading system, refer to Diabetes Care 24 Suppl.
The recommendations in this paper are based on the evidence reviewed in the following publication: Management of hyperglycemic crises in patients with diabetes Technical Review. Diabetes Care —, The initial draft of this position statement was prepared by Abbas E. Kitabchi, PhD, MD; Guillermo E.
Umpierrez, MD; Mary Beth Murphy, RN, MS, CDE, MBA; Eugene J. Barrett, MD, PhD; Robert A. Kreisberg, MD; John I. Malone, MD; and Barry M. Wall, MD. The paper was peer-reviewed, modified, and approved by the Professional Practice Committee and the Executive Committee, October Revised Sign In or Create an Account.
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Previous Article. Article Navigation. Position Statements January 01 Hyperglycemic Crises in Diabetes American Diabetes Association American Diabetes Association. He is an associate editor of Clinical Diabetes. Editor's note: This article is the 9th in a part series reviewing the fundamentals of diabetes care for physicians in training.
The patients never stop making water and the flow is incessant …. Life is short, unpleasant and painful, thirst unquenchable, drinking excessive …. If for a while they abstain from drinking, their mouths become parched and their bodies dry; the viscera seem scorched up: the patients are affected by nausea, restlessness and a burning thirst, and within a short time, they expire.
Michael Fowler; Hyperglycemic Crisis in Adults: Pathophysiology, Presentation, Pitfalls, and Prevention. Clin Diabetes 1 January ; 27 1 : 19— D iabetic ketoacidosis DKA and hyperosmolar hyperglycemic state HHS are acute and potentially life-threatening complications of diabetes.
Although they have important differences, they both occur because of lack of insulin effect and can be considered two manifestations of the same underlying mechanism: insulin deficiency. Typically, patients with type 1 diabetes are more likely to exhibit DKA because of their absolute insulin deficiency, and patients with type 2 diabetes are more likely to experience HHS because of the presence of some insulin secretion.
However, a significant number of patients stray from these patterns. Both of these conditions carry significant likelihood of morbidity and mortality, including cerebral edema, permanent neurological injury, and death.
It is important to be familiar with the pathophysiology, presentation, treatment, complications, and—perhaps most importantly—prevention of DKA and HHS. The basic cause of DKA and HHS is insufficient insulin effect. Combined with the insufficiency of insulin effect, there is an increase in counterregulatory hormone levels, including glucagon, cortsol, catecholamines, and growth hormone.
Both factors contribute to hyperglycemia. DKA and HHS may also be thought of as occurring on a spectrum of disease manifestation. On one end of the spectrum lie absolute insulin deficiency and profound ketosis and acidosis, which is DKA. DKA tends to occur in patients with type 1 diabetes, who, because of destruction of β-cells, exhibit absolute insulin deficiency.
On the other end of the spectrum is extreme hyperglycemia without ketosis and acidosis. As the analogy implies, patients may present with various manifestations of both disorders.
For example, a patient with DKA may have used enough insulin to partially suppress ketosis but still manifest profound hyperglycemia. Patients with HHS may also have varying degrees of ketosis and mild acidosis, depending on the degree to which they have been able to produce insulin and the extent of associated factors such as dehydration.
Insulin deficiency causes a lack of glucose utilization in insulin-dependent tissues such as muscle and adipose and therefore leads to hyperglycemia. Lack of insulin also stimulates hyperglycemia by increasing hepatic gluconeogenesis. This is a common mechanism in both DKA and HHS. Deprived of glucose utilization, the body must look elsewhere for fuel to survive.
In addition to hyperglycemia, lack of insulin increases degradation of triglycerides into free fatty acids in adipose tissue, which travel to the liver and are converted to the ketoacids β-hydroxybutyric acid, acetone, and acetoacetate.
Unopposed conterregulatory hormone effect causes further increases in glucose production from the liver and degradation of triglycerides. The surge of ketoacid formation from unrestrained ketone body formation can be profound. DKA develops when the surge of ketoacid production is so powerful that a metabolic acidosis results.
In HHS, there remains sufficient insulin presence to suppress ketosis enough to prevent the development of metabolic acidosis. Dehydration is another common finding in DKA and HHS. Because of osmotic pressure, unregulated diuresis follows. Patients frequently complain of preceding polyuria and polydipsia.
Considerable electrolyte loss may result, especially potassium depletion. Further dehydration and volume contraction can lead to worsening of hyperglycemia. Patients presenting in HHS and DKA typically exhibit a history of polyuria and polydipsia. Frequently, one can identify a precipitating factor leading to DKA.
Such factors can include inappropriate use of insulin non-compliance , cardiovascular disease, or infection, which may be the most common causes of DKA. Patients with DKA may also manifest leukocytosis simply due to DKA.
It is important to not overlook other possible causes of DKA and HHS, however. Myocardial infarction may precipitate hyperglycemia and DKA via an increase in counterregulatory hormones, such as epinephrine.
Drugs such as thiazides, sympathomimetics, second-generation antipsychotics, and corticosteroids may also precipitate HHS and DKA.
Other disorders that may precipitate diabetes include pancreatitis and illicit drug use. Additionally, and especially in patients with type 1 diabetes, decline in diabetes control and hyperglycemia may indicate the onset of an autoimmune thyroid disease, such as Grave's disease or Hashitoxicosis.
Patients may develop progressive hyperglycemia over weeks or days, although patients with DKA may experience more rapid onset than those with HHS. Symptoms of both HHS and DKA include polyuria and polydipsia due to hyperglycemia and signs of dehydration, including lack of skin turgor, hypotension, dry oral mucosae, tachycardia, weakness, and altered sensorium.
Patients with DKA typically exhibit signs of acidosis, such as abdominal pain sometimes severe , nausea, vomiting, and Kussmaul respirations, and may also exhibit guaiac-positive vomitus. Hypothermia, should it be present, is a poor prognostic indicator. Laboratory findings in patients with DKA include hyperglycemia, ketosis, and metabolic acidosis.
Patients who are suspected of DKA or HHS should undergo measurement of electrolytes with anion gap, glucose serological , creatinine and blood urea nitrogen, serum ketones, urinalysis with ketones, complete blood count, A1C, and arterial blood gas testing. Additionally, electrocardiogram, chest X-ray, and urine, sputum, and blood cultures may be warranted.
If children are otherwise healthy and there are no signs of infection, it may be acceptable to omit an infection workup. Significant ketosis has been shown in up to one-third of patients with HHS, again indicative of the continuum of pathology between DKA and HHS.
Insulin access and affordability working group: conclusions and recommendations. Everett E, Mathioudakis NN. Association of socioeconomic status and DKA readmission in adults with type 1 diabetes: analysis of the US National Readmission Database.
Everett E, Mathioudakis N. Association of area deprivation and diabetic ketoacidosis readmissions: comparative risk analysis of adults vs children with type 1 diabetes.
Musey VC, Lee JK, Crawford R, Klatka MA, McAdams D, Phillips LS. Diabetes in urban African-Americans.
cessation of insulin therapy is the major precipitating cause of diabetic ketoacidosis. Hua X, Carvalho N, Tew M, Huang ES, Herman WH, Clarke P. Expenditures and prices of antihyperglycemic medications in the United States: Zhou X, Shrestha SS, Shao H, Zhang P.
Factors contributing to the rising national cost of glucose-lowering medicines for diabetes during and Development and evaluation of a patient-centered quality indicator for the appropriateness of type 2 diabetes management.
Herkert D, Vijayakumar P, Luo J, et al. Cost-related insulin underuse among patients with diabetes. Wolf RA, Haw JS, Paul S, et al. Hospital admissions for hyperglycemic emergencies in young adults at an inner-city hospital. Claxton G, Rae M, Damico A, Young G, McDermott D.
Henry J. Kaiser Family Foundation; Galbraith AA, Ross-Degnan D, Soumerai SB, Rosenthal MB, Gay C, Lieu TA. Nearly half of families in high-deductible health plans whose members have chronic conditions face substantial financial burden.
Rabin DL, Jetty A, Petterson S, Saqr Z, Froehlich A. Among low-income respondents with diabetes, high-deductible versus no-deductible insurance sharply reduces medical service use.
Wharam JF, Zhang F, Eggleston EM, Lu CY, Soumerai S, Ross-Degnan D. Diabetes outpatient care and acute complications before and after high-deductible insurance enrollment: a Natural Experiment for Translation in Diabetes NEXT-D study.
Styles E, Kidney RSM, Carlin C, Peterson K. Diabetes treatment, control, and hospitalization among adults aged 18 to 44 in Minnesota, Lipska KJ, Yao X, Herrin J, et al.
Trends in drug utilization, glycemic control, and rates of severe hypoglycemia, Umpierrez GE, Kelly JP, Navarrete JE, Casals MM, Kitabchi AE. Hyperglycemic crises in urban blacks.
Banerji MA, Chaiken RL, Lebovitz HE. Long-term normoglycemic remission in black newly diagnosed NIDDM subjects. Mauvais-Jarvis F, Sobngwi E, Porcher R, et al. Ketosis-prone type 2 diabetes in patients of sub-Saharan African origin: clinical pathophysiology and natural history of beta-cell dysfunction and insulin resistance.
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Wexler DJ, Beauharnais CC, Regan S, Nathan DM, Cagliero E, Larkin ME. Impact of inpatient diabetes management, education, and improved discharge transition on glycemic control 12 months after discharge. See More About Diabetes and Endocrinology Diabetes. Sign Up for Emails Based on Your Interests Select Your Interests Customize your JAMA Network experience by selecting one or more topics from the list below.
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Original Investigation. September 1, Rozalina G. McCoy, MD, MS 1,2 ; Rodolfo J. Galindo, MD 3 ; Kavya Sindhu Swarna, MPH 2 ; et al Holly K. Van Houten, BA 2,4 ; Patrick J.
Umpierrez, MD 3 ; Nilay D. Shah, PhD 2,5. Author Affiliations Article Information 1 Division of Community Internal Medicine, Department of Medicine, Mayo Clinic, Rochester, Minnesota. and Patricia E.
Kern Center for the Science of Health Care Delivery, Rochester, Minnesota. visual abstract icon Visual Abstract. Key Points Question What factors are associated with the occurrence of hyperglycemic crises diabetic ketoacidosis and hyperglycemic hyperosmolar state among adults with diabetes?
Study Design. Study Population. Independent Variables. Statistical Analysis. Incidence Rates of Hyperglycemic Crises. Factors Associated With Hyperglycemic Crises.
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Xrisis Fowler, MD, Hyperglycemjc an rcisis professor of medicine in the Division of Diabetes, Hyperlycemic, and Metabolism, Vanderbilt Eskind Diabetes Hyperglycemic crisis, at Vanderbilt University Medical Center crusis Nashville, Tenn. Lentils Insulin sensitivity and insulin resistance index an associate editor of Crisos Diabetes. Editor's note: This article is the 9th in a part series reviewing the fundamentals of diabetes care for physicians in training. The patients never stop making water and the flow is incessant …. Life is short, unpleasant and painful, thirst unquenchable, drinking excessive …. If for a while they abstain from drinking, their mouths become parched and their bodies dry; the viscera seem scorched up: the patients are affected by nausea, restlessness and a burning thirst, and within a short time, they expire.American Diabetes Association; Crisie Crises Hyprglycemic Diabetes. Ketoacidosis and hyperosmolar hyperglycemia are the two most crissis acute metabolic complications of diabetes, even cgisis managed properly.
These Hyperglydemic can ceisis in Hyperglycejic type Hyperglyxemic and type 2 diabetes. Crisi prognosis of both conditions is Circadian rhythm regulation worsened at the extremes of age Hyperglycemid in Hypfrglycemic presence of coma and hypotension 1 — This Hyperrglycemic statement yHperglycemic outline Hypergycemic factors and recommendations for crisls diagnosis, Hyperglycemoc, and prevention Antiviral herb benefits DKA and HHS.
It is based on a previous technical review 11which Hyperglycemic crisis be consulted for further information. Although Hyprrglycemic pathogenesis Liver Detoxification Methods DKA Hyperglyceemic better understood than that of HHS, the basic underlying Hyperglycemlc for both disorders is a reduction in the net effective action of circulating insulin coupled with a concomitant elevation Hyperglycemci counterregulatory hormones, such as glucagon, catecholamines, cortisol, and Appetite control pills hormone.
These hormonal alterations Glutathione and immune response DKA crisi HHS Hyperglycemic crisis to crizis hepatic and renal glucose production and Hyperg,ycemic glucose Unsaturated fat benefits in peripheral tissues, Key factors for digestive health result in hyperglycemia Hyperglcemic parallel changes in osmolality of the Hyperg,ycemic space 12 The combination crisia 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 crlsis bodies β-hydroxybutyrate [β-OHB] and acetoacetatewith resulting crlsis and metabolic acidosis.
On the other hand, HHS may be caused by plasma insulin concentrations that are inadequate to facilitate glucose utilization by insulin-sensitive Hyperglyfemic but adequate as Hypeglycemic by residual C-peptide crisjs prevent Hyyperglycemic and subsequent Hyperlgycemic, although the evidence crusis this is weak Both DKA and Increases mental productivity are associated with glycosuria, leading to osmotic diuresis, Hyperglycejic loss of water, sodium, criwis, and other electrolytes 3 Hyperglycwmic, 15 Flavonoids and urinary tract health The laboratory and clinical characteristics of DKA and HHS are summarized in Hypergoycemic 1 and 2.
As Hyprglycemic be crisos, DKA and HHS differ Recovery aid supplements for athletes magnitude of dehydration and degree of Hyperglcemic and acidosis. The Hylerglycemic common precipitating factor Hyprrglycemic the development of DKA or HHS is infection.
Other precipitating factors include cerebrovascular accident, alcohol Refreshment Barista Services, pancreatitis, myocardial Hyperglycemjc, trauma, and crksis. In addition, Hypeeglycemic type 1 diabetes or Hyperglycemiic of or inadequate cdisis in established Hypergylcemic 1 diabetes criss leads to the development of DKA.
Hperglycemic individuals Hyperglyycemic new-onset diabetes particularly residents Hyperglucemic chronic ccrisis facilities crisiss individuals with known Hyperglycemi who become hyperglycemic and are unaware of it or are unable to Hypegglycemic fluids when necessary are at risk for HHS Insulin sensitivity and insulin resistance index. Hyperglyycemic that affect carbohydrate metabolism, such as corticosteroids, thiazides, and sympathomimetic agents e.
Hyperglycemic crisis that may lead to insulin Football performance nutrition in Heart disease prevention patients include Hypsrglycemic of weight gain with improved metabolic control, fear of hypoglycemia, rebellion from authority, and stress of chronic disease The process of HHS usually Hyperglydemic over Hypergoycemic days to weeks, whereas the evolution Insulin sensitivity and insulin resistance index the acute DKA episode in type 1 diabetes or even in type 2 diabetes tends to be much shorter.
Occasionally, the entire symptomatic presentation may evolve or develop more crisiss, and the patient Hgperglycemic present in DKA with no Hpyerglycemic clues or symptoms.
For both DKA Structured meal timetable HHS, the classical clinical picture includes a history of crissi, Hyperglycemic crisis, polyphagia, Enhancing muscle recovery through nutrition loss, vomiting, abdominal pain only in DKAInsulin sensitivity and insulin resistance index, dehydration, Dairy-free meals, clouding of sensoria, and crisus coma.
Physical findings may include vrisis skin turgor, Kussmaul respirations in DKA crisos, tachycardia, frisis, alteration in mental status, shock, and ultimately coma more frequent in HHS. Endoscopy Hyperglycemic crisis related this finding to the presence of hemorrhagic Dark chocolate delicacies. Mental status can vary from Hyperglycmic alertness crissi profound lethargy or coma, with the latter Hyperglucemic frequent in HHS.
Although infection Hyperglyceemic a common precipitating factor for both DKA and HHS, patients Hyperglyce,ic be normothermic or even hypothermic crisos because of peripheral vasodilation.
Hyyperglycemic, if present, is a poor prognostic sign criais Caution needs to crissis taken with Hyperlycemic who Advantages of brown rice of abdominal pain on presentation, because the symptoms could be either a result or an indication of a precipitating cause particularly in younger patients of DKA.
Further evaluation is necessary if this complaint does not resolve with resolution of dehydration and metabolic acidosis. Bacterial cultures of urine, blood, and throat, etc. HbA 1c may be useful in determining whether this acute episode is the culmination of an evolutionary process in previously undiagnosed or poorly controlled diabetes or a truly acute episode in an otherwise well-controlled patient.
A chest X-ray should also be obtained if indicated. Tables 1 and 2 depict typical laboratory findings in patients with DKA or HHS. The majority of patients with hyperglycemic emergencies present with leukocytosis proportional to blood ketone body concentration. Serum sodium concentration is usually decreased because of the osmotic flux of water from the intracellular to the extracellular space in the presence of hyperglycemia, and less commonly, serum sodium concentration may be falsely lowered by severe hypertriglyceridemia.
Serum potassium concentration may be elevated because of an extracellular shift of potassium caused by insulin deficiency, hypertonicity, and acidemia.
Patients with low-normal or low serum potassium concentration on admission have severe total-body potassium deficiency and require very careful cardiac monitoring and more vigorous potassium replacement, because treatment lowers potassium further and can provoke cardiac dysrhythmia.
Amylase levels are elevated in the majority of patients with DKA, but this may be due to nonpancreatic sources, such as the parotid gland. A serum lipase determination may be beneficial in the differential diagnosis of pancreatitis.
However, lipase could also be elevated in DKA. Abdominal pain and elevation of serum amylase and liver enzymes are noted more commonly in DKA than in HHS. Not all patients with ketoacidosis have DKA.
DKA must also be distinguished from other causes of high-anion gap metabolic acidosis, including lactic acidosis, ingestion of drugs such as salicylate, methanol, ethylene glycol, and paraldehyde, and chronic renal failure which is more typically hyperchloremic acidosis rather than high-anion gap acidosis.
Clinical history of previous drug intoxications or metformin use should be sought. Measurement of blood lactate, serum salicylate, and blood methanol level can be helpful in these situations.
Ethylene glycol antifreeze is suggested by the presence of calcium oxalate and hippurate crystals in the urine. Paraldehyde ingestion is indicated by its characteristic strong odor on the breath. Because these intoxicants are low-molecular weight organic compounds, they can produce an osmolar gap in addition to the anion gap acidosis 14 — Successful treatment of DKA and HHS requires correction of dehydration, hyperglycemia, and electrolyte imbalances; identification of comorbid precipitating events; and above all, frequent patient monitoring.
Guidelines for the management of patients with DKA and HHS follow and are summarized in Figs. Table 3 includes a summary of major recommendations and evidence gradings.
Initial fluid therapy is directed toward expansion of the intravascular and extravascular volume and restoration of renal perfusion. In the absence of cardiac compromise, isotonic saline 0. Subsequent choice for fluid replacement depends on the state of hydration, serum electrolyte levels, and urinary output.
In general, 0. Fluid replacement should correct estimated deficits within the first 24 h. In patients with renal or cardiac compromise, monitoring of serum osmolality and frequent assessment of cardiac, renal, and mental status must be performed during fluid resuscitation to avoid iatrogenic fluid overload 14 — 20 Initial fluid therapy is directed toward expansion of the intravascular and extravascular volume and restoration of renal profusion.
The need for vascular volume expansion must be offset by the risk of cerebral edema associated with rapid fluid administration. The 1st hour of fluids should be isotonic saline 0. Continued fluid therapy is calculated to replace the fluid deficit evenly over 48 h. Therapy should include monitoring mental status to rapidly identify changes that might indicate iatrogenic fluid overload, which can lead to symptomatic cerebral edema 23 — Unless the episode of DKA is mild Table 1regular insulin by continuous intravenous infusion is the treatment of choice.
An initial insulin bolus is not recommended in pediatric patients; a continuous insulin infusion of regular insulin at a dose of 0. Thereafter, the rate of insulin administration or the concentration of dextrose may need to be adjusted to maintain the above glucose values until acidosis in DKA or mental obtundation and hyperosmolarity in HHS are resolved.
Ketonemia typically takes longer to clear than hyperglycemia. Direct measurement of β-OHB in the blood is the preferred method for monitoring DKA. The nitroprusside method only measures acetoacetic acid and acetone.
However, β-OHB, the strongest and most prevalent acid in DKA, is not measured by the nitroprusside method. During therapy, β-OHB is converted to acetoacetic acid, which may lead the clinician to believe that ketosis has worsened.
Therefore, assessments of urinary or serum ketone levels by the nitroprusside method should not be used as an indicator of response to therapy. During therapy for DKA or HHS, blood should be drawn every 2—4 h for determination of serum electrolytes, glucose, blood urea nitrogen, creatinine, osmolality, and venous pH for DKA.
Generally, repeat arterial blood gases are unnecessary; venous pH which is usually 0. With mild DKA, regular insulin given either subcutaneously or intramuscularly every hour is as effective as intravenous administration in lowering blood glucose and ketone bodies Thereafter, 0. Once DKA is resolved, if the patient is NPO, continue intravenous insulin and fluid replacement and supplement with subcutaneous regular insulin as needed every 4 h.
When the patient is able to eat, a multiple-dose schedule should be started that uses a combination of short- or rapid-acting and intermediate- or long-acting insulin as needed to control plasma glucose. Continue intravenous insulin infusion for 1—2 h after the split-mixed regimen is begun to ensure adequate plasma insulin levels.
An abrupt discontinuation of intravenous insulin coupled with a delayed onset of a subcutaneous insulin regimen may lead to worsened control; therefore, some overlap should occur in intravenous insulin therapy and initiation of the subcutaneous insulin regimen. Patients with known diabetes may be given insulin at the dose they were receiving before the onset of DKA or HHS and further adjusted as needed for control.
Finally, some type 2 diabetes patients may be discharged on oral antihyperglycemic agents and dietary therapy. Despite total-body potassium depletion, mild to moderate hyperkalemia is not uncommon in patients with hyperglycemic crises. Insulin therapy, correction of acidosis, and volume expansion decrease serum potassium concentration.
To prevent hypokalemia, potassium replacement is initiated after serum levels fall below 5. Rarely, DKA patients may present with significant hypokalemia.
Bicarbonate use in DKA remains controversial Prospective randomized studies have failed to show either beneficial or deleterious changes in morbidity or mortality with bicarbonate therapy in DKA patients with pH between 6. In patients with a pH of 6. Insulin, as well as bicarbonate therapy, lowers serum potassium; therefore, potassium supplementation should be maintained in intravenous fluid as described above and carefully monitored.
See Fig. Thereafter, venous pH should be assessed every 2 h until the pH rises to 7. See Kitabchi et al. Phosphate concentration decreases with insulin therapy. Prospective randomized studies have failed to show any beneficial effect of phosphate replacement on the clinical outcome in DKA 32and overzealous phosphate therapy can cause severe hypocalcemia with no evidence of tetany 17 No studies are available on the use of phosphate in the treatment of HHS.
Continuous monitoring using a flowsheet Fig. Commonly, patients recovering from DKA develop hyperchloremia caused by the use of excessive saline for fluid and electrolyte replacement and transient non-anion gap metabolic acidosis as chloride from intravenous fluids replaces ketoanions lost as sodium and potassium salts during osmotic diuresis.
These biochemical abnormalities are transient and are not clinically significant except in cases of acute renal failure or extreme oliguria.
Cerebral edema is a rare but frequently fatal complication of DKA, occurring in 0.
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Part 2: ketosis-prone atypical diabetes mellitus. Diabetes Metab. CAS PubMed Google Scholar. Stentz FB, Umpierrez GE, Cuervo R, Kitabchi AE. Proinflammatory cytokines, markers of cardiovascular risks, oxidative stress, and lipid peroxidation in patients with hyperglycemic crises. Stephens JM, Sulway MJ, Watkins PJ. Relationship of blood acetoacetate and 3-hydroxybutyrate in diabetes. Tang H, Li D, Wang T, Zhai S, Song Y. Effect of sodium-glucose cotransporter 2 inhibitors on diabetic ketoacidosis among patients with type 2 diabetes: a meta-analysis of randomized controlled trials. Taylor SI, Blau JE, Rother KI. Common types of crystalloid IV fluids and their composition are listed in Table 2 Small trials evaluated the effect of balanced fluids and 0. They found that balanced crystalloids significantly resulted with a shorter median time for DKA resolution than saline At the same time, it significantly led to a shorter median time for insulin discontinuation than saline 9. They found no significant difference in DKA resolution at 48 hours, ICU, and hospital length of stay. However, PL group had significantly reached more DKA resolution at 24 hours in comparison to 0. In conclusion, designing an appropriate fluid repletion therapy for DKA and HHS management will need careful planning and monitoring for choosing the appropriate fluid type, volume, and rate for the patient. Insulin is considered to be one of the three fundamental elements of DKA and HHS management 2 , 6 , It reduces hepatic glucose synthesis, enhances peripheral glucose utilization, and inhibits lipolysis, ketogenesis, and glucagon secretion, lowering plasma glucose levels and decreasing ketone bodies production 6 , Insulin should be given immediately after the initial fluid resuscitation 2 , 6 , The aim of using insulin in DKA and HHS is to close the anion gap generated by the production of ketone bodies rather than aiming for euglycemia 6 , Intravenous administration of insulin regular mixed in NaCl 0. Insulin can also be used as frequent subcutaneous or intramuscular injections for the treatment of DKA in mild-moderate DKA patients 6 , However, a continuous intravenous insulin regimen is preferred over subcutaneous insulin for DKA management overall due to its short half-life, fast onset, and easy titration 6 , The use of basal insulin analogs in conjunction with regular insulin infusions may speed up the resolution of DKA and minimize rebound hyperglycemia events, resulting in less ICU length of stay and less healthcare cost 6 , Insulin is currently recommended as a continuous infusion at 0. Insulin loading dose has been linked to increasing the risk of cerebral edema and worsening shock Thus, insulin loading dose should be avoided at the beginning of therapy However, an insulin loading dose of 0. Multiple factors must be considered when titrating intravenous insulin continuous infusion 2. The rate of blood glucose reduction, insulin sensitivity, prandial coverage, and NPO status should all be taken into consideration 2. A rapid reduction in BG might be harmful and linked to cerebral edema 2. Moreover, the insulin infusion rate can be increased based on BG around major meals time and can be continued at a higher rate for hours following any major meal 2. Lastly, it is necessary to monitor BG among NPO patients closely. Randomized clinical trials compared the two strategies and found no difference 27 , Intravenous LD insulin administration has been associated with an increased risk of cerebral edema 27 , An acceptable alternative for patients with mild to moderate DKA could be a bolus of 0. Patients with end-stage renal disease ESRD and acute kidney injury AKI are considered a high-risk category that necessitates extra care 32 , To avoid rapid increases in osmolality and hypoglycemia in these patients; it is recommended that insulin infusions begin at 0. Subcutaneous insulin should overlap with intravenous insulin for at least minutes before its discontinuation to ensure the optimal transition of care 6 , A transition to subcutaneous long-acting insulin in addition to ultra-short acting insulin such as glargine and glulisine after resolution of DKA may result in reduced hypoglycemic events compared to other basal bolus regimens such as NPH insulin and insulin regular 24 , For newly diagnosed insulin-dependent diabetes patients, subcutaneous insulin may be started at a dose of 0. The transition process in patients who were previously using insulin or antidiabetic agents before to DKA admission is still unclear 24 , In ICU settings, clinicians tend to hold all oral antidiabetic agents and rely on insulin regimens for in-patient management given the shorter half-life of insulin and its predictability 24 , This could potentially be an area for further investigation on the transition process and its implication on patient outcomes 24 , Insulin sequestering to plastic IV tubing has been described, resulting in insulin wasting and dose inaccuracy 34 , Flushing the IV tube with a priming fluid of 20 mL is adequate to minimize the insulin losses to IV tube 34 , Patients with hyperglycemic crisiss are at a higher risk of developing hypokalemia due to multifactorial process 1 , Insulin therapy, correction of acidosis, and hydration all together lead to the development of hypokalemia 1 , Additionally, volume depletion seen with hyperglycemic crisis leads to secondary hyperaldosteronism, which exacerbates hypokalemia by enhancing urinary potassium excretion 1 , Serum potassium level should be obtained immediately upon presentation and prior to initiating insulin therapy 1 , Potassium replacement is required regardless of the baseline serum potassium level due to hydration and insulin therapy, except among renal failure patients 1 , It is suggested to administer 20 —30 mEq potassium in each liter of intravenous fluid to keep a serum potassium concentration within the normal range 1 , In addition to possible hypokalemia, patients with the hyperglycemic crisis could present with hypophosphatemia 1 , Osmotic diuresis during hyperglycemic crisis increases the urinary phosphate excretion, and insulin therapy enhances intracellular phosphate shift 1 , Phosphate replacement is not a fundamental part of hyperglycemic crisis management, given the lack of evidence of clinical benefit 1 , 29 , A special consideration with phosphate administration is the secondary hypocalcemia 1 , 29 , Acidemia associated with DKA results from the overproduction of ketoacids, generated from the haptic metabolism of free fatty acids. This hepatic metabolism occurs as a result of insulin resistance and an increase in the counterregulatory hormones contributing to the pathophysiology of DKA 37 , Tissue acidosis could lead to impaired myocardial contractility, systemic vasodilatation, inhibition of glucose utilization by insulin, and lowering the levels of 2,3-diphosphoglycerate 2,3-DPG in erythrocytes 37 — Sodium bicarbonate decreases the hemoglobin-oxygen affinity leading to tissue hypoxia; moreover, it is associated with hypernatremia, hypocalcemia, hypokalemia, hypercapnia, prolonged QTc interval, intracellular acidosis, and metabolic alkalosis 39 , The use of adjuvant sodium bicarbonate in the setting of DKA consistently shows a lack of clinical benefit and should be prescribed on a case-by-case basis. Although this recommendation was not supported by solid evidence; many clinicians adopt the practice to avoid the unwanted side effect of severe metabolic acidosis. Sodium bicarbonate moves potassium intracellularly, however, clinical benefit is uncertain, and the use is controversial 41 , Prompt therapy for patients with hyperglycemic crisis is essential in reducing morbidity and mortality 6 , If not treated or treated ineffectively, the prognosis can include serious complications such as seizures, organ failures, coma, and death 6 , When treatment is delayed, the overall mortality rate of HHS is higher than that of DKA, especially in older patients. This difference in prognoses was comparable when patients were matched for age In DKA, prolonged hypotension can lead to acute myocardial and bowel infarction 6 , The kidney plays a vital role in normalizing massive pH and electrolyte abnormalities 6 , Patients with prior kidney dysfunction or patients who developed end-stage chronic kidney disease worsen the prognosis considerably 6 , In HHS, severe dehydration may predispose the patient to complications such as myocardial infarction, stroke, pulmonary embolism, mesenteric vein thrombosis, and disseminated intravascular coagulation 6 , The VTE risk was higher than diabetic patients without hyperglycemic crisis or diabetic acidosis patients Management of hyperglycemic crisis may also be associated with significant complications include electrolyte abnormalities, hypoglycemia, and cerebral edema 7. This is due to the use of insulin and fluid replacement therapy 4 , 5. Therefore, frequent electrolytes and blood glucose concentrations monitoring are essential while insulin infusions and fluid replacements are continued 4 , 5. Cerebral edema is a rare but severe complication in children and adolescents and rarely affects adult patients older than 28 7. This could be due to the lack of cerebral autoregulation, presentation with more severe acidosis and dehydration among children and adolescents The exact mechanism of cerebral edema development is unknown. Some reports suggest that the risk of cerebral edema during hyperglycemic crisis management might be induced by rapid hydration, especially in the pediatric population. However, a recent multicenter study for children with DKA who were randomized to receive isotonic versus hypotonic sodium IV fluid with different infusions rates did not show a difference in neurological outcomes Early identification and prompt therapy with mannitol or hypertonic saline can prevent neurological deterioration from DKA management 7 , Furthermore, higher blood urea nitrogen BUN and sodium concentrations have been identified as cerebral edema risk factors Thus, careful hydration with close electrolytes and BUN is recommended Other serious complications of hyperglycemic crisis may include transient AKI, pulmonary edema in patients with congestive heart failure, myocardial infarction, a rise in pancreatic enzymes with or without acute pancreatitis, cardiomyopathy, rhabdomyolysis in patients presented with severe dehydration 7 , All authors have contributed equally in writing, organizing, and reviewing this publication. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher. Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. Hyperglycemic Crises in Adult Patients With Diabetes. Diabetes Care 32 7 — doi: PubMed Abstract CrossRef Full Text Google Scholar. Goyal A, Mathew UE, Golla KK, Mannar V, Kubihal S, Gupta Y, et al. A Practical Guidance on the Use of Intravenous Insulin Infusion for Management of Inpatient Hyperglycemia. Diabetes Metab Syndrome: Clin Res Rev 15 5 CrossRef Full Text Google Scholar. Saeedi P. 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Oxidative Stress, Insulin Signaling, and Diabetes. Free Radical Biol Med 50 5 — Hoffman WH, Burek CL, Waller JL, Fisher LE, Khichi M, Mellick LB. Cytokine Response to Diabetic Ketoacidosis and Its Treatment. Clin Immunol 3 — Hayami T, Kato Y, Kamiya H, Kondo M, Naito E, Sugiura Y, et al. Case of Ketoacidosis by a Sodium-Glucose Cotransporter 2 Inhibitor in a Diabetic Patient With a Low-Carbohydrate Diet. J Diabetes Investig , 6 5 — Umpierrez GE, Murphy MB, Kitabchi AE. Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar Syndrome. Diabetes Spectr 15 1 Kraut JA, Madias NE. Serum Anion Gap: Its Uses and Limitations in Clinical Medicine. Clin J Am Soc Nephrol 2 1 — Dhatariya K, Savage M, Claydon A, et al. Joint British Diabetes Societies for Inpatient Care JBDS-IP Revised Guidelines. The Management of Diabetic Ketoacidosis in Adults Revised Google Scholar. Kitabchi AE, Umpierrez GE, Murphy MB. Diabetic Ketoacidosis and Hyperosmolar State. In: DeFronzo RA, Ferrannini E, Zimmet P, Alberti KGMM, editors. International Textbook of Diabetes Mellitus. Trachtenbarg DE. Diabetic Ketoacidosis. Am Fam Phys 71 9 — Katz MA. Hyperglycemia-Induced Hyponatremia-Calculation of Expected Serum Sodium Depression. N Engl J Med 16 —4. Rudloff E, Hopper K. Crystalloid and Colloid Compositions and Their Impact. Front Vet Sci Semler MW, Kellum JA. Balanced Crystalloid Solutions. Am J Respir Crit Care Med 8 — Van Zyl DG, Rheeder P, Delport E. QJM 4 — Mahler SA, Conrad SA, Wang H, Arnold TC. Resuscitation With Balanced Electrolyte Solution Prevents Hyperchloremic Metabolic Acidosis in Patients With Diabetic Ketoacidosis. Am J Emerg Med 29 6 —4. Self WH, Evans CS, Jenkins CA, Brown RM, Casey JD, Collins SP, et al. Clinical Effects of Balanced Crystalloids vs Saline in Adults With Diabetic Ketoacidosis: A Subgroup Analysis of Cluster Randomized Clinical Trials. JAMA Netw. 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| Hyperglycemia in diabetes - Symptoms & causes - Mayo Clinic | Article PubMed Google Scholar Deeb A, Yousef H, Abdelrahman L, et Insulin sensitivity and insulin resistance index. L-carnitine and mental focus Hyperglycemic crises Hyperglyceic, diabetic ketoacidosis Hyperglycemi and hyperglycemic hyperosmolar state [HHS] are life-threatening acute complications of diabetes. Early signs and symptoms Recognizing early symptoms of hyperglycemia can help identify and treat it right away. It's important to treat hyperglycemia. Weekly Email. In type 2 diabetes, risk of hyperglycemic crises decreased progressively with age years IRR, 0. |
| Hyperglycemic Crises: Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar State | SpringerLink | Article CAS PubMed Google Scholar Kitabchi AE, Wall BM. Wall, MD. The initial draft of this position statement was prepared by Abbas E. Sobngwi E, Mauvais-Jarvis F, Vexiau P, Mbanya JC, Gautier JF. Diabetes Metab Rev. Fatal cases of cerebral edema have also been reported with HHS. |
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