ISPAD Clinical Practice Hypefglycemic Guidelines Diabetic ketoacidosis and the hyperglycemic hyperosmolar state. In Diabetes in America. Google Scholar. Common triggers of DKA include:.

Hyperglycemic crisis and insulin pump failure -

Skin and soft tissue complications can include any of the following: Local insulin reactions : These are particularly common at the beginning of insulin therapy. Newly diabetic patients can have cutaneous allergic reactions or edema while the body adjusts to the tighter glycemic control provided by the insulin pump.

The majority of these local reactions are harmless and do not require treatment, but can certainly worry patients. These areas are often associated with focal scarring. If lipohypertrophy occurs, patients should be instructed to change insertion site and avoid that area for 3 to 4 weeks to allow healing.

To minimize scarring, the infusion set should be inserted at 90 degrees. Previously scarred areas should be avoided during infusion set placement as they can impair insulin absorption. are often precipitated by poor site preparation before insertion.

If infection occurs, the area should be cleaned and the infusion site should be changed. Abscesses near the insulin pump infusion site should be drained and cultured to guide antibiotic therapy. Diabetic Ketoacidosis Definition : DKA is characterized by the classic triad of hyperglycemia, ketosis, and metabolic acidosis.

It is the result of a relative or absolute deficiency of insulin, and an excess of counter-regulatory hormones, resulting in hyperglycemia.

Hyperglycemic crises can be classified as either DKA or Hyperglycemic Hyperosmolar State HSS , however, HSS rarely presents as an acute complication of insulin pump therapy.

Less commonly, DKA can result from inadequate site changes and impaired insulin absorption. Management in Setting of Insulin Pump: Turn off the pump once IV access is established! Premature insulin administration can precipitate hypokalemia due to intracellular shifts.

Make sure the pump is completely shut down and turned to OFF. It is typically not necessary to remove the insertion needle in the acute setting, as doing so may result in misplacement or damage of the pump. Begin insulin at a continuous infusion rate of 0. The use of a correctional sliding insulin scale as sole therapy is associated with worse glycemic control.

However, it is important to allow a hour overlap between IV therapy and administration of subcutaneous therapy to prevent rebound hyperglycemia and complication. Severe hypoglycemia is a common occurrence of insulin pump therapy in Type 1 Diabetes, and to a lesser extent Type 2 Diabetes.

Type 1 Diabetics are completely dependent on exogenous insulin for glycemic control, but over time also lose the ability to effectively release glucagon and other regulatory hormones.

The result is that episodes of hypoglycemia beget more episodes. This can decrease the symptom severity, masking hypoglycemia and increasing the risk for hypoglycemic episodes to develop into severe events.

This is defined as the onset of neuroglycopenia before the appearance of sympathoadrenal symptoms. Give the patient 15 grams of oral carbohydrates half a cup of apple juice, half a sandwich, or 4 or 5 pieces of hard candies and check the serum glucose after 15 minutes.

Repeat as necessary. Monitor frequently! Insulin pump users should monitor their blood glucose levels before and after meals, before and after exercise, and before bed at a minimum.

Infusion site failures increase after 3 days of catheter use. Patients should check with their insurance to see if replacement parts are covered. Pumps are not a replacement for a functioning pancreas. Patients still need to exercise careful glucose intake and make appropriate dosing adjustments per a pre-set plan.

Upon resolution of DKA or hypoglycemia the patient should meet with the clinician managing their diabetes as an outpatient to fine tune their therapy program. Many community health systems have offered training programs and local support for insulin pump users. Future of Insulin Pumps Many insulin pumps on the market today are associated with a glucometer or continuous glucose monitor CGM.

However, closed loop systems still have limitations, including delays in response times, accurate signal feedback, software malfunctions, high cost, and user errors. Bedtime infusion complications are the most common culprit for both DKA and hypoglycemia.

Recurrent hypoglycemia blunts the normal counterregulatory response in patients with type 1 DM and can mask the early warning signs of hypoglycemic episodes. Careful blood glucose monitoring is key in the setting of insulin pumps!

Patient education is essential for prevention of insulin pump complications. Review of Evidence for Adult Diabetic Ketoacidosis Management Protocols. Front Endocrinol Lausanne. Published Jun Insulin Pump Class: Back to the Basics of Pump Therapy Diabetes Spectrum ; vol.

Pickup, JC. Insulin-pump therapy for type 1 diabetes mellitus. New England Journal of Medicine. Joseph, Josh. Endocrine-Metabolic, ALiEM. Chiang JL, Kirkman MS, Laffel LM, Peters AL, Type 1 Diabetes Sourcebook Authors. Type 1 diabetes through the life span: a position statement of the American Diabetes Association.

Diabetes Care. Hayek A, Robert A, Al Dawish M. Skin-Related Complications Among Adolescents With Type 1 Diabetes Using Insulin Pump Therapy.

Endocrinology and Diabetes. Ross P, Milburn J, Reith D, Wheeler B Clinical review: insulin pump-associated adverse events in adults and children. Acta Diabetol ; Saboo BD, Talaviya PA. Continuous subcutaneous insulin infusion: practical issues.

Indian J Endocrinol Metab. Kessinger H, Knezevich E, DeSimone E, Davidian M. Pumping it up: new advancements in insulin delivery.

Pharmacist Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. Hyperglycemic crises in adult patients with diabetes. Laufgraben M, Kaufman S. Acute Diabetic Emergencies, Glycemic Control, and Hypoglycemia. Critical Care Medicine: Principles of Diagnosis and Management in the Adult.

Wolfsdorf JI, Glaser N, Agus M, et al. ISPAD Clinical Practice Consensus Guidelines Diabetic ketoacidosis and the hyperglycemic hyperosmolar state. Pediatr Diabetes. Tsai SH, Lin YY, Hsu CW, Cheng CS, Chu DM.

Hypoglycemia revisited in the acute care setting. Yonsei Med J. Martín-Timón I, Del Cañizo-Gómez FJ. Mechanisms of hypoglycemia unawareness and implications in diabetic patients.

World J Diabetes. Drugs that affect carbohydrate metabolism, such as corticosteroids, thiazides, and sympathomimetic agents e. Factors that may lead to insulin omission in younger patients include fear of weight gain with improved metabolic control, fear of hypoglycemia, rebellion from authority, and the stress of chronic disease.

Before , the use of continuous subcutaneous insulin infusion devices had also been associated with an increased frequency of DKA 22 , but with improvement in technology and better education of patients, the incidence of DKA appears to have reduced in pump users.

However, additional prospective studies are needed to document reduction of DKA incidence with the use of continuous subcutaneous insulin infusion devices During the past decade, an increasing number of DKA cases without precipitating cause have been reported in children, adolescents, and adult subjects with type 2 diabetes.

Observational and prospective studies indicate that over half of newly diagnosed adult African-American and Hispanic subjects with unprovoked DKA have type 2 diabetes 24 — In such patients, clinical and metabolic features of type 2 diabetes include a high rate of obesity, a strong family history of diabetes, a measurable pancreatic insulin reserve, low prevalence of autoimmune markers of β-cell destruction, and the ability to discontinue insulin therapy during follow-up 28 , This variant of type 2 diabetes has been referred to in the literature as idiopathic type 1 diabetes, atypical diabetes, Flatbush diabetes, type 1.

At presentation, they have markedly impaired insulin secretion and insulin action 25 , 26 , 29 , but aggressive management with insulin significantly improves β-cell function, allowing discontinuation of insulin therapy within a few months of follow-up 25 — Furthermore, a novel genetic mechanism related to the high prevalence of glucosephosphate dehydrogenase deficiency has been linked with ketosis-prone diabetes The process of HHS usually evolves over several days to weeks, whereas the evolution of the acute DKA episode in type 1 diabetes or even in type 2 diabetes tends to be much shorter.

The classic clinical picture of patients with DKA includes a history of polyuria, polydipsia, weight loss, vomiting, abdominal pain, dehydration, weakness, mental status change, and coma. Physical findings may include poor skin turgor, Kussmaul respirations, tachycardia, hypotension, alteration in mental status, shock, and ultimately coma.

Mental status can vary from full alertness to profound lethargy or coma, with the latter more frequent in HHS. Although infection is a common precipitating factor for both DKA and HHS, patients can be normothermic or even hypothermic primarily because of peripheral vasodilation Severe hypothermia, if present, is a poor prognostic sign.

The abdominal pain usually resolves with correction of hyperglycemia and metabolic acidosis. The most common clinical presentation in patients with HHS is altered sensorium 4 , 8 , 11 , Physical examination reveals signs of dehydration with loss of skin turgor, weakness, tachycardia, and hypotension.

Fever due to underlying infection is common, and signs of acidosis Kussmaul breathing, acetone breath are usually absent. In some patients, focal neurologic signs hemiparesis, hemianopsia and seizures partial motor seizures more common than generalized may be the dominant clinical features 1 , 4 , 6 , 8.

The initial laboratory evaluation of patients with suspected DKA or HHS should include determination of plasma glucose, blood urea nitrogen, creatinine, serum ketones, electrolytes with calculated anion gap , osmolality, urinalysis, urine ketones by dipstick, as well as initial arterial blood gases and complete blood count with differential.

An electrocardiogram, chest X-ray, and urine, sputum, or blood cultures should also be obtained, if clinically indicated. 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.

The diagnostic criteria for DKA and HHS are shown in Table 1. DKA consists of the biochemical triad of hyperglycemia, ketonemia, and metabolic acidosis. Accumulation of ketoacids results in an increased anion gap metabolic acidosis.

The severity of DKA is classified as mild, moderate, or severe based on the severity of metabolic acidosis blood pH, bicarbonate, ketones and the presence of altered mental status 1. Significant overlap between DKA and HHS has been reported in more than one-third of patients 1 , 2 , The majority of patients with hyperglycemic emergencies present with leukocytosis proportional to blood ketone body concentration 2 , The admission serum sodium is usually low because of the osmotic flux of water from the intracellular to the extracellular space in the presence of hyperglycemia.

An increase in serum sodium concentration in the presence of hyperglycemia indicates a rather profound degree of water loss. Unless the plasma is cleared of chylomicrons, pseudonormoglycemia and pseudohyponatremia may occur in DKA 37 , Serum potassium concentration may be elevated because of an extracellular shift of potassium caused by insulin deficiency, hypertonicity, and acidemia 3 , 10 , 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.

The classic work of Atchley et al. Studies on serum osmolality and mental alteration have established a positive linear relationship between osmolality and mental obtundation 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.

Finally, abnormal acetoacetate levels may falsely elevate serum creatinine if the clinical laboratory uses a colorometric method for the creatinine assay 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.

A clinical history of previous drug abuse 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 10 , A recent report 44 suggested a relationship between low carbohydrate dietary intake and metabolic acidosis.

Finally, four case reports have shown that patients with undiagnosed acromegaly may present with DKA as the primary manifestation of their disease 45 — 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.

Protocols for the management of patients with DKA and HHS are summarized in Figs. Initial fluid therapy is directed toward expansion of the intravascular and extra vascular volume and restoration of renal perfusion. In the absence of cardiac compromise, isotonic saline 0. The subsequent choice for fluid replacement depends on the state of hydration, serum electrolyte levels, and urinary output.

In general, 0. Successful progress with fluid replacement is judged by hemodynamic monitoring improvement in blood pressure , measurement of fluid input and output, laboratory values, and clinical examination. 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 1 , 3 , 4 , 10 , 12 , 16 , Adequate rehydration with subsequent correction of the hyperosmolar state has been shown to result in a more robust response to low-dose insulin therapy If plasma glucose does not decrease by 50—75 mg from the initial value in the first hour, the insulin infusion may be doubled every hour until a steady glucose decline is achieved.

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 hyperosmolality in HHS are resolved. Prospective and randomized studies have reported on the efficacy and cost effectiveness of subcutaneous rapid-acting insulin analogs in the management of patients with uncomplicated DKA.

Patients treated with subcutaneous rapid-acting insulin received an initial injection of 0. There were no differences in length of hospital stay, total amount of insulin administration until resolution of hyperglycemia or ketoacidosis, or number of hypoglycemic events among treatment groups.

In addition, the use of insulin analogs allowed treatment of DKA in general wards or in the emergency department, avoiding admission to an intensive care unit.

Ketonemia typically takes longer to clear than hyperglycemia. Direct measurement of β-OHB in the blood is the preferred method for monitoring DKA and has become more convenient with the recent development of bedside meters capable of measuring whole-blood β-OHB The nitroprusside method, which is used in clinical chemistry laboratories, 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 during the treatment of DKA in hemodynamically stable patients.

Since venous pH is only 0. When the patient is able to eat, a multiple-dose insulin 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.

Intravenous insulin infusion should be continued for 1—2 h after the subcutaneous insulin is given 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 hyperglycemia or recurrence of ketoacidosis.

If the patient is to remain n. Patients with known diabetes may be given insulin at the dose they were receiving before the onset of DKA or HHS. In insulin-naïve patients, a multidose insulin regimen should be started at a dose of 0.

However, good clinical judgment and frequent glucose assessment are vital in initiating a new insulin regimen in insulin-naïve patients. Despite total-body potassium depletion 40 , 57 , mild to moderate hyperkalemia is not uncommon in patients with hyperglycemic crises.

Insulin therapy, correction of acidosis, and volume expansion decrease serum potassium concentration. Rarely, DKA patients may present with significant hypokalemia. Bicarbonate use in DKA remains controversial However, the administration of bicarbonate may be associated with several deleterious effects including an increased risk of hypokalemia 59 , decreased tissue oxygen uptake, and cerebral edema 60 , A prospective randomized study in 21 patients failed to show either beneficial or deleterious changes in morbidity or mortality with bicarbonate therapy in DKA patients with an admission arterial pH between 6.

The average pH in the bicarbonate group was 7. Therefore, if the pH is 6. Bicarbonate as well as insulin therapy lowers serum potassium; therefore, potassium supplementation should be maintained in the 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 reference 1 for further review. Despite whole-body phosphate deficits in DKA that average 1. Phosphate concentration decreases with insulin therapy.

Prospective randomized studies 63 , 64 have failed to show any beneficial effect of phosphate replacement on the clinical outcome in DKA, and overzealous phosphate therapy can cause severe hypocalcemia 63 , Therefore, the routine use of phosphate in the treatment of DKA or HHS has resulted in no clinical benefit to the patient The most common complications of DKA and HHS include hypoglycemia and hypokalemia due to overzealous treatment with insulin.

Low potassium may also occur as a result of treatment of acidosis with bicarbonate. Commonly, patients recovering from DKA develop a transient hyperchloremic non—anion gap acidosis 68 — The hyperchloremic acidosis is caused by the loss of large quantities of ketoanions that occur during the development of DKA.

Because ketoanions are metabolized with regeneration of bicarbonate, the prior loss of ketoacid anions in the urine hinders regeneration of bicarbonate during treatment Other mechanisms include the administration of intravenous fluids containing chloride that exceeds the plasma chloride concentration and the intracellular shifts of NaHCO 3 during correction of DKA 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 72 — Fatal cases of cerebral edema have also been reported with HHS.

Clinically, cerebral edema is characterized by deterioration in the level of consciousness, lethargy, decreased 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 may result from osmotically driven movement of water into the central nervous system when plasma osmolality declines too rapidly with the treatment of DKA or HHS 72 — However, a recent study 75 using magnetic resonance imaging to assess cerebral water diffusion and cerebral vascular perfusion during the treatment of 14 children with DKA found that the cerebral edema was not a function of cerebral tissue edema but rather a function of increased cerebral perfusion.

There is a lack of information on the morbidity associated with cerebral edema in adult patients; therefore, any recommendations for adult patients are based on clinical judgment 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 and Hispanics 2 , 76 , 77 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- or rapid-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 caregivers 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. Based on an annual average of , hospitalizations for DKA in the U.

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 earlier.

This has been shown to decrease the incidence of DKA at the onset of diabetes A recent study from a city hospital reports that active cocaine use is an independent risk factor for recurrent DKA Protocol for the management of adult patients with DKA.

Normal laboratory values vary; check local lab normal ranges for all electrolytes. Begin 1 liter of 0. Obtain electrocardiogram, chest X-ray, and specimens for bacterial cultures, as needed. Adapted from ref. Protocol for the management of adult patients with HHS. Diagnostic criteria and typical total body deficits of water and electrolytes in DKA and HHS.

Per kg body wt. Data adapted from refs. Studies cited by the authors were supported in part by USPHS grants RR to the General Clinical Research Center and AM , training grant AM of the National Institutes of Health, and grants from Novo-Nordisk, Eli Lilly, the American Diabetes Association, and the Abe Goodman Fund.

The initial draft of this position statement was prepared by the authors as listed above. The manuscript was then peer-reviewed, modified, and approved by the Professional Practice Committee and the Executive Committee, March The recommendations in this article are based on the evidence reviewed in the following publication: Management of hyperglycemic crises in patients with diabetes Technical Review.

Diabetes Care —, , as well as subsequent peer-reviewed publications since A table elsewhere in this issue shows conventional and Système International SI units and conversion factors for many substances.

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NOTE ADDED IN PROOF—. Article Information. Article Navigation. Hyperglycemic Crises in Adult Patients With Diabetes : A consensus statement from the American Diabetes Association Abbas E. Kitabchi, PHD, MD ; Abbas E. Kitabchi, PHD, MD.

This Site. Google Scholar. Guillermo E. Umpierrez, MD ; Guillermo E. Umpierrez, MD. Mary Beth Murphy, RN, MS, CDE, MBA ; Mary Beth Murphy, RN, MS, CDE, MBA. Robert A. Kreisberg, MD Robert A. Kreisberg, MD. Address correspondence and reprint requests to Dr.

Kitabchi, Director, Division of Endocrinology, Diabetes and Metabolism, University of Tennessee Health Science Center, Court Ave.

E-mail: akitabchi utmem. Diabetes Care ;29 12 —

A Vegan Mexican dishes criss is a failuree disorder that causes unconsciousness. If you have diabetes, dangerously high Vegan Mexican dishes sugar Cauliflower and black bean tacos or dangerously low crisid sugar hypoglycemia can lead to a diabetic coma. If you go into a diabetic coma, you're alive — but you can't wake up or respond purposefully to sights, sounds or other types of stimulation. If it's not treated, a diabetic coma can result in death. The idea of a diabetic coma can be scary, but you can take steps to help prevent it.

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Diabetic Ketoacidosis (DKA) \u0026 Hyperglycemic Hyperosmolar Syndrome (HHS)