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. Elevated hepatic transaminase levels may occur, especially in persons with fatty liver disease. Figure 1 4 , 29 provides the treatment approach for DKA in adults, and Figure 2 24 , 30 provides the treatment approach for DKA in persons younger than 20 years.

Both approaches are recommended by the American Diabetes Association. Specific issues for the adult patient are discussed in more detail below. For persons younger than 20 years, insulin should be administered gradually, and fluid and electrolyte replacement should be done cautiously because of limited data and concern for precipitating cerebral edema.

After determining the level of dehydration, intravenous fluid replacement should be started. In most persons, saline 0. Fluid status, cardiac status, urine output, blood pressure, and electrolyte level should be monitored.

As the patient stabilizes, fluids can be lowered to 4 to 14 mL per kg per hour, or to mL per hour. Once the corrected sodium concentration is normal or high greater than mEq per L [ mmol per L] , the solution can be changed to saline 0. Dextrose is added when the glucose level decreases to mg per dL To further correct hyperglycemia, insulin should be added to intravenous fluids one to two hours after fluids are initiated.

An initial bolus of 0. Glucose level should decrease by about 50 to 70 mg per dL 2. Physiologic and clinical outcomes were identical in all three groups. DKA is resolved when the glucose level is less than mg per dL, the pH is greater than 7. Once these levels are achieved and oral fluids are tolerated, the patient can be started on an insulin regimen that includes an intermediate- or long-acting insulin and a short- or rapid-acting insulin.

When intravenous insulin is used, it should remain in place for one to two hours after subcutaneous insulin is initiated. Persons known to have diabetes can be started on their outpatient dose, with adjustments to improve control.

Those new to insulin should receive 0. Although potassium is profoundly depleted in persons with DKA, decreased insulin levels, acidosis, and volume depletion cause elevated extracellular concentrations. Potassium levels should be monitored every two to four hours in the early stages of DKA.

Hydration alone will cause potassium to drop because of dilution. Improved renal perfusion will increase excretion. Insulin therapy and correction of acidosis will cause cellular uptake of potassium. If the potassium level is in the normal range, replacement can start at 10 to 15 mEq potassium per hour.

During treatment of DKA, the goal is to maintain serum potassium levels between 4 and 5 mEq per L 4 and 5 mmol per L. If the potassium level is between 3. If the potassium level is lower than 3.

If the potassium level is greater than 5. When the potassium level is between 3. Clinical trials are lacking to determine which is best, although in the face of phosphate depletion, potassium phosphate is used.

Bicarbonate therapy in persons with DKA is somewhat controversial. Proponents believe that severe acidosis will cause cardiac and neurologic complications. However, studies have not demonstrated improved clinical outcomes with bicarbonate therapy, and treatment has been associated with hypokalemia.

In one retrospective quasi-experimental study of 39 persons with DKA and a pH between 6. Current American Diabetes Association guidelines continue to recommend bicarbonate replacement in persons with a pH lower than 6.

This should be repeated every two hours until the patient's pH is 6. Phosphate levels may be normal to elevated on presentation, but decline with treatment as the phosphate enters the intracellular space.

Studies have not shown a benefit from phosphate replacement, and it can be associated with hypocalcemia and hypomagnesemia. However, because phosphate deficiency is linked with muscle fatigue, rhabdomyolysis, hemolysis, respiratory failure, and cardiac arrhythmia, replacement is recommended when the phosphate level falls below 1.

This can be achieved by adding 20 to 30 mEq of potassium phosphate to the intravenous fluid. DKA can cause a drop in magnesium, which can result in paresthesia, tremor, muscle spasm, seizures, and cardiac arrhythmia.

It should be replaced if it falls below 1. Cerebral edema is the most severe complication of DKA. It occurs in 0. Other complications of DKA include hypokalemia, hypoglycemia, acute renal failure, and shock.

Less common problems can include rhabdomyolysis, 41 thrombosis and stroke, 42 pneumomediastinum, 43 prolonged corrected QT interval, 44 pulmonary edema, 45 and memory loss with decreased cognitive function in children.

Physicians should recognize signs of diabetes in all age groups, and should educate patients and caregivers on how to recognize them as well eTable A. In one study, persons with DKA had symptoms of diabetes for This includes more frequent glucose monitoring; continuing insulin, but at lower doses, during times of decreased food intake; and checking urine ketone levels with a dipstick test if the glucose level is greater than mg per dL Nonadherence to medical regimens is often the cause of recurrent DKA.

Physicians need to recognize patient barriers to getting care, such as financial, social, psychological, and cultural reasons. Diabetes education with certified educators and pharmacists enhances patient care. Data Sources: In July , an initially broad search of PubMed, Essential Evidence Plus, and sources such as the Cochrane database and Clinical Evidence was conducted using the key term diabetic ketoacidosis.

In the fall of , another search was conducted using additional key terms, such as incidence and prevalence. As information was collected, individual questions were then searched to add finer points to the documentation.

The searches were repeated with each draft of the manuscript. Henriksen OM, Røder ME, Prahl JB, Svendsen OL. Diabetic ketoacidosis in Denmark incidence and mortality estimated from public health registries. Diabetes Res Clin Pract. Fritsch M, Rosenbauer J, Schober E, Neu A, Placzek K, Holl RW.

German Competence Network Diabetes Mellitus and the DPV Initiative. Predictors of diabetic ketoacidosis in children and adolescents with type 1 diabetes. Experience from a large multicentre database. Pediatr Diabetes. Wang J, Williams DE, Narayan KM, Geiss LS. Declining death rates from hyperglycemic crisis among adults with diabetes, U.

Diabetes Care. Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. Hyperglycemic crisis in adult patients with diabetes. Schober E, Rami B, Waldhoer T Austrian Diabetes Incidence Study Group.

Diabetic ketoacidosis at diagnosis in Austrian children in — a population-based analysis. Westphal SA. The occurrence of diabetic ketoacidosis in non-insulin-dependent diabetes and newly diagnosed diabetic adults. Am J Med. Kim MK, Lee SH, Kim JH, et al.

Clinical characteristics of Korean patients with new-onset diabetes presenting with diabetic ketoacidosis. Balasubramanyam A, Nalini R, Hampe CS, Maldonado M. Syndromes of ketosis-prone diabetes mellitus. Endocr Rev. Umpierrez GE, Smiley D, Kitabchi AE.

Narrative review: ketosis-prone type 2 diabetes mellitus. Ann Intern Med. Wilson DR, D'Souza L, Sarkar N, Newton M, Hammond C.

New-onset diabetes and ketoacidosis with atypical antipsychotics. Schizophr Res. Ragucci KR, Wells BJ. Olanzapine-induced diabetic ketoacidosis. Ann Pharmacother. Mithat B, Alpaslan T, Bulent C, Cengiz T.

Risperidone-associated transient diabetic ketoacidosis and diabetes mellitus type 1 in a patient treated with valproate and lithium. Nyenwe EA, Loganathan RS, Blum S, et al.

Active use of cocaine: an independent risk factor for recurrent diabetic ketoacidosis in a city hospital. Endocr Pract. Yan L. Nephrol News Issues. Can J Diabetes. Hyperglycemic Crises: Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar State.

In: Feingold KR, Anawalt B, Boyce A, Chrousos G, de Herder WW, Dhatariya K, Dungan K, Grossman A, Hershman JM, Hofland J, Kalra S, Kaltsas G, Koch C, Kopp P, Korbonits M, Kovacs CS, Kuohung W, Laferrère B, McGee EA, McLachlan R, Morley JE, New M, Purnell J, Sahay R, Singer F, Stratakis CA, Trence DL, Wilson DP, editors.

Endotext [Internet]. South Dartmouth MA : MDText. com, Inc. Controversies in the management of hyperglycaemic emergencies in adults with diabetes.

Management of Hyperglycemic Crises: Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar State. Med Clin North Am. Review of Evidence for Adult Diabetic Ketoacidosis Management Protocols. Front Endocrinol Lausanne. Euglycemic diabetic ketoacidosis: a diagnostic and therapeutic dilemma.

Endocrinol Diabetes Metab Case Rep. Diabetic ketoacidosis. Nat Rev Dis Primers. Evaluation and Management of the Critically Ill Adult With Diabetic Ketoacidosis. J Emerg Med. Diabetic ketoacidosis: A consensus statement of the Italian Association of Medical Diabetologists AMD , Italian Society of Diabetology SID , Italian Society of Endocrinology and Pediatric Diabetoloy SIEDP.

Nutr Metab Cardiovasc Dis. Clinical Effects of Balanced Crystalloids vs Saline in Adults With Diabetic Ketoacidosis: A Subgroup Analysis of Cluster Randomized Clinical Trials. JAMA Netw Open. Euglycemic diabetic ketoacidosis: Etiologies, evaluation, and management.

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Dec 10th, Joel Hamm categories: practice updates. Initial vitals: T Background The utilization of insulin pumps, or continuous subcutaneous insulin infusion CSII , has been on the rise for the management of both Type 1 and Type 2 Diabetes.

Complications from Insulin Pump Therapy The most common complications of insulin pump therapy involve the skin and soft tissue. 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. Ketoacidosis is a medical emergency that requires immediate medical attention. Always carry an insulin vial and syringe or an insulin pen with needle for backup.

Speak with your doctor and have a backup plan in case of pump malfunction. Self assessment quizzes are available for topics covered in this website.

To find out how much you have learned about Insulin Pumps , take our self assessment quiz when you have completed this section. The quiz is multiple choice. Please choose the single best answer to each question. At the end of the quiz, your score will display.

All rights reserved. University of California, San Francisco About UCSF Search UCSF UCSF Medical Center. Clin Cardiol. Mazer M, Chen E.

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search close. PREV Mar 1, NEXT. C 19 Serum ketone level should be used in the diagnosis and management of DKA. C 22 Subcutaneous insulin can be used for treatment of uncomplicated DKA. C 29 , 32 Bicarbonate therapy has not been shown to improve outcomes in persons with DKA, but is recommended by consensus guidelines for persons with a pH less than 6.

Diabetic ketoacidosis in infants, children, and adolescents: A consensus statement from the American Diabetes Association. Copyright American Diabetes Association. Additional information from reference Hyperglycemic crisis in diabetes.

PHOSPHATE AND MAGNESIUM. eTable A. Vanelli M, Chiari G, Ghizzoni L, Costi G, Giacalone T, Chiarelli F. Effectiveness of a prevention program for diabetic ketoacidosis in children. org Sick day management A7 Early contact with clinician Insulin reduction rather than elimination Measurement of urine or serum ketone level Backup insulin protocol in case of insulin pump failure Psychological counseling for those who eliminate insulin for body image concerns, and those who have major depression or other psychological illnesses that interfere with proper management Disparities in care Assess reasons for discontinuation of insulin e.

DYANNE P. At the time this article was written, she was chief of Family and Community Medicine at Cooper University Hospital, and vice chair of Family Medicine and Community Health at Robert Wood Johnson Medical School in Camden.

Westerberg, DO, FAAFP, Cooper University Hospital, Haddon Ave. Trachtenbarg DE. Am Fam Physician. Continue Reading. More in AFP. More in Pubmed.