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Hyperglycemic crisis and insulin pump failure

Hyperglycemic crisis and insulin pump failure

In addition, new-onset type 1 Hyperglyceimc or discontinuation of insulin in established type 1 diabetes commonly leads to the development of DKA. Sign in to annotate. Signs and Symptoms.

Hyperglycemic crisis and insulin pump failure -

K — Check for Ketones I — Give Insulin by Injection using an insulin pen or syringe — not through the pump S — Change the infusion Set S — Check blood Sugar.

If you have elevated ketones, insulin replacement must be delivered via an injection with an insulin pen or insulin syringe instead of the pump because the pump or infusion set may be malfunctioning and causing ketones to develop.

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. com Go to Settings , click My Devices, click View Settings , click Save Report Omnipod: my.

com Go to Create PDF report , click Devices , click Create PDF Medtronic: carelink. com Go to Reports , click Device Settings , click Generate Reports Without insulin, you may develop diabetic ketoacidosis DKA and need hospitalization.

The number of units will equal your total amount of daily basal insulin. The basic metabolic profile was monitored every 4 h, and serum glucose levels were checked every hour.

When her serum carbon dioxide levels were greater than or equal to 18 and her anion gap was less than 12, her insulin drip was switched off, and she was placed on long-acting insulin. Patient was discharged to home on long-acting and short-acting insulin and was advised to get her insulin pump fixed on her next appointment with her endocrinologist.

On physical examination at the time of admission, she had mild suprapubic tenderness, and her mucous membranes were dry. There was no renal angle tenderness, and the rest of the physical examination was normal. A working diagnosis of urinary tract infection was made, and a routine blood work-up was done, the results of which are given in Table 2.

Since clinical dehydration was out of proportion to the symptoms, based on our previous experiences with T1DM patients, we decided to evaluate the patient for DKA, and this revealed the patient to be suffering from concomitant EDKA secondary to urinary tract infection, starving and severe dehydration.

The urine analysis confirmed urinary tract infection, and the blood investigations revealed hemoconcentration, pre-renal failure, sepsis and partially compensated increased anion gap metabolic acidosis.

In both our patients, other causes of metabolic acidosis were excluded by testing for urine toxicology screen, blood salicylate, acetaminophen, lactic acid and alcohol levels, which were all within the normal limits.

There was no known ingestion of toxic substances in these patients. No history of SGLT-2 inhibitors usage in the above patients. She was treated with 5L of bolus IV normal saline to reverse the dehydration and was started on insulin drip according to the protocol for her blood glucose levels.

She was treated with IV ceftriaxone for her UTI. Her anion gap closed slowly and her acidosis resolved. Patient was started back on her regular insulin regimen with insulin glargine and insulin aspart and was discharged home. Glycemic control is achieved in our human body using a balance between the insulin levels and the levels of counter-regulatory hormones like glucagon, growth hormone, glucocorticoids and epinephrine.

DKA occurs when there is either a decrease in insulin or when there is an excess of counter-regulatory hormones both of which causes hyperglycemia.

Though there is hyperglycemia, the end organs are unable to utilize the available glucose due to the comparative lack of insulin, and this leads to lipolysis thereby leading to excessive production of ketone bodies 4. However, in this case series, we have reported 2 cases where there is DKA but no hyperglycemia.

The underlying mechanism of EDKA is either due to decreased hepatic production of glucose during fasting state or enhanced urinary excretion of glucose induced by an excess of counter-regulatory hormones, the former being the most common reason.

Thus, when a diabetic patient is exposed to any triggering factor for DKA and is fasting or starving while continuing the insulin treatment regularly, the liver will be in a state of glycogen depletion, thereby producing a lesser amount of glucose.

On the other hand, there will be lipolysis and fatty acid production, which finally leads to excessive ketone body production 3. Some of the common causes of EDKA that have been reported in literature so far are low caloric intake, fasting or starvation 5 , pregnancy 6 , pancreatitis 7 , cocaine intoxication, prolonged vomiting or diarrhea 8 , insulin pump use 9 and of late use of SGLT2 inhibitors like empagliflozin, canagliflozin and so forth Both our patients were type 1 diabetes mellitus patients on insulin therapy.

Burge et al had reported in their study that short-term fasting is a well-known mechanism of developing euglycemic ketoacidosis when there is insulin deficiency in type I diabetic patients They also subsequently went ahead to describe how dehydration can accelerate the development of DKA during periods of insulin deficiency.

Dehydration usually promotes the development of hyperglycemia. However, it is interesting to note its differential role in EDKA. Fasting primarily increases the secretion of counter-regulatory hormones especially the glucagon, which depletes the glycogen stores in the liver.

Dehydration acts as a stimulus for further glucagon secretion, which results in lipolysis and ketone body production in the background of decreased glucose production leading to EDKA. During insulin deficiency, dehydration also increases the secretion of other counter-regulatory hormones like catecholamines and cortisol, which further worsens EDKA In the case of our second patient, urinary tract infection in conjunction with nausea due to the infection caused a decreased calorie intake and led to ketoacidosis with euglycemia.

This is a classic presentation of EDKA. Diagnosis of EDKA is difficult as it is primarily a diagnosis of exclusion. Other forms of ketoacidosis like starvation ketoacidosis has to be ruled out. Also, other causes of increased anion gap metabolic acidosis like lactic acidosis, increased toxic serum alcohols methanol, ethylene glycol, etc.

Once diagnosed, management of EDKA is simple and is almost similar to the management of DKA. The mainstay of treatment involves rapid correction of dehydration using intravenous fluids The second most important step in the management is the use of insulin drip along with a dextrose containing solution until the anion gap, and bicarbonate levels normalize Periodic checking of urine for ketones and arterial blood gas analysis to estimate anion gap are warranted till the values normalize Here, we presented two patients diagnosed with euglycemic diabetic ketoacidosis both of whom were on regular insulin therapy.

Early detection and management are warranted as this condition may else prove fatal. It is best advised that the clinicians are aware of the possible etiological triggers of EDKA in susceptible patients and actively rule out other differentials thereby minimizing the time required for diagnosing EDKA.

If diagnosed early and management aggressively with fluids and insulin drip, EDKA may be easily reversed, thus minimizing morbidity and mortality. The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research reported.

This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors. Study design, drafting by P R, critical revisions and final approval by P R, A R V, S S B and J P R.

Metabolism 65 — BMJ 2 — Diabetes Care 32 — Laffel L Ketone bodies: a review of physiology, pathophysiology and application of monitoring to diabetes. Journal of General Internal Medicine 24 — Journal of Perinatology 28 — Endocrine Practice 1 e88 — e Case Reports in Critical Care Article ID: Current Diabetes Reviews 13 — Journal of Clinical Endocrinology and Metabolism 76 — Metabolism 50 — Diabetes Care 38 — Endocrinology, Diabetes and Metabolism Case Reports is committed to supporting researchers in demonstrating the impact of their articles published in the journal.

Diabetic ketoacidosis DKA continues to have high rates Hyperglycemic crisis and insulin pump failure ihsulin and mortality despite advances in the treatment Ginseng for stress relief diabetes Metabolism boosting drinks. In Hyperglycemic crisis and insulin pump failure study of 4, Hypergljcemic Belly fat reduction supplements DKA, 14 percent occurred Hyperblycemic persons older pumo 70 years, 23 percent in persons 51 to 70 years of ffailure, 27 percent Hyperglycemjc persons 30 to 50 years of age, and 36 percent in persons younger than 30 years. Although persons with DKA typically have a history of diabetes, 27 to 37 percent have newly diagnosed diabetes. Most persons with DKA have type 1 diabetes. There is also a subgroup of persons with type 2 diabetes who have ketosis-prone diabetes; this subgroup represents 20 to 50 percent of persons with DKA. DKA results from insulin deficiency from new-onset diabetes, insulin noncompliance, prescription or illicit drug use, and increased insulin need because of infection Table 1. Without the ability to use glucose, the body needs alternative energy sources. Hyperglycemic crisis and insulin pump failure

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