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 Table of Contents  
CASE REPORT
Year : 2017  |  Volume : 8  |  Issue : 3  |  Page : 92-93

Closing anion gap without insulin in euglycaemic diabetic ketoacidosis


1 Department of Internal Medicine, Western Reserve Health Education, Youngstown, OH, USA
2 Department of Public Health, Institute of Medicine, Kathmandu, Nepal

Date of Web Publication29-Dec-2017

Correspondence Address:
Resham Raj Poudel
Department of Internal Medicine, Western Reserve Health Education, Youngstown, OH
USA
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jod.jod_26_17

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  Abstract 


Euglycaemic diabetic ketoacidosis (euDKA) occurs in patients with poor carbohydrate intake who continue to take insulin. For these patients are not truly in the insulin-deficient state, intravenous fluid resuscitation alone can correct the ketoacidosis without any risk of hypoglycaemia. Diagnosis of euDKA can be missed in inexperienced settings; therefore, calculating anion gap and measuring ketone levels should be practiced in every sick diabetic patient regardless of glucose levels.

Keywords: Anion gap, euglycaemic diabetic ketoacidosis, insulin


How to cite this article:
Poudel RR, Kafle NK. Closing anion gap without insulin in euglycaemic diabetic ketoacidosis. J Diabetol 2017;8:92-3

How to cite this URL:
Poudel RR, Kafle NK. Closing anion gap without insulin in euglycaemic diabetic ketoacidosis. J Diabetol [serial online] 2017 [cited 2018 Jan 22];8:92-3. Available from: http://www.journalofdiabetology.org/text.asp?2017/8/3/92/222087




  Introduction Top


Euglycaemic diabetic ketoacidosis (euDKA) (blood glucose <250 mg/dL) represents initial spectrum of DKA, which requires similar management with intravenous (IV) fluids and insulin. euDKA was first described by Munro in 1973.[1] We report a case of euDKA in type 2 diabetes mellitus (DM) precipitated by poor food intake while continuing insulin use which was treated without Insulin.


  Case Report Top


A 65-year-old female with a history of type 2 DM on insulin, hypertension, poorly controlled depression and anxiety disorder presented with nausea, vomiting, polyuria, weakness and confusion for 3 days. She had no fever, abdominal pain or burning urination. She had decreased appetite and was eating poorly for more than a week; however, she was taking all her medications including insulin regularly. On examination, she was obese (body mass index 31 kg/m 2), somewhat confused and had mild bilateral pedal oedema. Blood pressure was 135/67 mmHg. Chemistries revealed: glucose 141 mg/dL, BUN 31 mg/dL, creatinine 0.7 mg/dL, sodium 135 mg/dL, chloride 98 mg/dL, potassium 4.7 mg/dL, pH 7.27, bicarbonate 14, anion gap (AG) 23 and β-OH butyrate 71. Urine was negative for glucose and protein, but positive for ketone. WBC count was 17.8, which came down to 9.2 the next day. Glycated haemoglobin 2 weeks back was 7.5%. No source of infection was identified. She received 1 L normal saline initially in the emergency department. After admission, she received 1 L Ringer's lactate followed by infusion at rate 150 cc/h. After 16 h, AG closed and glucose remained <200 mg/dL throughout. She was more alert and felt better. She was then started on diet and her usual dose of subcutaneous isophane/regular mixed insulin. Glucose was 132 at this time, other chemistries were normal except low phosphorous of 0.9 mg/dL which was treated with IV potassium-phosphate. Decreased food intake and continuing insulin precipitated euDKA in this patient.


  Discussion Top


The American Diabetes Association diagnostic criteria of DKA include plasma glucose >250 mg/dL, positive serum/urine ketone, AG metabolic acidosis (pH <7) and bicarbonate <18 mEq/L.[2] euDKA, defined as DKA without marked hyperglycaemia (250 mg/dL), is considered uncommon, but perhaps underreported.[1],[2] euDKA is particularly seen in patients with type 1 DM in the context of starvation (suppressed appetite from depression as seen in this case) and inter-current illness, where continuing insulin which suppresses hepatic glucose output resulting in low glucose levels.[3] Poor carbohydrate intake, inadequate hydration, while continuing insulin intake can lead to the development of euDKA in both types of diabetes. In fasting state, increased glucose utilisation and decreased glucose production can precipitate ketoacidosis, which is accelerated by dehydration and continuing insulin intake.[4],[5] euDKA differs from starvation ketosis where serum bicarbonate concentration is usually not <18 mEq/L.[6] DKA and euDKA must also be distinguished from other causes of high-AG metabolic acidosis, such as lactic acidosis, salicylate toxicity, methanol, ethylene glycol poisoning and renal failure. Adequate hydration could prevent hyperglycaemia in the presence of ketoacidosis by enhancing renal excretion of glucose and decreasing counterregulatory hormone release.[7] Diagnosis of euDKA can be delayed or even missed due to low plasma glucose levels. In type 2 DM patients, euDKA is also on increase with the use of sodium-glucose cotransporter 2 inhibitors.[8] Healthcare providers should be aware of the entity and have a low threshold for measuring ketone levels. The rational of insulin treatment in DKA is to close the AG, and insulin treatment is continued even after the glucose level falls below 200 mg/dL, whereas adding some dextrose to the IV fluids to prevent hypoglycaemia. In general, euDKA is treated the same as DKA albeit requiring lesser dose and duration of insulin treatment; AG in this patient closed without insulin and ketoacidosis resolved completely with IV fluid treatment. In a subset of patients who are apparently not in a state of insulin deficiency and the ketoacidosis is primarily from starvation resulting in ketoacids production from fat metabolism, an approach with IV fluids treatment with close monitoring can be attempted with less risk of hypoglycaemic episodes.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Munro JF, Campbell IW, McCuish AC, Duncan LJ. Euglycaemic diabetic ketoacidosis. Br Med J 1973;2:578-80.  Back to cited text no. 1
    
2.
Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. Hyperglycemic crises in adult patients with diabetes. Diabetes Care 2009;32:1335-43.  Back to cited text no. 2
    
3.
Joseph F, Anderson L, Goenka N, Vora J. Starvation-induced true diabetic euglycemic ketoacidosis in severe depression. J Gen Intern Med 2009;24:129-31.  Back to cited text no. 3
    
4.
Burge MR, Hardy KJ, Schade DS. Short-term fasting is a mechanism for the development of euglycemic ketoacidosis during periods of insulin deficiency. J Clin Endocrinol Metab 1993;76:1192-8.  Back to cited text no. 4
    
5.
Burge MR, Garcia N, Qualls CR, Schade DS. Differential effects of fasting and dehydration in the pathogenesis of diabetic ketoacidosis. Metabolism 2001;50:171-7.  Back to cited text no. 5
    
6.
Kitabchi AE, Umpierrez GE, Murphy MB, Kreisberg RA. Hyperglycemic crises in adult patients with diabetes: A consensus statement from the American diabetes association. Diabe tes Care 2006;29:2739-48.  Back to cited text no. 6
    
7.
Owen OE, Licht JH, Sapir DG. Renal function and effects of partial rehydration during diabetic ketoacidosis. Diabetes 1981;30:510-8.  Back to cited text no. 7
    
8.
Rosenstock J, Ferrannini E. Euglycemic diabetic ketoacidosis: A Predictable, detectable, and preventable safety concern with SGLT2 inhibitors. Diabetes Care 2015;38:1638-42.  Back to cited text no. 8
    




 

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