|Year : 2019 | Volume
| Issue : 1 | Page : 1-3
Clinical profiles and precipitating factors for diabetic ketoacidosis at a tertiary center in Dubai, United Arab Emirates
Saira Abbas, Zufana Nazir, Touseef Azhar, Abeer Alhaj, Khadija Hafidh
Department of Internal Medicine, Diabetology Unit, Rashid Hospital, Dubai Health Authority, Dubai, United Arab Emirates
|Date of Submission||10-Nov-2018|
|Date of Decision||10-Feb-2019|
|Date of Acceptance||19-Apr-2019|
|Date of Web Publication||11-Apr-2020|
Dr. Saira Abbas
Department of Internal Medicine, Rashid Hospital, Dubai Health Authority, P. O. Box: 114934, Dubai
United Arab Emirates
Source of Support: None, Conflict of Interest: None
Objectives: Our aim was to assess the clinical profiles and determine the precipitating factors for diabetic ketoacidosis (DKA) in adult patients admitted to a tertiary care center in United Arab Emirates (UAE). Materials and Methods: We conducted a retrospective analysis of all patients admitted with DKA at a tertiary care hospital in UAE during June 2014–December 2017. Variables recorded included gender, type of diabetes, and HbA1c on presentation and identified precipitating factors. Results: Data from a total of 255 patients with DKA were analyzed. One hundred and fifty-seven of these patients had type 1 diabetes (61.6%) whereas 69 patients were diagnosed with type 2 diabetes mellitus (T2DM) (27.1%), and 22 patients could not be classified as type 1 or type 2. A small number of patients (2.7%) were found to have secondary diabetes as their DKA was precipitated by acute pancreatitis. Around 12% of cases occurred in the setting of newly diagnosed diabetes. The most common precipitating factor for DKA was noncompliance to treatment (31.4%), followed by infections (22.7%). Pancreatitis was another important precipitating factor which accounted for 6.3% of the cases. Conclusions: DKA is not limited to patients with T1DM, and there seems to be a steady increase in its occurrence in patients with T2DM. Noncompliance to therapy is a major precipitating factor which needs to be addressed by offering better education programs to prevent hospitalization of these cases.
Keywords: Diabetes, diabetic ketoacidosis, hospitalizations, pancreatitis, precipitating factors, type 1 diabetes, type 2 diabetes
|How to cite this article:|
Abbas S, Nazir Z, Azhar T, Alhaj A, Hafidh K. Clinical profiles and precipitating factors for diabetic ketoacidosis at a tertiary center in Dubai, United Arab Emirates. J Diabetes Endocr Pract 2019;2:1-3
|How to cite this URL:|
Abbas S, Nazir Z, Azhar T, Alhaj A, Hafidh K. Clinical profiles and precipitating factors for diabetic ketoacidosis at a tertiary center in Dubai, United Arab Emirates. J Diabetes Endocr Pract [serial online] 2019 [cited 2021 Apr 16];2:1-3. Available from: https://www.jdeponline.com/text.asp?2019/2/1/1/282230
| Introduction|| |
Diabetic ketoacidosis (DKA) continues to be a life-threatening hyperglycemic emergency in people with diabetes. Recent trends have shown an increase in the rate of hospitalizations for DKA. DKA typically occurs in patients with type 1 diabetes mellitus although ketosis-prone diabetes in patients with type 2 diabetes is also now a well-recognized entity. Figures from the International Diabetes Federation revealed that, in 2017, 17.3% of the United Arab Emirates (UAE) population between the ages of 20 and 79 have type 2 diabetes. However, there is limited knowledge about the incidence of type 1 diabetes and the characteristics of patients presenting with DKA. Current trends have shown that there has been an increase in hospitalization rates for DKA while at the same time case fatality rates have declined from 1.1% to 0.4%., Several factors may be involved in precipitating an episode of DKA. Early diagnosis of diabetes and recognition of the precipitating factors can help to prevent these emergencies.
| Materials and Methods|| |
We performed a retrospective cross-sectional analysis of patients admitted to the medical wards and intensive care units of a tertiary care hospital in Dubai, UAE in the period of June 2014–December 2017. Variables recorded included age, gender, ethnicity, type of diabetes, HbA1c at presentation, precipitating factors, and time to resolution of DKA from the diagnosis. The patients included in the analysis fulfilled the criteria of DKA as per the Joint British Diabetes Societies guidelines which include significant ketonuria (>2+ on standard urine dipstick), blood glucose >250 mg/dl or known case of diabetes, pH <7.3, and/or serum HCO3<15 mmol/L., The study received approval by the hospital's research and ethics committee and conducted in accordance to the Helsinki declaration.
| Results and Discussion|| |
A total of 255 patients (n = 255) were admitted over the specified 3½-year period who satisfied the above criteria for DKA.
The characteristics of these patients are shown in [Table 1].
Although the majority (61%) of those presenting with DKA had type 1 diabetes, a significant number (27.1%) had a diagnosis of type 2 diabetes. This is close to the current trend in USA and Sweden where type 2 diabetes accounted for nearly a third of the cases. There is limited data in our region, but one study from Saudi Arabia (KSA) reported type 2 diabetes in only 7% of their patients presenting with DKA. A small number of our cases (8.6%) remained unclassified, as their antibody status could not be assessed due to logistical reasons. Antibody testing in our facility is quite expensive as it is performed in centralized laboratories abroad. It is thus financially challenging for those patients with basic medical insurance plans. Seven of the patients in our cohort were classified as secondary diabetes. All of these patients presented with acute pancreatitis (AP) without a prior history of diabetes and had biochemical indices that fulfilled a diagnosis of DKA.
Our cohort had 57.4% males and 42.7% females. There was a slightly higher occurrence in males in our patient population. The median age of presentation was 31 years. Majority of our patients were from the expatriate community (76.5%), which reflects the current demographics of this region.
The most common precipitating factor for the episode of DKA in our patients was interruption of treatment as either complete discontinuation, reduced frequency, or quantity of doses taken. This is similar to data reported by authors in KSA who also found that the most common precipitating factors were missed insulin doses (51.2%). Majority of our patients (72.5%) were poorly controlled as reflected by an HbA1c above 10%, which may explain why they rapidly progressed into DKA with minor interruptions in their treatment. Although financial reasons do account for lack of compliance in the expatriate population, analysis of our data revealed that similar percentages of UAE and expatriate population had reduced compliance (30% of UAE national and 31% of expatriates).
Infections accounted for 23% of cases. Majority of these were URTI followed by UTI and pneumonia [Table 2]. Another interesting observation was the number of patients presenting with DKA without a prior history of diabetes (12.2% of the total admissions). Of the newly diagnosed, 58% were type 1, 35.4% were type 2, whereas 6.4% could not be classified as type 1 or type 2.
Most of our patients had resolution of DKA within 48 h. Fifteen percent had a more prolonged course. Of these, 52.6% were type 1 and 34.2% were type 2.
Six percent of our patients had DKA precipitated by AP. The association of AP in the setting of DKA is quite challenging in terms of management. Prompt diagnosis of AP in DKA or vice versa is important for the proper management and follow-up of such patients. The concurrent diagnosis of these two conditions has several important clinical implications. First, the presence of AP aggravates the severity of DKA by increasing the intravascular volume depletion, and such patients may require more aggressive volume replacement. Second, as AP influences glucose homeostasis, control of hyperglycemia may be more difficult. On the other hand, DKA may mask coexisting AP. The pathogenesis of AP in DKA varies; but, at least in some, transient and profound hyperlipidemia is an identifiable factor. Most of our patients with DKA had a prompt diagnosis of pancreatitis as checking serum amylase and lipase is part of our initial laboratory package in DKA patients. However, we failed to note any increase in duration of resolution of DKA for these patients.
A number of our patients had nonspecific elevations of amylase and lipase, and in the presence of abdominal pain, a clinical diagnosis of AP became difficult unless supported by computed tomography findings of pancreatitis.
AP can also induce hyperglycemia and ketosis in a patient with DM and hence may be a primary event rather than a sequele to DKA. Thus, the clinical significance of this bidirectional cause and effect relationship of AP with DKA is a complex one and needs further analysis.
| Conclusions|| |
Our data collection spanned over a period of 3½ years during which time we observed that the number of admissions with DKA remained relatively constant year after year [Figure 1]. We had only one case of fatality (0.39% of the total cases), and this was in a patient who presented with a mixed picture of DKA with hyperosmolar hyperglycemic state.
The finding that 12% of DKA admissions occurred in individuals with previously undiagnosed diabetes draws our attention to the fact that we need to educate the public on the warning signs of diabetes, so people can seek medical attention early and avoid presenting in extremis with an extreme hyperglycemic emergencies. Noncompliance to therapy is also a major precipitating factor, which needs to be addressed by offering better education programs. Structured education program like DAFNE have been proven to reduce number of DKA episodes in patients with type 1 diabetes, and the development and implementation of similar programs in our region is needed.
AP is an important precipitating factor of DKA and should be looked for in a patient with DKA as these patients require more vigilant care to ensure rapid resolution of their acidosis.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. Hyperglycemic crises in adult patients with diabetes. Diabetes Care 2009;32:1335-43.
Vellanki P, Umpierrez GE. Increasing hospitalizations for DKA: A need for prevention programs. Diabetes Care 2018;41:1839-41.
Umpierrez GE, Smiley D, Kitabchi AE. Narrative review: Ketosis-prone type 2 diabetes mellitus. Ann Intern Med 2006;144:350-7.
International Diabetes Federation IDF Diabetes Atlas. 8th ed. Brussels, Belgium: International Diabetes Federation; 2017.
Benoit SR, Zhang Y, Geiss LS, Gregg EW, Albright A. Trends in diabetic ketoacidosis hospitalizations and in-hospital mortality – United States, 2000-2014. MMWR Morb Mortal Wkly Rep 2018;67:362-5.
Zhong VW, Juhaeri J, Mayer-Davis EJ. Trends in hospital admission for diabetic ketoacidosis in adults with type 1 and type 2 diabetes in England, 1998-2013: A retrospective cohort study. Diabetes Care 2018;41:1870-7.
Savage MW, Dhatariya KK, Kilvert A, Rayman G, Rees JA, Courtney CH, et al.
Joint British diabetes societies guideline for the management of diabetic ketoacidosis. Diabet Med 2011;28:508-15.
Nyenwe EA, Kitabchi AE. The evolution of diabetic ketoacidosis: An update of its etiology, pathogenesis and management. Metabolism 2016;65:507-21.
Almalki MH, Buhary BM, Khan SA, Almaghamsi A, Alshahrani F. Clinical and biochemical characteristics of diabetes ketoacidosis in a tertiary hospital in Riyadh. Clin Med Insights Endocrinol Diabetes 2016;9:7-11.
Al-Rubeaan KA, Aftab SA, Alotaibi MS, Alghamdi AA, Rafiullah MR. Clinico-laboratory characteristics of diabetic keto acidosis in adults in a tertiary hospital in Saudi Arabia. Eur Rev Med Pharmacol Sci 2011;15:1202-6.
Nair S, Yadav D, Pitchumoni CS. Association of diabetic ketoacidosis and acute pancreatitis: Observations in 100 consecutive episodes of DKA. Am J Gastroenterol 2000;95:2795-800.
Knight AH, Williams DN, Ellis G, Goldberg DM. Significance of hyperamylasaemia and abdominal pain in diabetic ketoacidosis. Br Med J 1973;3:128-31.
Warshaw AL, Feller ER, Lee KH. On the cause of raised serum-amylase in diabetic ketoacidosis. Lancet 1977;1:929-31.
Elliott J, Jacques RM, Kruger J, Campbell MJ, Amiel SA, Mansell P, et al
. Substantial reductions in the number of diabetic ketoacidosis and severe hypoglycaemia episodes requiring emergency treatment lead to reduced costs after structured education in adults with type 1 diabetes. Diabet Med 2014;31:847-53.
[Table 1], [Table 2]