dka case study type 1

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Severe diabetic ketoacidosis – a remarkable case study

Summarized from Van de Vyver C, Damen J, Haentjens C et al . An exceptional case of diabetic ketoacidosis. Case Reports in Emergency Medicine 2017.

Diabetic ketoacidosis (DKA) is a potentially life-threatening acute complication of type 1 diabetes caused by insulin deficiency. It is characterized by raised blood glucose (hyperglycemia), metabolic acidosis, and increased blood/urine ketones. Dehydration and electrolyte disturbance are common and affected patients may develop some degree of acute kidney injury (AKI) consequent on fluid loss (hypovolemia) due to osmotic diuresis associated with severe hyperglycemia. DKA evolves rapidly over a short time frame (hours rather than days) and can occur (rarely) in those with type 2 diabetes.  This DKA case study is particularly noteworthy because of the severity of the hyperglycemia and acid-base disturbance, and the fact that the patient survived such profound metabolic disturbance and associated life-threatening hemodynamic changes. The case concerns a 33-year-old woman with ”brittle” type 1 diabetes treated with continuous subcutaneous insulin infusion (insulin pump). She had, in common with many brittle diabetics, a history of gastroparesis (delayed stomach emptying).  Some 36 hours prior to emergency hospital admission she complained of abdominal pain and vomiting after attending a party. Her condition deteriorated before transfer to hospital. The ambulance team reported a rapid decline in Glasgow Coma Score (GCS) from 13 to 3 in only 10 minutes, sinus tachycardia, undetectable peripheral pulse, and hypotension (BP 99/52 mmHg). 

Clinical examination revealed severe dehydration and respiratory distress (respiration rate 40 breaths/min). Urgent intubation was necessary and systolic blood pressure dropped further to 55 mmHg. Initial (fingerstick) blood glucose was above the upper detection limit of the analyzer and blood ketones were >8.0 mmol/L. Blood gas analysis revealed severe metabolic acidosis (pH 6.74, bicarbonate 5 mmol/L, p CO 2 39.9 mmHg (5.3 kPa) and hypoxemia ( p O 2 50.2 mmHg, 6.7 kPa). Among other abnormal laboratory test results, perhaps the most remarkable was serum glucose 107 mmol/L (1924 mg/dL). (Serum glucose >33 mmol/L (600 mg/dL) is rarely seen in patients with DKA.)  White blood count (32.8x10 9 /L), C-reactive protein (789 nmol/L) and lactate (4.6 mmol/L) were also grossly elevated. Other laboratory testing revealed severe hyponatremia (sodium 113 mmol/L), severe hyperkalemia (6.7 mmol/L) and acute kidney failure (serum creatinine 332 µmol/L).  Following presumptive diagnosis of DKA, sepsis and acute renal failure, the patient was treated with aggressive IV fluids, norepinephrine, bicarbonate, and insulin, IV bolus and drip. Intensive investigation for evidence of infection proved fruitless. With treatment, the patient’s condition improved over the following days and she was extubated. Normal renal function was restored after 2 days.  In discussion of this case history, the authors briefly review the pathogenesis and treatment of DKA in general terms. They also highlight some interesting features of this case. One aspect discussed relates to the blood gas results on admission, in particular the curiously normal p CO 2 (39.9 mmHg, 5.3kPa). 

Metabolic acidosis usually provokes compensatory hyperventilation and reduced p CO 2 . The authors propose plausible theories to explain the much higher than expected p CO 2 in this case. They also propose that the remarkably high blood glucose in this case is the result of the combined effect of reduced glucose elimination consequent on renal failure and the presence of gastroparesis. 

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has a master's degree in medical biochemistry and he has twenty years experience of work in clinical laboratories.

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• Volume 9, Issue 2
• Clinical and biochemical profile of 786 sequential episodes of diabetic ketoacidosis in adults with type 1 and type 2 diabetes mellitus
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• http://orcid.org/0000-0002-6921-4395 Emma Ooi 1 ,
• Katrina Nash 2 ,
• Lakshmi Rengarajan 3 ,
• Eka Melson 3 , 4 ,
• Lucretia Thomas 2 ,
• Agnes Johnson 2 ,
• Dengyi Zhou 2 ,
• Lucy Wallett 3 ,
• Sandip Ghosh 3 ,
• Parth Narendran 3 , 5 ,
• Punith Kempegowda 3 , 4
• 1 Medical School , RCSI & UCD Malaysia Campus , Georgetown , Malaysia
• 2 Medical School, College of Medical and Dental Sciences , University of Birmingham , Birmingham , UK
• 3 Diabetes and Endocrinology , University Hospitals Birmingham NHS Foundation Trust , Birmingham , UK
• 4 Institute of Metabolism and Systems Research , University of Birmingham , Birmingham , UK
• 5 Institute of Immunology and Immunotherapy , University of Birmingham , Birmingham , UK
• Correspondence to Dr Punith Kempegowda; p.kempegowda{at}bham.ac.uk

Introduction We explored the clinical and biochemical differences in demographics, presentation and management of diabetic ketoacidosis (DKA) in adults with type 1 and type 2 diabetes.

Research design and methods This observational study included all episodes of DKA from April 2014 to September 2020 in a UK tertiary care hospital. Data were collected on diabetes type, demographics, biochemical and clinical features at presentation, and DKA management.

Results From 786 consecutive DKA, 583 (75.9%) type 1 diabetes and 185 (24.1%) type 2 diabetes episodes were included in the final analysis. Those with type 2 diabetes were older and had more ethnic minority representation than those with type 1 diabetes. Intercurrent illness (39.8%) and suboptimal compliance (26.8%) were the two most common precipitating causes of DKA in both cohorts. Severity of DKA as assessed by pH, glucose and lactate at presentation was similar in both groups. Total insulin requirements and total DKA duration were the same (type 1 diabetes 13.9 units (9.1–21.9); type 2 diabetes 13.9 units (7.7–21.1); p=0.4638). However, people with type 2 diabetes had significantly longer hospital stay (type 1 diabetes: 3.0 days (1.7–6.1); type 2 diabetes: 11.0 days (5.0–23.1); p<0.0001).

Conclusions In this population, a quarter of DKA episodes occurred in people with type 2 diabetes. DKA in type 2 diabetes presents at an older age and with greater representation from ethnic minorities. However, severity of presentation and DKA duration are similar in both type 1 and type 2 diabetes, suggesting that the same clinical management protocol is equally effective. People with type 2 diabetes have longer hospital admission.

• diabetes mellitus type 1
• diabetes mellitus type 2
• diabetic ketoacidosis
• endocrine system diseases

Data availability statement

Data are available upon reasonable request.

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See:  http://creativecommons.org/licenses/by-nc/4.0/ .

https://doi.org/10.1136/bmjdrc-2021-002451

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Significance of this study

What is already known about this subject.

Diabetic ketoacidosis (DKA) is generally associated with type 1 diabetes mellitus (T1DM) but can also develop in people with type 2 diabetes mellitus (T2DM).

Common precipitants of DKA in T1DM and T2DM are intercurrent illness and suboptimal treatment.

DKA in people with T1DM and T2DM are currently managed using the same clinical protocols.

What are the new findings?

DKA in those with T2DM is more common in people of ethnic minority background.

Severity of DKA at presentation as assessed by pH, glucose and lactate does not differ between T1DM and T2DM, although people with T2DM have longer hospital stays than those with T1DM.

Management of DKA as assessed by insulin requirements did not differ between T1DM and T2DM, but people with T1DM have more episodes of hypoglycemia during their DKA treatment.

How might these results change the focus of research or clinical practice?

The existing DKA guidelines are appropriate for both type 1 and type 2 diabetes, thus minimizing the need to create further individualized pathways.

Ethnic minority populations with T2DM are at greater risk of DKA and may benefit from specific education around DKA as a potential complication of their diabetes.

Introduction

Diabetic ketoacidosis (DKA) is a life-threatening complication of diabetes which requires rapid assessment and treatment. 1 It is characterized by the triad of hyperglycemia, acidemia and ketosis and results from insulin deficiency. 2 Treatment involves correction of hyperglycemia and hypovolemia and replacement of electrolytes. 2 The incidence of DKA ranges from 4.6 to 8 episodes per 1000 people with type 1 or type 2 diabetes. 3 4 While mortality associated with DKA appears to have significantly decreased over the last 20 years (from 7.96% to 0.67%), 5 DKA still represents a considerable risk in adults, adolescents and young children. 1

Diabetes is usually classified into type 1 and type 2 diabetes and most people with diabetes have type 2 diabetes (90%–95%). 6–8 It is traditionally accepted that DKA is characteristic of type 1 diabetes. 6 In fact, it has previously been considered that DKA is indicative, or diagnostic, of type 1 diabetes. 1 However, it is also recognized that those with type 2 diabetes can also develop DKA; a retrospective cohort study recently estimated that the incidence of DKA in type 2 diabetes has increased by 4.24% annually between 1992 and 2013. 9 Unfortunately, data reporting on DKA in people with type 2 diabetes are sparse and guidelines for managing DKA in people with type 2 diabetes are based on those for type 1 diabetes.

Newton and Raskin 10 studied the clinical and biochemical characteristics of 176 episodes of DKA in people with type 1 diabetes compared with 20 with type 2 diabetes. They found a greater proportion of patients with type 2 diabetes experiencing DKA were Latino-American or African-American and required a longer period of treatment to achieve ketone-free urine. Balasubramanyam et al 11 also compared 141 people with type 1 diabetes and 55 people with type 2 diabetes presenting with DKA and identified differences in ethnicities, body mass index and age of onset at presentation. These studies are small and there are currently no published studies comparing DKA in type 1 and type 2 diabetes in the UK.

This descriptive study aimed to compare the demographics and clinical course of DKA in type 1 and type 2 diabetes. We also explored the hypothesis on whether DKA treatment algorithm is as effective in people with type 2 diabetes as in those with type 1 diabetes.

Study design, setting and population

The study was undertaken at a large tertiary care center in West Midlands, UK, which serves an ethnically diverse population of over one million people. All people admitted with DKA from April 2014 to September 2020 were included in the study. DKA was defined as blood glucose >11 mmol/L, pH ≤7.3 or bicarbonate ≤15 mmol/L and ketonemia ≥3 mmol/L. 1 The list of people admitted with DKA was initially screened based on those who meet one of the following criteria: electronic records with pH <7.3 and blood glucose >11 mmol/L or referral with DKA to the specialist team or discharged with a diagnosis of DKA. 1 This list was further manually verified for confirmed diagnosis of DKA and only those who met the criteria as per national guidelines were included in the study. Classification (type 1/2) of diabetes was based on a clinical diagnosis as per National Institute of Health and Care Excellence (NICE) guidelines, although may have been confirmed through islet autoantibody or C peptide testing. Patients who had DKA were identified using an automatic monitoring system, and data regarding various aspects of DKA were collected manually. We reviewed patients’ health records to confirm the type of diabetes diagnosis. Patients were excluded from analysis if the diabetes classification was unclear or if this information was unavailable.

DKA management guidelines

The guidelines for management of DKA at our center are based on the Joint British Diabetes Societies guidelines and are the same for both type 1 and type 2 diabetes. 1 Treatment of DKA includes administering fluids to correct the deficit and replacement glucose infusion when serum glucose drops less than 14 mmol/L but ketosis persists. A fixed rate intravenous insulin infusion was administered based on the patient’s body weight at a rate of 0.1 unit/kg/hour to switch of lipolysis. Hourly glucose and ketone measurements are done to check treatment progress. Venous blood gases are done during infusion bag change to ensure the next bag of fluid has appropriate potassium replacement. While the guidelines for DKA management have evolved to ensure simplicity and end-user satisfaction over the last 7 years in our institute, the principles have not changed ( figure 1 ).

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Guidelines for DKA treatment at our center. BP, blood pressure; DKA, diabetic ketoacidosis; GCS, Glasgow Coma Scale; HbA1c, glycated haemoglobin; SGLT2, sodium-glucose cotransporter-2; ITU, intensive treatment unit.

Data collection

Patient demographics.

The following variables were registered: age, sex and ethnicity. Data were based on self-identification or from medical records. Ethnicity was categorized as white, Asian, black, mixed and others.

Etiology of DKA

The precipitating cause was categorized as alcohol-related, intercurrent illness, new diagnosis of diabetes mellitus, suboptimal compliance to diabetes treatment, cancer therapy-associated, sodium-glucose cotransporter-2 (SGLT2) inhibitors-related or unknown.

DKA severity

The following data were collected as indicators of DKA severity: serum sodium, serum potassium, serum glucose, lactate, pH, bicarbonate, urea and serum osmolality. Serum ketone data were unavailable.

In addition, serum osmolality was calculated to explore whether there was an element of hyperosmolar hyperglycemic state in any of the episodes. HHS was defined as a calculated serum osmolality of greater than 320 mOsm/L.

Progression of treatment

Progression of DKA was measured in several ways: number of episodes of hypoglycemia (blood glucose <4 mmol/L), hypokalemia (potassium <3.5 mmol/L) and hyperkalemia (potassium >5.5 mmol/L) during the DKA episode. Total insulin infused was calculated as the product of fixed rate intravenous insulin infusion rate and the total DKA duration. It does not include the dose of any subcutaneous basal insulin therapy that may have been initiated/maintained during the DKA episode. DKA duration (days) was calculated as the time difference between DKA diagnosis and DKA resolution (pH >7.3 and bicarbonate >15 mmol/L; ketones <0.6 mmol/L). Length of stay (days) was calculated as the difference between admission and discharge.

Data analysis

Data were analyzed using Stata/SE V.16.1 for Mac. Descriptive statistics were used to characterize the type 1 and type 2 diabetes groups by outcome. The Shapiro-Wilk test was used to determine continuous data normality. Continuous data are presented as mean and SD if normally distributed, and as median and IQR if data were skewed. Categorical data are presented as frequency and proportions. The χ 2 significance test, Wilcoxon rank-sum test and independent t-test were used to analyze the differences between variables, as appropriate. We used linear regression model with length of stay as outcome and type of diabetes as exposure, with age, sex and ethnicity as covariates. The findings of this model are presented as a coefficient and 95% CI. Statistical significance was accepted at a 95% confidence level (p<0.05).

Analyses on presentation, management, complications and outcome parameters were repeated in subgroups according to sex (male and female), age groups (<30, 30–49, 50–69, >70), ethnicity (white, South Asian, black, mixed, others), concurrent presence of hyperosmolality (>320 mOsm/L) and year of presentation (2014, 2015, 2016, 2017, 2018, 2019, 2020).

A total of 786 DKA episodes were identified for the study. Of these, 18 were excluded due to issues with access to clinical data or lack of clarity on diabetes classification. The final analysis included 768 episodes ( table 1 ). Shapiro-Wilk tests indicated all outcomes were non-normally distributed and thus descriptive results are presented in median and interquartile range (IQR) and Wilcoxon rank-sum test was used.

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Baseline characteristics by type of diabetes (N=768)

The median age was 38.2 years (IQR 23.8–56.8) and the male to female ratio was 1:1.04. Of the patients, 583 (78.7%) were white Caucasian, 70 (9.5%) South Asian, 51 (6.9%) black, 25 (3.4%) mixed and 12 (1.6%) other ethnicities.

Of the 768 episodes, 583 (75.9%) had type 1 diabetes and 185 (24.1%) had a prior diagnosis of type 2 diabetes. A summary of the baseline characteristics for the type 1 and type 2 groups is presented in table 1 . People with type 2 diabetes were older and had greater representation from ethnic minority populations compared with those with type 1 diabetes.

Intercurrent illness (n=306/768, 39.8%), including any infection or inflammation, and suboptimal compliance to diabetes treatment (n=206/768, 26.8%) were the two most common precipitating causes of DKA. Jointly they contributed to two-thirds of all episodes. No clear precipitating event could be identified in 16.2% (n=124/768) of the DKA episodes, and this was the third most common precipitant of DKA in the cohort ( figure 2A ). There was no difference in the common precipitating factors between the two groups ( figure 2B,C ). COVID-19 was identified to be the precipitating factor in two (type 1 diabetes n=1/2; type 2 diabetes n=1/2) of the DKA episodes (n=2/768, 0.3%). Figure 2D illustrates the change in the trends of etiology over the years.

Proportion of various precipitating causes of DKA from 2014 to 2020: (A) overall, (B) people with type 1 diabetes, (C) people with type 2 diabetes and (D) year-wise. DKA, diabetic ketoacidosis; SGLT2, sodium-glucose cotransporter-2 inhibitors; T1DM, type 1 diabetes mellitus.

There was no significant difference in severity of DKA at presentation between type 1 and type 2 diabetes regarding pH, glucose, lactate or osmolality. However, urea was higher in those with type 2 diabetes.

Furthermore, there was no difference in intravenous insulin requirements to treat the DKA or the total volume of fluid administered between type 1 and type 2 diabetes ( table 2 ). DKA management was associated with more episodes of hypoglycemia in patients with type 1 diabetes than type 2 diabetes. There was no difference between the groups in the number of episodes of hypokalemia or hyperkalemia during treatment for DKA.

Biochemical profiles for severity on admission and management, complications and outcomes of DKA management by type of diabetes

The duration of DKA treatment was the same between patients with type 1 diabetes and type 2 diabetes, although those with type 2 diabetes required longer hospital stay ( table 2 ). People with type 2 diabetes had stayed 4.8 (1.2–8.4) days longer compared with people with type 1 diabetes, after controlling for age, sex and ethnicity ( online supplemental table 1 ).

Supplemental material

Sex-based differences.

Men with type 1 diabetes had higher blood glucose at presentation. Women with type 2 diabetes had higher urea and serum osmolality at presentation. There was no other difference in the biochemical parameters at presentation with DKA. Women with type 1 diabetes had more episodes of hypoglycemia during DKA treatment. There was no difference in DKA duration between men and women ( online supplemental table 2 ).

Ethnicity-based differences

Non-Caucasian and mixed ethnicities were more likely to have type 2 diabetes (proportion of white in type 1 diabetes 80.3% vs type 2 diabetes 73.5%; p=0.030). In those of white Caucasian ethnicity, people with type 1 diabetes were more hyperglycemic on admission with DKA than people with type 2 diabetes; however, people with type 2 diabetes had higher urea than people with type 1 diabetes. People of Asian ethnicity with type 2 diabetes had higher lactate and urea levels on admission than people of Asian ethnicity with type 1 diabetes. Conversely, people of black ethnicity with type 2 diabetes were more hyperglycemic and had higher urea and serum osmolality on admission than people of black ethnicity with type 1 diabetes. In people of mixed ethnicity, bicarbonate was higher in those with type 2 diabetes than those with type 1 diabetes. When outcomes of DKA management were compared by type of diabetes based on ethnicity, there were no differences in total DKA duration between type 1 and type 2 diabetes, while length of hospitalization was longer in people with type 2 diabetes across all ethnicities apart from those of an Asian ethnicity ( online supplemental table 3A ).

Data were then compared between ethnicities by diabetes type. In those with type 1 diabetes, there were statistically significant differences in only urea levels on admission between ethnicities. However, in the type 2 diabetes group, there were statistically significant differences in bicarbonate, lactate and serum osmolality in type 2 diabetes mellitus between ethnicities. However, there were no differences in hypoglycemic, hypokalemic or hyperkalemic episodes between ethnicities in either type of diabetes. There were also no differences between ethnicities in DKA duration or length of hospitalization ( online supplemental table 3B ).

Age-based differences

All DKA episodes in the <30 years age group ( online supplemental table 4 ) with available biochemical parameters at presentation were accounted for by people with type 1 diabetes and thus no comparison could be made between types of diabetes. There was no difference in biochemical profile on admission in the other age groups other than people with type 1 diabetes presenting more hyperglycemic and with higher serum osmolality in the 50–69 age group. People in the 50–69 age group with type 2 diabetes had more episodes of hypokalemia than people with type 1 diabetes. Otherwise, there were no differences in complications of DKA management between age groups. There was no difference in DKA duration in people with type 1 and type 2 diabetes in any of the age groups. Length of hospitalization was significantly longer in people with type 2 diabetes in the 30–49 and 50–69 age subgroups ( online supplemental table 4 ).

Serum osmolality-based differences

We also undertook an analysis of the influence of serum osmolality on the presentation and clinical outcome of DKA to explore if those who presented with a ‘mixed DKA/HHS’ picture fared differently. 12 Overall, people with a higher serum osmolality (>320 mmol/L) had higher glucose, lactate and urea levels on admission ( online supplemental table 5 ). While there was no difference in the number of hypoglycemia episodes during the management of DKA, people with higher serum osmolality (>320 mmol/L) experienced more hyperkalemic episodes, while people with lower serum osmolality (<320 mmol/L) had more hypokalemic episodes. There was no significant difference in DKA duration between the two groups, but length of hospitalization was significantly higher in people with serum osmolality >320 mmol/L ( online supplemental table 5 ).

In the type 1 diabetes cohort, those with a higher serum osmolality had lower pH, higher glucose, lactate and urea, and an increased DKA duration and length of hospital stay. People with type 2 diabetes and higher serum osmolality had higher glucose, lactate and urea, compared with those with serum osmolality <320 mmol/L. There was no difference in DKA duration and length of hospitalization between the two groups by serum osmolality ( online supplemental table 5 ).

Year-based differences

Over the years, there was an increase in DKA admissions due to SGLT2 inhibitors and cancer immunotherapies in type 2 and type 1 diabetes, respectively, in addition to COVID-19 as a precipitating factor in 2020 ( figure 2 ). There was a significant reduction in duration of DKA in comparison with 2014, in all subsequent years. In 2015, there was a reduction in duration of DKA by 49.8% (2014 median 21.9 (15.2–38.7); 2015 median 11.0 (7.1–16.0); p<0.0001). There was an upward trend from 2017 to 2019; however, DKA duration was still significantly lower in comparison with 2014. In 2020, DKA duration decreased to a median of 11.7 (IQR 9.3–19.2; p<0.0001). While duration in DKA decreased over the years ( figure 3A ), length of hospitalization increased ( figure 3B ) as compared with that in 2014. This increase was significant in 2015, 2017 and 2019.

Differences in diabetic ketoacidosis (DKA) duration in hours (A) and length of hospitalization in days (B) based on the year of the episode compared with 2014 (*p<0.05).

In this large observational single-center study of 786 DKA episodes, we show that DKA more commonly affects people with type 1 diabetes; however, we also noted a trend toward ethnic minorities preponderance and those of an older age, especially in type 2 diabetes. Importantly, however, nearly a quarter of admission with DKA were in people with a clinical diagnosis of type 2 diabetes. Wang et al 13 reported type 2 diabetes accounted a third of overall DKA cases in Swedish population. However, the results were limited by a small study population. The most common precipitants were intercurrent illness and suboptimal compliance, although no clear precipitating etiology could be ascertained for 16.5% of our cohort. There was no difference between type 1 and type 2 diabetes in DKA severity at presentation, insulin requirements for DKA treatment or complications of DKA treatment. South Asian or black ethnicities admitted with DKA were more likely to have type 2 diabetes, while those of white Caucasian ethnicity with DKA were more likely to have type 1 diabetes. People with type 2 diabetes were found to have a significantly longer hospital stay than those with type 1 diabetes. We noted a graded difference in length of hospitalization as age increased, which plateaued after 70 years.

The strengths of this study are that this is a single-center study of long duration with comprehensive data collection of demographics, presentation and outcome of DKA management. To our knowledge, our cohort is the largest consecutive DKA episodes ever reported, with inclusion of all people with DKA over a 6-year time period. However, we note lack of ketone measurement data, intensive care unit admission and mortality data, which limit our assessment between those with type 1 and type 2 diabetes. Previous studies showed higher mortality in type 2 diabetes with DKA compared with type 1 diabetes 14 15 and mortality is reported to relate to the precipitating cause of DKA. Additionally, antibody and C peptide data were also unavailable and thus we relied on a clinical diagnosis of type 1 diabetes and type 2 diabetes.

Our findings on the precipitating etiology are similar to previous studies which have found that intercurrent illness and suboptimal compliance were the two most common presentations. 16 No identifiable precipitating factor could be found in half of patients with type 2 diabetes for DKA in a similar study in the past, akin to our study. 11 Identifying the precipitating factor is important in order to avoid future episodes. We also identified a small proportion of DKA related to SGLT2 inhibitors, in line with building evidence in this drug class, 17 18 as well as increasing contribution with time from causes such as checkpoint inhibitor cancer therapy and COVID-19 virus infection. We recently reported that in people with type 1 diabetes, those with COVID-19 presented more hyperglycemic episodes, and in those with type 2 diabetes those with COVID-19 were more likely to require intensive care support and had higher mortality rates. 19 Other studies have also identified changes in presenting characteristics of patients with DKA during the COVID-19 pandemic, most notably an increase in presentation of DKA in patients with type 2 diabetes. 20 21

Our analysis did not show any differences in serum osmolality between DKA in type 1 and type 2 diabetes. We do show however that higher calculated osmolality across the cohort, driven by higher glucose, lactate and urea, indicated more severe dehydration and a longer length of hospitalization, but not longer DKA duration. However, those with higher serum osmolality and type 1 diabetes had an increased DKA duration and longer hospital stay when compared with those with a lower serum osmolality and type 1 diabetes.

The longer hospital stay we observed in those with type 2 diabetes may be indicative of a more complex requirement for care in this cohort. People with type 2 diabetes tend to have more comorbidities, experience macrovascular and/or microvascular complications, and have worse diabetic control compared with people with type 1 diabetes, which will add to disease burden and recovery from DKA. 14 22–25 On the other hand, those with type 2 diabetes who experience DKA may represent a more complex cohort, as studies have identified increased risk of complications, such as stroke, in this group in comparison with patients with type 2 diabetes who do not experience DKA. 26 Although our analyses did not find a significant difference in clinical parameters, multiple studies have indicated greater severity and mortality of DKA in patients with type 2 diabetes in comparison with those with type 1 diabetes. 14–16

Balasubramanyam et al 11 reported a high proportion of DKA episodes in non-Caucasian adults occur in persons with type 2 diabetes, similar to our findings. 11 These findings may be representative of the population diagnosed with these diseases, as minority ethnic groups are at a higher risk of type 2 diabetes. 27 However, this may also be in part due to the fact that those who are South Asian or black are more likely to have worse diabetes control, have a genetic predisposition or to be of a lower socioeconomic and/or educational status, all factors which associate with an increased risk of DKA. 28–30 It is also increasingly recognized that non-Caucasian ethnics are more likely to be diagnosed with ketosis-prone type 2 diabetes and this may contribute to some of the DKA episodes seen. 31

Over the years, our analysis identified a reduction in DKA duration but an increase in length of hospitalization. During this time period, multiple changes to DKA management have been implemented in our hospital trust as part of an ongoing quality improvement. 32 33 These interventions have been effective at reducing DKA duration and have included development of a real-time audit tool, automatic referral to a specialist team, electronic surveillance of blood gas results, education and redesigning of local guidelines, and monthly feedback meetings. Nevertheless, an increase in length of hospitalization was seen which contradicts reports from other centers. 9 We are still not clear of the reasons for the increased median length of stay, although this has been stable for a number of years.

The findings of this study can help inform policy and practice to reduce morbidity and mortality associated with DKA. Patient education among at-risk groups, particularly those of non-Caucasian ethnicity, can increase awareness of the potential of DKA as a complication of both type 1 and type 2 diabetes. Increasing awareness will prevent DKA occurrence and enable rapid identification of warning signs to reduce DKA-associated morbidity. Furthermore, although no differences were observed in management requirements, it is important to consider factors which may affect length of hospitalization in those with type 2 diabetes. Additionally, our subgroup analysis which confirmed that those with a higher serum osmolality are sicker may inform medical practice to alert front-line workers to patients who are likely to require more care.

Our study contributes to the understanding of DKA in people with type 1 and type 2 diabetes. We are able to confirm previous reports that DKA can present in people with a clinical diagnosis of type 2 diabetes, that DKA in type 2 diabetes is over-represented by older people and those from ethnic minority populations, and that the most common precipitants of DKA remain poor compliance with insulin and intercurrent illness.

We contribute new knowledge in that the clinical protocol for managing DKA in those with type 1 and type 2 diabetes appears equally effective, that those with higher serum osmolality appear to be more unwell and may require more support, and that new therapies such as SGLT2 inhibitors and cancer immunotherapies are increasingly contributing to the etiology of DKA in type 2 diabetes and type 1 diabetes, respectively.

Ethics statements

Patient consent for publication.

Not required.

Ethics approval

The study was approved as part of service improvement by the Department of Information Governance, University Hospitals Birmingham NHS Foundation Trust (CARMS approval number: 12074).

Acknowledgments

We thank all the staff of the department of diabetes and endocrinology, University Hospitals Birmingham NHS Foundation Trust for their assistance and support to this study.

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Supplementary materials

Supplementary data.

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EO and KN are joint first authors.

PN and PK are joint senior authors.

Contributors PK and PN conceptualized the study. EO, LR, EM, LT, AJ, DZ, LW and PK collected the data. EO and KN conducted statistical analysis. SG, PN and PK supervised the study. EO, KN, LR, EM and PK wrote the original draft. All authors reviewed and edited the final draft. PN and PK are the guarantors and joint senior authors taking responsibility for the content of this article.

Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

Competing interests None declared.

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Diagnosis and problem identification, planning and intervention, case presentation, case study: a patient with type 1 diabetes who transitions to insulin pump therapy by working with an advanced practice dietitian.

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Claudia Shwide-Slavin; Case Study: A Patient With Type 1 Diabetes Who Transitions to Insulin Pump Therapy by Working With an Advanced Practice Dietitian. Diabetes Spectr 1 January 2003; 16 (1): 37–40. https://doi.org/10.2337/diaspect.16.1.37

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Registered dietitians (RDs) who have earned the Board Certified–Advanced Diabetes Manager (BC-ADM) credential hold a master’s or doctorate degree in a clinically relevant area and have at least 500 hours of recent experience helping with the clinical management of people with diabetes. 1 They work in both inpatient and outpatient settings, including diabetes or endocrine-based specialty clinics, primary care offices, hospitals, and private practices. Advanced practice dietitians provide all components of diabetes care, including advanced assessment (medical history and physical examination), diagnosis, medical management, education, counseling, and overall case management.

The role of RDs in case and disease management was explored in a recent article 2 that included interviews with three dietitians who work as case managers or disease managers. All three reported experiencing challenges in practice and noted that the meaning of “case management” varies from one health care setting to another. This is also true for RD, BC-ADMs. Advanced practice dietitians specializing in diabetes require case management expertise that stresses communication skills, knowing the limits of your own discipline, knowing how to interact with other health care professionals, and knowing when to seek the expertise of other members of the diabetes care team.

Clinical practice includes assessment and data collection, diagnosis and problem identification, planning, and intervention. In many cases, diabetes educators who are dietitians and those who are nurses are cross-trained to perform the same roles. The first one to meet with a client handles that client’s assessment, and cases are discussed and interventions planned at weekly team meetings.

For advanced practice dietitians, the first session with a client often involves a complete physical assessment, not just a nutrition history. This includes a comprehensive medical history of all body systems. The diabetes-focused physical examination, just as performed by clinicians from other disciplines, includes height and weight measurement, body mass index (BMI) calculation, examination of injection sites, assessment of injection technique, and foot assessment.

Assessment also includes reviewing which medications the client is taking, evaluating their effectiveness and side effects, and determining the need for adjustment based on lifestyle, dietary intake, and blood glucose goals.

When carbohydrate counting is added to therapy, dietitians calculate carbohydrate-to-insulin ratios and teach clients how to use carbohydrate counting instead of a sliding-scale approach to insulin. Medications are adjusted based on clients’ lifestyles until blood glucose goals are achieved.

The therapeutic problem solving, regimen management, case management, and self-management training performed by advanced practice dietitians exceeds the traditional role of most dietetics professionals. 3  

A role delineation study for clinical nurse specialists, nurse practitioners, RDs, and registered pharmacists, 4 conducted in 2000 by the American Nurses Credentialing Center, reported equal findings among all four groups for the skills used to identify pathophysiology, analyze diagnostic tests, and list problems. Assessment for medical nutrition therapy typically includes evaluation of food intake, metabolic status, lifestyle, and readiness to change. For people with diabetes, monitoring glucose and measuring hemoglobin A 1c (A1C), lipids, blood pressure, and renal status are essential to evaluating nutrition-related outcomes.

The U.S. Air Force health care system conducted a pilot test giving RDs clinical privileges and evaluating their clinical judgment in patient nutritional care. A protocol was approved, and dietitians were allowed to order and interpret selected outpatient laboratory tests independently. The higher-level clinical judgments and laboratory privileges were linked to additional certifications. 5  

The Diabetes Prevention Program (DPP) also provided a unique opportunity for dietitians to demonstrate advance practice roles. 6 Dietitians served as lifestyle coaches, contacting participants at least once a month to address intervention goals. As case managers, they interviewed potential volunteers, assessed past experience with weight loss, and scheduled quarterly outcome assessments and weekly reviews of each participant’s progress at team meetings. Within the DPP’s central management, dietitians served as program coordinators and served on national study committees related to participant recruitment and retention, quality control, the use of protocols, and lifestyle advisory groups. 7  

Dietitians now play key roles in translating DPP findings and serving as community advocates to reduce the incidence of obesity and the health care burden of type 2 diabetes. This includes serving in a consultative role to other health care team members on issues regarding weight loss and risk factor reduction.

Advanced practice RDs offer comprehensive diabetes patient care services, including identifying patient goals and expected outcomes, selecting nonpharmacological and pharmacological treatments, and developing integrated plans of care. Problems discussed with patients range from acute and chronic diabetes complications to comorbid conditions, other conditions, preventive interventions, and self-management education. Advanced practice RDs also review patients’ health care resources and order laboratory tests if information is not available from referral sources. They provide supportive counseling and referral to specialists, as needed. And, they provide a full report of their findings and any regimen changes and recommendations they make to referring clinicians after each visit.

These activities and responsibilities go beyond the scope and standards of practice for the RDs and for RD, CDEs. 8 They will be included in the scope of practice document for RD, BC-ADMs that is now being developed by the Diabetes Care and Education Practice Group of The American Dietetic Association.

The following case study illustrates the clinical role of advanced practice dietitians in the field of diabetes.

B.C. is a 51-year-old white man who was diagnosed with type 1 diabetes 21 years ago. He believes that his diabetes has been fairly well controlled during the past 20 years and that his insulin needs have increased. He was recently remarried, and his wife is now helping him care for his diabetes.

His endocrinologist referred him to the RD for an urgent visit because 4 days ago he had a hypoglycemic event requiring treatment in the emergency room (ER). He has come to see the dietitian because his doctor and his wife insisted that he do so.

B.C. has had chronic problems with asymptomatic hypoglycemia. His last doctor’s visit was 3–4 weeks ago, when areas of hypertrophy were found. His endocrinologist asked him to change his injection sites from his thigh to his abdomen after the ER incident.

He does not think he needs any diabetes education but would like help in losing 10 lb. His body mass index is 25 kg/m 2 .

His medications include pravastatin (Pravacol), 10 mg daily; NPH insulin, 34 units in the morning and 13 units at bedtime; and regular insulin at breakfast and dinner following a sliding-scale algorithm. He also takes lispro (Humalog) insulin as needed to correct high blood glucose.

Before his ER visit, B.C. monitored his blood glucose only minimally, testing fasting and sometimes before dinner but not keeping records. Since his severe hypoglycemia 4 days ago, he has begun checking his blood glucose four times a day, before meals and bedtime.

Lab Results

B.C.’s most recent laboratory testing results were as follows:

A1C: 8.3% (normal 4.2–5.9%)

Lipid panel

    • Total cholesterol: 207 mg/dl (normal: 100–200 mg/dl)

    • HDL cholesterol: 46 mg/dl (normal: 35–65 mg/dl)

    • LDL cholesterol: 132 mg/dl (normal: <100 mg/dl)

    • Triglycerides: 144 mg/dl (normal: <150 mg/dl)

Creatinine: 0.9 mg/dl (normal: 0.5–1.4 mg/dl)

Microalbumin: 4 μg (normal: 0–29 μg)

At his initial visit with the RD for crisis management of asymptomatic hypoglycemia, she examined his injection sites and asked if he had made the changes recommended by his clinician. She reviewed his injection technique, diet history, incidence of hypoglycemia, and hypoglycemia treatment methods. She discussed with B.C. ways to reduce his risks of hypoglycemia, including food choices, insulin timing, and absorption variations at different injection sites.

The RD reinforced his clinician’s instruction to avoid old injection sites and added a new recommendation to lower insulin doses because of improved absorption at the new sites.

B.C. was now checking his blood glucose and recording results in a handheld electronic device in a form that could be downloaded, e-mailed, or faxed, but he was not recording his food choices. The dietitian asked him to keep food records and started his carbohydrate-counting education. A follow-up visit was scheduled for 1 week later.

At the second visit, B.C.’s mid-afternoon blood glucose was <70 mg/dl. He did not respond to treatment with 15 g carbohydrate from 4 oz. of regular soda. His blood glucose continued to drop, measuring 47 mg/dl 15 minutes later. He drank another 8 oz. of soda, and his blood glucose increased to 63 mg/dl 1 hour later. He then drank another 8 oz. of soda and ate a sandwich before leaving the dietitian’s office. He called in 1 hour later to report that his blood glucose was finally up to 96 mg/dl.

B.C.’s records showed a pattern of mid-afternoon hypoglycemia. He was willing to add a shot of lispro at lunch to his regimen, so the RD recommended reducing his morning NPH to prevent lows later in the day.

The RD also calculated insulin and carbohydrate ratios for blood glucose correction and meal-related insulin coverage using the “1500 rule” and the “500 rule.”

The 1500 rule is a commonly accepted formula for estimating the drop in a person’s blood glucose per unit of fast-acting insulin. This value is referred to as an “insulin sensitivity factor” (ISF) or “correction factor.” To use the 1500 rule, first determine the total daily dose (TDD) of all rapid- and long-acting insulin. Then divide 1500 by the TDD to find the ISF (the number of mg/dl that 1 unit of rapid-acting insulin will lower the blood glucose level). B.C.’s average TDD was 41 units. Therefore, his estimated ISF was 37 mg/dl per 1 unit of insulin. The RD rounded this up to 40 mg/dl to be prudent, given his history of hypoglycemia.

The 500 rule is a formula for calculating the insulin-to-carbohydrate ratio. To use the 500 rule, divide 500 by the TDD. For B.C., the insulin-to-carbohydrate ratio was calculated at 1:12 (1 unit of insulin to cover every 12 g of carbohydrate), but again this was rounded up to 1:14 for safety. Later, his carbohydrate ratio was adjusted down to 1:10 based on blood glucose monitoring results before and 2 hours after meals.

The RD taught B.C. how to use the insulin-to-carbohydrate ratio instead of his sliding scale to adjust his insulin and asked him to try to follow the new recommendations. With his endocrinologist’s approval, she reduced his NPH doses to 34 units and added a shot of lispro at lunchtime, the dose to be based on the amount of carbohydrate in the meal and his before-meal blood glucose level.

The RD asked B.C. to return in 1 week for evaluation and review of his new regimen. However, 3 days later, he returned after having had another severe episode of hypoglycemia.

In the course of these early visits, a good rapport developed between B.C. and the dietitian. B.C. learned that his judgment on how hypo- and hyperglycemia felt was often inaccurate and led him to make insulin adjustments that contributed to his hypoglycemia problems. By improving B.C.’s understanding of insulin doses and blood glucose responses, the RD hoped to help him become more skilled at making insulin dose adjustments. For the time being, however, he was still at risk for asymptomatic hypoglycemia. He had recently filled a prescription for glucagon, but the RD needed to review and encourage its proper use. She also provided literature to support his wife in case she needed to administer glucagon for him.

At this third visit, the RD reduced B.C.’s morning NPH dose to 22 units because of his rapid drop in blood glucose between noon and 1:00 p.m. This reduction finally eliminated his mid-afternoon lows.

B.C. had started using carbohydrate counting to make his decisions about lunchtime insulin doses. He liked carbohydrate counting because it gave him a more viable reason for testing his blood glucose frequently. Over the years, B.C.’s glycemia had become increasingly difficult to control. He had stopped checking his blood glucose because he felt unable to improve the situation once he had the information. In the early 1990s, his endocrinologist had started him self-adjusting insulin doses using the exchange system, but he found that he was always “chasing his blood sugars.” Carbohydrate counting changed everything. He now knew what to do to improve his blood glucose levels, and that made him feel more in charge of his diabetes.

Still, although carbohydrate counting led to more frequent testing and better blood glucose control than his old sliding scale, it was not perfect. At home, he had mastered this technique, but he ate many of his meals in restaurants, where carbohydrate counting was more challenging.

B.C. found it difficult to carry different types of insulin. This and his lifestyle suggested the need to change his multiple daily injections from regular to lispro insulin. He continued checking his blood glucose before and 2 hours after meals. His insulin-to-carbohydrate ratio of 1:10 g and his ISF of 1:40 mg/dl allowed him to stay within his goal of no more than a 30-mg/dl increase in blood glucose 2 hours after meals. He continued to be asymptomatic of hypoglycemia, but lows occurred less frequently. The new goal of therapy was to recover his hypoglycemia symptoms at a more normal level of about 70 mg/dl. He was scheduled for another visit 2 weeks later.

Between visits to the RD, BC-ADM, his clinician identified problems with the timing of his long-acting insulin peak, resulting in early nocturnal lows. Based on the clinician’s clinical experience of lente demonstrating a slightly smoother peak, she changed B.C.’s long-acting insulin unit-for-unit from NPH to lente.

At B.C.’s next visit, he and the RD reviewed his insulin doses of 22 units of lente in the morning and 11 units of lente at night. His TDD including premeal lispro now averaged 49 units. His average blood glucose levels were 130 mg/dl fasting, 100 mg/dl mid-afternoon, 127 mg/dl before dinner, and 200 mg/dl at bedtime.

The bedtime levels were higher because of late meals, the fat content of restaurant meals, his meat food choices, and his inexperience at counting carbohydrates for prepared foods. The dietitian suggested mixing regular and lispro insulin to try and get the average bedtime blood glucose level to 140 mg/dl. Mixing his calculated dose to be one-third regular and two-third lispro would provide coverage lasting a little longer than that of just lispro to cover higher-fat foods that took longer to digest. At the same time, the dietitian encouraged B.C. to choose lower-fat foods to help reduce his LDL cholesterol and assist with weight loss. B.C. now had an incentive to keep accurate food records to help evaluate his accuracy at calculating insulin doses.

B.C. and the RD also reviewed his decisions for treating lows. At his first meeting, B.C. ate anything and everything when he experienced hypoglycemia, which often resulted in blood glucose levels >400 mg/dl. Now, he was appropriately using 15–30 g of quick-acting glucose—usually 4–8 oz. of orange juice. He based this amount on his blood glucose level, expecting about a 40-mg/dl rise over 30 minutes from 10 g of carbohydrate. He checked his glucose level before treating when possible and always checked 15–30 minutes after treating to evaluate the results. Once his glucose reached 80 mg/dl or above, he either ate a meal or ate 15 g of carbohydrate per hour to prevent a recurrence of hypoglycemia until his next meal.

In completing her assessment during the next few meetings with B.C., the RD identified a problem with erectile dysfunction. She notifed his clinician and referred him to a urologist. Eventually, the urologist diagnosed reduced blood flow and started B.C. on sildenafil (Viagra).

B.C. wanted to resume exercise to help his weight loss efforts. Because exercise improves insulin sensitivity and can acutely lower blood glucose, the dietitian taught B.C. how to reduce his insulin doses by 25–50% for planned physical activity to further reduce his risks of hypoglycemia. He learned to carry his blood glucose meter, fluids, and carbohydrate foods during and after exercise. His pre-exercise blood glucose goal was set at 150 mg/dl. The dietitian instructed B.C. to test his blood glucose again after exercise and to eat carbohydrate foods if it was <100 mg/dl.

She also gave instructions for unplanned exercise. He would require additional carbohydrate depending on his blood glucose level before exercise, his previous experience with similar exercise, and the timing of the exercise. Education follow-ups were scheduled with the dietitian for 1 month later and every 3 months thereafter.

At his next annual eye exam, B.C. discovered that he had background retinopathy. He also reported feeling that his daily injection regimen had become too complicated. Still feeling limited in his ability to control his diabetes and looking for an alternative to insulin injections, he wanted to discuss continuous subcutaneous insulin infusion therapy (insulin pump therapy).

He, his endocrinologist, and his dietitian discussed the pros and cons of pump therapy and how it might affect his current situation. They reviewed available insulin pumps and sets and agreed on which ones would best meet his needs. The equipment was ordered, and a training session was scheduled with the dietitian (a certified pump trainer) in 1 month.

B.C. started using an insulin pump 2 years after his first visit with the dietitian. His insulin-to-carbohydrate ratio was adjusted for his new therapy regimen, and a new ISF was calculated to help him reduce high blood glucose levels. His endocrinologist set basal insulin rates at 0.3 units/hour to start at midnight and 0.5 units/hour to start at 3:00 a.m. This more natural delivery of insulin based on B.C.’s body rhythms and lifestyle further improved his diabetes control.

One week after starting pump therapy, B.C. called the dietitian to report large urine ketones and a blood glucose level of 317 mg/dl. His endocrinologist had changed his basal rates, but he wanted to meet with the dietitian to review his sites, set insertion, troubleshooting skills, and related issues. Working together, they eventually discovered that problems with his pump sites required using a bent-needle set to resolve absorption issues.

B.C’s relationship with his endocrinologist and dietitian was seamless. He met with the dietitian when his clinician was unavailable or when he needed more time to work through problems.

B.C. has met with the RD 15 times over 3 years. Eventually, he recovered symptoms of hypoglycemia when his blood glucose levels were 70 mg/dl. After 6 months of education meetings, his lab values had reached target ranges. Most recently, his LDL cholesterol was <100 mg/dl, his A1C results were <7%, his hypoglycemia symptoms were maintained at a blood glucose level of 70 mg/dl, and his blood glucose had been stabilized using the square-wave and dual-wave features on his insulin pump.

B.C. learned how to achieve recommended goals and to self-manage his diabetes with the help of his care team: endocrinologist, cardiologist, ophthalmologist, podiatrist, urologist, and advanced practice dietitian.

Advanced practice dietitians in diabetes work in many settings and see clients referred from many different types of medical professionals. They may see clients either before or after their appointments with other members of the health care team, depending on appointment availability and their need for nutrition therapy and diabetes education. Referring clinicians rely on their evaluations and findings. When necessary, clinician approval can be obtained for immediate interventions, enhancing the timeliness of care.

Why would an RD want to obtain the skills and certification necessary to earn the BC-ADM credential? The answer, as illustrated in the case study above, lies in their routine use of two sets of skills and performance of two roles: patient education and clinical management.

Dietitians who specialize in diabetes often find that their role expands beyond provider of nutrition counseling. As part of a multidisciplinary team, they become increasingly involved with patient care. As they move patients toward self-management of their disease, they necessarily participate actively in assessment and diagnosis of patients; planning, implementation, and coordination of their diabetes care regimens; and monitoring and evaluation of their treatment options and strategies. They find that their daily professional activities go beyond diabetes education, crossing over into identifying problems, providing or coordinating clinical care, adjusting therapy, and referring to other medical professionals. They often work independently, providing consultation both to people with diabetes and to other diabetes care team members.

The BC-ADM credential acknowledges this professional autonomy while promoting team collaboration and thus improving the quality of care for people with diabetes. The new certification formally recognizes advanced practice dietitians as they move beyond their traditional roles and into clinical problem solving and case management.

Claudia Shwide-Slavin, MS, RD, BC-ADM, CDE, is a private practice dietitian in New York, N.Y.

Note of disclosure: Ms. Shwide-Slavin has received honoraria for speaking engagements from Medtronic Minimed, which manufactures insulin pumps, and Eli Lilly and Co., which manufactures insulin products for the treatment of diabetes.

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COVID-19 vaccination and diabetic ketoacidosis

Academic Center, Sanitation1 Medical Academic Center, Bangkok 1033300, Thailand. moc.liamtoh@boojyueb

Viroj Wiwanitkit

Community Medicine, DY Patil Vidhyapeeth, Pune 233230, India

Corresponding author: Beuy Joob, PhD, Adjunct Associate Professor, Academic Center, Sanitation1 Medical Academic Center, Bangkok 1033300, Thailand. moc.liamtoh@boojyueb

An efficient coronavirus disease 2019 (COVID-19) vaccine is urgently required to fight the pandemic due to its high transmission rate and quick dissemination. There have been numerous reports on the side effects of the COVID-19 immu-nization, with a focus on its negative effects. Clinical endocrinology is extremely interested in the endocrine issue that arises after receiving the COVID-19 vaccine. As was already mentioned, after receiving the COVID-19 vaccine, many clinical problems could occur. Additionally, there are some compelling reports on diabetes. After receiving the COVID-19 vaccine, a patient experienced hyperosmolar hyperglycemia state, a case of newly-onset type 2 diabetes. There has also been information on a potential connection between the COVID-19 vaccine and diabetic ketoacidosis. Common symptoms include thirst, polydipsia, polyuria, palpitations, a lack of appetite, and weariness. In extremely rare clinical circumstances, a COVID-19 vaccine recipient may develop diabetes complications such as hyperglycemia and ketoacidosis. In these circumstances, routine clinical care has a successful track record. It is advised to give vaccine recipients who are vulnerable to problems, such as those with type 1 diabetes as an underlying illness, extra attention.

Core Tip: There has also been information on a potential connection between the coronavirus disease 2019 (COVID-19) vaccine and diabetic ketoacidosis. Common symptoms include thirst, polydipsia, polyuria, palpitations, a lack of appetite, and weariness. In extremely rare clinical circumstances, a COVID-19 vaccine recipient may develop diabetes complications such as hyperglycemia and ketoacidosis.

INTRODUCTION

Because of the pandemic's high transmission rate, an effective coronavirus disease 2019 (COVID-19) vaccine is urgently needed[ 1 ]. The available literature indicates that both vaccines help prevent severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. However, given that the vaccination is new, any potential side effects are of greater concern[ 2 - 3 ]. When a handful of novel vaccines created in response to the COVID-19 pandemic got emergency approval and were widely distributed in late 2020[ 2 ], pharmacovigilance was unwittingly thrust into the spotlight. An effective global post marketing safety surveillance system was emphasized due to the employment of cutting-edge technologies and the anticipated rapid and widespread deployment of the vaccinations. The vaccinations went through extensive clinical evaluation and regulatory authority review. Many reports on the adverse effects of the COVID-19 vaccination have focused on how diverse they are. Clinical endocrinology is quite concerned about the endocrine issue that manifests after receiving the COVID-19 vaccination. The main concern expressed by the authors of this paper is that diabetes can become a medical problem after receiving the COVID-19 vaccine. After getting the COVID-19 vaccination, numerous clinical issues could arise, as was already mentioned. There are also some interesting reports regarding diabetes. The key words are provided here with a brief explanation.

Diabetes and COVID-19 have a well-established association. There is a bidirectional causal relationship between COVID-19 and type 2 diabetes. Diabetes may exacerbate COVID-19 severity, and COVID-19 vulnerability may increase diabetes risk[ 4 ]. Diabetes patients should receive the COVID-19 vaccine, just like everyone else, to protect themselves from the disease. It is critical to discuss the risks of vaccination for those who currently have diabetes mellitus. Piccini et al [ 5 ] evaluate the likelihood of glycemic control modification, insulin dose adjustment, and adverse effects following COVID-19 vaccination in young people with type 1 diabetes who use varying degrees of technology[ 5 ]. Piccini et al [ 5 ] came to the conclusion that receiving the OVID-19 immunization did not significantly increase the risk of glycemic control disturbance in type 1 diabetes adolescents and young adults[ 5 ]. This information may be helpful clinically[ 6 ] when counseling families about the SARS-CoV-2 vaccine for young people with type 1 diabetes. In a study by D'Addio et al [ 6 ] that investigated the immunogenicity and security of SARS-CoV-2 mRNA vaccines, a cohort of individuals with type 1 diabetes took part[ 5 ]. The vaccination demonstrated both dependability and security, according to D'Addio et al [ 6 ].

Several reports claim that COVID-19 vaccine recipients have problems with their diabetes. The exacerbation of hyperglycemia in people with type 2 diabetes after receiving the COVID-19 vaccination is the first problem that needs to be addressed[ 7 ]. Mishra et al [ 7 ] claim that an early inflammatory reaction to the vaccine and a subsequent immunological response are likely to be the causes of a minor and transient rise in blood sugar levels[ 7 ]. Mishra et al [ 7 ] published a case series that substantiated the etiology of transient immuno-inflammation because all episodes of hyperglycemia were self-limited and did not require significant treatment modifications[ 7 ]. A rapid jump in blood sugar levels appears to be caused by a vaccine. The possibility of a mild to moderate rise in blood sugar levels following vaccination has been theorized[ 7 ]. One patient experienced new-onset type 2 diabetes after receiving the COVID-19 vaccine, which is known as hyperosmolar hyperglycemia state[ 8 ].

COVID-19 VACCINATION AND DIABETIC KETOACIDOSIS

Clinical diabetology has an intriguing discussion regarding the COVID-19 vaccine and diabetic ketoacidosis. As was already indicated, the immunization may cause hyperviscosity and have unintended side effects. Additionally, reports of a connection between the COVID-19 immunization and diabetic ketoacidosis have been made. Three days after the first dose of COVID-19 RNA-based vaccines, the patient typically experiences thirst, polydipsia, polyuria, palpitations, a lack of appetite, and exhaustion without a prior history of diabetes[ 9 ]. Hyperglycemia, anion gap metabolic acidosis, and ketonuria are the three main signs of classic diabetic ketoacidosis[ 9 ]. It is possible to detect insulin autoantibody positivity and latent thyroid autoimmunity[ 10 ]. Ganakumar et al [ 11 ] advised that people with diabetes, particularly those with type 1 diabetes mellitus and inadequate glycemic control, be constantly monitored for hyperglycemia and ketonemia for at least two weeks after receiving the COVID-19 vaccine[ 11 ]. Autoimmunity and genetic predisposition may have contributed to the onset of the disease, even if the precise pathophysiologic mechanisms underlying type 1 diabetes are still unknown[ 12 ].

According to Tang et al [ 12 ], vaccination could result in type 1 diabetes, irreversible islet beta cell loss, and autoimmunity in persons with susceptible genetic backgrounds[ 12 ]. The problem might be more serious and more likely to occur in situations where type 1 diabetes is already present. Yakou et al [ 13 ] advised that the immunization be cautiously administered to type 1 diabetes patients receiving strict insulin therapy and a sodium-glucose transporter[ 13 ] due to the increased risk of ketoacidosis. In the affected case, despite hyperglycemia and diabetic ketoacidosis (DKA) after SARS-CoV-2 immunization, low glycohemoglobin levels are a crucial indicator of COVID-19 vaccine-related DKA[ 14 ]. As a preventive measure, it is essential to counsel patients to continue getting insulin injections[ 13 ]. Due to the significant risk of ketoacidosis, the vaccination should be cautiously given to type 1 diabetes patients receiving rigorous insulin therapy and a sodium-glucose transporter[ 15 ]. When a patient becomes ill, it's crucial to remind them to continue taking their insulin injections and to drink enough fluids[ 13 ]. A similar preventative concern should be used in the case of the patient with poorly controlled type 2 diabetes, in addition to the patient with underlying type 1 diabetes. According to Kshetree et al [ 15 ], Type I or dysglycemia in Type 2 diabetes mellitus is becoming more frequently documented following COVID-19 vaccinations or infection[ 16 ]. The mechanisms could be autoimmunity following mRNA vaccinations, cytokine-mediated beta-cell injury, or as a component of an autoimmune syndrome brought on by vaccine adjuvants[ 15 ]. Further investigation into the negative effects of people prone to life-threatening illnesses is required, as suggested by Lin et al [ 14 ]. Also, there might be a need for postvaccination surveillance on both hyperglycemia and DKA problems[ 16 ].

Concerning the reported cases of a link between COVID-19 vaccination and diabetes ketoacidosis, an important clinical question is whether ketosis in type 1 diabetes is related to the use of sodium-glucose transport protein 2 (SGLT2) inhibitors. The clinical history of the vaccine recipients in the published articles on the clinical association usually revealed no use of SGLT2 inhibitors, which could be a clue to support the possible clinical association between COVID-19 vaccination and ketoacidosis. Last but not least, it should be noted that the mRNA COVID-19 vaccine is primarily associated with most findings on the relationship between COVID-19 immunization and diabetic ketoacidosis. There are, however, a few reports of clinical associations with other vaccination types (viral vector and inactivated COVID-19 vaccines) that have been documented[ 11 ]. The fact that the mRNA vaccination is currently the primary recommended COVID-19 vaccine may be the cause of the higher number of reported cases in the mRNA vaccine group. As previously stated, the COVID-19 vaccination may cause diabetic ketoacidosis in patients with type 1 or type 2 diabetes mellitus (Table ​ (Table1 1 ).

Table summarizing the key information of coronavirus disease-19 vaccine related diabetic ketoacidosis in recipients with background type 1 and type 2 diabetes mellitus

There are significant differences in COVD-19 vaccine-induced diabetes ketoacidosis between recipients with type 1 and type 2 diabetes. COVID-19 vaccine induced diabetes ketoacidosis usually occurs in adolescent male cases with inadequate glycemic control in cases with background type 1 diabetes mellitus[ 11 ]. This is the same pattern seen in diabetic ketoacidosis caused by COVID-19 in type 1 diabetes patients[ 17 ]. There are fewer reported cases of COVID-19 vaccine-induced diabetes ketoacidosis in people with type 2 diabetes mellitus, and the patient is usually an elderly man with a long history of diabetic illness[ 15 ]. The background hemoglobin A1C level, on the other hand, has not been identified as a risk factor for the development of COVID-19 vaccine-induced diabetic ketoacidosis[ 18 ].

In general, the COVID-19 immunization should be given to the diabetic patient because it has been proven to be effective. Generally, it has been confirmed that it is secure. In exceedingly uncommon clinical situations, a COVID-19 vaccination recipient may experience diabetes-related problems such as hyperglycemia and ketoacidosis. Routine clinical care has a history of success in some situations. Users of vaccines who are more likely to develop problems, such as those who already have type 1 diabetes as an underlying illness, are advised to receive additional attention. Because there is a possible link between the COVID vaccine and ketoacidosis, the risk diabetic case must be closely monitored. There is still a need for more clinical research on this subject because there isn't any in vivo or in vitro experimental data at this time.

Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.

Provenance and peer review: Invited article; Externally peer reviewed.

Peer-review model: Single blind

Peer-review started: December 15, 2022

First decision: January 17, 2023

Article in press: April 12, 2023

Specialty type: Endocrinology and metabolism

Country/Territory of origin: Thailand

Peer-review report’s scientific quality classification

Grade A (Excellent): 0

Grade B (Very good): B

Grade C (Good): C, C, C

Grade D (Fair): D

Grade E (Poor): 0

P-Reviewer: Cai L, United States; Dong Z, China; Moreno-Gómez-Toledano R, Spain; Wu QN, China; Zhang F, China S-Editor: Li L L-Editor: A P-Editor: Zhang XD

Contributor Information

Beuy Joob, Academic Center, Sanitation1 Medical Academic Center, Bangkok 1033300, Thailand. moc.liamtoh@boojyueb .

Viroj Wiwanitkit, Community Medicine, DY Patil Vidhyapeeth, Pune 233230, India.