A case report of diabetic keto-acidosis post intra-articular steroid injection in patient with type 1 diabetes mellitus: a rare complication
Highlight box
Key findings
• This case report highlights the potential risk of development of diabetic ketoacidosis (DKA) in patients with known diabetes mellitus.
What is known and what is new?
• Patients with known diabetes mellitus are at elevated risk of complications from steroids. Studies have shown elevation in blood glucose levels following intra-articular steroid injection.
• DKA is one of the rare and underreported complications post intra-articular steroid injection and there are very few reported cases available is literature. This report would add to existing body of evidence about the possibility of this complication and will allow physicians to safety net patients, so that prompt treatment can be started.
What is the implication, and what should change now?
• This case highlights the importance of promptly diagnosing and treating patients with DKA post intra-articular corticosteroid (IACS) injection. Enhanced monitoring of diabetic patients for hyperglycaemia or DKA following IACS is highly recommended, especially in first week and patients should get safety netting advise about signs and symptoms of DKA as well.
Introduction
Diabetic ketoacidosis (DKA) is the definition of an absolute deficiency of insulin in the body. DKA is characterised by uncontrolled hyperglycaemia, metabolic acidosis, and increased concentration of ketones in the body (1). It is more common among those with type 1 diabetes though it may also occur in type 2 diabetics, and the use of sodium-glucose co-transporter-2 (SGLT-2) inhibitors in this group further increases the risk of DKA, especially euglycemic DKA (2).
DKA is a life-threatening complication of diabetes. Catabolic stresses such as infection or surgery, poor diabetic control or an initial presentation of diabetes are the most common causes of DKA. It is less commonly caused by intra-articular steroid injections as presented further in this case report.
The use of intra-articular corticosteroid (IACS) injection is common in orthopaedic settings due to their anti-inflammatory and pain-relieving benefits (2). Whilst infection, swelling and pain are the most common complications (3), corticosteroids have a significant effect on blood sugar levels as well. Studies have found that 43% of non-diabetic patients experience hyperglycaemia just two hours after intra-articular steroid injection (4,5). Steroids are known to inhibit the hypothalamic-pituitary axis, patients with poor glycaemic control and those at higher risk or prone to DKA are at an even higher risk of developing complications post intra-articular steroid (6). We present this article in accordance with the CARE reporting checklist (available at https://acr.amegroups.com/article/view/10.21037/acr-24-290/rc).
Case presentation
A 76-year-old gentleman presented to the Emergency Department with a one-day history of lethargy and abdominal pain. He had a past medical history inclusive of type 1 diabetes mellitus, asthma, hypertension, and osteoarthritis, all of which were well controlled. He was normally independent with activities of daily living and mobilised unaided. Three days prior to this presentation, he had received an IACS injection (80 milligrams of depomedrone) to his right hip as part of pain management.
On arrival, vital signs were stable: respiratory rate was 20 breaths/min with oxygen saturation of 98% on air, his blood pressure was 135/50 mmHg, his heart rate was 93 beats per minute, and he had a temperature of 36.7 degree Celsius. Physical examination was generally unremarkable.
An initial venous blood gas showed a pH of 7.264 with bicarbonate of 14.4 mmol/L. Blood glucose was 27.4 mmol/L and capillary ketones was 3.3 mmol/L. A diagnosis of DKA was made and treatment according to local protocol was commenced.
Laboratory blood results are outlined in Table 1.
Table 1
| Biochemistry | Value |
|---|---|
| Haemoglobin | 101 g/L |
| White cell count | 16.2×109/L |
| Platelets | 367×109/L |
| Sodium | 121 mmol/L |
| Potassium | 6.4 mmol/L |
| Urea | 3.0 mmol/L |
| Creatine | 174 μmol/L |
| C-reactive protein | 22 mg/L |
An ECG was done which showed normal sinus rhythm with no ST segment changes and echocardiogram was done which showed normal left and right ventricle size and function with no significant valvular pathology. A full sepsis screen was performed. Blood and urine cultures were negative. His chest X-ray showed no consolidation, infective changes or any suspicious pathology and urine dip was negative for leucocytes and nitrites. The patient was afebrile throughout admission and had no focal symptoms suggestive of infection. The mild elevation in inflammatory markers was deemed nonspecific in the context of DKA.
The patient used an Insulin pump which was firmly in place on arrival and reported having good glycaemic control with no prior admissions for any acute diabetic complication. The interrogation of the pump history confirmed regular basal insulin delivery in the days leading up to admission. There was no evidence of pump malfunction, occlusion, or interruption of insulin administration. The patient also confirmed appropriate bolus dosing for meals. His HbA1C was 56 mmol/mol on admission.
The patient improved rapidly following commencement of local DKA protocol and was switched to his regular subcutaneous Insulin (via Insulin pump) following review by the diabetic team. He was discharged a few days later. In the absence of other identifiable triggers, the intra-articular steroid injection was considered the likely precipitant. Table 2 highlights the timeline of main events related to the case.
Table 2
| Day | Event |
|---|---|
| Day –3 | Received 40 mg depomedrone IACS injection |
| Day 0 | Presented to ED with lethargy, abdominal pain |
| Day 0 | DKA diagnosis (blood glucose 27.4 mmol/L, pH 7.264, ketones 3.3 mmol/L) |
| Day 1–3 | Treated as per DKA protocol |
| Day 4 | Reviewed by Endocrine & Rheumatology teams |
| Day 5 | Discharged with no complications |
DKA, diabetes ketoacidosis; ED, emergency department; IACS, intra-articular corticosteroid.
All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Helsinki Declaration and its subsequent amendments. Written informed consent was obtained from the patient for publication of this case report. A copy of the written consent is available for review by the editorial office of this journal.
Discussion
DKA is a recognised acute complication of diabetes mellitus. It is more common in patients with type 1 diabetes mellitus. The association of British Clinical Diabetologists outline the diagnostic criteria for DKA as a blood glucose concentration of more than 11 mmol/L, a capillary or blood ketone concentration of >3.0 mmol/L or significant ketonuria (2+ or more on standard urine sticks) and a bicarbonate concentration of <15.0 mmol/L and/or venous pH <7.3 (7).
Insulin deficiency, increased insulin counter-regulatory hormones; which include cortisol, glucagon, growth hormone, and catecholamines; and peripheral insulin resistance lead to hyperglycaemia, dehydration, ketosis, and electrolyte imbalance which underlie the pathophysiology of DKA. Hyperglycaemia causes osmotic diuresis leading to fluid and electrolyte loss and dehydration. Increased lipolysis because of Insulin deficiency leads to elevated free fatty acids (which are later converted to ketones) and develops into metabolic acidosis. This results in vomiting which subsequently leads to loss of fluids and electrolytes. Processes that increase insulin resistance, counter-regulatory hormones, or impair carbohydrate metabolism can precipitate DKA (8).
With regards to triggering factors, omission of insulin and infection are the two most common precipitants of DKA. Non-adherence may account for up to 44% of DKA presentations, while infection is less frequently observed in DKA patients. Other known precipitants include acute medical illnesses involving the cardiovascular system (myocardial infarction, stroke, acute thrombosis) and gastrointestinal tract (bleeding, pancreatitis), diseases of endocrine axis (acromegaly, Cushing’s syndrome, hyperthyroidism) and impaired thermoregulation or recent surgical procedures are also common precipitants. Certain medications, such as beta-blockers, corticosteroids, sodium-glucose cotransporter-2 SGLT-2 inhibitors, could precipitate DKA (8). Although infection is a common precipitant of DKA, this was deemed unlikely in this case. The patient had no clinical signs of infection, remained afebrile, and had negative blood and urine cultures. Imaging, including chest x-ray, revealed no infective source.
IACS is a quite common procedure particularly in pain management and is often done for patients with severe osteoarthritis. Studies have shown changes in blood glucose levels following intra-articular steroid injection (9,10). Moon et al. in 2014 had shown elevated blood glucose levels soon after procedure; in all subgroups, fasting plasma glucose levels were significantly higher one day after injection but returned to baseline seven days after the injection (9). Another study done to assess impact of IACS on glycaemic control revealed nearly 16% of patients experienced a greater-than-expected rise in HbA1c following IACS (10).
However, literature search revealed that there were not many known cases of DKA following IACS. There is case report published in the Journal of Urgent Care Medicine which describes a case of a known diabetic presenting with DKA following IACS a few days prior (11). The patient in this case report had a similar scenario—presenting with a history of lethargy and abdominal pain and was found to be in DKA. The patient had no obvious evidence of infection; he was not started on any new medications and had good glycaemic control prior to presentation. Studies have shown that IACS can lead to elevated glucose levels and even rises in HbA1c post procedure. This results in further risks of patients with diabetes receiving IACS injections.
This case report is limited by its single-patient design, which restricts generalizability. While clinical and laboratory workup did not reveal signs of infection or insulin pump malfunction, the possibility of undetected factors cannot be entirely ruled out. Additionally, we did not quantify systemic absorption of corticosteroids following IACS. Future studies should explore the pharmacokinetics of IACS in diabetic patients and assess risks across larger cohorts. Prospective tracking of glycaemic trends and HbA1c pre- and post-IACS would be helpful in stratifying patients at higher risk.
Conclusions
Given that studies have shown that IACS injection can cause hyperglycaemia in diabetic (and even nondiabetic) patients, it stands to reason those patients with diabetes mellitus are at risk of developing acute complications but instances of patients developing these complications are rare (or under-reported). While causality cannot be definitively established, this case highlights the need to consider IACS injections as a potential trigger for DKA) in at-risk patients, particularly when other common precipitants are excluded. Enhanced monitoring should include daily self-monitoring of blood glucose and ketones for at least one-week post-IACS, and earlier clinical review if patients report symptoms such as nausea, vomiting, abdominal pain, or unexplained fatigue. Clear safety netting advice should be provided at the time of steroid administration.
Acknowledgments
None.
Footnote
Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://acr.amegroups.com/article/view/10.21037/acr-24-290/rc
Peer Review File: Available at https://acr.amegroups.com/article/view/10.21037/acr-24-290/prf
Funding: None.
Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://acr.amegroups.com/article/view/10.21037/acr-24-290/coif). The authors have no conflicts of interest to declare.
Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Helsinki Declaration and its subsequent amendments. Written informed consent was obtained from the patient for publication of this case report. A copy of the written consent is available for review by the editorial office of this journal.
Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.
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Cite this article as: Pabani UK, Osondu M, Jones KLC, Kumar V. A case report of diabetic keto-acidosis post intra-articular steroid injection in patient with type 1 diabetes mellitus: a rare complication. AME Case Rep 2025;9:140.
