1
Introduction
There is scarce data on diabetic ketoacidosis (DKA) in Covid-19 infection. We report
a case of DKA precipitated by Covid-19 in a patient with newly diagnosed diabetes
mellitus.
A 37 year-old, previously healthy man presented with 1 week history of fever, vomiting,
polydipsia and polyuria.
On admission, his temperature was 38.5°C. He was haemodynamically stable but mildly
tachycardic. He did not display Kussmaul’s breathing and did not require supplemental
oxygen. His body mass index was 22.6 kg/m2 with no evidence of insulin resistance.
Given positive contact history, he was tested and confirmed to be infected with severe
acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Laboratory investigations (Table
1
) were significant for hyperglycemia, high anion gap metabolic acidosis and ketonemia,
confirming the diagnosis of DKA.
Table 1
Laboratory results
Investigation
Result
Reference Range
Venous glucose (mmol/L)
39.7
-
Arterial blood gaspH (mmHg)Bicarbonate (mmol/L)pCO2 (mmHg)
7.281225
7.25 – 7.3522 – 2835 - 45
Sodium (mmol/L)
128
135 - 145
Chloride (mmol/L)
86
95 - 110
Anion gap
30
8 – 16
Ketones (mmol/L)
6.4
< 0.6
Creatinine (umol/L)
95
67 – 112
Glycated haemoglobin (%)
14.2
-
He received 6 litres of intravenous fluids and intravenous insulin infusion in the
first 24 hours. Serum electrolytes were closely monitored. DKA resolved the following
day and he was transitioned to subcutaneous insulin therapy.
DKA occurs as a result of insulin deficiency and increased counterregulatory responses,
which favour the production of ketones. The interactions between SARS-CoV-2 and the
renin-angiotensin-aldosterone system (RAAS) might provide another mechanism in the
pathophysiology of DKA.
Angiotensin-converting enzyme 2 (ACE2), a key enzyme in the RAAS, catalyzes the conversion
of angiotensin II to angiotensin (1-7)[1]. ACE2 is highly expressed in the lungs,
pancreas and serves as the entry point for SARS-CoV-2[1]. After endocytosis of the
virus complex, ACE2 expression is downregulated[2]. There are 2 implications of these
interactions. Firstly, entry of SARS-CoV-2 into pancreatic islet cells may directly
aggravate beta cell injury[3]. Secondly, downregulation of ACE2 after viral entry
can lead to unopposed angiotensin II, which may impede insulin secretion[4]. These
2 factors might have contributed to the acute worsening of pancreatic beta cell function
and precipitated DKA in this patient.
In addition, the relationship between SARS-CoV-2 and the RAAS can complicate DKA management.
Excessive fluid resuscitation may potentiate acute respiratory distress syndrome as
angiotensin II increases pulmonary vascular permeability and worsens damage to lung
parenchyma[5]. Furthermore, angiotensin II stimulates aldosterone secretion, potentiating
the risk of hypokalemia, which may necessitate more potassium supplementation in order
to continue intravenous insulin to suppress ketogenesis.
In conclusion, it is possible that SARS-CoV-2 may aggravate pancreatic beta cell function
and precipitate DKA. Further studies will help delineate the pathophysiology. We also
highlight the pertinent clinical considerations in the concurrent management of two
life-threatening conditions – DKA and Covid-19.
The authors do not have any financial associations or conflicts of interests to disclose.
Funding: None.
Declaration of Competing Interest
The authors declare that they have no known competing financial interests or personal
relationships that could have appeared to influence the work reported in this paper.