Growing epidemiological data has revealed that patients with diabetes are at higher risk for severe clinical outcomes of Covid-19. Hyperglycemia (high blood sugar) can impair host defences, and poor glycemic control has been associated with infections. As the pandemic continues to evolve, it has also become clear that the interplay between Covid-19 and diabetes entails a complex pathophysiology. Not only are Covid-19 complications more severe in diabetes patients, but recent data also suggests that Covid-19 can precipitate diabetic complications like hyperglycemia and diabetic ketoacidosis (build-up of acids in blood).
The mechanisms are likely to involve the angiotensin converting enzyme receptor 2 (ACE2), a binding site for SARS-CoV-2, which is expressed in key metabolic organs like the pancreas and beta cells. The SARS-CoV-2 tropism for beta cells causes cell damage and impairment in insulin secretion, causing ketoacidosis and hyperglycemia.
In June 2020, an international group of experts announced the formation of CoviDiab, a global registry for Covid-19 diabetes cases. It aims to investigate the extent and pathogenesis of new onset diabetes and metabolic dysfunction in pre-existing diabetes to help uncover novel mechanisms of the disease and define the best interventions.
Recently, I had a patient—John (name changed)—who was admitted for Covid-19. He had a prior history of diabetes, which was fairly well controlled with analogue insulin—metformin and empagliflozin. But he was on the obese side. On the day of admission, I noticed that apart from high sugar level, he had a fast breathing rate and also a drop in oxygen saturation below 95 per cent. I promptly started oxygen via face mask, but as the saturation did not stabilise, I initiated high flow nasal oxygen. I realised that conventional premix insulin would not work for him as he had gone into a cytokine storm induced by the virus. I started him on intravenous remdesivir and steroids, both of which again raise sugars. The spike was brought under control using intravenous insulin and after 48 hours using subcutaneous basal bolus insulin. His insulin requirement had tripled from 30 to more than 120 units/day! By the time of discharge 10 days later, he still had an insulin requirement of above 60 units, met by the basal bolus insulin regimen.
In stark contrast, another diabetes patient with Covid-19—Anitha (name changed)—had an uneventful course after admission. She was a model and part-time actor. She maintained a healthy BMI of 22 and was regular with medications. She did not develop the cytokine storm and her sugars were well maintained with her oral drugs—sitagliptin and metformin. She had only mild symptoms. I did not have to initiate insulin and after seven days she was discharged with her same oral medications.
The take-home message is poorly controlled diabetes and obesity are a prognostic factor for Covid-19 worsening in admitted patients. This holds true if HbA1c is above 9 and the BMI above 28. Such patients require oxygen via face mask initially, then high-flow nasal oxygen. About 10 per cent of them require non-invasive ventilation and about 3 per cent intubated ventilation. Sadly, the mortality rate of those who are intubated is quite high—more than 50 per cent—unless the ICU is equipped with ECMO machine and other support measures.
As a member of a team that treated over 470 cases, I must inform the public to maintain a healthy BMI by exercise and for those who have diabetes to maintain an HbA1c of less than 7.5. For those who have comorbidities, get the vaccine as quickly as possible.
The writer is consultant, internal medicine, VPS Lakeshore Hospital, Kochi.