The Critical Role of Insulin Therapy in the Management of Stress Hyperglycaemia in Sepsis Secondary to Community-Acquired Pneumonia with Impending Respiratory Failure and Acute Severe Asthma Exacerbation: A Case Report from a Secondary-Level Indonesian Hospital

Abstract

Introduction. Stress hyperglycaemia is a common but frequently overlooked metabolic derangement in acutely ill patients without diabetes, arising from catecholamine and glucocorticoid surges, cytokine-mediated insulin resistance, and accelerated hepatic gluconeogenesis. It independently predicts adverse outcomes in both sepsis and community-acquired pneumonia (CAP). Recognition becomes particularly challenging when severe dyspnoea dominates, leucocyte count is normal, and chest radiography is non-specific—a combination common when acute asthma exacerbation and lower respiratory tract infection coexist.

Case Illustration. A 58-year-old Indonesian woman with lifelong asthma, hypertension, and remote cardiovascular and cerebrovascular history, but no known diabetes, presented with three days of progressive dyspnoea, productive cough, fever, nausea, and epigastric pain. She was orthopnoeic, agitated, speaking in single words, with respiratory rate 62/min, heart rate 116/min, oxygen saturation 87% on room air, and a normal leucocyte count of 5.1 × 10³/µL. Random blood glucose was markedly elevated at 248 mg/dL. Chest radiography showed a bronchitic pattern, cardiomegaly without congestion, and aortic atherosclerosis. She was diagnosed with sepsis secondary to CAP with impending respiratory failure, acute severe asthma with life-threatening features, and newly detected stress hyperglycaemia. Management comprised high-flow oxygen, empirical ceftriaxone and levofloxacin, systemic corticosteroid, nebulised bronchodilator and corticosteroid, intravenous magnesium sulphate, and basal insulin glargine 8 units subcutaneously at night. Fasting plasma glucose the following morning was 150 mg/dL. She improved steadily without intubation and was discharged on day four speaking in full sentences, saturating 95% on room air.

Discussion. This case demonstrates the convergence of three hyperglycaemic mechanisms: endogenous stress response, high-dose corticosteroid, and β₂-agonist therapy. Hyperglycaemia impairs neutrophil function, elevates airway surface glucose promoting bacterial proliferation, amplifies cytokine release, and contributes to respiratory muscle dysfunction—each aggravating dyspnoea. Insulin was the only rational glucose-lowering agent: rapidly titratable, anti-inflammatory, and avoiding organ-specific hazards in sepsis.

Conclusion. Random blood glucose should be measured in every patient presenting with severe dyspnoea, regardless of diabetes history. Early recognition and prompt basal insulin, delivered alongside guideline-directed therapy in a secondary-level hospital without intensive care facilities, accompanied rapid clinical recovery and avoided invasive ventilation. Glycaemic assessment deserves integration into emergency evaluation of the severely breathless patient.