Diabetic Ketoacidosis and Hyperosmolar Hyperglycaemia 

Words By Taneisha Beckton 

Diabetes mellitus (diabetes) is a common, and important endocrine disorder characterised by defective insulin production and/or action¹. Whilst there are several subtypes of diabetes, it is largely categorised into Type 1 and Type 2. Type 1 diabetes is most commonly caused by a failure to produce insulin as a result of autoimmune destruction of pancreatic beta cells. On the other hand, the development of type 2 diabetes has been attributed to increased insulin resistance and reduced insulin production as a result of adaptive changes to target tissues^1,2. 

The prevalence of diabetes is increasing and is becoming a major global health problem^3,4. In Australia, 1.24 million people are registered as having diabetes and an additional 500,000 are estimated to have undiagnosed diabetes³. The progressively increasing number of people diagnosed with diabetes requires the development and provision of more resources to manage the disease and its complications⁴. The implications of diabetes on the health system are widespread and include both acute and chronic complications. Patients experiencing acute glycaemic complications, most frequently severe hypoglycaemia and hyperglycaemic crises, will often seek emergency medical assistance³. 

Recent research has highlighted the increasing demand for Australian emergency service attendance to hyperglycaemic cases³. The seven-year community-based observational study identified that although prehospital emergency service attendances for hyperglycaemia were less frequent than for hypoglycaemia, the frequency of transport to hospital for hyperglycaemia was higher than for other conditions and much higher than for hypoglycaemia⁵. This may be strongly correlated with the high mortality rates associated with the incidence of hyperglycaemic emergencies, such as Diabetic Ketoacidosis (DKA) and Hyperglycaemia Hyperosmolar State (HHS)⁶. 

In the prehospital environment, DKA and HHS are potentially fatal medical emergencies which often present in the context of uncontrolled diabetes⁵. A paramedics ability to recognise the incidence of DKA or HHS is imperative to facilitate timely management and reduce the risk of adverse health outcomes including myocardial infarction, stroke, sepsis, and trauma^{1, 5, 6}. 

DKA occurs most commonly in individuals with type 1 diabetes but may occasionally occur in those with type 2 diabetes². DKA results from an absolute insulin deficiency, or relative insulin deficiency in the presence of the increased release of counterregulatory hormones (glucagon, catecholamines, cortisol and growth hormone)^{2, 7}. The release of these hormones worsens insulin resistance and causes further impairment of insulin secretion^{2, 7}. Insufficient insulin concentration impairs the uptake of glucose into cells for energy, thereby resulting in a shift to metabolise triglycerides and amino acids instead of glucose^{2, 8}. The consequential release of ketone bodies lowers blood pH leading to the onset of metabolic acidosis². 

As a result, there are distinctive clinical signs and symptoms which may manifest in the onset of DKA. Upon assessment, DKA should be suspected when blood glucose levels (BGL) are greater than 10mmol/L and blood ketone levels are greater than 1.5mmol/L ^{2, 9}. The provisional diagnosis of DKA is further justified in the presence of polyuria, polydipsia, and evidence of dehydration^{2, 10}. Moraes and Surani⁹ suggest that a combination of the aforementioned signs and symptoms, combined with gastrointestinal, neurological, and cardiovascular involvement are pertinent indicators of the onset of metabolic acidosis. Such signs and symptoms may include nausea and/or vomiting, abdominal pain, altered level of consciousness, tachycardia, and hypotension. Once metabolic acidosis is prevalent, compensatory mechanisms such as tachypnoea, and in severe circumstances, the presence of Kussmaul respirations may evolve^{2, 8, 9}.

Contrastingly, HHS is most prevalent in individuals with type 2 diabetes, or in some instances, in those without a diagnosis of diabetes². In HHS, there is a sufficient concentration of circulating insulin which prevents the onset of ketosis and consequent acidosis⁷. However, the acceleration of glycogenolysis, gluconeogenesis and reduced peripheral uptake of glucose results in a significant hyperglycaemia state². The clinical manifestations of HHS are in some ways similar to that of DKA, in that an incidence of polyuria, polydipsia and evidence of dehydration are pertinent indicators of HHS¹⁰. These symptoms, combined with a BGL of greater than 30mmol/L without significant blood ketone levels, should elicit an index of suspicion of HHS among clinicians². Generally, the impacts of extreme dehydration and hypernatremia and in severe cases, renal failure, causes an altered mental status of patients suffering from HHS^{2, 7}. Prehospitally, the management of HHS is very similar to DKA with replacing fluid deficits and transporting to an appropriate hospital for ongoing management. 

Diabetes is a highly prevalent chronic disease within Australia and requires large amounts of resourcing, education, and treatment regimes. Diabetic emergencies, including hyperglycaemia, are frequently encountered by paramedics in the prehospital environment. Whilst they are often a result of poor diabetic management, it is crucial that paramedics are able to recognise the pertinent signs and symptoms of both DKA and HHS to facilitate prompt treatment and management of such medical emergencies. 

References 

1. Luciano-Feijoo M, Cabanas J, Brice J. Diabetic Emergencies. In: Cone D, Brice J, Delbridge T, Myers J, editors. Emergency Medical Services: Clinical Practice and Systems Oversight. 1: Clinical Aspects of EMS. Third ed. NAEMSP: John Wiley & Sons, Inc.; 2021. p. 188-93.
2. Williams B, Ross L. Paramedic Principles and Practice: A Clinical Approach 2E: Elsevier; 2021.
3. Villani M, Earnest A, Nanayakkara N, Smith K, De Courten B, Zoungas S. Time series modelling to forecast prehospital EMS demand for diabetic emergencies. BMC Health Services Research. 2017;17(1).
4. Davis WA, Peters KE, Makepeace A, Griffiths S, Bundell C, Grant SFA, et al. Prevalence of diabetes in Australia: insights from the Fremantle Diabetes Study Phase II. Internal Medicine Journal. 2018;48(7):803-9.
5. Villani M, Nanayakkara N, Ranasinha S, Earnest A, Smith K, Soldatos G, et al. Utilisation of prehospital emergency medical services for hyperglycaemia: A community-based observational study. PLoS One. 2017;12(8):1-12.
6. Zelihic E, Poneleit B, Siegmund T, Haller B, Sayk F, Dodt C. Hyperglycemia in emergency patients – prevalence and consequences: results of the GLUCEMERGE analysis. Eur J Emerg Med. 2015;22(3).
7. Umpierrez G, Korytkowski M. Diabetic emergencies — ketoacidosis, hyperglycaemic hyperosmolar state and hypoglycaemia. Nature Reviews Endocrinology. 2016;12(4):222-32.
8. Turan C, Yurtseven A, Basa EG, Gökşen D, Ulaş Saz E. The Effects of Prehospital Care on Outcome in Pediatric Diabetic Ketoacidosis. Journal of Clinical Research in Pediatric Endocrinology. 2020;12(2):189-96.
9. Moraes AGD, Surani S. Effects of diabetic ketoacidosis in the respiratory system. World Journal of Diabetes. 2019;10(1):16-22.
10. Practitioners. RACoG. Emergency management of hyperglycaemia in primary care The Royal Australian College of General Practitioners website2022 [Available from: https://www.racgp.org.au/clinical-resources/clinical-guidelines/key-racgp-guidelines/view-all-racgp-guidelines/emergency-management-of-hyperglycaemia.