Paul is a 19-year-old male with Type 1 Diabetes Mellitus (T1DM) with acute symptoms of polyuria and polydipsia for two days. He presents to the emergency department with complaints of abdominal pain. On assessment, he is observed to have labored breathing. His lab report reveals (urinalysis 2++) ketonuria and blood glucose level of 20 mmol/L. Further investigation reveals hyperkalemia. He is non-compliant to insulin therapy from the past few days and is diagnosed with diabetic ketoacidosis (DKA).
DKA is the commonest precipitating factor in the case of T1DM patients. If left untreated, it can lead to life-threatening complications such as dehydration, episodes of syncope, coma, and even death (Cooper et al., 2016). Hyperglycaemia, metabolic acidosis, and ketonuria form a characteristic triad in cases of DKA, the metabolic imbalances occur due to severe deficiency and of insulin in the body and increase in the level of counter-regulatory hormones such as glucagon and catecholamines and leading to a variety of infections such as pneumonia and urinary tract infection which serve as primary risk factors in triggering DKA (French, Donihi & Korytkowski, 2019).
The second most vital risk factor includes renal failure. Since it is the kidneys that regulate the water in the body and when the kidneys are unable to function properly, they re-absorb the sugar and circulating back to the bloodstream, which results in polyurea and polydipsia, causing severe dehydration.
The third risk factor includes cerebral edema, which occurs due to increase water intake or by external administration of body fluids for compensating dehydration.
In the case study, it can be seen that Paul is non-compliant with his insulin therapy. This drop in the level of insulin causes a decrease in the level of glucose reaching the tissues, and the majority of the glucose to remain in the blood (Cooper et al., 2016). This causes metabolic acidosis at the cellular level causing the release of counter-regulatory hormones, which are glucagon and catecholamines, growth hormone, cortisol, and epinephrine (Fayfman, Pasquel, & Umpierrez, 2017). These hormones increase the level of glucose furthermore to compensate for the loss of glucose to the cells by the process of glycogenesis by acting of lipids and proteins, instead of carbohydrates, which eventually leads to more glucose in the blood as the cells are not able to absorb it. It also leads to osmotic diuresis, when glucose flows out through urine taking along electrolytes such as potassium, chlorine, and sodium with it. This mechanism causes increased urinary output (polyuria) and leading to increased thirst and dehydration (polydipsia).
The body also undergoes lipolysis, which means metabolizing fat instead of glucose as a substitute for energy. This increases the number of fatty acids in the liver and produces ketones which reach the brain by blood-brain barrier unlike glucose and provide energy, but when produced in large amounts, it leads to metabolic acidosis (pH <7.3). The body tries to compensate for the acidity by exhaling more carbon dioxide, leading to labored breathing, also known as Kussmaul breathing (Cooper et al., 2016). Furthermore, the cells exchange the hydrogen ions with potassium ions to deal with acidosis, causing an increased level of potassium in the blood, which results in hyperkalemia.
Together, these three mains namely hyperglycemia, ketosis, and metabolic acidosis characteristics form the triad for DKA (Cooper et al., 2016).
For improving the airways and breathing, mechanical ventilation or oxygen mask is provided to decrease the effort of the patient. (Mbugua et al., 2005)
Circulation: Increase in providing body fluids such as electrolytes through intravenous mode. Switching to 0.45 percent of saline with 5.0 percent of dextrose is suggested when the glucose level drops to <14mmol/L in the urinalysis. (Umpierrez, 2015)
Cooper, H., Tekiteki, A., Khanolkar, M., & Braatvedt, G. (2016). Risk factors for recurrent admissions with diabetic ketoacidosis: a case–control observational study. Diabetic Medicine, 33(4), 523-528.
Fayfman, M., Pasquel, F. J., & Umpierrez, G. E. (2017). Management of hyperglycemic crises: diabetic ketoacidosis and hyperglycemic hyperosmolar state. Medical Clinics, 101(3), 587-606.
French, E. K., Donihi, A. C., & Korytkowski, M. T. (2019). Diabetic ketoacidosis and hyperosmolar hyperglycemic syndrome: review of acute decompensated diabetes in adult patients. Bmj, 365.
Mbugua, P. K., Otieno, C. F., Kayima, J. K., Amayo, A. A., & McLigeyo, S. O. (2005). Diabetic ketoacidosis: clinical presentation and precipitating factors at Kenyatta National Hospital, Nairobi. East African medical journal, 82(12).
Umpierrez, G. E. (2020). Hyperglycemic Crises: Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar State. Diabetes Complications, Comorbidities and Related Disorders, 595-614.
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