Case Study: Diabetic ketoacidosis (DKA)

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Case study

A 17-year-old male presented to the Emergency Department in a coma. He has type I diabetes mellitus (DM). His mother reported that he kept “throwing up” all night and that his blood glucose was very high, and urine was positive for ketones early this morning. Currently, his respirations are deep and rapid; blood pressure is 88/64 and his pulse weak and rapid (120).

Give an example of what his ABG’s and electrolytes would be prior to treatment. Explain the abnormal values associated with this complication of Type I DM. Explain the various signs and symptoms he presented with as well as those reported by his mother.


Response

The patient has presented to the ER in a coma. It was reported from his mother that he was vomiting the prior night, that he had a high blood sugar, and that his urine was positive for ketones. In the ER he is found to be hypotensive and tachycardic, with deep and rapid respirations. The combination of vomiting, hypotension, and tachycardia may be the result of hypovolemia and dehydration. However, McCance and Huethe (2014) state that the additional hallmark symptoms of ketonuria, hyperglycemia, coma, vomiting, and Kussmaul respirations suggest that the patient is presenting with diabetic ketoacidosis (DKA), and would also expect to find polyuria and an elevated anion gap. McCance and Huethe state that DKA is more prevalent in patients with type I diabetes. McCance and Huethe state that a reason that patients in DKA present with polyuria and dehydration is a result of the hyperglycemic state. The authors state that glucose in the blood will begin to be excreted by the kidneys, increasing the osmotic pressure of the urine and creating diuresis (McCance & Huethe, 2014).

Arterial Blood Gases (ABGs)

Große et al. (2018) state that common ABGs found in the setting of DKA are aligned with those of metabolic acidosis. Große et al. state that these signs include an acidic pH below 7.3, and a bicarbonate less than 15 mmol/l. The authors that as the severity of DKA increases, the acidity and bicarbonate drop lower with a pH of less than 7.1 and a bicarbonate of lower than 5 mmol/l in severe DKA (Große et al., 2018).

For this patient, a hypothetical ABG would be a pH of 7.1, a bicarbonate of 5 mmol/l, and a carbon dioxide of 20 mmHg. Considering the patient is in a coma, it is assumed that the pH would severely low. The reason for the lowered carbon dioxide level is that the patient appears to be attempting to compensate for the metabolic acidosis by expelling carbon dioxide from the lungs with Kussmaul respirations. The reduction in bicarbonate is not only associated with metabolic acidosis but can also result from vomiting (McCance & Huethe 2014).

Treatment

Hirsch & Emmett (2017) state that treatment for DKA firstly involves fluid replacement. The authors state that this intervention will treat both the patient’s hyperosmolar state as well as their hypovolemia. Hirsch and Emmett state that the initial fluid therapy of choice is isotonic saline. After the first 2-3 hours of rapid fluid replacement, the authors suggest continuing with isotonic saline if the patient’s sodium is less than normal range but switch to half normal saline if the sodium is normal or elevated. Hirsch and Emmett also state that patients in DKA often present with hypokalemia and that potassium levels should be replaced on an as-needed basis based on severity, with more aggressive repletion if the patient is severely hypokalemic.

In addition to fluid and electrolyte replacement, Hirsch and Emmett (2017) state that treatment for DKA requires the administration of insulin, typically in the form of regular insulin given intravenously. The authors state that the only reason to consider delaying the administration of insulin is if the patient has severe hypokalemia since the infusion of insulin would worsen the problem by pushing more potassium into the cells. Furthermore, the authors state that in severe cases of metabolic acidosis where the pH is less than 6.9, bicarbonate replacement can be administered. Hirsche and Emmett suggest that patients should be monitored closely during treatment and laboratory findings of an anion gap under 12 would indicate a resolution of the ketoacidosis, and blood glucose levels hopefully have stabilized by this point as well.

References

Große, J., Hornstein, H., Manuwald, U., Kugler, J., Glauche, I., & Rothe, U. (2018). Incidence of Diabetic Ketoacidosis of New-Onset Type 1 Diabetes in Children and Adolescents in Different Countries Correlates with Human Development Index (HDI): An Updated Systematic Review, Meta-Analysis, and Meta-Regression. Horm Metab Res, 50(3), 209–222. https://doi.org/10.1055/s-0044-102090

Hirsch, I. B., & Emmett, M. (2017). Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Treatment. Retrieved March 14, 2018, from https://www.uptodate.com/contents/diabetic-ketoacidosis-and-hyperosmolar-hyperglycemic-state-in-adults-treatment

McCance, K. L., & Huethe, S. E. (2014). Pathophysiology: The biologic basis for disease in adults and children (7th ed.). Mosby.