Diabetic ketoacidosis: pathophysiology, clinical presentation, and management

The patient is in a diabetic ketoacidosis (DKA) state if the following conditions apply: (a) Hyperglycemia—blood glucose > 11mmol/L, and (b) Metabolic acidosis— venous pH < 7.3 or plasma HCO3 < 15 mmol/L plus (c) ketosis—ketones in the blood or urine or beta-hydroxybutyrate concentration > 3 mmol/L (Wolfsdorf et al., 2014). The patient’s deep respirations are perfectly normal given the condition of the patient: the respirations are explained by the lungs working to expel CO2 from the body. The body does not want CO2 levels to rise too highly, which happens during the event of ketoacidosis.
Because the patient is a type 1 diabetic—also known as a juvenile diabetic as Type 1 is found primarily in children and young adults—the condition with which the patient has presented is most likely diabetic ketoacidosis, probably caused by an illness or infection which compels the body to produce more hormones (adrenaline, cortisol) to fight the infection. The problem is that the hormones counteract the insulin’s work, which is to help cells absorb blood sugar. If the hormones prevent the insulin from doing its job, the blood glucose levels will rise sharply because the body’s cells are not absorbing them. This will trigger commonly a DKA.
The arterial blood gases (ABGs) likely to be seen in this state, therefore, would be consistent with metabolic acidosis. DKA pH would be around 7.36 for a mild DKA, and PaCO2 would be 25 mm Hg. The carbon dioxide level is explained by the fact that the patient’s body is implementing a compensatory mechanism because of the metabolic acidosis. Blowing off CO2 (acid)—i.e., releasing carbon dioxide from the lungs via Kussmaul respirations (hyperventilation in an attempt to compensate for the acidosis)—is the body’s line of defense. HCO3 would be 9 mEq/L in a mild DKA. The patient would be in metabolic acidosis, fully compensated.
One likely explanation for what happened is that the patient probably had an infection prior to getting sick with the diabetic ketoacidosis. The patient’s mother might be in a position to confirm or deny this hypothesis. Even if unknown, to the mother, a quick examination of the anion gap would help to clarify the state of the patient’s helath with respect to acidosis severity. The hyperventilation is compensation for the acidosis and should not be viewed as a cause of immediate concern for the mother or the nurse. The patient has ketonuria (a high amount of ketone bodies in the urine), anorexia, nausea, abdominal pain, thirst, and polyuria.  Bicorbanate could be used to facilitate the CO2 reduction process, but this is not without its own risks: as Leung, Perlman, Rumantir and Freedman (2015) indicate, bicarbonate reduction, while commonly linked with acidosis, could also be associated with the vomiting that the patient has been doing—so bicarbonate might not be a proper intervention strategy.
When DKA occurs, the body is depleted of potassium. Estimated loss is 6-7 mol/kg (Wolfsdorf et al., 2014). Sodium levels can range widely in DKA patients, so levels have to be compared to baseline. Typically, DKA patients will present with a degree of sodium loss within a range of 5-13 mmol/kg. Low phosphate levels can also be found and can be made worse by insulin. And though phosphate levels should be corrected, the DKA patient should also be checked for hypocalcemia which can occur if phosphate levels rise too high.
The patient’s vomiting, tachycardia and hypotension could be caused by a combination of dehydration and hypovolemia, and in accordance with the diagnosis of DKA, it would be expected that the patient would also exhibit polyuria and a higher anion gap, which measures the body’s ion balance (Wolfsdorf et al., 2014). Insulin and fluids can help to eliminate the ketone bodies. The anion gap should be monitored because it is typically associated with a better overall improvement in the acidosis state for a patient suffering even from mild DKA, whiles the HCO3 levels are not so immediately associated with an improved state. For that reason, monitoring the anion gap provides nurses with the better indicator of the patient’s status.
Differential diagnosis of the patient would include other possible explanations for the metabolic acidosis. For example, hyperosmolar hyperglycemic state may present with similar symptoms, but the ketone levels will not be so high; therefore, high ketone levels in the blood or urine indicate DKA. Still, there may be other explanations for a high anion gap metabolic acidosis, which include lactic acidosis, alcoholic ketoacidosis, methanol intoxication, and uremia.
DKA classification is based on the severity of the blood pH and HCO3 mmol/L. Mild DKA would have a blood pH of 7.2-7.3 and HCO3 between 10 and 15. For the patient, his levels indicate that mild DKA is to be treated for, following a procedure of fluid replacement and insulin infusion following an hour or two of rehydration therapy. This will help to counter the dehydration and to reduce the blood glucose levels. Introducing insulin into the body prematurely could risk the onset of cerebral edema, which could be fatal for the patient (Wolfsdorf et al., 2014). Therefore, proper steps should be taken to ensure that the patient is properly hydrated before insulin infusion begins.

References
Leung, J. S., Perlman, K., Rumantir, M., & Freedman, S. B. (2015). Emergency
department ondansetron use in children with type 1 diabetes mellitus and vomiting. The Journal of Pediatrics, 166(2), 432-438.
Wolfsdorf, J. I., Allgrove, J., Craig, M. E., Edge, J., Glaser, N., Jain, V., ... & Hanas, R.
(2014). Diabetic ketoacidosis and hyperglycemic hyperosmolar state. Pediatric Diabetes, 15(S20), 154-179.