NUR 4220 Module 5 Pediatric DKA Paper: Fluids, Insulin and Watching for Cerebral Edema Example

Thirsty for Weeks: A Teenager's First Diagnosis of Diabetes Arrives as Ketoacidosis

Student Name

B.S.N., Accelerated Second Degree, Thomas Edison State University

NUR-4220: Nursing Care of Infants, Children, and Adolescents

Mentor Name

Month Day, Year

Thirsty for Weeks: A Teenager's First Diagnosis of Diabetes Arrives as Ketoacidosis

The Patient

Maya is invented for this paper. She is 14, plays travel soccer and lives with her mother and grandmother. For three weeks she has been drinking large amounts of water, getting up at night to urinate and losing weight, which her coach praised. For two days she has had abdominal pain and vomiting. In the emergency department she was drowsy but answered questions, breathed deeply and quickly and had a fruity smell on her breath. Her glucose was 512 mg/dL, venous pH 7.08, bicarbonate 6 and blood ketones high. She weighed 48 kilograms, down from 53 a month earlier.

What Ketoacidosis Is

Type 1 diabetes is autoimmune: the body's own defenses wipe out the pancreatic cells that make insulin. Without insulin, cells cannot use glucose, sugar accumulates in the bloodstream and overflows into the urine, dragging water out with it and causing thirst, urination and dehydration. Starved of usable glucose, the body burns fat, and the ketones this produces are acids. The blood becomes acidic, and deep, rapid breathing, known as Kussmaul breathing, blows off carbon dioxide to compensate. Vomiting worsens dehydration.

The Guideline

Wolfsdorf et al. (2018) wrote the 2018 international consensus guideline on ketoacidosis in children and teens. It defines DKA as high glucose plus acidosis, meaning a venous pH under 7.3 or a bicarbonate under 15, plus ketones, with severe DKA at a pH below 7.1 or bicarbonate below 5. It recommends careful fluid replacement to restore circulation and correct dehydration over 24 to 48 hours, beginning a continuous low-dose insulin infusion once fluids are running, adding potassium as soon as urine output and potassium levels allow, avoiding routine bicarbonate and monitoring glucose, electrolytes, fluid balance and neurologic status closely.

Fluids and the Brain

For years, clinicians feared that giving fluids too quickly caused cerebral edema, brain swelling, which causes most DKA deaths in children. Kuppermann et al. (2018) tested this in the PECARN FLUID trial, randomly assigning more than 1,300 episodes of DKA in children to faster or slower fluid replacement and to normal-strength or half-strength saline. There were no significant differences in declines in mental status during treatment, clinically apparent brain injury or memory after recovery. Brain injury was uncommon in all groups. The trial suggested that clinicians can choose fluid rates within this range without fear that rate alone causes brain injury.

Who Is at Risk

Glaser et al. (2001) compared children with DKA who developed cerebral edema with those who did not. Risk was greater in children with lower partial pressure of carbon dioxide and higher blood urea nitrogen at presentation, signs of more severe acidosis and dehydration, and in those treated with bicarbonate. These findings guide which children need the closest neurologic monitoring.

Nursing Diagnoses

The main diagnoses were deficient fluid volume from glucose-driven urine loss and vomiting, risk for unstable blood glucose and electrolytes related to insulin therapy and risk for decreased intracranial adaptive capacity related to cerebral edema.

Nursing Care

Two intravenous lines were placed. Fluids started as ordered, and the insulin infusion began an hour later. The student helped with hourly glucose checks, recorded intake and output and drew electrolytes every two hours. Because insulin drives potassium into cells, potassium was added to the fluids once Maya urinated and her level was known. As her glucose fell toward 250 to 300, dextrose was added to the fluids to keep glucose steady while insulin continued to clear ketones.

Every hour the student assessed her level of consciousness, pupils, headache and heart rate, looking for warning signs of cerebral edema such as a new headache, slowing heart rate, rising blood pressure, change in mental status or incontinence. Her low carbon dioxide and severe acidosis placed her at higher risk, so the team had mannitol available.

Her Family and the Diagnosis

Maya's mother was shocked and asked whether she had caused this. The student explained that type 1 diabetes is an autoimmune condition, not caused by diet or anything she did. Maya cried about soccer, and the student told her that many athletes, including professionals, play with type 1 diabetes.

Beginning Education

Once she was out of DKA, teaching began with survival skills: checking glucose or using a continuous glucose monitor, giving insulin, recognizing and treating low blood sugar and checking ketones when sick. Her grandmother, who would be home after school, joined the sessions. A diabetes educator, dietitian and social worker were part of the team, and her school nurse was contacted with her mother's permission.

Why Not Bicarbonate

Maya's pH was very low, and her mother asked why the team did not give something to correct the acid directly. The student learned that bicarbonate is not given routinely because it has not been shown to help and has been linked to cerebral edema, as Glaser and colleagues found. Fluids and insulin correct the acidosis by stopping ketone production.

Evaluation

Within 18 hours her acidosis had resolved, she was alert and eating and she had no signs of cerebral edema. She was switched to injected insulin and discharged on day three with a follow-up appointment at the diabetes clinic.

Limits

The fluid trial did not test rates outside the protocol range. Guidelines vary in details between institutions. A student helps monitor and teach but leaves insulin and fluid changes to the team. Maya is invented.

Conclusion

Maya's weeks of thirst and weight loss ended in severe DKA. The ISPAD guideline set the order of fluids, insulin and potassium, the PECARN FLUID trial eased fears that fluid rate alone causes brain injury and Glaser and colleagues identified the children who need the closest watch. Hourly glucose and neurologic checks, careful electrolyte monitoring and teaching for a frightened family at the start of a lifelong condition completed the nursing role.

References

Glaser, N., Barnett, P., McCaslin, I., Nelson, D., Trainor, J., Louie, J., Kaufman, F., Quayle, K., Roback, M., Malley, R., & Kuppermann, N. (2001). Risk factors for cerebral edema in children with diabetic ketoacidosis. New England Journal of Medicine, 344(4), 264-269. https://doi.org/10.1056/NEJM200101253440404

Kuppermann, N., Ghetti, S., Schunk, J. E., Stoner, M. J., Rewers, A., McManemy, J. K., Myers, S. R., Nigrovic, L. E., Garro, A., Brown, K. M., Quayle, K. S., Trainor, J. L., Tzimenatos, L., Bennett, J. E., DePiero, A. D., Kwok, M. Y., Perry, C. S., Olsen, C. S., Casper, T. C., . . . Glaser, N. S. (2018). Clinical trial of fluid infusion rates for pediatric diabetic ketoacidosis. New England Journal of Medicine, 378(24), 2275-2287. https://doi.org/10.1056/NEJMoa1716816

Wolfsdorf, J. I., Glaser, N., Agus, M., Fritsch, M., Hanas, R., Rewers, A., Sperling, M. A., & Codner, E. (2018). ISPAD clinical practice consensus guidelines 2018: Diabetic ketoacidosis and the hyperglycemic hyperosmolar state. Pediatric Diabetes, 19(Suppl. 27), 155-177. https://doi.org/10.1111/pedi.12701