Week 2 – Pediatrics

Longterm concerns and preventive care for DKA

For preventive care in these patients, education is extremely important. These patients should be informed of proper dieting, exercising, and psychosocial maintenance. Greater parental involvement in the child’s diabetes care, check-ups, and treatments may also be needed.

When dealing with the patients’ nutrition, it may depend on whether or not they are on insulin. It is suggested that there should be controlled carbohydrate intake to lower the amount of sugars taken in; as well as education on proper foods/drinks.

The patient’s growth and development should be noted when starting insulin. Initially, the patients likely had weight loss from the uncontrolled diabetes. When insulin is started, the weight may be regained. If excessive insulin is given, the dose is not reduced after puberty, or the dose is not reduced after patient gains back the initial lost weight, the patient may become hypoglycemic. Therefore, it is important to keep monitoring the patient, and adjust the insulin dose if necessary. 

Exercise is encouraged in these patients, however, they need to be educated that the amount and intensity of exercise can lead to the body responding, and causing hypoglycemia within the following hours. It is suggested to have additional blood glucose monitoring around the time of exercise, as well as insulin dose adjustment.

Psychological issues should also be monitored. Children may run into issues from living with their chronic condition, and they may have stresses in school and their family. This can risk poor self-care, diet, and treatment adherence. It is important to address these sources of conflict in order to decrease the risk of hospitalizations and DKA.

Patients and their family should also be informed of the risk of untreated diabetes, or noncompliance with treatment. They should be educated that it can lead to the buildup of ketones and acids in the body, which can lead to DKA, and serious complications, like cerebral edema, cognitive impairment, pulmonary edema, DVT risk, organ damage, arrhythmias, or even death.

 

Reflection on the case presentations

DKA is a life-threatening complication seen in diabetics. I found it helpful when we reviewed its pathophysiology so that we could thoroughly understand how this problem occurs within the body. It mostly occurs in DM1 patients, whose bodies are unable to produce insulin. Insulin is important to allow glucose to enter cells for its usage. When the body lacks insulin, it will produce counterregulatory hormones (ie: glucagon, cortisol, GH) in order to produce alternative forms of energy. The liver will undergo gluconeogenesis, further increasing the glucose circulating in the blood. Triglycerides will get broken down into free fatty acids, which then will break down into ketones. The buildup of ketones can be seen in blood and urine, making the blood acidic. The complications of DKA were also covered: cerebral edema, cognitive deficits, DVT risk, and increased pancreatic enzymes.

We reviewed the treatment goals of DKA, which included: correcting dehydration with IV fluids, giving insulin to reduce ketosis and hyperglycemia, and correcting electrolyte imbalances. Learning how to calculate the amount of NS or LR to give when treating dehydration and fluid maintenance was challenging, but useful as an introduction of how to do it. Some takeaways were: 1kg of weight loss = 1L of fluid depleted; 10-20mL/kg via IV bolus is given initially in pediatric DKA, while 15-20mL/kg can be given in adults; 0.1unit/kg/hr IV insulin infusion should be given in peds, while 0.1 units/kg IV bolus of regular insulin, followed by 0.1 units/kg/hour continuous infusion should be given in adults; electrolyte imbalances (ie: Na, K, phosphate, Ca, Mg) need to be monitored for and corrected; and that bicarbonate can be given in adults with DKA, but not in pediatric DKA patients.

Last but not least, we covered the concept of anion gap. In our plasma, we need the charges to add up to be electrically neutral. The measurement of anions and cations concentrations in the plasma is difficult, so the equation of anion gap is used. Na – (HCO3- + Cl-). It describes how much more positive cations there are from negative anions, which is usually 8-12mEq/L. The gap is present since Na+ accounts for the majority of positive charges, while the equation does not account for some of the negative charges that exist beyond Cl- and HCO3- concentrations, such as organic acids and negatively charged proteins.

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