Presentations classic silent and diabetic ketoacidosis

The presentation of new-onset T1D is distributed among three typical patterns: classic new onset, silent diabetes, and diabetic ketoacidosis (DKA). Although most children present with classic new-onset diabetes, in many locations, DKA still accounts for 20% to 40% of all new diagnoses [78]. Silent diabetes, which is less commonly seen at diagnosis, is typically seen in children either involved in diabetes research studies or picked up by families in which one member already has the disease.

Children who have classic new-onset T1D typically present with polydipsia, polyuria, polyphagia, weight loss, and lethargy. Classic-onset T1D is differentiated from DKA because children who have classic onset have enough preserved beta cell function to avoid metabolic decompensation with resultant acidosis. The symptoms of classic diabetes are caused by prolonged hyper-glycemia. Once blood glucose concentrations exceed the renal threshold for reabsorption (approximately 180mg/dL), glycosuria ensues with the resultant osmotic diuresis, dehydration, and thirst. Over time, increasingly poor glucose uptake by tissues, resultant chronic glycosuria, and breakdown of amino acids for gluconeogenic substrate with fat breakdown to supply fatty acids for ketogenesis all contribute to weight loss.

Classic T1D is usually diagnosed in the outpatient setting when a slightly ill-appearing child presents to the pediatrician for evaluation of weight loss and other nonspecific symptoms. A high index of suspicion for diabetes should be a concern for all physicians. The classic polyuria is not told to the physician, but recurrence of bedwetting, unusually wet diapers in a child who seems to be dehydrated, recurrent monilial infection in the diaper area, and persistent thirst should arouse suspicion. Glucosuria and hyperglycemia are easily confirmed in a physician's office by test strips and glucose meters. Children who have silent (ie, diagnosed early in the course of) T1D are typically diagnosed by families or physicians with a high index of suspicion. Often these children have other family members with T1D and their parents are more likely to have them undergo testing or have them screened in research studies. Children with a silent presentation often require little insulin because they have greater residual beta cell mass.

Most patients who have new-onset diabetes without DKA can receive initial management and education as outpatients in a tertiary care setting. In areas without a pediatric referral hospital, inpatient management may be needed to facilitate proper education and initiation of therapy. Outpatient management with early teaching of basic diabetes management tasks often gives the family a sense of being in control and reduces the initial emotional impact for the child and family.

The clinic setting is much more comfortable for education than the emotionally highly charged hospital environment. Outpatient management greatly reduces the initial cost of T1D management.

DKA is characterized by complete lack of insulin production such that glucose use is crippled and triglycerides must be broken down to provide the body with energy. The resulting byproducts of fatty acid metabolism—the ketones aceto-acetate and beta-hydroxybutyrate—further exacerbate the osmotic diuresis and cause acidosis. Dehydration and poor perfusion also may lead to lactic acidosis. The consequences of insulin deficiency are shown in Fig. 2.

Children who present with DKA require immediate hospitalization, insulin replacement, and rehydration. An initial arterial pH of < 7.3, serum bicarbonate concentration of < 15 mEq/L, and clinical signs of dehydration, vomiting, or mental status changes dictate hospitalization. Rapid deep respirations, known as Kussmaul breathing, often are present when significant acidosis occurs. Kussmaul breathing results from the body's attempt to compensate for the metabolic acidosis by exhaling excess CO2. Kussmaul respiration must be distinguished from reactive airways disease (asthma) or other causes of respiratory distress. Glucocorticoids and sympathomimetics given in the mistaken belief that the

Sympathomimetics Classification Table
Fig. 2. Pathogenesis of DKA. This figure outlines the pathophysiology of insulin deficiency leading to hyperglycemia, hyperketonemia, dehydration, and acidosis.

deep, sighing respirations of acidosis are caused by airway obstruction are a common cause of exacerbating DKA.

The overall mortality rate from pediatric DKA in the United States is approximately 0.5%. More than 90% of the deaths associated with pediatric T1D are related to DKA and cerebral edema, which occurs almost exclusively in children and adolescents [79]. Approximately 1% of DKA episodes are complicated by cerebral edema with its extremely high morbidity and mortality.

Initial management of DKA includes fluid resuscitation, close monitoring of vital signs, securing intravenous access, and obtaining blood and urine specimens for laboratory analysis. Urine ketones, pH (arterial or venous), electrolytes, and blood glucose are usually the only laboratory tests needed to provide proper management. Based on the pathophysiology of DKA, successful management involves rehydration, appropriate replacement of electrolytes, and correction of the underlying defect, namely, insulin deficiency. (For an in-depth discussion of DKA management, please see the article by Glaser elsewhere in this issue.) Once acidosis has resolved, subcutaneous insulin regimens can be started.

Management

Overall the goals for management of T1D in children are as follows:

• Setting of realistic goals for each child and family. Factors to be considered include a patient's age, developmental status, family involvement and social situation, economic factors, and hypoglycemic history in persons with established disease

• Near normalization of blood glucose levels and HbA1c measurements or, where not possible, improvement on subsequent follow-up

• Prevention of DKA

• Avoidance of severe hypoglycemia

• Assuring as near normal quality of life as is possible within the constraints of the factors outlined in the first goal

• Maintaining normal growth, development, and maturation

• Providing readily available multidisciplinary support, including nutritional education and psychological support

• Maintaining close surveillance and prevention of microvascular and macro-vascular complications (see article by Glastras and colleagues elsewhere in this issue)

Management in new-onset diabetes

For almost all children and their families, the diagnosis of diabetes is overwhelming. The initial management and education can be divided into two phases:

(1) stabilization and the teaching of survival skills over the first few days and

(2) ongoing diabetes management skills designed to teach a patient and family day-to-day management. All patients are seen on the day of diagnosis. If a patient is stable metabolically (ie, without DKA), has a stable social situation, and is older than 5 years, we manage the situation on an outpatient basis. Initially, the family is asked to return daily until education is completed and the family feels comfortable with their ability to manage the basics of their child's diabetes. After this intensive teaching, the family maintains close contact with the nurse and doctor on a daily basis until they seem able to cope with the situation.

Stabilization and teaching of survival skills

On the day the diagnosis is confirmed, families are given a simple overview of diabetes. Because there are often feelings of guilt, we reassure the family that there is no known cause of diabetes and that no food, activity, or anything they did contributed to its development. Survival skills are taught. All patients are started on insulin therapy. If stable, we typically start a patient on a total dose of insulin of 0.5 to 1 U/kg/d (see later discussion).

The next day the family returns for further education from the diabetes nurse. Information is provided on the pathophysiology of hyperglycemia and hypoglycemia and the ''do's'' and ''don'ts'' of living with diabetes. This education usually takes 2 to 3 days. The family is taught about the insulin types, how to mix and inject the insulin, and how to rotate sites. They are also taught the importance and mechanics of monitoring blood glucose levels and checking the urine for ketones at times of illness and elevated blood glucose measurements (> 250 mg/dL). The child and family are taught to test the blood glucose initially before each mealtime, before bed, and once a week between 2am and 4am. Hypoglycemia recognition and treatment (including the use of glucagon) is taught, as is sick day management. A basic guideline is given for planning meals and snacks and what must be done if the blood glucose level is too high or low. Carbohydrate counting is not taught at this time. The importance of a healthy, balanced nutritional plan with various foods from all the basic food groups is emphasized.

Once the health care team is comfortable with a family's ability to manage the diabetes at home, the child is allowed to return to home and school. The family is instructed to call daily in the morning for the first week after diagnosis for insulin dose adjustment. The frequency of contact abates as the family becomes more confident with diabetes management abilities. It is imperative that the school be apprised of the child's diagnosis and written materials be provided on the essential skills necessary for the detection and management of hypoglycemia and hyperglycemia. Contact numbers are also provided in cases of an emergency.

Ongoing diabetes management

Within the next 4 to 6 weeks, two to three additional sessions are scheduled with a diabetes nurse and nutritionist and with a psychologist and social worker as necessary. Clearly, education relating to the pathophysiology of diabetes, the causes of hyperglycemia and hypoglycemia, target glucose levels, how different insulin preparations work, the importance of 2-hour postprandial blood glucose testing, the interaction of food, exercise, and insulin, and the impact of stress and illness is critical to good control. These concepts and the importance of good control are stressed repeatedly. Approximately 2 months after diagnosis, an in-depth review of the topics takes place, and short- and long-term treatment goals are mutually agreed upon by the family and multidisciplinary team. Potential barriers (eg, familial, psychosocial, and school) are identified and appropriate intervention instituted.

Subcutaneous insulin regimens: neutral protamine Hagedorn and rapid acting analogs

Although multiple insulin regimens exist, we prefer to start new-onset T1D patients on a simple combination of neutral protamine Hagedorn (NPH) insulin and a rapid-acting analog, such as aspart or lispro given two or three times daily (see the article by Daneman elsewhere in this issue on details of insulin types and mixtures available). Most children who have symptomatic T1D at diagnosis require a total insulin dose of approximately 1 U/kg/d at diagnosis. Pubertal children typically are more insulin resistant and often require 1 to 1.5 U/kg/d. When using NPH with short-acting insulin regimens, the total daily insulin dosage is typically divided into two thirds in the morning and one third in the evening. The morning dose is usually given as two thirds NPH and one third rapid-acting analog. The evening dose is usually given as one half NPH and one half rapid-acting analog. NPH insulin begins to work 2 hours after injection, peaks 5 to 7 hours after injection, and lasts 13 to 16 hours. Rapid-acting analogs, such as lispro or aspart, begin to work 15 minutes after injection, peak 1 to 3 hours after injection, and last 3 to 5 hours (Table 3) [80].

In addition to scheduled insulin doses, supplemental short-acting insulin should be given to bring elevated glucose values into the target range. Once patients and their families have developed a rudimentary understanding of diabetes management, we teach them to apply a correction factor to determine how much additional insulin is needed to correct elevated blood glucoses. The correction factor can be estimated by dividing 1600 by the total daily dose of insulin. The result gives an approximation of the glucose lowering effect of 1 U

Table 3

Insulin preparations

Table 3

Insulin preparations

Type

Onset (h)

Peak (h)

Duration (h)

Short acting

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Responses

  • Asmara
    Is it dm type 1 or 2 in new onset dka?
    7 years ago

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