bubble_chart Overview

Diabetes mellitus is a disorder caused by absolute or relative insulin deficiency, leading to metabolic disturbances of carbohydrates, fats, and proteins, resulting in elevated blood sugar and increased urinary glucose. Pediatric patients are prone to developing ketoacidosis, which can become an emergency condition. The vascular complications in its late stage [third stage] often affect the eyes and kidneys. Diabetes can be classified into:

1. Insulin-dependent diabetes mellitus (ID-DM), also known as type I diabetes: commonly seen in adolescents, characterized by absolute insulin deficiency, frequent ketoacidosis, and requiring insulin therapy.
2. Non-insulin-dependent diabetes mellitus (NIDDM), also known as type II diabetes: more common in adults. Fasting insulin levels are normal or elevated but fail to synchronize with postprandial blood sugar, and ketoacidosis is rare.
3. Other types: including secondary diabetes, such as pancreatic diseases, endocrine disorders (e.g., hypercortisolism), drug- or chemical-induced diabetes, malnutrition-related diabetes, certain genetic syndromes, and insulin receptor abnormalities.

Pediatric diabetes is mostly type I, with a minority being type II. The disease cause of type I diabetes is not fully understood but may involve genetic predisposition combined with exogenous triggers (e.g., viral infections) leading to autoimmune dysfunction, destruction of pancreatic β-cells, reduced insulin secretion, and ultimately IDDM. This section focuses on IDDM.

bubble_chart Diagnosis

(1) Clinical Manifestations

The typical manifestations include polyuria, polydipsia, polyphagia, and weight loss; infants and young children may present with enuresis or increased nocturia. The onset is often preceded by triggers such as fever, infection, emotional stress, or other stressful conditions. Some cases have a more gradual onset, presenting with weakness, progressive weight loss, and impaired vision. In other cases, children may present with ketoacidosis as the prominent symptom, with younger children more likely to exhibit ketoacidosis at onset. In such cases, in addition to polyuria, polydipsia, and weight loss, symptoms may include nausea, vomiting, abdominal pain, loss of appetite, confusion, drowsiness, or even unconsciousness. Physical examination may reveal severe dehydration, acidosis, deep and labored breathing (Kussmaul respiration), and a ketotic odor on the breath.

(2) Laboratory Findings

1. Urinalysis: Morning and pre-meal urine tests show glycosuria. In early or mild cases, glycosuria may only appear postprandially or during infections. The presence of ketonuria suggests ketosis or ketoacidosis. For long-standing cases, regular urine protein testing is necessary to detect kidney involvement early.
2. Blood glucose: Fasting blood glucose is elevated, with plasma glucose ≥7.8 mmol/L (140 mg/dL). Random blood glucose at any time of the day is ≥11.1 mmol/L (200 mg/dL).
3. Glucose tolerance test: After oral administration of glucose (1.75 g/kg, maximum 75 g), the 2-hour blood glucose level is ≥
4. 11.1 mmol/L (200 mg/dL).
5. Glycosylated hemoglobin (HbA1c) test: Significantly higher than normal (normal HbA1c ≤10%).
6. Other tests: Cholesterol, triglycerides, and free fatty acids are elevated. Serum insulin and C-peptide levels are decreased, and islet cell antibodies may be positive (up to 85%).

(3) Diagnostic Criteria

1. The diagnosis can be made without a glucose tolerance test if the patient exhibits diabetic symptoms and has a random blood glucose level ≥11.0 mmol/L (200 mg/dL) or a fasting blood glucose level ≥7.8 mmol/L (≥140 mg/dL).
2. If diabetic symptoms are present but blood glucose levels do not meet the above criteria, a glucose tolerance test is required (oral glucose dose: 2 g/kg for children under 3 years, 1.75 g/kg for older children, maximum 75 g). A diagnosis is supported if blood glucose levels rise excessively or recovery is delayed (2-hour blood glucose ≥11.0 mmol/L or 200 mg/dL).

bubble_chart Treatment Measures

IDDM requires insulin therapy and proper dietary management. Treatment should meet the following requirements:

1. Control diabetic symptoms.
2. Prevent ketoacidosis and hypoglycemia.
3. Postprandial 2-hour blood glucose should be controlled below 11.2mmol/L (200mg/dl); urine glucose below ++; 24-hour urine glucose <5g為理想，不得>25g; glycosylated hemoglobin <10%。
4. normal lipid levels.
5. Normal or near-normal growth and development, including puberty.
6. Ability to participate in normal activities with peers.

(1) Insulin Therapy

1. **Types and Administration of Insulin** Before the 1980s, insulin extracted from animal pancreases was used, which had many drawbacks. In the 1970s, purer "single-peak insulin" and "single-component insulin" were developed. Later, semi-synthetic human insulin was produced, and in recent years, biosynthetic human insulin has been created using DNA recombination technology. The types of insulin currently used in pediatrics and their durations of action are shown in Table 9-2:
   **Table 9-2. Types of Insulin and Their Durations of Action**

   Duration of Action After Injection (hours)

   Type

   Route

   Onset

   Peak

   Duration

   Regular Insulin (RI)

   SubQ

   1/2

   2～4

   6～8

   IV

   Immediate

   1/2

   2

   NPH Insulin

   SubQ

   2

   4～12

   24

   Protamine Zinc Insulin (PZI)

   SubQ

   4～8

   14～20

   24～36

   For newly diagnosed patients, regular insulin (RI) is generally used. For mild cases, the initial dose should be small, approximately 0.5 U/(kg·d). For severe cases, especially during the convalescence stage of ketoacidosis, the daily requirement is higher, 1–1.5 U/(kg·d). The daily dose is divided into 3–4 subcutaneous injections, administered 15–30 minutes before meals or once before bedtime after a snack (the bedtime dose should not exceed 4 U). The dose is adjusted based on pre-meal urine glucose levels and the previous day's response: maintain the dose for urine glucose ++, increase for higher levels, decrease for +, and skip a dose if urine glucose is negative, while monitoring for hypoglycemia. Adjustments are typically made every 2–3 days, with changes of 10% or 2 U per dose, and no more than two adjustments per day. Once the condition stabilizes and insulin requirements decrease, a combination of NPH and RI can be used (NPH at 2/3 of the total dose and RI at 1/3), administered twice daily (morning and evening). Alternatively, RI and PZI can be mixed in a 3:1 or 4:1 ratio. PZI is rarely used alone in children due to the risk of nocturnal hypoglycemia. However, for long-term patients with pancreatic beta-cell failure, significant fasting hyperglycemia in the morning, and uncontrolled post-breakfast hyperglycemia or morning urine glucose, 4–6 U of PZI may be added to the evening RI or mixed injections may be given twice daily (morning and evening).
2. **Precautions During Insulin Therapy**
   1. The injection site is generally selected on the thigh, upper arm, or abdominal wall, with each injection point spaced 2 cm apart to avoid subcutaneous fat atrophy caused by long-term injections at the same site.
   2. Beware of hypoglycemia.
   3. A few may experience allergic reactions, redness and itching at the injection site, or develop angioedema and urticaria, which usually do not require discontinuation and often resolve on their own.
   4. Insulin antibody production and resistance.
   5. Chronic insulin overdose: Hypoglycemia occurs between midnight and 4 a.m., leading to the secretion of glucagon, cortisol, adrenaline, etc., resulting in reactive hyperglycemia, known as the Somogyi phenomenon. This manifests as persistent morning glycosuria and hyperglycemia despite insulin doses of 1.5 U/(kg·d), along with grade I ketosis. Upon confirmation, the dosage should be reduced.

(II) Dietary Control

Since children are in a stage of growth and development, their diet should meet nutritional and caloric needs, maintain stable blood sugar, and avoid excessive dietary restrictions. However, meals should be timed and portion-controlled.

1. Daily caloric intake: For infants under 1 year, calculate 460 kJ (100 kcal)/kg per day, then reduce by 4.2 kJ (10 kcal) every 3 years until reaching 290 kJ (60 kcal)/kg per day by age 15.
2. Caloric distribution: Carbohydrates 50%, protein 20%, fat 30%. Meal distribution: Breakfast, lunch, and dinner at 1/5, 2/5, and 2/5, respectively; or breakfast at 2/10, lunch and dinner at 3/10 each, with afternoon and bedtime snacks at 1/100 each.
3. To evaluate dietary adequacy, refer to growth in height and weight, blood sugar levels, and glycated hemoglobin. <9.5%為佳。

(III) Exercise

Under basic diabetes control with insulin and dietary therapy, exercise is generally not restricted. However, the optimal time for exercise is 1 hour after meals and within 2–3 hours. Avoid exercising on an empty stomach. If hypoglycemic symptoms occur after exercise, a snack may be added.

(IV) Treatment of Concurrent Diabetic Ketoacidosis (DKA)

1. Insulin: Small-dose continuous intravenous infusion. RI 0.1 U/kg per hour. First, add a 4-hour dose to 240 ml of normal saline and infuse at 1 ml per minute. When blood sugar drops below 16.8 mmol/L (300 mg/dl), add glucose to the infusion (to make a 2.5% glucose solution) along with RI, calculated as 1 U RI per 3–4 g glucose. After improvement, administer subcutaneous RI 30 minutes before meals, referencing the usual dose. For new cases, start with 0.25–0.5 U/kg and adjust based on response.
2. Correct dehydration, acidosis, and electrolyte imbalances.
   1. Typically, another intravenous line is needed to rapidly correct dehydration. For clinically significant dehydration and acidosis, calculate as grade II dehydration with 10% fluid loss.
   2. Cumulative loss: First, administer 20 ml/kg of normal saline within 1–1.5 hours for volume expansion. The second batch uses 0.5% NaCl, with half the calculated cumulative loss infused over 8–10 hours and the remainder over the next 16–24 hours, mostly within 24 hours. Oral rehydration is also an option.
   3. Maintenance fluids can be calculated at 1500 ml/(m ² .d), using 1/3 tonicity fluids containing Na 30 mmol/L and K 20–40 mmol/L. Intravenous rehydration is preferred in the first 24 hours. The total actual volume is 70% of the cumulative loss plus maintenance needs.
   4. Pay attention to timely potassium supplementation.
   5. Alkaline drugs, generally for grade III acidosis with pH <7.2時給NaHCO₃1–2 mmol/kg, which translates to 5% NaHCO₃1.6–3.2 ml/kg. Administer as an isotonic solution after dilution. Avoid sodium lactate.

(4) Strengthen protection to prevent infection.

bubble_chart Differentiation

The main differentiation is from other diseases that can cause glycosuria, such as temporary glycosuria in infants due to severe infections or trauma, renal glycosuria caused by a decreased renal threshold for glucose excretion, and glycosuria in hyperthyroidism. In these cases, fasting blood glucose and glucose tolerance tests are normal. When diabetic children experience unconsciousness, the following conditions should be distinguished:

1. Ketoacidosis unconsciousness: This is a common and severe complication, particularly in younger children. It can be the initial symptom of diabetes or occur due to insufficient insulin dosage or secondary infections or trauma. Symptoms include anorexia, nausea, vomiting, abdominal pain, severe dehydration, and acidosis. Blood glucose is elevated, blood pH decreases, blood HCO₃^- decreases, blood ketones may exceed 200 mg/dl, serum sodium and chloride ions are low, and serum potassium decreases after fluid infusion. Urine ketones are strongly positive.
2. Hyperosmolar unconsciousness: Blood glucose is extremely high, plasma osmolality is significantly elevated, but urine ketones are negative.
3. Hypoglycemic unconsciousness: Caused by excessive insulin injection, symptoms include hunger, pallor, cold sweating, unconsciousness, and spasms, with a significant drop in blood glucose. For children with long-standing diabetes, attention should be paid to the following complications: diabetic dwarfism (Mauriac syndrome), white internal visual obstruction, diabetic nephropathy, retinal membrane lesions, peripheral neuropathy, joint lesions, stirred pulse atherosclerosis, skin changes, etc.