Type 1A: Autoimmune

Type 1B: Idiopathic

Permanent neonatal diabetes PNDM

Transient neonatal diabetes mellitus TNDM

secondary diabetes

Causes: Acute infection, delayed diagnosis, overeating, or interruption of insulin therapy

Pathophysiology: 1. Starvation or insufficient sugar supply---Weakening of sugar metabolism---Free fatty acids entering liver cells mainly enter mitochondria for β-oxidation---Increased ketone body production 2. Decreased insulin secretion and increased secretion of glucagon hormone--- -Severe lack of insulin action---increased lipolysis, hyperglycemia

Clinical manifestations: 1. Exacerbation of diabetes symptoms: polyuria, polydipsia, fatigue, dehydration 2. Gastrointestinal symptoms: loss of appetite, nausea and vomiting, abdominal pain 3. Deep and fast breathing or sighing breathing, and the exhalation smells like rotten apples [ Acetone is excreted in the urine, and is exhaled directly from the lungs when blood ketones increase significantly] 4. Headache, drowsiness, irritability, and progressive disturbance of consciousness

Laboratory tests: 1. Determination of blood ketones and urine ketones: β-hydroxybutyric acid, the main component of blood ketones ≥0.6mmol/L---decompensated state 2. Accumulation of anions β-hydroxybutyric acid and acetoacetate in plasma- --Anion gap rises 3. In the case of healthy renal function, blood ketone (β-hydroxybutyric acid acetoacetate): (1) reaches 0.8mmol/L---urine routine (2) reaches 1.3mmol/L---urine Normal (crisis value)

Diagnosis: 1. Blood sugar>11.1mmol/L 2. Blood pH<7.3, HCO3-<15mmol/L (<15 indicates acid substitution) 3. Blood ketone bodies, urine ketone bodies and urine sugar ( )

Treatment: 1. Infusion: mainly for dehydration (generally isotonic), acidosis, and electrolyte imbalance: (1) Mild dehydration: oral rehydration at 50ml/kg (2) Moderate dehydration: calculated rehydration at 5% to 7% (3) Severe dehydration: Calculate fluid rehydration at 7% to 10%. 2. Alkali replenishment: (1) Blood pH＜7.1, HCO3-＜12mmol/L---1.4% sodium bicarbonate solution intravenously, use half the amount first-- - HCO3 supplementation amount = (12-measured HCO3-mmol/L) × body weight kg × 0.6 (2) Blood pH ≥ 7.2---discontinue to avoid rapid correction of acidosis and aggravation of cerebral edema 3. Insulin treatment: ( 1) Add 25 U of insulin to 250 ml of isotonic saline at a rate of 0.1 U/kg per hour (2) Continue intravenous infusion of low-dose insulin until DKA is corrected [2 consecutive negative urine ketones, blood pH > 7.3, and blood sugar dropped to 11 mmol/L] Change to subcutaneous injection of insulin (3) Short-acting insulin---control postprandial hyperglycemia, medium-acting insulin---control fasting basal blood sugar (4) Adverse insulin reactions: ① Hypoglycemia (the most common) ② Allergy ③ Insulin antibodies Generation ④ lipodystrophy at the injection site ⑤ edema ⑥ blurred vision 4. Diet therapy, exercise therapy, diabetes education

Cause: Too much insulin or failure to eat on time after injecting insulin

Features: 1. Blood sugar of normal people <2.8mmol/L 2. Blood sugar of children with diabetes <3.9mmol/L

Diagnosis: 1. In children with diabetes, blood glucose <3.9mmol/L reaches the threshold for clinical intervention, and <3.0mmol/L may cause central nervous system and cognitive dysfunction. 2. Severe hypoglycemia = hypoglycemia attack accompanied by cognitive dysfunction.

1. Blood sugar is usually >28~54mmol/L 2. Blood sodium >145mmol/L 3. Plasma osmotic pressure >310mmol/L 4. Dehydration and coma occur, but blood and urine ketones do not increase significantly, and there is no acidosis

1. Coronary heart disease 2. Ischemic or hemorrhagic cerebrovascular disease 3. Renal arteriosclerosis 4. Limb arteriosclerosis

1. Diabetic nephropathy 2. Diabetic retinopathy 3. Diabetic cardiomyopathy

1. Peripheral neuritis 2. Cranial neuropathy 3. Autonomic neuropathy

Peripheral N lesions---Insufficient arterial blood supply to the lower limbs Bacterial infection---foot pain, deep skin ulcers, gangrene of the extremities