Diabetic ketoacidosis (DKA) is a complex endocrine condition caused by an absolute or relative lack of insulin. It is characterized by hyperglycemia, dehydration, ketosis, and metabolic acidosis.
DKA is often insidious in onset, with slow progression of the illness.
Definition of DKA by biochemical criteria includes the following:
Hyperglycemia: Blood glucose >200 mg/dL
Venous pH <7.3 or bicarbonate <15 mmol/L
Ketonemia and ketonuria
Treatment of DKA consists of rapid assessment, replacement of the patient’s fluid and electrolyte deficit, and reversal of the central pathophysiologic process by the administration of insulin.
Type 2 diabetes mellitus, hyperglycemic hyperosmolar state (HHS) can occur and is defined by the following:
Plasma glucose concentration >600 mg/dL
Arterial pH >7.30
Serum bicarbonate >15 mmol/L
Small ketonuria and absent or mild ketonemia
Serum osmolarity >320 mOsm/L
Stupor or coma
Newborns and young infants with hypoglycemia may be asymptomatic or may manifest nonspecific symptoms. Older children exhibit more classic symptoms of hypoglycemia, including sweating, tachycardia, tremor, anxiety, tachypnea, and weakness.
Treatment of hypoglycemia
In newborns, give 10% dextrose 2 mL/kg (0.2 g/kg) as a bolus, followed by infusion at 6 to 9 mg/kg/min.
In children, give 10% dextrose at 5 mL/kg (0.5 g/kg) as a bolus, followed by continuous infusion at 6 to 9 mg/kg/min. Alternatively, follow the “50 rule” in which the mL/kg multiplied by the dextrose % equals 50. For example, 1 mL/kg of D50, 2 mL/kg of D25, 5 mL/kg of D10, etc.
If an intravenous (IV) line is not possible, then give glucagon 0.03 mg/kg (maximum dose 1 mg) subcutaneously.
Admission of the hypoglycemic patient is indicated when there is no obvious cause, toxic ingestion as with oral hypoglycemic agents is suspected, administration of long-acting insulin was the cause, or if there are persistent neurological deficits.
DKA is a complex endocrine condition caused by an absolute or relative lack of insulin. It is characterized by hyperglycemia, dehydration, ketosis, and metabolic acidosis.
The annual incidence of DKA in the United States ranges from 4.6 to 8 episodes per 1000 patients with diabetes. Diabetes is one of the most common diseases occurring in teenagers. DKA is seen as the initial presentation of diabetes in approximately 25% of young children.1 The risk of DKA in children and adolescents with type 1 diabetes is 1 to 10 per 100 persons per year.2–5 In young patients, DKA accounts for 70% of diabetes-related deaths.
In DKA, a lack of insulin and stress lead to increases in the levels of counterregulatory hormones—glucagon, epinephrine, cortisol, and growth hormone. Gluconeogenesis and glycogenolysis occur in the liver, and proteolysis occurs in peripheral tissues. Lipolysis occurs in fatty tissues, forming the ketoacids, β-hydroxybutyrate, and acetoacetic acid. The combination of hyperglycemia and ketoacidosis causes a hyperosmolar diuresis that results in loss of fluids and electrolytes. The combination of ketonemia and hypoperfusion then results in a high anion gap metabolic acidosis.
DKA is precipitated by a variety of causes. DKA at diagnosis is more common in younger children <5 years and families with poor access to health care.2 In adolescents, noncompliance with insulin is a main cause of DKA. The risk of DKA is increased in peripubertal and adolescent girls, children with clinical depression or eating disorders, and those on insulin pump therapy (due to the use of short-acting insulin).2,5,6
DKA is often insidious in onset with slow progression of the illness. Symptoms can include fatigue and malaise, nausea/vomiting, abdominal pain, polydipsia, polyuria, polyphagia, significant weight loss, and sometimes fever.
Physical findings can include altered mental status characterized by drowsiness, progressive obtundation, and loss of consciousness without evidence of head trauma. The patient will usually have tachycardia, tachypnea, or deep, rapid, sighing respirations (Kussmaul respiration), and normal or low blood pressure. The child may also have poor perfusion, delayed capillary refill, and other signs of dehydration. The child may have lethargy and weakness and an acetone odor of the breath, reflecting metabolic acidosis. Fever may be present if infection precipitated the episode.
Initial laboratory studies include a complete blood count, serum electrolytes, glucose, calcium, phosphorus, and serum acetone. The patient may have a nonspecific elevation of serum amylase. A venous or arterial blood gas and bedside tests for blood sugar and urine ketones can be done for rapid diagnosis of DKA. An initial electrocardiogram can be performed to assess for T-wave changes.
The definition of DKA (biochemical criteria)7 is as follows: hyperglycemia with a blood glucose >200 mg/dL; venous pH <7.3 or bicarbonate <15 mmol/L; ketonemia and ketonuria.
DKA can be classified by the degree of acidosis into mild, moderate, and severe.8
Mild: Venous pH <7.3 or bicarbonate <15 mmol/L
Moderate: pH <7.2, bicarbonate <10 mmol/L
Severe: pH <7.1, bicarbonate <5 mmol/L
In type 2 diabetes mellitus, HHS can occur.9 This is defined by the following: plasma glucose concentration >600 mg/dL; arterial pH >7.30; serum bicarbonate >15 mmol/L; small ketonuria and absent or mild ketonemia; serum osmolarity >320 mOsm/kg; stupor or coma.
Treatment of DKA consists of rapid assessment, replacement of the patient’s fluid and electrolyte deficit, and reversal of the central pathophysiologic process by the administration of insulin.
Assessment includes performing a quick clinical assessment and bedside tests to confirm the diagnosis. Weigh the patient and use this weight for calculation of fluid and electrolyte therapy, as well as to assess the level of dehydration. Assess the level of consciousness using the Glasgow Coma Scale. Then obtain blood samples, start peripheral IV line, and obtain an ECG. Provide supportive measures including airway management for obtunded or comatose patients and oxygen at 100% concentration to patients in respiratory or circulatory failure and shock. Maintain good peripheral or central IV access. Continuous cardiac monitoring is to be used for assessment of T-wave changes.
After obtaining samples for cultures, intravenous antibiotics are to be started as soon as possible for patients with DKA precipitated by febrile illness. As soon as hemodynamic stability is achieved, the child should be transferred to an intensive care unit to be managed by a pediatric intensive care specialist with consultation from a pediatric endocrinologist.
Based on old studies, children with DKA are at least 5% to 10% dehydrated.10,11 Because clinical estimates are usually inaccurate,12 it is practical to estimate for moderate DKA, 5% to 7% dehydration, and for severe DKA, 7% to 10% dehydration.1 The initial fluid resuscitation is with normal saline or similar at a dose of commonly recommended at 20 mL/kg over 1 to 2 hours; however, reduced and slower fluid volumes are often recommended.13–15 The patient’s cardiovascular status is continuously reevaluated to modify fluid administration. The association between the rate of fluid resuscitation and development of cerebral edema is not convincing.13–17
After the initial fluid resuscitation, rehydration is continued with normal saline or Ringer lactate for 4 to 6 hours depending on the state of hydration, serum sodium, and hemodynamic status of the patient.18 Subsequently, the remaining fluid deficit should be replaced slowly over 48 hours with a solution of tonicity greater than equal to half normal saline with added potassium chloride, potassium phosphate, or potassium acetate.18–20
In addition to assessment of dehydration, calculation of effective osmolarity can guide fluid and electrolyte therapy. In patients with extreme hyperosmolarity, some recommend continuing therapy with normal saline or Ringer lactate until serum osmolarity decreases below 320 mOsm/L. The formula for serum osmolality is as follows (blood urea is not included because of low osmolality):
The absolute or relative lack of insulin and increase in counterregulatory hormones causes hyperglycemia and DKA. With initial fluid resuscitation, there is some decrease in blood glucose21,22; however, normalization of blood glucose and suppression of lipolysis requires low-dose continuous intravenous insulin infusion.23 This provides slow, reliable, and titratable systemic absorption of insulin. An initial bolus of insulin is unnecessary and can increase the risk of cerebral edema.24,25 The starting dose is commonly recommended at 0.1 U/kg/h; however, lower doses (e.g., 0.05 U/kg/h) are often recommended and utilized,13–15 and this should continue until resolution of DKA (pH >7.3, bicarbonate >15 mmol/L). On occasion, the infusion may have to be decreased to 0.05 U/kg/h when there is marked sensitivity to insulin. The goal of therapy is to decrease the serum glucose by 75 to 100 mg/dL/h. When the serum glucose reaches 250 mg/dL, 5% glucose is added to the infusing fluid. If the serum glucose is dropping precipitously, a glucose solution of ≥10% may need to be administered. It is dangerous to discontinue the insulin infusion completely if the patient has moderate-to-large serum ketones, since this can worsen the ketoacidosis.
During the initial resuscitation phase, the patient should be given nothing by mouth. As the patient improves, oral intake of water or ice may be provided and advanced to clear liquids as tolerated. When the serum glucose normalizes, metabolic acidosis improves and serum ketones decrease to trace, the insulin infusion is discontinued and switched to subcutaneous insulin and oral intake of liquids or solids. Subcutaneous insulin is administered 30 minutes prior to discontinuing the insulin infusion to allow for absorption of the subcutaneous insulin dose and hence prevent rebound hyperglycemia and ketoacidosis.
Children with DKA are potassium-depleted with a deficit of 3 to 6 mEq/L/kg.11 This loss is primarily intracellular potassium, which is drawn out of the cells by hypertonicity, in exchange for hydrogen ions, and also by efflux during glycogenolysis and proteolysis. Potassium is also lost by vomiting and osmotic diuresis.26 Although there is total body depletion of potassium, the initial serum potassium can be normal, increased, or decreased.27 When the insulin infusion is started, potassium is driven back into the cells with decrease in serum levels.28 Hypokalemia is most common after several hours of rehydration. Both severe hypo- and hyperkalemia can cause life-threatening cardiac arrhythmias; therefore it is essential that the patient’s serum potassium be determined as soon as possible. Serum potassium levels should be checked every 2 to 4 hours. Replacement therapy is started once normal or low serum potassium is ensured and urine output is established. The usual dose of potassium is twice-daily maintenance (Table 77–1) or 3 to 4 mEq/kg per 24 hours provided as 40 mEq/L in the IV fluids, with half as potassium chloride or potassium acetate and half as potassium phosphate. The maximum recommended rate of IV potassium is usually 0.5 mEq/kg/h.
| Average Loss (Per kg) | 24-h Maintenance Requirements (Per kg) | |
|---|---|---|
| Water | 70 mL (30–100) | <10 kg: 100 mL/kg/24 h |
| 11–20 kg: 1000 mL + 50 mL/kg/24 h for each kg over 10 | ||
| >20 kg: 1500 mL + 20 mL/kg/24 h for each kg over 2019 | ||
| For children over 10 kg: body surface area can be used (1500 mL/m2/24 h) | ||
| Sodium | 6 mEq (5–13) | 2–4 mEq |
| Potassium | 5 mEq (3–6) | 2–3 mEq |
| Chloride | 4 mEq (3–9) | 2–3 mEq |
| Phosphate | 1.5–7.5 mEq | 3–6 mEq |
The osmotic diuresis usually induces sodium depletion in patients with DKA. In DKA, both the hyperglycemia and hyperlipidemia cause pseudohyponatremia. In addition, the osmotic movement of water into the extracellular space causes dilutional hyponatremia.29,30 Therefore, corrected serum sodium should be used for monitoring changes during therapy. The formula for corrected serum sodium is as follows:
The corrected serum sodium should not be allowed to drop faster than 10 to 12 mEq/L per 24 hours. If significant hyponatremia is present, the first 6 to 8 hours of correction should occur with normal saline. During the continuing resuscitation, sodium levels are monitored every 4 hours, and as the glucose falls, the reported level of serum sodium should increase. A fall in serum sodium during continued fluid resuscitation may indicate excess accumulation of free water and may be a risk factor for the development of cerebral edema. If this happens, the sodium content of the fluid may need to be increased.31,32
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