DKA is characterised by hyperglycaemia with increased levels of circulating ketones in the body leading to ketoacidosis. The ISPAD guidelines stress that since beta-hydroxybutyrate is found at the onset of DKA, measurement of blood beta-hydroxybutyrate (BOHB) concentration can be helpful.

Diabetic ketoacidosis (DKA) is a common but preventable complication of diabetes, which occurs as a result of insulin deficiency. DKA is a hallmark of type 1 diabetes; however, DKA is increasingly recognised in patients with type 2 diabetes. DKA at diagnosis is commonly observed in younger children, minority race, and male gender.

Diabetic ketoacidosis management has been in practice for several decades, however, the complications and cost associated with it is ever increasing. Prompt treatment with proper resource utilisation is the key to appropriate management of DKA.

The International Society for Paediatric and Adolescent Diabetes (ISPAD) clinical practice guideline lays down some important recommendations regarding the management of diabetic ketoacidosis.

---

Biochemical Criteria for Diabetic Ketoacidosis

The biochemical criteria for the diagnosis of DKA include the following:

1. Hyperglycaemia (blood glucose >11 mmol/L [200 mg/dL]): It should be noted that some paediatric patients may present with modestly elevated blood glucose levels, a condition termed euglycaemic DKA. Starvation, a low-carbohydrate, high-fat diet, or the off-label use of SGLT2-inhibitors are some reasons for euglycemic DKA.
2. Venous pH <7.3 or serum bicarbonate <15 mmol/L: Serum bicarbonate concentration alone is suggested as an alternative to venous pH (vpH) in settings where access to vpH measurement is limited.
3. Ketonemia or ketonuria: Urine ketones are typically ≥2+ “moderate or large” positive. As beta-hydroxybutyrate is a predominant ketone body found at the onset of DKA, measurement of blood beta-hydroxybutyrate (BOHB) concentration can be helpful. A BOHB concentration of ≥3 mmol/L is indicative of DKA.

---

Categorisation of DKA severity

The degree of acidosis is used to categorise the severity of DKA:

• Mild: Venous pH <7.3 or serum bicarbonate <15 mmol/L
• Moderate: pH <7.2, serum bicarbonate <10 mmol/L
• Severe: pH <7.1, serum bicarbonate <5 mmol/L

---

Management of DKA

The first step in managing DKA includes assessing the clinical history, clinical signs and biochemical features.

• Assessing the Clinical History: Polyuria, polydipsia, nocturia, enuresis, weight loss, nausea, vomiting, abdominal pain, weakness, fatigue, confusion, decreased level of consciousness
• Clinical signs such as dehydration, deep sighing, respiration (Kussmaul), smell of ketones, lethargy/drowsiness
• Biochemical features & investigations: Ketones in urine, increased blood glucose, Acidaemia (vpH <7.3, HCO3 <15 mmol/L), Urea, electrolytes

After Diabetic Ketoacidosis has been confirmed

1. Resuscitation should be performed in cases with shock (reduced peripheral pulses) and reduced conscious level/coma.
2. In cases with dehydration >5%, (not in shock), acidotic (hyperventilation) and vomiting, IV Therapy of Saline 0.9% 10 mL/kg over 1 h should be initiated; which may also be repeated. The fluid requirements should be calculated and fluid deficit should be corrected over 24-48 hours. ECG should be looked to assess T-waves for evidence of hyper- or hypokalaemia. KCl 40 mmol per litre fluid should be added in hypokalaemia.
3. If the patient presents with minimal dehydration and can tolerate oral fluid, start with SC insulin and continue oral hydration. If there is no improvement with this strategy, IV therapy should be started.
4. After IV therapy, continuous insulin infusion should be administered at 0.05 - 0.1 unit/kg/hour starting 1 hour after fluids initiated.

Critical observations to be noted

• Hourly blood glucose
• Hourly fluid input & output
• Neurological status at least hourly
• Electrolytes 2 hourly after starting IV fluid therapy
• Monitor ECG for T-wave changes

The following should be re-evaluated if acidosis is not improving

• IV fluid calculations
• Insulin delivery system & dose
• Need for additional resuscitation
• Consider sepsis

 

If Blood glucose ≤17 mmol/L (300 mg/dL); Blood glucose falls >5 mmol/L/hour (90 mg/dL)

• Change IV Therapy to 0.45% or 0.9% saline; add glucose to fluids (5% - 12.5%) to prevent hypoglycaemia
• Adjust sodium infusion to promote an increase in measured serum sodium

If a patients shows signs of improvement (clinically well, ketoacidosis resolved, tolerating oral fluids) consider transition to SC Insulin; IV insulin administration should be gradually decreased

If case shows signs of neurological deterioration such as headache, slowing heart rate, irritability, confusion, decreased consciousness, incontinence, specific neurological signs; diagnosis for cerebral edema should be considered.

---

Cerebral oedema management

• Give mannitol 0.5-1g/kg or 3% hypertonic saline
• Adjust IV fluids to maintain normal BP, but avoid overhydration
• Call senior staff and move to ICU
• Consider cranial imaging only after patient stabilised

---

Introduction of oral fluids and transition to SC insulin

Oral fluids should be introduced only when substantial clinical improvement has occurred. Absence of ketonuria should not be used as an end‐point for determining resolution of DKA as persistent ketonuria occurs for several hours after serum BOHB levels have returned to normal.

Once ketoacidosis has resolved, oral intake can be tolerated, and the change to SC insulin can be initiated. The best time to transition to SC insulin is just before a mealtime.

A dose of basal (long‐ or intermediate‐acting) insulin should be administered in addition to rapid‐ or short‐acting insulin. Earlier administration of a dose of basal insulin while the patient is still receiving IV insulin infusion can prove beneficial. The regimen, dose and type of SC insulin should be as per the local preferences and circumstances.

---

To prevent rebound hyperglycaemia

• The first SC injection should be given 15 to 30 minutes (with rapid‐acting insulin) or 1 to 2 hours (with regular insulin) before stopping the insulin infusion to allow sufficient time for the insulin to be absorbed
• With intermediate‐ or long‐acting insulin, the overlap should be longer and the rate of IV insulin administration gradually decreased

After transitioning to SC insulin, the blood glucose should be monitored frequently to avoid marked hyperglycaemia and hypoglycaemia.

---

Preventing recurrent DKA

Management of an episode of DKA is incomplete until the definite cause has been identified. Following are some common causes for the development of DKA

• Insulin omission - Inadvertently or deliberately
• The most common cause in insulin pump users is the failure to take extra insulin with a pen or syringe when hyperglycaemia and hyperketonaemia or ketonuria occur

An infection is rarely the cause of DKA when the patient or his caregivers are properly educated in diabetes management and is receiving appropriate follow‐up care.

Home measurement of blood BOHB concentrations decreases diabetes‐related hospital visits as it helps in early identification and treatment of ketosis. Blood BOHB measurements may be especially valuable to prevent DKA in patients who use a pump because interrupted insulin delivery rapidly leads to ketosis.

Psychosocial reasons for insulin omission includes attempt to lose weight, a means of escaping an intolerable or abusive home situation and depression or inability of the patient to manage the diabetes unassisted. In such cases, help should be sought from a psychiatric social worker or clinical psychologist.

Insulin omission can be prevented by comprehensive programs that provide education, psychosocial evaluation and treatment combined with adult supervision of the entire process of insulin administration. Parents and patients should be taught how to recognise and treat ketosis and impending DKA with additional rapid‐ or short‐acting insulin and oral fluids.