Diabetic Ketoacidosis (DKA)

Diabetic ketoacidosis (DKA) is a complex disordered metabolic state characterised by hyperglycaemia, acidosis, and ketonaemia. DKA has been considered to be indicative, or even diagnostic, of type 1 diabetes, but increasingly there are cases of ketone-prone type 2 diabetes being recognised. However, the initial treatment is the same.

Diagnostic Criteria (all three must be present):

Capillary blood glucose > 11 mmol/L
Ketonaemia > 3 mmol/L or Ketonuria > ++
Bicarbonate (HCO3-) < 15 mmol/L and/or venous pH < 7.3

Pathophysiology

DKA usually occurs as a consequence of absolute or relative insulin deficiency that is accompanied by an increase in counter regulatory hormones (i.e. glucagon, cortisol, growth hormone, catecholamines). This hormonal imbalance enhances hepatic gluconeogenesis and glycogenolysis resulting in severe hyperglycaemia. Enhanced lipolysis increases serum free fatty acids that are then metabolised as an alternative energy source in the process of ketogenesis. This results in accumulation of large quantities of ketone bodies and subsequent metabolic acidosis.

There is initial compensation for the metabolic acidosis by hyperventilation and a respiratory alkalosis but as the condition progresses, the combination of acidosis, hyperosmolality and dehydration leads to coma. There are several mechanisms responsible for fluid depletion in DKA. These include osmotic diuresis due to hyperglycaemia, vomiting and eventually, inability to take in fluid due to a diminished level of consciousness. Electrolyte shifts and depletion are in part related to the osmotic diuresis. Hyperkalaemia and hypokalaemia need particular attention.

Precipitating Factors

Infection (for example pneumonia or a urinary tract infection)
Physiological stress (such as trauma or surgery)
Non-adherence to insulin treatment regimen or intentional insulin omission in order to lose weight (diabulimia)
Other medical conditions (such as hypothyroidism or pancreatitis)
Drug treatment (such as corticosteroids, diuretics, and sympathomimetic drugs)

Clinical Features

Suspect diabetic ketoacidosis (DKA) in a person with known diabetes or significant hyperglycaemia (finger-prick blood glucose level greater than 11 mmol/L) and the following clinical features:

Increased thirst and urinary frequency
Weight loss
Inability to tolerate fluids
Persistent vomiting and/or diarrhoea
Abdominal pain
Visual disturbance
Lethargy and/or confusion
Fruity smell of acetone on the breath
Acidotic breathing — deep sighing (Kussmaul) respiration
Dehydration, which can be classified as:
- Mild — only just clinically detectable.
- Moderate — dry skin and mucous membranes, and reduced skin turgor.
- Severe — sunken eyes and prolonged capillary refill time.
Shock (resulting from severe dehydration). The person is severely ill with:
- Tachycardia, poor peripheral perfusion, and (as a late sign) hypotension (indicating decreased cardiac output)
- Lethargy, drowsiness, or decreased level of consciousness (indicating decreased cerebral perfusion)
- Reduced urine output (indicating decreased renal perfusion)

Complications

Cerebral oedema (more common in children)
Cardiac dysrhythmias, usually secondary to electrolyte disturbance
Pulmonary oedema
Acute renal failure
Severe hypokalaemia
Acute respiratory distress syndrome (ARDS)
Comorbid states e.g. pneumonia, acute myocardial infarction, sepsis

Investigations

Blood tests:
- Capillary and laboratory glucose
- Ketones
- Venous blood gas
- U&Es
Urine dipstick for glucose and ketones
ECG and continuous cardiac monitoring (and pulse oximetry)
Infection screen if indicated:
- FBC, CRP
- Blood cultures
- Chest x-ray
- Urinalysis, culture and sensitivities
- Throat swab
- Lumbar puncture
Pregnancy test if appropriate

Management in Adults

Intravenous Fluids

Initial fluids:

Systolic BP < 90 mmHg:

500 mL 0.9% sodium chloride over 10–15 minutes
Repeat if BP remains < 90 mmHg
Consider ITU involvement

Systolic BP ≥ 90 mmHg:

1 L 0.9% sodium chloride over 60 minutes

Potassium Replacement

Add KCl to all fluids unless anuria suspected
Monitor K+ levels:
- K+ >5.5 = nil replacement
- K+ 3.5-5.5 = 40 mmol/L
- K+ <3.5 = senior review
Monitor pH and HCO3 at 60 min, 2h, then 2-hourly

Insulin

Fixed rate: 0.1 units/kg/hour
Continue SC long-acting insulin
Monitor hourly:
- Ketones should fall ≥0.5 mmol/L/hour
- Glucose should fall ≥3 mmol/L/hour
Continue until ketones <0.6 mmol/L and pH >7.3

Glucose

Add 10% glucose when BG <14 mmol/L
Rate: 125 mL/hour
Consider reducing insulin to 0.05 units/kg/hour
Continue 0.9% NaCl alongside glucose

Management in Children

Note:

For 16-18 year olds, use pediatric guidelines if managed by pediatric diabetes team, otherwise follow adult guidelines.

Severity Classification:

Severity	pH / Bicarbonate	Dehydration
Mild	pH 7.2-7.29 or HCO3 < 15	5%
Moderate	pH 7.1-7.19 or HCO3 < 10	5%
Severe	pH < 7.1 or HCO3 < 5	10%

Fluid Management:

Shock: 10 ml/kg isotonic crystalloid over 15 min (max 40 ml/kg)
Non-shocked: 10 ml/kg 0.9% saline over 30 min
Deficit: 5-10% × weight(kg) × 10 (replace over 48h)
Maintenance: Holliday-Segar formula

Insulin:

Start 1-2 hours after beginning IV fluids
Rate: 0.05-0.1 units/kg/hour
No bolus doses
Reduce to 0.05 units/kg/hour when BG <14 mmol/L

Cerebral Oedema Management

Early Signs

Headache
Agitation or irritability
Unexpected bradycardia
Hypertension

Late Signs (Immediate Treatment)

Decreased consciousness
Abnormal breathing pattern
Oculomotor palsies
Abnormal posturing
Pupillary changes

Treatment:

Immediate:
- Hypertonic saline (2.7-3%): 2.5-5 ml/kg over 10-15 min OR
- Mannitol (20%): 0.5-1 g/kg over 10-15 min
Restrict fluids to 50% maintenance
Immediate senior/ICU involvement

DKA Summary

Diagnostic Criteria

Fluid Management

Insulin Protocol

Potassium

Pediatric Specific

Cerebral Edema