DIABETIC

KETOACIDOSIS
PRESENTED BY DR. PATRICK MAILA (MBCHB)
DEPARTMENT OF PAEDIATRICS-LUTH
OCTOBER 21, 2024
Outline

1. definitions
2. risk factors
3. pathophysiology
4. investigations
5. management
Definition

 Diabetic ketoacidosis is a life-threatening complication of childhood diabetes

(mainly associated with type 1 or insulin-dependent diabetes).
 The prevalence of DKA at T1DM diagnosis varies greatly worldwide and ranges
between 13% and 80% in different countries
 30% of children with new-onset type 1 diabetes present with diabetic ketoacidosis,
and an additional 6% to 8% develop diabetic ketoacidosis each year (ISPAD 2022)

 It occurs when there is an absolute or relative insulin deficiency that inhibits the
ability of glucose to enter cells for utilization as a metabolic fuel.

 DKA is a leading cause of death in children with diabetes

DEFINITION-
ISPAD 2022
DKA is defined by the presence of all of the following in a patient
with diabetes:
 Hyperglycemia – Blood glucose >11 mmol/L (200mg/dl)
 Ketosis – Presence of ketones in the blood; >3 mmol/L beta-
hydroxybutyrate or urine >=2+ ("moderate or large“)
 Metabolic acidosis – Venous pH <7.3 or serum bicarbonate
<15 mmol/L
CLASSIFICATION

 Mild DKA if blood pH is below 7.3 or plasma bicarbonate is below 15 mmol/L

 Moderate DKA if blood pH is below 7.2 or plasma bicarbonate is below 10
mmol/L
 Severe DKA if blood pH is below 7.1 or plasma bicarbonate is below 5 mmol/L
RISK FACTORS

NEW ONSET DIAGNOSED DM

 younger age  omission of insulin for various reasons

 delayed diagnosis,  limited access to medical services
 lower socioeconomic status  unrecognized interruption of insulin
delivery in patients using an insulin pump
 residence in a country with a low
prevalence of type 1 diabetes mellitus
Pathogenesis of type 1 DM

GENETIC FACTORS

REDUCED INSULIN
AUTOIMMUNITY PRODUCTION DUE TO
PANCREATIC BETA CELL
DESTRUCTION

ENVIRONMENTAL
FACTORS
FUNCTIONS OF INSULIN ?
An anabolic hormone

CARBOHYDRATES LIPIDS PROTEINS

1. ACTIVATGE
GLYCOLYSIS
1. INCREASE LIPID
2. ACTIVATE
SYNTHESIS 1. STIMULATION OF
GLYCOGENESIS
2. INCREASE PROTEIN SYNTHESIS
(LIVER, MUSCLE)
LIPOPROTEIN 2. INHIBITION OF
3. INHIBIT
LIPASE PROTEIN
GLYCOGENOLYSIS
3. INHIBIT HORMONAL DEGRADATION
4. INHIBIT
LIPASE
GLUCONEOGENESI
S
Pathophysiology
 In a patient with new-onset diabetes, the cause for the insulin deficiency is the progressive
deterioration in beta cell reserve and function.
 In patients with established diabetes, insulin omission (intentional, as a result of insulin
pump failure or other technical problems, or related to lack of access to medical care) is a
major cause.
 Acute stress, commonly induced by an intercurrent illness, might precipitate DKA. During
stress, counterregulatory hormone (glucagon, cortisol, growth hormone, and epinephrine)
levels increase, causing hyperglycemia and an increased requirement for insulin. If this
increased need for insulin is not met, DKA may ensue.
 Insulin deficiency leads to hyperglycemia as a result of decreased utilization of glucose
at the same time of increased hepatic and renal glucose production. Hyperglycemia
increases serum osmolality, and in response, thirst is induced and osmotic diuresis
occurs.
 The increased fluid loss further promotes polydipsia.
 Because of the unavailability of glucose to tissues, compensatory mechanisms are
activated. Counterregulatory hormones are secreted, leading to increased glucose
production by gluconeogenesis and glycogenolysis.
 Insulin resistance increases and lipolysis is promoted, resulting in production of free
fatty acids (FFAs). FFAs are metabolized into ketone bodies, particularly β-
hydroxybutyrate, by the liver as an alternative energy source. The accumulation of
ketones leads to metabolic acidosis
 As the condition progresses, ketones further accumulate, ketonuria occurs, and eventually
the metabolic acidosis becomes evident.
 The ketoacidosis causes decreased bowel motility, particularly of the small bowl,
accompanied by nausea and vomiting. At this stage, the patient may be unable to
compensate for the urinary fluid losses.
 In a vicious cycle, dehydration impairs the renal ability to clear glucose and ketoacids,
thus further worsening the hyperglycemia and acidosis.
 The increasing osmolality, dehydration, and acidosis decrease cerebral function. This
might be manifested as lethargy, or even an altered level of consciousness, further
impairing the patient’s ability to rehydrate.
 Serum hyperglycemia and hyperosmolarity together with the acidosis and osmotic diuresis
lead to significant electrolyte deficiencies and imbalances
 Electrolyte losses
 Total body stores of potassium are depleted in basically every patient with DKA, and the
average potassium loss is 5 mmol/kg body weight
1. Acidosis.
2. The osmotic diuresis
3. Aldosterone
4. Emesis
 The osmotic diuresis in DKA results in urinary loss of sodium, and the hyperosmolar state
drives water out of cells into the extracellular space, leading to dilutional hyponatremia.
The average sodium loss is 6 mmol/kg body weight.
 Phosphate shifted extracellularly by the acidosis is then lost in the urine. Phosphate losses
can be substantial and are estimated to be about 0.5–2.5 mmol/kg body weight. Significant
hypophosphatemia has the potential to impair oxygen delivery to tissues and cause muscle
weakness.
CLINICAL FEATURES

 Polyuria
 Polydipsia
 polyphagia
 nausea or vomiting
 abdominal pain
 Hyperventilation (kusmaul’s breathing)
 dehydration
 reduced level of consciousness.
MANAGEMENT
Goals of Management

1. Correct acidosis and reverse ketosis

2. Correct dehydration
3. Restore blood glucose to near normal
4. Monitor for complications of DKA and its treatment
5. Identify and treat any precipitating event
Emergency management

1. General Resuscitation: A, B, C
2. Initial fluid bolus:
For patients who are volume depleted but not in shock, volume
expansion (resuscitation) should begin immediately with 0.9%
saline, 10 to 20 mL/kg infused over 20-30 minutes to restore the
peripheral circulation. If tissue perfusion is poor the initial fluid
bolus volume should be 20 ml/kg.
Initial Investigations

 Blood glucose
 FBC, Urea and electrolytes
 Blood gases (venous or capillary)-including anion gap
 Ketones -blood ketones (beta-hydroxybutyrate)

 IF INDICATED; CXR, CSF, throat swab, blood cultures, urinalysis, culture and
sensitivity etc.
(Presence of fever in DKA should raise a high index of suspicion for infection;
other features being hypothermia, hypotension, refractory acidosis, lactic
acidosis)
SPECIFIC
MANAGEMENT
FLUID/ELECTROLYTE AND INSULIN THERAPY
1. FLUIDS

 Treat DKA with intravenous fluids and intravenous insulin if the child is not alert,
is nauseated or vomiting, or is clinically dehydrated.
 Once circulating blood volume has been restored and the child adequately
resuscitated, calculate fluid requirements as follows:

➢ Fluid Requirement = Deficit + Maintenance

Fluid to be administered is 0.45% or 0.9% NS
 For children who are not shocked, the initial fluid bolus is subtracted from the
deficit fluid.
Hourly rate = ({Deficit – initial bolus} / 48hr) + Maintenance per hour
What is the fluid deficit?
 This is a calculated fluid value n patients who are fluid depleted (dehydrated), it is a percentage of
the body weight, calculated as Volume in liters.
fluid deficit:
➢ in mild-to-moderate DKA (blood pH 7.1 or above), assume 5% dehydration (e.g. a 10 kg child
needs 500 ml)
➢ in severe DKA (blood pH below 7.1), assume 10% dehydration (e.g. a 10kg child needs 1L)
Maintenance fluid

Maintenance fluid volumes should be calculated using the Holliday – Segar formula
➢ 100 ml/kg/day for the first 10 kg body weight, plus
➢ 50 ml/kg/day for 10 to 20 kg and
➢ 20 ml/kg/day for each additional kilogram above 20 kg
NB- Maximum weight of 75kg or 97th centile weigh for age (which ever is lower)
POTASSIUM

Children with DKA suffer from total body potassium deficits of approximately 3-
6mmol/kg
Start potassium at 40 mmol/L (or 20 mmol/500 ml). KCl is added to the intravenous
fluids only if:
 their potassium is less than 5.5 mmol/l or
 Passing urine (renal impairment)
INSULIN THERAPY
Use soluble Insulin (e.g. Actrapid), infusion rate between 0.05 and 0.1 units/kg/hour.

 Once rehydration fluids and potassium are running, blood glucose levels will start to fall. There is
some evidence that cerebral oedema is more likely if insulin is started early
 Therefore, start an intravenous insulin infusion 1-2 hours after beginning intravenous fluid
therapy.
 Aim to drop glucose by 5mmol/hour
 When the plasma glucose concentration falls below 14 mmol/L or >5mmol/hour,
change fluids to 0.9% NaCL with 5% glucose and KCl
 If the blood beta-hydroxybutyrate level is not falling within 6 to 8 hours think
about increasing the insulin dosage to 0.1 units/ kg/hour or more.
 Consider stopping intravenous fluid therapy if:
➢ ketosis is resolving and their blood pH has reached 7.3
➢ they are alert and
➢ they can take oral fluids without nausea or vomiting.
 Start subcutaneous insulin at least 30 minutes before stopping intravenous insulin
Monitoring during fluid and inulin therapy

One to one nursing in severe DKA or <2 years

A. Every 30 minutes
level of consciousness- check very 30 minutes
B. Every hour
1. capillary blood glucose
2. heart rate, blood pressure, temperature, respiratory rate
3. fluid balance, with fluid input and output charts
c. From 2nd hour to 4 hourly
1. glucose (laboratory measurement)
2. blood pH and pCO2
3. plasma sodium, potassium and urea
4. beta-hydroxybutyrate (urine ketones if not available)
5. ECG tracing
6. Cumulative fluid balance
Complications of DKA
CEREBRAL EDEMA

Signs and symptoms of cerebral edema

➢ Headache, irritability
➢ Neurological changes
deterioration in level of consciousness (41%)
cranial nerve (oculomotor) palsies (35%)
abnormal posturing (15%)
papilloedema
➢ Cushing’s triad (41%)
Bradycardia
Elevated blood pressure
abnormal respirations
Management of cerebral edema

➢ Exlude hypoglycemia and elevate head of bed

➢ Restrict fluids to half of maintenance

1. Mannitol (20%), 0.5 g/kg to 1 g/kg over 10 to 15 minutes or

2. Hypertonic NaCl (2.7% or 3%, 2.5 ml/kg to 5 ml/kg over 10 to 15 minutes)

➢ Document carefully
Other complications

➢ Hypoglycemia
➢ hypokalemia
➢ Acute renal failure
➢ Thromboembolic complications
References

1. BSPED Guideline for the Management of Children and Young People under the
age of 18 years with Diabetic Ketoacidosis – 2021
2. ISPAD Clinical Practice Consensus Guidelines 2022
3. Diabetes (type 1 and type 2) in children and young people: diagnosis and
management 2018 (updated 2023)
4. Robert M. Kliegman (2020) Nelson textbook of pediatrics, 21st edition, Elsevier,
Inc, Philadelphia, PA 19103-2899