Pediatrics Diabetic Ketoacidosis

PEDIATRIC DIABETIC KETOACIDOSIS

Dr Tariq Al thobaiti ,MBBS

Pediatric Diabetic Ketoacidosis

• Children with Diabetes specially type I, remain at risk for developing diabetic ketoacidosis (DKA).
• Children who are type I diabetics have incidence of DKA of 8/100 patients.
• In children younger than 19 years old, DKA is the admitting diagnosis in 65% of all hospital admissions of patients with diabetes mellitus.

Pediatric Diabetic Ketoacidosis

• The overall mortality rate for children in DKA is not unimpressive.
• Range of mortality is between 0.15 – 0.31 %
• The mortality associated with cerebral edema may approach 20-50 %
• The incidence of neurologic morbidity is significant and reported in 35-40% of survivors.
• Cerebral edema has largely been a complication of treatment in the pediatric population.

Pathophysiology of Diabetes Type I

Pediatric Diabetic Ketoacidosis

DEFINITION:

• Hyperglycemia >200mg/dl = 11 mmol/l

• Acidosis ph<7.3

• Bicarbonate < 15 meq/l

• Ketonemia (Beta hydroxy butyrate and acetoacetate) >3 mmol/l

• Ketonuria

ETIOLOGY:

• Error in insulin management at home or inadequate insulin administration.
• Secondary to child or parental non-compliance because of emotional and psychological stress
• Insulin pump malfunction
• Infections any stress
• Pre-pubertal and pubertal phase

* 1 ^st presentation

Assessment of severity of diabetic ketoacidosis in children

	Mild	Moderate	Severe
Defining features
Venous pH	7.2-7.3	7.1-7.2	<7.1
Serum bicarbonate (mEq/L)	10-15	5-10	<5

Clinical Presentation:

• Sometimes can be challenging and subtle requiring high degree of suspicion.
• Classically: Polyuria, Polydipsia, weight loss also abdominal pain, nausea, vomiting.
• Physical examination:
  • • Dehydrated
• Dry mucous membranes, tachycardia, delayed capillary refill, hypo-perfusion, hypothermia, kussmaul’s breathing, diffuse abdominal pain.

Management:

1- Fluids:

• 1^st ABCD

• 2^nd Look For the Cause

• 3^rd Treat the Cause

• 1- Fluids: Carefully regulated treatment plan to prevent the most lethal complication of DKA → cerebral edema & electrolytes

• pediatric dose: 10-20 ml x Kg until normalize the vital sign

• in adult: 1 l

• then calculate deficit (4, 2, 1)

• give 1 1/2 maintenance

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2- Electrolytes:

check for K before you start insulin

A- serum sodium:

• As serum glucose fall with therapy, serum sodium should rise to normal or above normal level.
• Clinicians should consider the possibility of pseudohyponatremia that may result from elevated glucose.
• Corrected Na level: Na decreased 1.6mEq/l for each 100mg/dl rise in glucose

B- serum potassium:

• At initial presentation in DKA, normally they have high or normal potassium level even though total body potassium stores are depleted (extra-cellular shift of potassium)
• Potassium is lost from the body via 3 routes: vomiting, urinary loss.
• Massive volume depletion $\to$ 2ry hyperaldosteronism $\to$ increased excretion of potassium through kidney.

CAUSES: because of high acid (Pseudohyperkalemia) but need K+ after insulin dose because will back into cell

• High plasma osmolality $\to$ osmotic shift of water to ECF $\to$ potassium follows this gradient $\to$ hyperkalemia
• Acidosis
• Insulin deficiency $\to$ glycogenolysis and proteolysis $\to$ worsen osmotic gradient.

C- Serum phosphate:

• Renal excretion of phosphate + rapid entry of phosphate intracellularly $\to$ hypophosphatemia

• Phosphorus replacement if level below 1 mg/dl as it may cause muscle weakness and insult diaphragmatic tissues.

• Always keep in mind that phosphorus administration may cause hypocalcemia.

Insulin as infusion $0.1\times \text{kg}/\text{h}$

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3- Insulin and glucose:

• Although there is consensus that blood sugar level must be greater than 200 mg/dl for patient to be in DKA, there are some infrequent reports of euglycemic DKA.

Reasons:

1. Fasting child.
2. Poor nutrient intake

• Insulin is crucial in the treatment of pediatric DKA as it suppresses lipolysis and ketogenesis.
• Care should be taken to avoid precipitous drop in glucose level, should not drop at a rate faster than 100mg/dl/hr to decrease the risk of cerebral oedema.

4- Acidosis and bicarbonate:

• There is absolutely no role for bicarbonate administration in DKA patients $\to$ leads to cerebral oedema (paradoxical CNS acidosis).

Indications for bicarbonate administration:

1. Severe academia with $\text{pH}<<6.9$
2. Life threatening hyperkalemia with ECG changes.
   • Causing arrhythmia

Complications of DKA:

1- Hypoglycemia:

• 2ry to insulin infusion→ Do hourly blood glucose check.

• Treatment: various types of IV dextrose

• if BG

• $300-250$ now change fluid to dextrose 5%.

2- Hypokalemia:

• 2ry to insulin therapy which shifts potassium intracellularly.

• Potassium losses from the body via: vomiting, urinary loss.

• Massive volume depletion→2ry hyperaldosteronism→increased excretion of potassium through kidney.

• It is prudent to add some potassium chloride to IVF according to protocol.

3- Cerebral edema:

• treat it by hypertonic saline

• It is a multifactorial process

• (cerebral oligemia, hyperemia, inflammation, cyto-toxic insult)

• Overhydration leads to cerebral edema.

• bicarbonate administration in DKA patients $\to$ leads to cerebral oedema (paradoxical CNS acidosis).

• Rapid drop in glucose level leads to osmotic shift $\to$ cerebral edema

• Failure of correction of Na with treatment

• Epidemiologically patients with high blood urea concentrations are at risk.

• Epidemiologically patients with severe hypocapnia are at risk for cerebral edema.

Clinically:

• Altered mental status
• Headache
• Vomiting
• Bradycardia
• Hypertension
• Irregular breathing
• Seizures
• Anisocoria

maybe alter DKA protocol

• Hypoglycemia is defined as a plasma glucose level of <45 milligrams/dL in any symptomatic patient or <35 milligrams/dL in an asymptomatic neonate.
• Evaluation of urine for ketones is the second important step. Ketonuria is characteristic of ketotic hypoglycemia, adrenal or growth hormone deficiency, and other inborn errors of metabolism.

Hypoglycemia

TABLE 137-1 Management of Hypoglycemia in the ED

Patient Age	Dextrose Bolus Dose	Dextrose Maintenance Dosage	Other Treatments to Consider
Neonate	D10 5 mL/kg PO/NG/IV/IO → give 5	6 mL/kg/h D10	Glucagon, 0.3 milligram/kg IM Hydrocortisone, 25 grams PO/IM/IV/IO
Infant	D10 5 mL/kg PO/NG/IV/IO or D25 2 mL/kg	6 mL/kg/h D10	Glucagon, 0.3 milligram/kg IM Hydrocortisone, 25 grams PO/IM/IV/IO
Child	D25 2 mL/kg PO/NG/IV/IO → give 2 to reach 50	6 mL/kg/h D10 for the first 10 kg + 3 mL/kg/h for 11–20 kg + 1.5 mL/kg/h for each additional kg >20 kg	Glucagon, 0.3 milligram/kg IM Hydrocortisone, 50 grams PO/IM/IV/IO
Adolescent	—	6 mL/kg/h D10 for the first 10 kg + 3 mL/kg/h for 11–20 kg + 1.5 mL/kg/h for each additional kg >20 kg	Glucagon, 0.3 milligram/kg IM Hydrocortisone, 100 grams PO/IM/IV/IO
adult	D50