Diabetic ketoacidosis (peds)

This page is for pediatric patients. For adult patients, see: diabetic ketoacidosis

Background

• DKA + altered mental status = cerebral edema until proven otherwise

Clinical Features

Frequency of signs and symptoms among 37 pediatric patients with diabetic ketoacidosis in Nigeria.

• May be the initial presenting of an unrecognized Type-1 diabetes mellitus patient
• Signs/symptoms may include:
  • Tachypnea, Kussmaul's breathing
  • Polyuria, polydipsia, polyphagia, poor weight gain/weight loss
  • Signs of dehydration
  • Abdominal pain, nausea/vomiting
  • Altered mental status, drowsiness, lethargy
  • Breath fruity odor (acetone)
    • Perform a thorough neurologic exam as cerebral edema increases mortality significantly, especially in children
• +/- signs/symptoms of precipitating trigger for decompensation (e.g. pneumonia, cellulitis)
• Keep in mind that the initial presentation of sepsis with dehydration can look very similar to DKA

Differential Diagnosis

Hyperglycemia

Diabetic Emergencies

• Diabetic ketoacidosis (DKA)
• Diabetic ketoacidosis (peds)
• Hyperosmolar hyperglycemic state (HHS)
• Nonketotic hyperglycemia
• Euglycemic DKA (SGLT-2 inhibitors, pregnancy, fasting)

Diabetes Mellitus (New or Known)

• Type 1 diabetes mellitus (new-onset or uncontrolled)
• Type 2 diabetes mellitus (new-onset or uncontrolled)
• Medication noncompliance or insulin pump malfunction
• Gestational diabetes
• Latent autoimmune diabetes of adults (LADA)

Medication/Drug-Induced

• Corticosteroids (most common drug-induced cause)
• Thiazide diuretics
• Atypical antipsychotics (olanzapine, clozapine, quetiapine)
• Beta-blockers (especially non-selective)
• Phenytoin
• Tacrolimus, cyclosporine (transplant patients)
• Protease inhibitors (HIV antiretrovirals)
• Catecholamines (epinephrine, norepinephrine infusions)
• SGLT-2 inhibitors (paradoxical DKA with euglycemia)
• Total parenteral nutrition (TPN)
• Dextrose-containing IV fluids (iatrogenic)
• Niacin
• Pentamidine (initially hyperglycemia, then hypoglycemia from beta-cell destruction)

Physiologic Stress Response

• Sepsis / critical illness (stress hyperglycemia — very common in the ED)
• Trauma / major surgery / burns
• Acute coronary syndrome / myocardial infarction
• Stroke (especially hemorrhagic)
• Pancreatitis (both a cause and consequence)
• Shock (any etiology)
• Pain (catecholamine surge)
• Seizure (postictal)
• Physiologic stress alone rarely causes glucose >200 mg/dL in non-diabetics; glucose >200 in a "stress response" should prompt evaluation for undiagnosed diabetes or prediabetes

Endocrine

• Cushing syndrome / Cushing disease (cortisol excess)
• Pheochromocytoma (catecholamine excess)
• Hyperthyroidism / thyroid storm
• Acromegaly (growth hormone excess)
• Glucagonoma (rare)
• Somatostatinoma (rare)

Pancreatic

• Pancreatitis (acute or chronic — destruction of islet cells)
• Pancreatic malignancy (adenocarcinoma, neuroendocrine tumors)
• Post-pancreatectomy
• Cystic fibrosis-related diabetes
• Hemochromatosis (iron deposition in pancreas — "bronze diabetes")

Toxic/Overdose

• Iron toxicity (hepatic injury → impaired glucose regulation)
• Salicylate toxicity (can cause both hyper- and hypoglycemia)
• Sympathomimetic toxicity (cocaine, methamphetamine)
• Calcium channel blocker toxicity (impairs insulin secretion)
• Carbon monoxide toxicity (stress response)

Other

• Renal failure (chronic kidney disease, acute kidney injury — impaired insulin clearance AND insulin resistance)
• Cirrhosis / hepatic failure (impaired glycogenolysis regulation)
• Pregnancy (gestational diabetes, steroid administration for fetal lung maturity)
• Parenteral nutrition (TPN, dextrose-containing fluids)
• Post-transplant diabetes (immunosuppressants)

Complications of Diabetes (Not Causes of Hyperglycemia)

These are associated conditions that may be present alongside hyperglycemia but do not themselves cause elevated glucose:

• Diabetic foot infection
• Diabetic peripheral neuropathy
• Cerebral edema in DKA
• Diabetic retinopathy
• Diabetic nephropathy

Evaluation

Workup

• Point of care glucose (and potassium, if available)
• VBG
• Chem 7
• Magnesium
• Phosphorus
• Serum ketones (or beta-OH and acetone)
• Urinalysis
• CBC
• Urine pregnancy (if appropriate)
• Consider infectious workup to identify trigger

Diagnosis

• Hyperglycemia (>200)
• Acidosis
  • pH <=7.30 or bicarb <=15
• +ketonemia (>1:2 serum dilution)

General Treatment

• Initial bolus 20ml/kg NS x 1 (repeat boluses only for shock or poor perfusion)

Manage Hydration

• If K+<5.5
  • 0.45% NS (or NS) + 20 KPhosat 1.5 x maintenance rate
    • When BS <300, change to D5/0.45%NS (or NS) +20 KPhos at 1.5 x maintenance rate (maintain BS 150-250)
• In a retrospective study, lactated ringers when compared with normal saline was associated with lower total cost and rate of development of cerebral edema.

Manage Acidosis

• Insulin 0.1 units/kg/hr IV drip IV drip — Do not start if K+ <4.0; decrease to 0.05 units/kg/hr when transitioning to SC
  • Do not start if K+ <4.0 (replete K+ first)
  • Continue until HCO3 >15 and pH >7.3, then transition to SC insulin
    • Decrease infusion to 0.05 units/kg/hr until 1hr after SC insulin initiated

Potassium

• if <2.5, hold insulin and give 1 meq/kg potassium KCL in IV over 1hr
  • No insulin until K >2.5
• if >2.5 but <3.5 give 40-60 meq/L in IV until K >3.5
• if >3.5 but <5.5 give 30-40 meq/L in IV for K = 3.5 - 5
• if >5.5, then check K q1hr

Bicarbonate

• No evidence supports the use of sodium bicarb in DKA, with a pH >6.9
• However, no studies have been performed for patients with pH <6.9 and the most recent ADA guidelines recommend it for patients with pH <7.1
• Only consider for:
  • Critically ill (hemodynamic compromise from decreased contractility) AND
  • pH <7.0
• Sodium bicarbonate 0.5-2 mEq/kg over 1-2 hr IV — Correction should never exceed pH >7.1 or bicarb >10
  • Correction should never exceed pH > 7.1 or bicarb >10

Monitor for Complications

• Cerebral edema (1% of DKA)
  • Acute change in mental status
  • Signs of herniation
• If present, see Cerebral Edema in DKA

Disposition

• Admit all (usually to PICU, if on insulin drip) unless
  • Known diabetes
  • pH >7.35 and bicarb >20
  • Known and resolving precipitant for DKA

Complications

• Cerebral Edema in DKA

See Also

• Diabetes mellitus (main)
• Diabetic ketoacidosis (main)
• EBQ:Sodium Bicarbonate use in DKA
• Clinical Trial of Fluid Infusion Rates for Pediatric Diabetic Ketoacidosis

External Links

• Pediatric Emergency Playbook -- Vomiting in the Young Child: Nothing or Nightmare