Rosen & Barkin's 5-Minute Emergency Medicine Consult (205 page)

• CXR if any suggestion of pneumonia
  
• Head CT if there are concerns about cerebral edema
  

• Infection (may precipitate):
  
  • UTI
    
  • Gastroenteritis
    
  • Appendicitis
    
  • Sepsis
    
• Ingestion (salicylates, alcohols, glycols)
  
• Diabetes insipidus
  

TREATMENT

For DKA:

• ABCs
  
• Airway protection
  
• Establish IV access and initiate fluid therapy.
  

For DKA:

• Oxygen
  
• Cardiac monitor
  
• IV access and volume resuscitation
  

• For DKA:
  
  • Fluid replacement:
    
  • Assume fluid deficit of 10% of body weight.
    
  • Initial volume expansion with 10–20 mL/kg of 0.9% NaCl or lactated Ringer; may repeat to achieve hemodynamic stability
    
  • Correct 50% of fluid deficit over 1st 8 hr, remainder over 24–48 hr.
    
  • Do not give >3 L/m
    ²
    over 1st 24 hr.
    
• Begin IV insulin infusion after ketoacidosis confirmed:
  
  • Initial rate of continuous infusion (regular insulin) 0.1 U/kg/h IV
    
  • Adjust rate to drop serum glucose 50–100 mg/dL/h.
    
  • Add dextrose to infusion fluid when serum glucose <300 mg/dL.
    
  • Change to SC insulin when no longer significantly acidotic and able to eat.
    
• Some clinicians prefer IM route, commonly initially using regular insulin at a dose of 0.1–0.2 U/kg/h.
  
• Replace potassium and phosphate losses:
  
  • Verify adequate urine output.
    
  • Add to fluids as K-acetate (or KCl if acetate not available) and K
    ₃
    PO
    ₄
    in equal amounts.
    
  • Large doses of K
    ⁺
    may be necessary; guide therapy by frequent monitoring of K
    ⁺
    .
    
• Monitor serum sodium:
  
  • Risk for cerebral edema if Na
    ⁺
    fails to rise as glucose falls
    
• Bicarbonate therapy:
  
  • Not recommended in most cases since generally it does not alter outcome and it increases risk for cerebral edema with its use
    
  • Use it with caution in patients with severe acidosis (pH <6.9) in whom peripheral vasodilation and decreased cardiac contractility may further impair tissue perfusion and in potentially life-threatening hyperkalemia.
    
• Cerebral edema:
  
  • Treat cerebral edema as soon as the condition is suspected due to its high mortality and morbidity rates: 21–25% and 10–26%, respectively.
    
  • Decrease fluid administration rate.
    
  • Mannitol (0.25–1 g/kg over 20 min): No large studies to date demonstrate definitive beneficial or detrimental effects. Consider its use in patients with signs of cerebral edema before impeding respiratory failure. Dose can be repeated in 2 hr if there is no initial response.
    
  • Endotracheal intubation and ventilation: Avoid aggressive hyperventilation since it has been associated with poor outcome in DKA-related cerebral edema (similar to that found in head trauma).
    

• Insulin drip: Start regular insulin 0.1 U/kg/h IV (some clinicians prefer the IM dosing and route).
  
• Mannitol: 0.25–1 g/kg IV
  

FOLLOW-UP

For DKA:

• ICU:
  
  • Altered mental status
    
  • Shock or cardiac dysrhythmia
    
  • Initial glucose >700 mg/dL
    
  • Initial pH <7
    
  • Risk factors for cerebral edema (age <5 yr, prolonged symptoms, high BUN)
    
• Inpatient unit:
  
  • Stable new-onset diabetic patients requiring intensive education
    
  • Patients with ketoacidosis not meeting requirements for ICU care
    
  • Compliance concerns or other social issues
    

• Known diabetic patients who respond well to therapy with normalization of glucose, pH, and ketosis
  
• Tolerating oral fluids
  
• Reliable parents
  
• Reliable follow-up within 24 hr including appropriate education
  

• Critically ill
  
• Persistent abnormal mental status
  
• Poorly controlled diabetes
  

• Close follow-up with the primary care physician is important even after the resolution of DKA to ensure appropriate management of the patient’s diabetes to prevent further occurrence of DKA.
  
• Many children with diabetes are followed at comprehensive diabetes centers in collaboration with primary care physician.
  

• Mortality from DKA is predominately related to the occurrence of cerebral edema. Therefore, early and appropriate treatment is of most importance in managing children with DKA.
  
• In children, avoid using an insulin bolus since it increase the risk of cerebral edema. Recently, some data suggest that starting insulin drip at 0.05 U/kg/h may reduce the risk for rapid fluid shifts and theoretically for cerebral edema.
  

• Al Hanshi S, Shann F. Insulin infused at 0.05 versus 0.1 units/kg/hr in children admitted to intensive care with diabetic ketoacidosis.
  Pediatr Crit Care Med.
  2011;12:137–140.
  
• Cebeci AN, Guven A, Kirmizibekmez H, et al. Clinical features and management of diabetic ketoacidosis in different age groups of children: Children less than 5 years of age are at higher risk of metabolic decompensation.
  J Pediatr Endocrinol Metab.
  2012;25(9–10):917–925. doi:10.1515/jpem-2012-0110.
  
• de Vries L, Grushka Y, Lebenthal Y, et al. Factors associated with increased risk of insulin pump discontinuation in pediatric patients with type 1 diabetes.
  Pediatr Diabetes.
  2011;12(5):506–512. doi:10.1111/j.
  
• Glaser N, Barnett P, McCaslin I, et al. Risk factors for cerebral edema in children with diabetic ketoacidosis. The Pediatric Emergency Medicine Collaborative Research Committee of the American Academy of Pediatrics.
  N Engl J Med
  . 2001;344:264–269.
  
• Kamat P, Vats A, Gross M, et al. Use of hypertonic saline for the treatment of altered mental status associated with diabetic ketoacidosis.
  Pediatr Crit Care Med
  . 2003;4:239–242.
  
• Roberts JS, Vavilala MS, Schenkman KA, et al. Cerebral hyperemia and impaired cerebral autoregulation associated with diabetic ketoacidosis in critically ill children.
  Crit Care Med
  . 2006;34:2217–2223.
  
• Toledo JD, Modesto V, Peinador M, et al. Sodium concentration in rehydration fluids for children with ketoacidotic diabetes: Effect on serum sodium concentration.
  J Pediatr
  . 2009;154:895–900.
  
• Wolfsdorf J, Craig ME, Daneman D, et al. Diabetic ketoacidosis in children and adolescents with diabetes.
  Pediatr Diabetes.
  2009;10(suppl 12):118–133.
  
• Wolfsdorf J, Glaser N, Sperling MA. Diabetic ketoacidosis in infants, children, and adolescents: A consensus statement from the American Diabetes Association.
  Diabetes Care.
  2006;29:1150–1159.
  

CODES

• 250.01 type I diabetes mellitus [insulin dependent type] [IDDM] [juvenile type], not stated as uncontrolled, without mention of complication
  
• 250.03 Diabetes mellitus without mention of complication, type I [juvenile type], uncontrolled
  
• 250.11 type I diabetes mellitus [insulin dependent type] [IDDM] [juvenile type], not stated as uncontrolled, with ketoacidosis
  

BASICS

Insulin deficiency and excess of counterregulatory hormones (catecholamines, glucagon, growth hormone, and cortisol) resulting in:

• Dehydration (osmotic, hyperglycemic, diuresis, and decreased oral intake)
  
• Acidosis (anion gap metabolic acidosis)
  
• Ketone formation (unrestrained lipolysis and ketogenesis)
  
• Hyperglycemia (unrestrained glycogenolysis and gluconeogenesis)
  
• Electrolyte disturbances (hypokalemia, hypo/hypernatremia, hypophosphatemia)
  

• Medication noncompliance (>50%)
  
• New-onset diabetes (type I or II)
  
• Underlying medical illness (increased counterregulatory hormones and insulin resistance):
  
  • Infectious process
    
  • MI
    
  • GI bleed
    
  • CNS event
    
• Pregnancy (relative insulin deficiency and counterregulatory hormone excess)
  
• Medications (protease inhibitors and atypical antipsychotics: Olanzapine, clozapine)
  
• Alcohol abuse
  

DIAGNOSIS