DKA Flashcards
Diabetic ketoacidosis
• (ISPAD) defined the following biochemical criteria for the
diagnosis of diabetic ketoacidosis (DKA): • Hyperglycemia [blood glucose (BG) >11mmol/L (≈200 mg/dL)] • Venous pH<7.3 or bicarbonate<15mmol/L . • Ketonemia and ketonuria. Blood beta-hydroxy-butyrate (BOHB)
concentration ≥3mmol/L, or Urine ketones are typically ≥2+ .
Severity
Severity
• Mild: venous pH < 7.3 or bicarbonate <
15mmol/L.
• Moderate: pH < 7.2, bicarbonate < 10mmol/L.
• Severe: pH < 7.1, bicarbonate < 5mmol/L.
Pathophysiology
Pathophysiology
• DKA (hyperglycemia + ketones + Acidosis)
• Glucose homeostasis : the blood sugar kept
under tight control and that because of very
precise and efficient secretion of insulin and
the counter-regulatory hormone
Diabetic ketoacidosis (DKA) results from
deficiency of circulating insulin and increased
levels of the counterregulatory hormones :
catecholamines, glucagon, cortisol and growth
hormone.
The risk factors of DKA
Children who omit insulin. • Children with poor metabolic control or previous
episodes of DKA. • Gastroenteritis with persistent vomiting and inability
to maintain hydration. • Children with psychiatric disorders.
• Children with difficult family circumstances .
• Children with limited access to medical
services.
• Insulin pump therapy
Clinical presentation
Clinical presentation
• Classical diabetes presentation ( 86%) • Vomiting but no diarrhea ( gastroenritis) • Abdominal pain (Acute abdomen) • Respiratory distress (chest infection) • Dehydration
Main Goals of therapy are
Main Goals of therapy are
1. Emergency assessment (PALS). 2. Correct dehydration (fluid therapy , electrolyte). 3. Correct acidosis and reverse ketosis ( insulin therapy). 4. Slowly correct hyperglycemia and restore BG to near normal, ( adjusting
the insulin and fluid). 5. Monitor for complications of DKA and its treatment. ( clinical and
biochemical monitoring). 6. Identify and treat any complications. (cerebral edema).
Wolfsdorf et al. 2018
Emergency assessment (PALS).
1- Emergency assessment (PALS). • Emergency assessment should follow the general guidelines for Pediatric Advanced Life Support (PALS) and includes: Air-way, Breathing and Circulation assessment. Immediate measurement of BG, Blood or urine ketones, Serum electrolytes. Blood gases and full blood count. Assessment of severity of dehydration. Assessment of level of consciousness . A second peripheral IV catheter should be inserted . Wolfsdorf et al. 2018
Assessment of severity
Assessment of severity
• Assess The severity of DKA by determining the degree of acidosis : • Mild: venous pH < 7.3 or bicarbonate < 15mmol/L.
5% dehydration
• Moderate: pH < 7.2, bicarbonate < 10mmol/L.
7% dehydration
• Severe: pH < 7.1, bicarbonate < 5mmol/L.
10% dehydration
2- Correct Dehydration (fluid therapy , electrolyte).
• The data from the available studies are
consistent with the following average losses in
severe DKA: • Water — 100 to 125 mL/kg • Sodium — 5 to 13 meq/kg • Potassium — 6 to 7 meq/kg
fluid therapy
ISPAD recommended that initial fluid
management of children with DKA be based upon
the assumption that patients present with a 7 to
10 percent fluid deficit. • Treatment should be initiated with a maximal
volume of 10 mL/kg of isotonic solution over one
hour, unless the patient is hypotensive. • Hypovolemic shock is a rare occurrence in DKA.
• The rate of fluid deficit administration should
be calculated to fully replete the patient over
48 hours.
• The rate over the first 24 hours should not
exceed 1.5 to 2 times the maintenance fluid.
Serum sodium
Hyperglycemia has a variable effect on the serum sodium concentration:
• By raising the plasma osmolality, hyperglycemia
results in osmotic water movement out of the
cells, thereby lowering the serum sodium
concentration by dilution. • This direct effect of hyperglycemia is often
counteracted by the glucosuria-induced osmotic
diuresis. • Sodium loss — 5 to 13 meq/kg
Normally, during dropping of blood sugar due to
insulin therapy, the serum sodium level will rise. • A failure of measured serum sodium levels to rise
or a further decline in serum sodium levels with
therapy is thought to be a potentially ominous
sign of impending cerebral edema . Glaser et al 2001 • The corrected serum sodium should be carefully
monitored and be plotted on a nomogram.
Potassium
Potassium
• Serum potassium — Both renal and
gastrointestinal losses can contribute to an often-
marked degree of potassium depletio n in DKA. • On the other hand, the combination of insulin
deficiency, and hyperosmolality, tend to raise the
serum potassium. • Total body Potassium loss — 6 to 7 meq/kg
• Potassium replacement will almost always be
required within one to two hours of the
initiation of fluid and insulin therapy in
children with DKA who do not have renal
failure.
Potassium
• If the patient is hypokalemic, potassium replacement needs to start
immediately, using a potassium concentration of 60 meq/L as insulin will
further reduce the serum potassium.
• For the same reason, if the patient is normokalemic, potassium
replacement should be given with the start of insulin therapy (eg, adding
40 meq/L of potassium to the saline solution ).
• If the patient is hyperkalemic, potassium replacement should be initiated
when the serum potassium falls to normal.
• The maximum recommended rate of IV potassium replacement is usually
0.5 mmol/kg/h.
Make sure good UOP =rule of thumb
Insulin therapy
Insulin therapy
• Insulin therapy as infusion: begin with 0.05–0.1 U/kg/h 1–2 h AFTER starting
fluid replacement therapy. • The lower dose should be used initially in younger
children who are more sensitive to insulin. • The insulin infusion should continue until the
venous pH is >7.3 and/or the serum HCO3 is >15
meq/L.
An Insulin IV bolus should not be used at the start
of therapy; it may increase the risk of cerebral
edema. • It can precipitate shock by rapidly decreasing
osmotic pressure and can exacerbate
hypokalemia.
• In a study of 635 episodes of DKA the mean
time to correction of DKA and complete
restoration of the circulation was 11.6±6.2
hours.
• At this point, patients were started oral intake and transitioned to subcutaneous insulin .
Fiordalisi et al 2007
Bicarbonate administration
• Bicarbonate therapy may cause paradoxical CNS
acidosis. Assal et al. 1974 • Bicarbonate administration is not recommended
except for treatment of life-threatening
hyperkalemia.