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Athina Sikavitsas DOChildren's Emergency ServicesUniversity of Michigan

Discuss DKA Presentation Assessment Treatment

I have no financial disclosures

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6 Y/O male presents with vomiting and abdominal pain for past couple of days

Felt “warm” Had been feeling tired

prior to vomiting Clothes look looser on

him

Appears distressed Alert and somewhat anxious Noted tachypnea RR: 30 HR: 170, BP: 85/45 Cool extremities Diffuse abdominal pain Dry mucous membranes

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Vomiting: Viral illness Appendicitis Other GI illness Sepsis Dehydrated

IV obtained : 20 cc/kg bolus Labs: glucose: 497 Bicarb:5 Lactate: 5, ph:7.01 WBC:25K,HB:15

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DKA New onset ?

Per 2014 International Society for Pediatric and Adolescent Diabetes guidelines, pediatric DKA will be defined as patients < 18 YO(cared for by pediatric services) with presenting serum glucose of > 200, venous pH < 7.30 or serum bicarbonate of < 15 with presence of ketones in either the blood and urine.

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Polyuria, polydipsia, polyphagia Weight loss Fatigue Nausea/ vomiting Abdominal pain (paralytic ileus) Fruity odor to breath Hyperventilation (Kussmaul resp.) Evidence dehydration-HR, cap refill,

turgor Mental status- altered, coma

The clinical disturbances seen in kids in

DKA are manifestations of loss of normal

hormonal control of:

1. carbohydrate metabolism

2. protein metabolism

3. Fat metabolism

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Hyperglycemia Acidosis Increased K (however low actual stores) Lactic acidosis Pseudohyponatremia

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Dehydration: most DKA are about 10% dehydrated

Kussmaul breathing Electrolyte abnormalities Mental status changes: Cerebral edema

Cerebral edema is the most devastating and overt form of cerebral injury in DKA (CIDKA), accounting for up to 90% of pediatric DKA deaths.3,4

Thoughts that there potential contributing mechanisms for CIDKA .inflammation and vasogenic factors

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The figure is excerpted from Dr. Elliot Krane’s publication and indicates that the peak onset of cerebral edema is oft 6-18 hours after initiation of treatment. These data were confirmed by Glaser et al in 2001.

Case control studies indicate that pediatric patients receiving sodium bicarbonate in the early phases of DKA, those presenting with severe acidosis and dehydration and those whose corrected serum sodium decrease during treatment (Glaser et al 2001, Durward et al 2011) are at highest risk of developing overt cerebral edema.

Hyperglycemia raises osmolality of ECF

Lowers serum sodium by dilution

As insulin corrects hyperglycemia, serum sodium should rise

Failure of serum sodium to rise appropriately may be sign of increased risk for cerebral edema

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For each 100 mg /dL increase in blood glucose, serum Na+ will measure 1.6 mEq/dL lower

If glucose is 497 ,serum sodium may be 132 for our patient on lab results

All pts in DKA are potassium depleted Insulin and correction of acidosis will drive K+

back into cells Serum K+ levels will drop Almost all pts will require K+ replacement Close monitoring is needed

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Prevent depletion of RBC 2,3 DPG which will improve tissue oxygenation as acidosis is resolving

May be useful in patients with anemia, CHF, pneumonia, hypoxia

Phosphate therapy increased 2,3 DPG in treated group at 48 hrs. (N/S)

Glucose and acidosis rates of correction were not improved

Treated group had significantly lower plasma ionized calcium

Tetany has been reported in pediatric patients given all replacement as KPO4

Fisher and Kitabihi 1983

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Correct dehydration IV Fluids Stop catabolism/ restore normoglycemia Insulin

Correct electrolytes replacement (Na, Cl, K, phos)

Correct acidosis/ reverse ketosis Insulin and IVF,

Avoid complications of treatment

▪ Establish IV (2 if possible).

▪ Labs – venous blood gas with electrolytes, CBC, Comp, Magnesium, Phosphorus, HgbA1C.

▪ Fluid bolus with isotonic fluids – NS - 20ml/kg. Consider repeat 20 mL/kg ONLY if hemodynamics (especially blood pressures) are unstable. ▪ Goal of fluid resuscitation is to assure perfusion and

restore blood pressure NOT to normalize HR and mentation.

▪ NO insulin bolus.

▪ NO sodium bicarbonate UNLESS patient hypotensive or in cardiopulmonary arrest.

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Very important to monitor Q1 hour neuro checks in initial resuscitation Cerebral edema is a most worrisome

outcome/presentation

If concern for neuro status: consider 3%saline bolus (5cc/kg)

▪ Recheck blood glucose (hourly)

▪ Goal glucose 120-250 mg/dL.

▪ Start/continue insulin infusion – DO NOT bolus insulin

▪ Regular Humulin Insulin at 0.1 units/kg/hour. Consider start at 0.05 units/kg/hr in infants or toddlers < 3yo with new onset DKA or in patients demonstrating extreme insulin sensitivity.

▪ IV fluids with electrolytes at 1.5 x Maintenance

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▪ Infusion rates:

▪ If Glucose > 250 run Bag #1 at 100% of ordered fluid rate

▪ (1.5 x Maintenance)

▪ If Glucose between 120 - 250, run Bag #1 at 50% of ordered fluid rate (0.75 x Maintenance) and Bag #2 at 50% of ordered fluid rate (0.75 x Maintenance)

▪ If Glucose between 100 – 119, run Bag #2 at 100% or ordered fluid rate (1.5 x Maintenance)

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▪ Insulin infusion is NOT to be discontinued while the patient is in DKA.

▪ For patients with rapidly dropping glucose, dextrose content should be increased so that infusion can be maintained.

▪ If, after dextrose concentration is increased, glucose remains low, consider dropping infusion to 0.05 U/kg/hr but all attempts should be made NOT to stop the infusion until DKA is resolved.

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Treated with above protocol guidelines Time for correction? Up to 24 hours

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In children with diabetes

▪ Risk 1-10/100 person years

▪ Poor metabolic control/history of DKA

▪ Psychiatric disorders

▪ Peripubertal and adolescent girls

▪ Unstable family situation

▪ Pump therapy failure

Patients are told to check all three sites

Do nut disconnect pump unless sure they are in DKA

TROUBLESHOOTING:1. TUBING

2. INFUSION SET3.NEEDLE4.PUMP

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Recognition of DKA Rehydration is important Insulin helps to restore catabolic state and not

stopped until DKA resolved Careful monitoring of electrolytes and

replacement Risk of Cerebral edema is most concerning

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Koves,IH,Leu,MG et al; Improving Care for Pediatric Diabetic Ketoacidosis. Pediatrics 2014;134;e848

Glaser N,Barnett,P et al; Pediatric Emergency Medicine Collaborative Research Committee of the American Academy of Pediatrics. Risk factors for cerebral edema in children with diabetic acidosis. N Engl J Med 2001;344(4):264-269

Wolfsdorf JI,Allgrove J,Craig ME,etal; ISPAD Clinical practice Consensus Guideline 2014 Compendium: Diabetic ketoacidosis and hyperglycemic hyperosmolar state. Pediatr Diabetes 2014(suppl20): 154-179

Dunger DB,Sperling MA et al; Predicting Cerebral edema during diabetic ketoacidosis. N Engl J Med. 2001;344 (4) 302-303

Decourcey DD, Steil GM,etal; Increasing use of hypertonic saline over mannitol in the treatment of symptomatic cerebral edema in pediatric diabetic ketoacidosis: an 11-year Retrospective Analysis of Mortality. Pediatric Critical Care Medicine 2013:14(7)694-700