Pediatrics Diabetic Ketoacidosis (DKA) from Primary to Intensive Care Wendy Nasser MSN, CPNP-AC/PC...

Pediatrics

Diabetic Ketoacidosis (DKA)from Primary to Intensive CareWendy Nasser MSN, CPNP-AC/PC

Mark Riccioni MSN, CPNP-AC/PC

Pediatrics

We have no conflicts of interest to disclose

xxx00.#####.ppt 04/19/23 05:55 PMPediatrics

Objectives1. Describe classic signs and symptoms of DKA in the new onset diabetic.

2. Summarize pertinent lab studies and acute management of DKA.

3. Identify the diabetic child in crisis

4. Describe various fluid management options

4.Explain the role of parental involvement in the care of puberty-aged diabetic children and the effect of decreased readmissions.


Case Study


Let’s talk about pathophysiology

•Diabetes Mellitus (DM) is a syndrome that occurs secondary to the body’s inability to maintain energy homeostasis.

•DM type 1 results from insulin deficiency caused by autoimmune destruction of islet cells in the pancreas and is then manifested by decreased uptake of glucose resulting in high serum glucose.


A closer look at Pathophysiology of DM type 1

Due to lack of insulin hormone, Glucose draws water into the serum and into the kidneys. As the osmotic force of glucose builds in the kidneys (above 180), urine output increases (polyuria) and thirst is sensed (polydypsia) along with hunger (polyphagia) and weight loss occurs.

As the body becomes more and more dehydrated, increased release of Growth Hormone, Glucagon and epinephrine ensues.

Breakdown of fat stores and creation of ketones then results from the imbalance between catabolic (glucagon and epinephrine) and anabolic (insulin) hormones. The buildup of ketones results in ketoacidosis

The body senses stress (i.e. acidosis, hyperglycemia, lactic acidosis and poor tissues perfusion) and responds by releasing cortisol, catecholamines and more growth hormone . The worsening imbalance restarts the cycle and the patient becomes more and more intravascularly depleted and symptomatic.


Pathophysiology:

•DM type 2 typically results from insulin resistance and relative insulin deficiency leading to abnormal metabolism of carbohydrates, protein and fat. Type 2 is becoming more prevalent in children with obesity on the rise.


Diabetic Ketoacidosis is the most common endocrine metabolic disorder in childhood and adolescence(add bar graph)


When all the of the symptoms coalesce Severity on presentation dictates treatment of DKA and degree of treatment required…

• pH < or > 7.15

• HCO3 > or < then 10

• Glasco Coma Score (GCS<13)

• Respiratory status

• Level of dehydration

• Electrolyte derangements

• Age less than 5


We can’t forget to correct for lab values!•Corrected Na+= Na+ + 0.016 x (Glucose-100)

•Osmolarity = 2x (Na+) + (Glu/18) + (BUN/2.8)

•K+ elevated in 1/3 of cases, do not add to IV fluids if no UOP or serum K+>5.5


Fluid Protocol Controversies

The common concern during DKA treatment is the potential risk of brain injury to the patient as he/she undergoes correction of acidosis resulting in fluid shifts in the brain

In the US, treatment of DKA across institutions varies widely with different fluid protocols in place and no consensus on which protocol is best at protecting patients from harm.


But is it all about lab correction?

•Lab values can be corrected…over time

•The true question is: can we protect the affected children from the effects of DKA and improve their brain’s recovery and development?


•Scan and Insert cover of DKA study paper here


Concerning data

•1% of patients in DKA have clinically overt signs of cerebral edema

•50% of affected children die or sustain permanent neurological injury.

•(Ref 5, 6 from k&G)


DKA Fluid Protocol (Kuppermann and Glaser) 2011•Reported that Cerebral edema (CE) resulting from diabetic ketoacidosis (DKA) is the most frequent diabetes-related cause of death in children.

•Ref (2,4 from k &g)


Kuppermann and Glaser’s Preliminary Animal Studies

Data from rat studies suggested that decreased cerebral blood flow during DKA may be part of the cause behind DKA-related brain injury

The rat models also indicated that the brain metabolic state actually worsens initially during DKA treatment, theorized to be a result of reperfusion injury


CT evidence of cerebral edema(Krane, 1985)


What is the cause of Cerebral Edema?

•The study aims to look at the two varying treatment strategies

•1. Conservative fluid therapy protocols: CE may result from osmotic shifts caused by rapid rehydration with intravenous fluids drives

•2. More liberal and rapid correction of DKA: Cerebral hypo-perfusion may play a prominent role in the development of cerebral injury and CE

•Best practice has not yet been determined


Aspiring for Safe Change

•Several institutions across the country are currently collaborating in Kuppermann and Glaser’s study with the overall goal to optimize DKA treatment and prevent neurological injury.

•The hope is that collaboration of data acquisition will improve therapy and enhance long-term neurocognitive outcomes for children with diabetes


Determining “best practice” is complicated at best

•Children in the study are assigned to one of several fluid protocols all of which are used at some hospitals in the US

•The aim is to determine which protocol has the best outcomes while nothing new or “experimental” is utilized


DKA Fluid Study ProtocolKuppermann and Glaser

A1 A2 B1 B2

Standard bolus 10cc/kg NS 10cc/kg NS 10cc/kg NS 10cc/kg NS

Additional bolus

10cc/kg NS 10cc/kg NS ----- -----

Assumed fluid deficit

10% of body weight

10% of body weight

5% of body weight

5% of body weight

Deficit replacement

½ over 12 hrs, ½ over next 24 hrs (plus maintenance)

½ over 12 hrs, ½ over next 24 hrs (plus maintenance)

evenly over 48 hrs (plus maintenance)

evenly over 48 hrs (plus maintenance)

Fluid for deficit replacement

½ NS NS ½ NS NS


DKA Fluid Study Overview:

Child is diagnosed with DKA and consented to participate in study

Child is randomized to 1 of 4 fluid treatment protocols

Child’s mental status is closely monitored for overt signs of cerebral edema or DKA complications

DKA is converted and treatment terminated

3-month follow up for neurocognitive testing is obtained


Traditional Texas Children’s Hospital DKA Protocol

The Two-Bag System


Calculating IVF rate in DKA

•Determine the number of IV boluses the patient received prior to start of correction

•Subtract the total amount of fluid given from the total 24h volume to be given for correction

•(2500/m2/d – total IV boluses)=correction volume to be given in 24h. Divide the result by 24 to reveal the hourly rate in ml/h


TCH 2-bag system protocol• Bag A: LR + KPO4 2mmol/100ml + KCL 1.5mEq/100ml

• Bag B: D10LR + KPO4 2mmol/100ml + KCL 1.5mEq/100ml

• Total IVF ml/h= Bag A ml/h + Bag B ml/h dependent on blood glucose

• Blood Glucose >300__ml/h (100% bag A)

• 251-300__ml/h (75% bag A) __ml/h (25% bag B)

• 201-250__ml/h (50% bag A) __ml/h (50% bag B)

• 151-200__ml/h (25% bag A) __ml/h (75% bag B)

• Blood Glucose <150__ml/h (100% bag B)


Insulin Administration

•Insulin drips are recommended for patients less than or equal to 5yo if HCO3 </=15mEq/L or if </= 12mEq/L and older than 5 years of age

•Recommended dose is 0.1units/kg/hr

•If patient is less than 5 years of age or “Hyper osmolar” the recommended dose is 0.05units/kg/hr


Extenuating Circumstances that Affect the Titration of Correction

•When pH is not improving, the insulin gtt may have to be titrated up

•If glucose is decreasing too quickly (more than 100mg/dL per hour), the correction must be slowed down and the patient must be monitored closely


Intensive Monitoring

•Labs required for IVF titration and correction:

• Gucose q1h

• Lytes q2h x2 then q4h

• Initial blood gas

• Q1h vitals and neuro vitals

• Strict I&Os


Insulin Administration

•Without mental status changes on initial presentation, subcutaneous insulin can be given if HCO3 is greater than 15mEq/L in patients 5yo or younger, or greater than 12mEq/L in patients older than 5yo

•If 2-bag system is required, once HCO3 is greater than or equal to 15, the patient can be converted to subcutaneous therapy


•The role of parental involvement in the care of puberty-aged diabetic children and the effect of decreased readmissions


Criteria for Discharge

•Corrected acidosis and return to “neurological baseline”

•Completion of Diabetes education and agreement of responsible adult who assumes responsibility of minor’s welfare

•Completed Endocrine Social Work consult to determine barrier to resources and medications

•Follow up appointment is scheduled with Endocrinologist


Case Study


Questions??


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