Neonatal Hypoglycemia NICU Night Team Curriculum 1.

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Transcript of Neonatal Hypoglycemia NICU Night Team Curriculum 1.

Neonatal Hypoglycemia

NICU Night Team CurriculumNICU Night Team Curriculum

1

Objectives

• Define neonatal hypoglycemia • Know the causes of neonatal

hypoglycemia• Know signs and symptoms of

hypoglycemia • Understand treatment

Case

39 wk F born by NSVD to a 22 y/o G1P0 mom with diet controlled GDM A1. Mom’s blood

sugars throughout the pregnancy ranged from 120-160. Maternal serologies were negative,

pregnancy otherwise unremarkable. APGARS were 8 and 9 at 1 and 5 minutes,

respectively. BW was 4,000 g.

Physical Examination

VS: T 36.5 P 148 RR 80 BP 55/38 mmHg HC 34 cm (75%), Lt 50 cm (75%), BW 4,000 (>97%)

GA: Well appearing F, NAD, no cyanosisHEENT: AF 2x2 cm, no cleft lip and palateHeart: RR, no murmurLungs: Tachypneic breathing with even breath sounds

throughout, no retractions, no flaring Abdomen: Soft ND, no hepatosplenomegaly Genitalia: Normal female genitalia Extremities: No deformities, MAEE

Labs

1 hour of life:Hematocrit 56%

Dexi 30 mg%Serum glucose 34 mg%

What is your What is your primary concern in primary concern in

this patient?this patient?

Neonatal HypoglycemiaNeonatal Hypoglycemia

Impaired glucose metabolism

Serum blood glucose < 40 mg/dLOR

Point of Care testing (accucheck, Dexi) <45

Why was a Dexi checked in Why was a Dexi checked in this patient?this patient?

She is at risk for developing hypoglycemia

Definition: A plasma glucose of less than 40 Definition: A plasma glucose of less than 40 mg/dlmg/dl

Plasma glucose is higher than whole blood Plasma glucose is higher than whole blood glucose by 15%glucose by 15%

Hypoglycemia

Fetal Glucose MetabolismFetal Glucose Metabolism

• Fetus does not produce glucoseFetus does not produce glucose• Maternal glucose is the only source of Maternal glucose is the only source of

fetal glucosefetal glucose• Baseline fetal blood glucose is 60-70% Baseline fetal blood glucose is 60-70%

of maternal serum glucoseof maternal serum glucose

Physiology

Glucose metabolism after birthGlucose metabolism after birth

Cessation of maternal glucose supply

Blood glucose Nadir( ~1-2 hrs after birth)

Physiology

Glucose Metabolism After BirthGlucose Metabolism After Birth

Cessation of maternal glucose supply

Surge in glucagon, catecholamineDecrease insulin

Gluconeogenesis: Hepatic glycogen, amino acid, fatty acid metabolism

Normal blood glucose

Etiology of neonatal Etiology of neonatal hypoglycemiahypoglycemia

1.1. Increased utilization Increased utilization (e.g.: (e.g.: hyperinsulinism)hyperinsulinism)

2.2. Decreased production/storesDecreased production/stores

3.3. Increased utilization and/or Increased utilization and/or decreased productiondecreased production

Increased UtilizationIncreased Utilization

• Diabetic motherDiabetic mother• Large for gestational age (LGA) infantLarge for gestational age (LGA) infant• ErythroblastosisErythroblastosis• Islet cells hyperplasiaIslet cells hyperplasia• Beckwith-Wiedemann syndromeBeckwith-Wiedemann syndrome• Insulin producing tumorsInsulin producing tumors• Maternal tocolytic therapy with B-Maternal tocolytic therapy with B-

sympathomimetric agentssympathomimetric agents• Malposition of umbilical artery catheterMalposition of umbilical artery catheter

Decreased Decreased Production/StoresProduction/Stores

• PrematurityPrematurity• Intrauterine growth retardation(IUGR)Intrauterine growth retardation(IUGR)• Inadequate caloric intakeInadequate caloric intake• Delayed onset of feedingDelayed onset of feeding

Increased utilization AND Increased utilization AND Decreased productionDecreased production

• Perinatal stress eg. shock, sepsis, asphyxiaPerinatal stress eg. shock, sepsis, asphyxia• Enchange transfusionEnchange transfusion• Defect in carbohydrate metabolism eg. glycogen Defect in carbohydrate metabolism eg. glycogen

storage diseasestorage disease• Endocrne deficiency eg. adrenal insufficiency, Endocrne deficiency eg. adrenal insufficiency,

hypopituitarismhypopituitarism• Defect in amino acid metabolismDefect in amino acid metabolism• PolycythemiaPolycythemia• Maternal therapy with B-blockerMaternal therapy with B-blocker

When do you screen? When do you screen?

1.1. Symptoms that could be due to Symptoms that could be due to hypoglycemia.hypoglycemia.

2.2. At risk infants.At risk infants.

What are signs and symptoms of

hypoglycemia?

Signs and Symptoms of Hypoglycemia

Symptoms are NON-SPECIFIC

• Jitteriness• Apnea • Irritability• Grunting• Lethargy• Seizures

Who is Who is at risk?at risk?

• Infants of diabetic mothersInfants of diabetic mothers• Maternal use of B-adrenergic agonist/ antagonistMaternal use of B-adrenergic agonist/ antagonist• IUGRIUGR• LGALGA• PretermPreterm• PolycythemiaPolycythemia• AsphyxiaAsphyxia• Sick infantSick infant

When is the ideal time to screen high risk infants?

ScreeningScreening

Blood glucose or point of care testing Blood glucose or point of care testing (POC) should be done in high risk (POC) should be done in high risk

infants within the first 1 to 2 hours infants within the first 1 to 2 hours after birthafter birth

Back to our case:

1. Term LGA infant2. IDM with poor blood glucose control3. Tachypnea 4. Hypoglycemia

Why do you think she developed hypoglycemia?

Hyperinsulinism

Pathophysiology : infants of diabetic mothers

•Feeding?• IV therapy?•Medication?

How do you treat this patient?

Management – Oral Management – Oral FeedsFeeds

• Can be used in asymptomatic infantsCan be used in asymptomatic infants• Only formula (never administer glucose water!!)Only formula (never administer glucose water!!)• Follow up blood glucose within 1 hour of feeding.Follow up blood glucose within 1 hour of feeding.• If the glucose level doesn’t rise, a more If the glucose level doesn’t rise, a more

aggressive therapy may be needed.aggressive therapy may be needed.

Management – IV Management – IV therapytherapy

Indications:Indications:• Inability to tolerate oral feedingInability to tolerate oral feeding• Symptomatic infantSymptomatic infant• Lack of response with oral feedsLack of response with oral feeds• Glucose < 25 mg/dL, regardless of patient’s Glucose < 25 mg/dL, regardless of patient’s

symptomssymptoms

Management – IV Management – IV therapytherapy

Urgent treatmentUrgent treatment• Bolus 2 ml/kg of D10WBolus 2 ml/kg of D10W• Do not use 25% or 50% glucose !!Do not use 25% or 50% glucose !!• Follow bolus with continuous dextrose fluidFollow bolus with continuous dextrose fluid

Continuing IV fluid Continuing IV fluid • Start infusion of glucose at a rate of 6-8 Start infusion of glucose at a rate of 6-8

mg/kg/minmg/kg/min• Glucose infusion rate formula (GIR):Glucose infusion rate formula (GIR):

GIR = %IV fluid x rate(ml/hr)GIR = %IV fluid x rate(ml/hr)

6 x BW(kg)6 x BW(kg)

Management – IV Management – IV therapytherapy

Management – IV Management – IV therapytherapy

• Re-check serum glucose 20-30 min after bolus Re-check serum glucose 20-30 min after bolus and hourly until stableand hourly until stable– If glucose is normal and stable, feeding may be If glucose is normal and stable, feeding may be

continued and glucose infusion taperedcontinued and glucose infusion tapered– If glucose can’t be maintained > 50 mg/dL, increase GIR If glucose can’t be maintained > 50 mg/dL, increase GIR

by 1-2 mg/kg/hrby 1-2 mg/kg/hr– If glucose can’t be maintained > 50 mg/dL, with a GIR If glucose can’t be maintained > 50 mg/dL, with a GIR

12 mg/kg/min, medication should be added.12 mg/kg/min, medication should be added.

Management – Management – MedicationMedication

Persistent hypoglycemia despite a GIR > 12 Persistent hypoglycemia despite a GIR > 12 mg/kg/min.mg/kg/min.

• Work up – Critical Labs:Work up – Critical Labs:– Serum cortisol, insulin, growth hormone when glucose is Serum cortisol, insulin, growth hormone when glucose is

low and prior to treatmentlow and prior to treatment– DO NOT wait >5 minutes for labs prior to treating DO NOT wait >5 minutes for labs prior to treating

hypoglycemiahypoglycemia

• MedicationMedication– Hydrocortisone Hydrocortisone – GlucagonGlucagon– Diazoxide Diazoxide

HydrocortisoneHydrocortisone

• Dose: 10 mg/kg/day IV q 12 hrsDose: 10 mg/kg/day IV q 12 hrs• Indication: Hypoglycemia despite GIR > 12 Indication: Hypoglycemia despite GIR > 12

mg/kg/minmg/kg/min• Send hormone level before starting Send hormone level before starting

hydrocortisone!!!hydrocortisone!!!

GlucagonGlucagon

• Dose: 0.025-0.3 mg/kg IM/IV Dose: 0.025-0.3 mg/kg IM/IV (maximum 1 mg)(maximum 1 mg)

• Should cause recovery of hypoglycemiaShould cause recovery of hypoglycemia• May not work ifMay not work if

– Reduced glycogen storesReduced glycogen stores– Glycogen storage diseaseGlycogen storage disease

DiazoxideDiazoxide

• Dose: 2-5 mg/kg/dose PO q 8 hrs.Dose: 2-5 mg/kg/dose PO q 8 hrs.• Indication: Infants who have persistent Indication: Infants who have persistent

hyperinsulinemia (e.g.. hyperinsulinemia (e.g.. Nesidioblastosis)Nesidioblastosis)

Remember, he was tachypneic

Urgent treatment:D10W 2 mL/kg IV bolus followed by continuous IV fluid

Back to our case: How would you treat our patient?

Board Question

A term infant was born to a pre-ecclamptic mother. BW was 2,000 g (<10th%). Physical exam was normal.

Blood glucose at 2 hour of age was 30 mg/dL

What is your next step in management?

a. D10W bolus of 4 mL

b. D10W continuous IV infusion at 6.5 ml/hr

c. 20 mL of oral glucose water

d. 20 mL of infant formula

Board Question

A term infant was born to a pre-ecclamptic mother. BW was 2,000 g (<10th%). Physical exam was normal.

Blood glucose at 2 hour of age was 30 mg/dL

What is your next step management?

a. D10W bolus of 4 mL

b. D10W continuous IV infusion at 6.5 ml/hr

c. 20 mL of oral glucose water

d. 20 mL of infant formula

ReferenceReference• Wilker RE. Hypoglycemia and hyperglycemia. In: Cloherty JP, Eichenwald EC, Stark AR, eds. Manual Wilker RE. Hypoglycemia and hyperglycemia. In: Cloherty JP, Eichenwald EC, Stark AR, eds. Manual

of Neonatal care. 5of Neonatal care. 5thth ed. Lippincott Williams & Wilkins; Philadelphia; 2008: 540-549 ed. Lippincott Williams & Wilkins; Philadelphia; 2008: 540-549• Cornblath M, Ichord R. Hypoglycemia in the neonate. Semin Perinatol 2000;24:136-149Cornblath M, Ichord R. Hypoglycemia in the neonate. Semin Perinatol 2000;24:136-149• Sperling MA, Menon RK. Differential diagnosis and management of neonatal hypoglycemia. Pediatr Sperling MA, Menon RK. Differential diagnosis and management of neonatal hypoglycemia. Pediatr

Clin North Am 2004;51:703-723Clin North Am 2004;51:703-723