HYPOGLYCEMIA AND HYPERGLYCEMIA

Izaskun C. Ganao

Hypoglycemia

Almost all fetal glucose is derived from the maternal circulation

The severing of the umbilical cord abruptly interrupts the source of glucose

To maintain adequate glucose levels Glycogenolysis of hepatic stores inducing

gluconeogenesis Feeding

During this transition, glucose levels fall in the first 1 to 2 hours and then increase and stabilize at 65 to 70 mg/dl by the age of 3 to 4 hours

Incidence 16% of LGA 15% of SGA

Definition of hypoglycemia: Operational Threshold Indication for action; not diagnosis Lower than therapeutic goal Dependent on clinical state and age Do not define normal or abnormal Provide margin of safety

Cornblath’s description of operational thersholds Healthy term infant

<24 hours of age – 30 to 35 mg/dl is acceptable; should be raised to 45 mg/dl after feeding

>24 hours – 45-50mg/dl Infant with abnormal signs of symptoms – 45 mg/dl Asymptomatic infants with risk factors for low

blood sugar – 36 mg/dl For any baby, if glucose levels are <20 to 25ml/dl –

IV glucose is needed to raise plasma glucose to >45mg/dl

There is no single value by which brain injury definitely occurs

Normal asymptomatic babies may have a transient glucose level in the 30s that will increase spontaneously or with feeding

Goal 45 mg/dl in the 1st day >50 mg/dl after the 1st day

Etiology

1. Hyperinsulinemic hypoglycemia Infants of diabetic mothers Congenital genetic hyperinsulnism Secondary to other conditions:

Birth asphyxia Developmental syndromes such as Beckwith-Wiedemann syndrome) Congenital disorders of glycosylation Erythroblastosis Maternal tocolytic therapy with beta-sympathomimetic agents

(terbutaline) Malposition umbilical artery catheter used to infuse glucose in high

concentration into the celiac and superior mesenteric arteries – stimulating insulin release from the pancreas

Abrupt cessation of high glucose infusion After exchange transfusion with blood containing high glucose

concentration Insulin-producing tumors

Etiology

2. LGA3. Decreased production/stores

Prematurity IUGR Inadequate caloric intake Delayed onset of feeding

Etiology

4. Increased utilization / decreased production

a. Perinatal stress Sepsis Shock Asphyxia Hypthermia Respiratory disetress Postresuscitation

b. Defects in carbohydrate metabolism

Glycogen storage disease Fructose intolerace Galactosemia

c. Endocrine deficiency Adrenal insufficiency Hypothalamic deficiency Congenital hypopituitarism Glucagon deficiency Epinephrine deficiency

d. Defects in amino acid metabolism Maple syrup urine disease Propionic acidemia Methylmalonic acidemia Tyrosinemia Glutaric acidemia type II Ethylmalonic adipic aciduria

e. Polycythemia - higher glucose utilization

f. maternal therapy with beta-blockers

Diagnosis

Symptoms Tremors, jitteriness, irritability Seizures, coma Lethargy, apathy, limpness Poor feeding, vomiting Apnea Weak or high-pitched cry Cyanosis asymptomatic

Diagnosis

Screening Done in infants with risk factors and with

symptoms 30 to 60 minutes of life IGDM SGA Erythroblastosis fetalis (hyperinsulinism)

Differential Diagnosis

Sepsis CNS disease Toxic exposure Metabolic abnormalities (hypocalcemia,

hypo or hypernatremia, hypomagnesemia, pyridoxine deficiency)

Adrenal insufficiency Heart, renal, and liver failure

Management

Well infants at risk (IGDM) Measure blood glucose levels and treat

accordingly Other asymptomatic infants at risk

HGT on the 1st 1 to 2 HOL Breastfeed or give formula ASAP then every

2 to 3 hours 20 to 25 mg/dl – IV glucose. Goal is to

maintain the glucose >45 mg/dl in the 1st 24 hours and >50 thereafter

Management

Feeding Asymptomatic with hgt 30mg/dl

Breastfeeding or formula Repeat hgt 1 hour after onset of feeding Glucose water not recommended

IV therapy

Indications Inability to tolerate oral feeding Symptoms Oral feedings do not maintain normal glucose

levels Glucose levels less than 25mg/dl

Urgent treatment 200mg/dl of glucose over 1 minute, to be

followed by continuing therapy Equivalent to 2ml/kg of dextrose 10% in water

(D10W) IV

IV therapy

Continuing therapy Glucose infusion at 6 to 8 mg of

glucose/kg/minute D10W at a rate of 86.4ml/kg/day or 3.6

ml/kg/hr gives 6 mg/kg/minute of glucose Glucose infusion rate (GIR)

(GIR) in mg/kg/min= dextrose % concentration x ml/kg/day

144

e.g.: an infant receiving D10W at 80ml/kg/dayGIR= 10 x 80 = 5.6 mg/kg/min.

144

IV therapy

Continuing therapy Repeat hgt after 20 to 30 minutes then hourly until

stable to determine if IV therapy still needed Additional bolus infusions of 2mg/kg of D10W may

be needed If glucose is stable and in acceptable range,

continue feedings and taper infusions as permitted by glucose levels prior to feeding

May give D10W at maintenance rate Infants with hyperinsulinism or IUGR – 12 to 15

mg of dextrose per kg per minute (often as 15% or 20% dextrose water)

IV therapy

May give hydrocortisone at 5mg/kg/day to reduce peripheral glucose utilization

Diazoxide – for persistently hyperinsulinemic infants

Octreotide – if diazoxide not effective Glucagon – for mobilization of glucose (if

the infant has good glycogen stores) Imaging studies for pancreatic function

Hyperglycemia

Whole blood glucose level of >125mg/dl or plasma glucose level of >145mg/dl

Common in infants with LBW receiving parenteral glucose

Clinical problems Hyperosmolarity Osmotic diuresis if osmolarity >300

mOsm/L Possible diabetes mellitus

Etiology Exogenous parenteral glucose Drugs

Steroids Caffeine Theophylline Phenytoin Diazoxide

ELBW infants Lipid infusion

Etiology Sepsis – due to depressed insulin release,

cytokines, endotoxin resulting in decreased glucose utilization

“stressed” premature infants Hypoxia Surgical procedures Neonatal DM – usually SGA term infants, no

gender predilection, with family hx of DM Diabetes due to pancreatic lesions

Etiology Transient hyperglycemia associated with

ingestion of hyperosmolar formula Hepatic glucose production Immature development of glucose

transport proteins (GLUT-4)

Treatment

Hgt monitoring in premature infants and infants with abnormal symptoms

ELBW infants should start with a GIR of at least 4 to 6 mg/kg/min

Parenteral nutrition ASAP in LBW infants. Some amino acids promote insulin secretion

Feeding Exogenous insulin therapy of glucose

levels >250mg/dl Oral sulfonylureas (long term therapy)

Thank you!