1. IMPLICATIONS FOR THE NEONATE By: Nicole Stevens
DIABETES IN PREGNANCY
IMPLICATIONS FOR THE NEONATE
By: Nicole Stevens

2. DIABETES IN PREGNANCY Makes a pregnancy high risk
Can have negative effects on mother & baby
Glucose is the food source which passes from the mother, across the placenta to the fetus
Complications for the fetus/neonate are most significant when the glucose control is poor
Careful glucose control decreases risk to the mother & developing fetus and improves outcomes for the neonate

3. Diabetes in pregnancy
When a mothers blood glucose levels are too high the fetus also receives excessive amounts of glucose
The fetus has the abiltiy to increase their production of insulin substantially in order to use the large amounts of glucose
This abnormal cycle of events can result in several complications
The complications can be dependent on the period of time that the glucose was not well controlled.

4. Diabetes in pregnancy Glucose crosses the placenta by diffusion
Glucose concentration 70-80% maternal
Insulin does not cross the placenta
Insulin secretion is influenced by glucose and amino acid concentration, but as the fetus matures they become more glucose sensitive
↑Glucose sensitivity  ↑ β-cell mass
↑ insulin production
Anabolism
Rapid fetal growth and laying down of fat
Anabolism: constructive metabolism characterized by the conversion of simple substances into more complex compounds.

5. Diabetes in pregnancy
If a woman has pre exisiting diabetes there can be high levels of glucose at the beginning of the pregnancy (during the crucial period of organ development), as well as at any other stage through the pregnancy
In gestational diabetes the elevation may only happen later in the pregnancy
The implications for the fetus/neonate can be dependent on when there was exposure to high levels of glucose

6. Diabetes in pregnancy
Increase in glucose causes increases in insulin production
This causes an increase in catabolism which requires energy, which in turn requires oxygen
Depleted oxygen stores leads to fetal hypoxia which causes the release of a flood of adrenal catecholamines
This in turn causes hypertension, cardiac hypertropy, stimulation of erythropoietin, RBC hyperplasia and increased hematocrit levels
Catabolism: metabolic breakdown of complex molecules into simpler ones
Adrenal catecholamines: hormones produced in adrenal gland (epinephrine/adrenaline, norepinephrine, dopamine)
Erythropoietin: a hormone produced in the kidneys that promotes the formation of RBCs in the bone marrow

7. EMBRYOLOGY
An understanding of embryology helps to explain why poor glucose control early in pregnancy can have devastating implications
Organogenesis occurs between weeks 3 – 8 of pregnancy
It is the series of organised integrated processes that transforms an amorphous (undifferientated) mass of cells into a complete organ; it continues until the definitive characteristics of the organ are achieved
Concurrent with this process is histogenesis: which is the formation of different tissues from undifferentiated cells

8. Embryology
These undifferientated cells are constituents of 3 primary germ layers (endoderm, mesoderm and ectoderm)
Different parts of the body form from different layers, eg: endoderm: GI tract, respiratory tract, endocrine glands and organs; mesoderm: bones, muscles, urinary system; ectoderm: CNS, eyes, skin
The end result of organogesesis and histogenesis is a structurally and functionally complete organ
The accomplishment of organogenesis ends the period where the developing organism is known as and embryo and begins the period during which it is known as a fetus

9. Embryology
The hormonal and metabolic changes that can occur with diabetes can adversely affect the developing embryo/fetus
This abnormal metabolic environment is considered to be teratogenic
There is a higher incidence of congenital malformations, such as cardiac, musculoskeletal, and CNS anomalies in neonates of mothers with diabetes
The mechanism by which hyperglycaemia disturbs embryonic development is multifactorial and remains controversial
Teratogen: a drug or other substance capable of interfering with the development of a fetus, causing birth defects

10. Embryology
There are theories that altered levels of arachidonic acid and myoinositol levels or fetal hypergylcaemia promote excessive formation of oxygen radicals in cells, which damage mitochondria, inhibits prostacyclin, and leads to oxidative stress
This results in an overabundance of thromboxanes and other prostaglandins which disrupts vascularisation of developing tissues
Hyperglycaemia alters the expression of regulating genes, resulting in altered cellular mitosis and normal apoptosis (programmed cell death); exaggerated apoptosis results in fetal anomalies
Arachidonic acid (long chain omega 6 fatty acid): required in small amounts by the body, but large amounts can be toxic; elevated insulin levels appear to stimulate an increase in the level in AA; it is present in the phospholipids of membranes of the bodys cells and is abundant in the brain, muscles and liver.
Cellular mitosis: cell division
Apoptosis:normal component of the development and health of multicellular organisms
Myoinositol: humans can make it from their glucose stores, major nutritionally active form of inositol, vital to many biological processes of the body
Mitochondria: the cells power producers: they convert energy into forms that are useable by the cells.
Prostacylin: a prostaglandin produced in the walls of blood vessels that acts as a vasodilator and inhibits platelet aggregation

11. NEONATAL COMPLICATIONS
Macrosomia
Increase in adipose tissue
Increase in skin fold thickness
Visceromegaly (liver)
Phlethoric appearance due to polycythaemia
RDS
Hypoglycaemia (most common problem)
Hypocalcaemia
Hyperbilirubinaemia
Hyperviscosity syndrome
Hypertrophy cardiomyopathy
Later effects:
Obesity in childhood and development of type 2 diabetes.
Visceromegaly: enlargement of an organ

12. CARDIAC ABNORMALITIES
Congenital anomalies occur more commonly in infants born to mothers with diabetes
Cardiac defects are dominant
The incidence of abnormalities is highest in the group where mothers were on insulin at the time of conception
The most frequent cardiac anomalies are ventricular septal defect, transposition of the greater arteries and aortic stenosis
Defects involving the great arteries, including truncus arteriosus and double outlet right ventricle, are also more prevalent.
Truncus arteriosus: where a single vessel overrides both ventricles and splits to form aorta and pulmonary artery, a large VSD will also be present.
Double outlet right ventricle: Both major vessels arise from the right ventricle, will also be a large VSD present

13. Hypertrophic cardiomyopathy
The incidence of hypertrophic cardiomyopathy is increased in infants of mothers with diabetes; fetal hyperinsulinaemia, triggered by maternal hyperglycaemia during the 3rd trimester can be the causative factor
The left ventricular mass will usually be significantly bigger and there will be hypertrophy, or thickening, of the septal wall.
The problem is usually transitory and generally resolves after a few weeks.
The hypertrophy of the wall and the septum reduces the stroke volume and hence cardiac output; the infant will usually present with tachypnoea and tachycardia and a systolic murmur.

14. Chest X-ray showing significant cardiomegaly and pulmonary venous congestion as a result of hypertrophic cardiomyopathy in an infant of diabetic mother

15. RESPIRATORY COMPLICATIONS
RDS requiring admission to SCN/NICU is 6 times more likely in the infant of a mother with diabetes
Delayed maturation of surfactant synthesis has been observed in these infants, but it is unclear if the cause is hyperglycaemia or hyperinsulinaemia inutero
Glycogen is normally depleted from the lungs as part of the maturation process and this coincides with an increase in surfactant synthesis
Insulin inhibits glycogen breakdown
Glycogen is a polysaccharide that is the principal storage form of glucose in human cells.
The most common disease in which glycogen metabolism becomes abnormal is diabetes, in which, because of abnormal amounts of insulin, liver glycogen can be abnormally accumulated or depleted.

16. HEMATOLOGY COMPLICATIONS
Hyperglycaemia decreases fetal oxygen tension, this stimulates fetal erythropoietin production, which increases RBC’s
Fetal hyperglycaemia & hyperinsulinaemia increase total body oxygen consumption by up to 30%, leading to accelerated erythropoiesis, polycythaemia and hypervisocosity
The increase in fetal RBC’s leads to greater iron demands and depletion of iron stores in the liver, brain and heart: this can lead to myopathies and altered neurodevelopment
Myopathy is a muscular disease in which the muscle fibers do not function for any one of many reasons, resulting in muscular weakness.

17. Hematology complications
Sludging of hyperviscous blood in the cerebral microcirculation can be responsible for symptoms of irritability, jitteriness and high-pitched cry – symptoms which are usually attributed to hypoglycaemia or hypocalcaemia
Infants of mothers with diabetes are also at risk of hyperbilirubinaemia because of the increase in RBC’s, decrease in RBC life, and immature hepatic bilirubin conjugation and excretion

18. NEUROLOGICAL COMPLICATIONS
Brain development may be altered if the mother has poor glycaemic control
In the short term these infants may present with symptoms of lethargy, poor feeding and decreased muscle tone
Discharge from hospital may be delayed because of issues with establishment of suck feeds
Long term studies have shown subtle developmental concerns across the domains of motor (fine & gross) & cognitive skills, coordination, language development and memory tasks

19. MACROSOMIA
The maternal hyperglycaemic state results in the delivery of excess fuels (carbohydrates) to the fetus
This stimulates fetal pancreatic β-cell hyperplasia and increases fetal insulin and insulin-like growth factors
These growth factors stimulate protein, lipid and glycogen synthesis, causing a high rate of growth, increased deposition of fat, and visceral enlargement

21. Birth trauma/complications
A macrosomic infant can be a causative factor of:
Obstructed labour (eg. CPD), &
Shoulder dystocia
Shoulder dystocia can result in birth trauma such as
Brachial plexus injury
Fractured clavicle or humerus
An obstructed labour or shoulder dystocia can have life threatening implications for the neonate, such as:
Perinatal hypoxia-ischaemia (reduced oxygen levels and reduced blood flow)
Hypoxic–ischemic brain damage is an evolving process, which begins during the insult and extends into the recovery period after resuscitation (reperfusion interval). 3Tissue injury takes the form of either selective neuronal necrosis or infarction, the latter with destruction of all cellular elements including neurons, glia, and blood vessels.

22. Shoulder dystocia
Shoulder dystocia occurs after delivery of the head, when the babys anterior shoulder gets stuck behind the mothers pubic bone

23. Shoulder dystocia Increased risk of fracture of clavicle and humerous
Following shoulder dystocia deliveries, 20% of babies will suffer some sort of injury, either temporary or permanent. The most common of these injuries are damage to the brachial plexus nerves, fractured clavicles, fractured humeri, contusions and lacerations, and birth asphyxia.

24. Large hypotonic infant of diabetic mother, lying in a frog-like position, with some bruising of the left arm due to shoulder dystocia

25. BABY A: A Case Study 36+6/40 Em LUSCS for fetal distress
Maternal Type 1 DM – poorly controlled - Insulin (1u/kg/d)
BW4740g (off the scale on the growth charts!)
30 sec IPPV; 5 mins PEEP for grunting/hypoxia
Apgars 7, 8, 10
SCN admission (due to high risk of hypoglycaemia, mild respiratroy issues, slight prematurity)

26. Baby A: A Case Study
Ongoing O2 requirement (managed with cot oxygen, no significant distress, just saturating low.
Unrecordable BSL (<1.1) taken before 1 hour of life.
IV access gained, baby 40 mins old by this time.
IV dextrose bolus (3ml/kg) + 60ml/kg/d infusion commenced
TBG 30 mins later still < 1.1 (further 3mL/kg bolus, TFI increased to 90mL/kg)
TBG 30 mins later still < 1.1 (further 3ml/kg bolus, TFI increased to 120mL/kg)
Preparation by medical staff to insert umbilical lines
Conversation with NETS consultant regarding situation
Baby noted to have continuous jittery movements

27. Baby A: A Case Study
TBG repeated 30mins later now recordable number of (further 3mL/kg bolus and concentration of dextrose increased to 12.5%)
Remained hypoglycaemia 1st 5hrs of life despite 5x3ml/kg 10% dex bolus
TFI inc from ml/kg at 12.5% dex
UVC inserted: inc to 15% dex at 120mL/kg
NETS called again, coming to retrieve baby, requested glucagon to be given
Glucagon 1mg IM given
BSL stabilised by 7hours of age at 15% dex – 100mls/kg/d

28. Baby A: A Case Study IV benpen & gentamycin for ?sepsis
Delay in NETS retrieval because of other cases being triaged as more critical
NETS T/F at 15hrs of age to MMC
Progress at MMC
Hypoglycaemia: weaned from 15% dex at 100ml/kg/d (10.4mg/kg/min) to 12.5% with gradual intro of oral feeds and stabilisation of BSL

29. Baby A: A Case Study
Respiratory: Cot Oxygen initially, CPAP for transfer, 23% FiO2 – weaned to SVIA at MMC
Sepsis: LP performed day 3 due to inc CRP – cefotaxime added to benpen + gent – CSF NAD; anti’s ceased day 6
Heart murmur: ESM LSE ?flow murmur – resolved pre discharge
Thrombocytopenia: plt 63 on day 3; spont improved to 102 by day 5

30. Baby A: A Case Study
Transferred to SJOG day 7 due to bed shortage at BHS
TF to BHS day 9 to continue establishment of feeds
DC home day 13, CA: 38.4wks. Weight: 4410g
For paediatric follow up, cranial ultrasound, enhanced M&CHN program
This was a very severe case of neonatal hypoglycaemia due to gestational diabetes.
But this isn’t the only reason babies can have problems hypoglycaemia……..

31. HYPOGLYCAEMIA
There is a lack on consensus on what defines hypoglycaemia in the neonate.
A clinical trial is not an option/possible.
Clinical guidelines should be defined by operational thresholds (ie. blood glucose levels at which clinical interventions should be considered).
Profound hypoglycaemia (TBG <1.5mmol/L) is more likely to result in long term sequelae, with longer durations adding to the risk.
Symptomatic neonates have a worse prognosis.

32. Hypoglycaemia
Which babies should we routinely monitor for hypoglycaemia?
Maternal indications: mother who has diabetes (up to 50% of these infants may become hypoglycaemic, the incidence is also related to glucose control in pregnancy/HbA1C, medications and dextrose in labour)
Infant indications: SGA (<10th centile), LBW (<2500g), macrosomic (>90th centile), prematurity, NBM, RDS, sepsis, hypothermia, asphyxia (arterial cord pH<7.2) – in fact most babies admitted to a SCN/NICU will have blood glucose monitoring initially.

33. Hypoglycaemia
For the neonate of the mother with diabetes the biggest risk time is the first 1 – 3 hrs of life
Maternal supply of glucose abruptly ceases, but there is a lag in the reduction of circulating insulin
But problems can continue to occur over the first week of life
The macrosomic baby is at greatest risk (47% will have issues with hypoglycaemia, compared to 20% of those that are non-macrosomic)

34. Signs & symptoms Signs & symptoms are non-specific
Abnormal muscle tone
Abnormal level of consciousness, lethargy
Poor oral feeding
Seizures
Jitteriness
Tachypnoea
Cyanotic episodes
High pitched cry, irritabiltiy
MANY BABIES WILL HAVE NO SIGNS OF HYPOGLYCAEMIA

35. Measuring blood glucose
Blood glucose levels (BSL’s) are measured by a blood glucose monitor and reagent strips – these are not considered to be reliable outside of the ranges of 2.5 – 8.0 mmol/L
Preferable to have low results confirmed with a TBG (from the lab, or a blood gas analyser that some units will have); the length in delay of obtaining a TBG would need to be considered with regard to prompt treatment in case the low result is correct.

36. Management of hypoglycaemia
Early, frequent and adequate milk feeds
IV glucose (10%): maintenance, +/- bolus
If increases in TFI are not correcting the problem the concentration of glucose can be increased to 12.5%, 15% & 20% (anything over 12.5% needs to be through a central line)
IV/IM glucagon
Hydrocortisone, diazoxide, octreotide
Diazoxide: used as an insulin suppressor
Octreotide: is an octapeptide that mimics natural somatostatin pharmacologically, though it is a more potent inhibitor of growth hormone, glucagon, and insulin than the natural hormone.

37. MANEGEMENT: DIAZOXIDE
Commonly used in adults as an antihypertensive agent in acute situations.
Used in neonates as an insulin suppressor.
Has become a first line drug for the management of hyperinsulinaemia (administered at 5 – 15 mg/kg/day).
Can be effective in controlling insulin secretion and promoting mobilization of glycogen stores.
Can take up to 7 days to be effective.
Doses < 20mg/kg/day appear to be safe and can be used long term.
Acts to inhibit closure of the Katp (potassium-adenosine triphosphate) pump. When there is an existing mutation of this pump it is usually not effective; this is often the case with persistent HH.
Can reduce serum IgG levels so can increase infection risk.

38. CALCULATING GLUCOSE LOAD
Average glucose consumption should be between 4- 6mg/kg/min
Some preterm & SGA infants may require 6-8mg/kg/min to maintain normal plasma glucose levels
If a neonate is requiring more than 10mg/kg/min to maintain adequate glucose levels further investigation is required
Caluculating glucose load (mg/kg/min):
Daily volume (mL/kg/day) x %dextrose/144=glucose load
(for breast milk you can assume the % is about 7%)

39. PERSISTENT HYPOGLYCAEMIA
If hypoglycaemia continues for longer than expected and does not respond to appropriate management further studies may be required:
Insulin levels,
Ketones (serum and urine),
Cortisol,
Growth hormone,
Lactate,
Pyruvate &
Serum electrolytes.
The optimum time to perform these tests is when the infant is having a hypoglycaemic episode.

40. CAUSES OF HYPOGLYCAEMIA
The causes of hypoglycaemia can be divided into
several broad categories based on the mechanisms
producing the hypoglycaemia:
Inadequate substrate supply,
Abnormal endocrine regulation of glucose
utilization &
Increased rate of glucose utilization.
There are also several etiological conditions for which
mechanisms are not well defined.

41. INADEQUATE SUBSTRATE SUPPLY
If supply is inadequate hepatic glucose output will not meet metabolic demands.
Usually results from subnormal fat and glycogen stores.
Infants born preterm have diminished glycogen stores.
Infant with IUGR secondary to placental insufficiency also at risk for decreased glycogen accumulation.
Glycogenolysis and gluconeogenesis can be impaired in premature infants for a prolonged period.
The subnormal fat and glycogen stores do not provide sufficient energy to maintain glucose homeostasis until gluconeogenesis reaches adequate levels.
Infants born preterm have diminished glycogen stores because most of the hepatic glycogen is accumulated during the 3rd trimester.
IUGR: presumably causes problems because of diminished transfer of glycogen precursors (eg. glucose and lactate) across the placenta; the limited supply of these is then used for oxidative metabolism rather than building up the fat or glycogen stores in utero.
Up to 18% of preterm infants have problems in maintaining normoglycaemia at the time of discharge if a feed is omitted or delayed.
Inadequate cortisol secretion in very preterm infants, particulary during periods of stress, also has been cited as a cause of limited activation of gluconeogenic enzymes.

42. INCREASED GLUCOSE UTILISATION
Normal stores, intact regulating mechanisms but an increased energy demand, such as in cases:
That cause a shift from aerobic to anaerobic metabolism (asphyxia, hypotension, severe lung disease, septic shock);
Hypothermia: rapid depletion of brown fat stores for non- shivering thermogenesis and secondary breakdown and exhaustion of glycogen stores.
Asphyxia results in anaerobic metabolism, this is inefficient and more glucose is used than would be under normal aerobic conditions; hypoxic damage to liver can impair normal postnatal onset of gluconeogenesis; may also be elevated insulin levels present in these situations.

43. ENZYMATIC AND GENETIC DISORDERS
Hormone deficiencies (such as growth hormone and cortisol)
Enzyme deficiency conditions
Defective carbohydrate metabolism
Defects in amino acid metabolism
Defects in fatty acid metabolism
Growth hormone and cortisol oppose the action of insulin; they increase blood glucose concentrations by reducing glucose uptake in muscle tissue and they stimulate lipolysis and gluconeogenesis.
Hereditary disorders associated with a deficiency of specific enzymes involved with substrate mobilization and utilization of carbohydrate, fat or amino acids.
A number of disorders characterised by a deficient or abnormally functioning enzyme that results in an interuption to the normal processes of gluconeogenesis and glycogenolysis.
Fatty acid metabolism releases ketone bodies and these can partly replace glucose as energy in the body. Defects in fatty acid metabolism are rare, but severe, metabolic disorders resulting in hypoglycaemia and hypoketonaemia.

44. THE ENDOCRINE SYSTEM Comprises:
the hypothalymus (the pituitary, pineal, thyroid, parathyroid and adrenal glands);
the gonads;
and the pancreatic islet cells.
Some of the problems that occur in the newborn are related to the metabolism of glucose, calcium, phosphorous and magnesium that are regulated by the endocrine system.

45. ABNORMALITIES OF ENDOCRINE REGULATION
Hyperinsulinaemia is the most common endocrinological disturbance producing neonatal hypoglycaemia.
Excessive insulin secretion in the newborn increases glucose utilization by stimulating cellular glucose uptake in insulin- dependent tissues.
The most common clinical situation where hyperinsulinaemia occurs is in the neonate of a mother with IDDM.
Beckwith-Weidermann syndrome.
Prolonged neonatal hypoglycaemia.
Persistent hyperinsulinaemic hypoglycaemia.
High circulating insulin concentration promotes continued glycogen synthesis and inhibits both glycogenolysis and gluconeogenesis, impairing the infants glucogenic response to the increased glucose demand and decreasing plasma glucose concentration.
IDDM: In utero the foetus becomes hyperglycaemic secondary to increased levels of glucose crossing the placenta; the foetal pancreatic beta cells produce increased quantities of insulin; after delivery the source of glucose is removed, but the increased insulin secretion continues; hypoglycaemia results from continued high glucose uptake and inhibition of gluconeogenesis and glycogenolysis (secondary to high insulin levels).
BW syndrome: inherited disorder involving numerous organ systems; also known as EMG disorder (E: exomphalos, 36% of cases; M: macroglossia, or hypertrophy of the tongue, 100% of cases; G: gigantism, 100% of cases). Other common presenting features are ear lobe abnormalities and hepatomegaly. It is an autosomal dominant syndrome; incidence is 1 in 13,700 live births; on karyotyping there may be subtle abnormalities on chromosome 11.
I’ll explain prolonged hypoglycaemia and persistent hyperinsulinaemic hypoglycaemia in more detail.

46. PROLONGED NEONATAL HYPOGLYCAEMIA
Common, but not well recognised or understood
Usually associated with stress before of during birth
May present as IUGR; birth asphyxia; secondary to maternal pre-eclamsia
Usually manifests in the first few days and often may be severe
May last up to 4 weeks
Does not respond well to glucocorticoids or frequent feeds
May be treated with diazoxide at doses of 5 – 10mg/kg/day.

47. Avoiding harm/reducing risk
Hospitals should have written protocols for prevention and management of potential neonatal complications
If complications are expected babies should be delivered in hospitals that have the expertise to manage these complications
Aim to avoid iatrogenic harm by avoiding unnecessary preterm delivery or caesarean section and unnecessary separation of mother and baby
Iatrogenic: caused by treatment or diagnostic procedures. An iatrogenic disorder is a condition that is caused by medical personnel or procedures, or that develops through exposure to the environment of a health care facility.

48. Iatrogenic complications
Routine admission of babies to neonatal units
Routine supplementation or replacement of breast feeds with formula
Delayed skin to skin and first feed
Poor management of temperature control
Blood glucose tested and acted upon too soon after birth

49. REFERENCES
Hawdon J. M. NICE guidance for neonatal care after diabetes in pregnancy. Infant 2008; 4(5):
Narchi H. & Kulaylat N. Heart disease in infants of diabetic mothers. Images in paediatric cardiology 2000;3:17-23.
Miller M.Q. & Morris L.A. Devlopmental considerations in working with newborn infants of mothers with diabetes. Neonatal Network 2011; 4:37-45.
Powell L.L. Infants of diabetic mothers: The effects of hyperglycaemia on the fetus and neonate. Neonatal Network 2007; 26:

50. References cont....
Cresto, J.C., Abdenur,J.P., Bergada,I., & Martino, R. (1998). Long term follow up of persistent hyperinsulinaemic hypoglycaemia of infancy. Arch Dis Child. 79:
(pancreatectomy)
Gallager, M.P., Chung, W.K., & Oberfield, S.E. (2007). Endocrinology and metabolism. In R.A. Polin & A.R. Spitzer (Eds.), Fetal and neonatal secrets, (2nd ed., pp ). Philadelphia, Pennsylvania: Mosby, Elsevier.
Glanze, W.D. (ed), (1986). Mosby’s Medical and Nursing Dictionary. St.Louis: The C.V. Mosby Company.
Helwick, C.A. (2002). Pancreatectomy. Gale encyclopedia of medicine. The Gale Group:
Hussain, K. (2007). Diagnosis and management of hyperinsulinaemic hypoglycaemia of infancy. Hormone Research, 69: 2-13.
Kenner, C., & Wright Lott, J. (2004). Neonatal Nursing Handbook. St.Louis, Missouri: Saunders.
McGowan, J.E., Price-Douglas, W. & Hay, W.W. (2006). Glucose homeostasis. In G.B. Merenstein & S.L. Gardner (Eds.), Handbook of neonatal intensive care, (6th ed., pp ). St.Louis, Missouri: Mosby, Elsevier.
Mims Online:
Normal Physiology of Insulin release – Athena Diagnostics:
Stockowski, L. (2004). Endocrine disorders. In M.T. Verklan & M. Waldan (Eds.), Core curriculum for neonatal intensive care nursing, (3rd ed., pp ). St. Louis, Missouri: Elsevier, Saunders.

52. CASE STUDIES
32 yr old multi presented to hospital in the Gippsland region, with history of decreased fetal movements (32.4wks gestation), CTG showed sinusoidal trace – EM LUSCS performed
Antenatal history: poorly controlled GDM on insulin; pregnancy induced cholestasis; antenatal depression (medicated); fetus estimated to be on the 98th centile and polyhydramnios evident
Steroids given just prior to delivery

53. Case study cont… Baby Beau born at 1530hrs via EM LUSCS (3300gs)
Noted to be pale, irregular respirations/periods of apnoea – CPAP/IPPV given intermittently until breathing regularly.
Nasal CPAP commenced at 40 mins of age with a PEEP of 5cm H20, FiO2: 45%
Umbilical pH 7.13 venous, 7.21 arterial
FBE, CRP, BC, electrolytes, ABG and BSL taken
APGARS: 5, 4, 4, 1, 5, 10 & 15mins

54. Case study cont…
Results of interest: (at 1&1/2 hrs of age) Hb 64, ph 7.12, CO PEEP increased to 10 at this point
Initial BSL’s: 1.5 & 1.8 (received 2 x 2.5mL/kg of 10% dextrose bolus’), BSL 1 hour later 2.6mmol/L. Infusion of 45mL/kg 10% dextrose commenced.
Issues: anaemia, prematurity, hypoglycaemia, LGA, respiratory distress requiring CPAP
NETS called and t/f planned to RWH
Mother and baby both A+ve, Kleihauer positive (fetal- maternal haemorrhage)

55. Case study cont… 12.5% dextrose commenced by NETS
Transferred to RWH (at 6 hrs of age) with NETS intubated, received x1 dose surfactant before t/f and one at RWH – extubated the following day.
Received a transfusion of PRBC’s
TBG’s stabilised 3.5, 3.8, 2.9,3.4, 4.4, 4.4, 4.0 etc
Hb checked post transfusion 145, next day 158

56. Case study cont…
What were this babies risk factors for hypoglycaemia?

57. Case study continued Neonate of gestational diabetic mother
Poor control of diabetes in pregnancy
Prematurity
Large for gestational age (? High levels of circulating insulin): above the 97th centile for a baby of this gestation
Respiratory distress
Sick baby/anaemic

58. Case Study No. 2
Multipara, NVB at 40wks gestation, born at 2044hrs. Mec liquor present, but baby vigorous, nil resus required
Apgars of 9 and 9
Birth weight: 4090gs
Mother planning to breastfeed
Transferred to postnatal ward, good breast feed noted at 2130hrs
Baby normothermic
Hep B and Vit K given

59. Case study cont..
On commencement of day shift, midwife noted that baby had not fed since 2130hrs in the evening, mother confirmed same
BSL taken at 0845hrs: 1.2, TBG performed in SCN: 2.3
Baby breastfed and topped up, received 0.5mL EBM and 8mL Nan via syringe
TBG repeated at 1045hrs: 1.5; baby admitted to SCN
Attempt made at suck feed, too sleepy, NGT inserted and 60mL/kg feed given.

60. Case study cont…
TBG at 1210hrs: 2.1; d/w paeds further 30mL/kg feed given via NGT
TBG at 1315hrs: 2.1; d/w paeds, for insertion of IV bung
1400hrs IVB inserted 2mL/kg bolus of 10% dextrose given and IVT commenced at 60mL/kg
Baby made NBM
1445hrs TBG 2.6, NBM infusion continued
1600hrs TBG 3.6, NBM infusion continued
2000hrs TBG 3.5, baby breast fed, IVT continued

61. Case study cont…
Plan from this point would be to continue breastfeeding on demand, or 3-4/24
Continue dextrose infusion overnight
Plan to wean dextrose next day and continue to establish breastfeeding/supply
No set rules on how to wean the dextrose, could go down by 2mL/hr with each feed, checking an AC BSL; or could be more ‘aggressive’ and half it initially, half again and then cease. Each hospital and doctor will be different, but as long as the BSL’s are monitored as the dextrose is weaned either option above would be acceptable, or variations of the same.

62. What are the risk factors for this baby?
Case study cont..
What are the risk factors for this baby?

63. Case study cont.. Large for gestational age
Did not have blood sugar monitoring, and any baby who is greater than 4kgs or > than the 90th centile should have monitoring of BSL’s initially until stable
Did not receive a feed for 12hrs
Incident report completed relating to care on post natal ward.