Sweet Nothings? Hypoglycaemia in the Neonate

This post has been submitted by paediatric registrar Dr Abiramy Saravanamuthu, with consultant input from Dr Prabhakaran Kalaivanan.

Babies with low blood sugars are a frequent worry for the poor overburdened SHO on the postnatal ward. Often a low blood sugar is harmless, but we rightly take notice given that it is a potential sign of something more serious going on.

The formal definition of neonatal hypoglycaemia is a blood glucose (BG) <2.6mmol/L

Does every baby with hypoglycaemia need further investigations? How do you decide? Follow this guide when the midwife calls.

A bit of physiology…

Blood glucose falls rapidly within the first few hours of life, as the infant loses the continuous supply of glucose the foetus had derived from the placenta. During this time there is a metabolic transition to independent glucose production from glycogenolysis and gluconeogenesis. There are a small portion of infants who are at increased risk of failure of this adaptation, and so at risk of symptomatic hypoglycaemia. Those infants identified ‘at risk’ are subject to routine blood glucose monitoring post-delivery. Monitoring begins pre- the 2nd feed, unless the infant is symptomatic prior to this.

Causes of neonatal hypoglycaemia

The majority of neonatal hypoglycaemia is transient.

* denotes those causes of persistent hypoglycaemia, which are also more likely to require higher glucose infusion rates (GIR). Normal postnatal glucose requirements are between 5-8mg/kg/min.

Focused clinical history and examination

Think beyond ‘poor feeding’ – there are many potential causes of hypoglycaemia in the neonatal period – and if you don’t consider them, you may miss an important diagnosis. It is helpful to think about causes divided into antenatal, perinatal and postnatal categories:

 

 

Antenatal

There are plenty of antenatal risk factors for hypoglycaemia and these babies will often have been identified already for BG monitoring.

  • What is in the mum’s medical history? Gestational diabetes, pregnancy induced hypertension and pre-eclampsia can all be related to low blood sugar in a baby.
  • Is mum on any medications? Ask specifically (or check drug charts) for beta blockers and oral hypoglycaemic agents.
  • What did the antenatal scans show? Is there evidence of intra-uterine growth restriction (IUGR) or macrosomia?
  • Think about potential medical conditions causing neonatal hypoglycaemia and whether there is a family history of metabolic conditions, previous neonatal hypoglycaemia or parental consanguinity.

 Perinatal

Birth can be a stressful event for everyone involved… including baby.

  • Were there any risk factors for sepsis (maternal fever, maternal GBS, prolonged rupture of membranes, fetal tachycardia)?
  • Was the baby born prematurely, or have an unexpectedly low birth weight?
  • Hypoxia associated with a difficult delivery can also cause blood sugars to drop – what were the Apgar scores?

Postnatal

Now think about the baby in front of you…

  • How does their weight plot; are they growth restricted (<2nd centile) or macrosomic (>90th centile)?
  • We all know a good feeding history can tell you a lot, never more so than in this context. Is the baby breast or bottle fed? If breast fed how is the baby latching, how long and frequent are the feeds, is mum’s milk supply in? If bottle fed, what is the volume and frequency of feeds? Does the baby tolerate the feeds? All these questions can help establish if hypogycaemia is simply due to a supply issue, which is often the commonest cause on postnatal wards.
  • Clinically examine the baby. Firstly, do they have any risk factors for hypoglycaemia such as wasting, severe jaundice or polycythaemia? Are there any clues to an underlying metabolic, endocrine or genetic condition (particularly looking for dymorphism, ambiguous genitalia or other midline defects).
  • Secondly, do they have any signs and symptoms of hypoglycaemia such as:

CNS excitation:      irritability, jitteriness, seizures

CNS depression:    hypotonia, lethargy, poor feeding, apnoeas

Non-specific:        temperature instability, sweating, tachycardia, cyanosis

Piecing all of this information together can help to build a much clearer picture of whether hypoglycaemia is due to a transient phenomenon, or potentially pathological.

Management

When faced with hypoglycaemia, think about the BG value and the clinical picture.

  • BG <1.5mmol/L or symptomatic hypoglycaemia requires immediate action.
  • Volumes and concentrations of dextrose are increased to maintain normoglycaemia.
  • Glucose infusion rate (GIR) >10mg/kg/min suggests significant pathology (see below for how to calculate this)
  • BG 1.5-2.5mmol/L is a borderline area which can be managed with a clear feeding plan.
  • Evidence of persistent borderline hypoglycaemia despite these plans, requires investigation.

Follow the flow chart below to guide your management decisions.

Calculating the Glucose Infusion Rate (GIR)

It is important to calculate the GIR for babies on the neonatal unit, particularly those admitted for hypoglycaemia.

Normal postnatal glucose requirements are between 4-8mg/kg/min. Requirements >10mg/kg/min ring alarm bells for a pathological cause of hypoglycaemia.

The hypoglycaemia screen

The dreaded hypo screen. When to do one? It’s a difficult question. The majority of neonatal hypoglycaemia is transient, and we want to avoid over-medicalising these infants, but no one wants to miss a potentially serious condition. Common consensus is that infants with severe hypoglycaemia (<1.5mmol/L) or symptomatic hypoglycaemia should be screened, as should those with less severe hypoglycaemic episodes which persist beyond the transitional period.

The aim of the basic hypoglycaemia screen is to identify the more prevalent metabolic and endocrine conditions that can cause hypoglycaemia – so as to appropriately treat them – and prevent fatal hypoglycaemia in the community.

The table below details the basic hypoglycaemia screen:

Interpreting the hypoglycaemia screen

Interpretation can be tricky, but we can also try and think it through logically before the obligatory call to tertiary services.

Insulin: when BG is low insulin should be undetectable. If in the context of hypoglycaemia there is any detectable insulin- that is an abnormal result and indicates hyperinsulinism.

Cortisol and GH: these are stress hormones and in the hypoglycaemic state their production should be triggered. Low levels indicate deficiency of these hormones and/or a problem along their production pathway.

Ammonia and lactate: high levels of these are always abnormal, alerting us to potential metabolic conditions. Lactate of course can be very non-specific, indicating generalised sepsis.

3β-Hydroxybutyrate and NEFA: in hypoglycaemia infants turn to alternative fuel sources such as ketones and fatty acids- we would expect these may be slightly raised. Low levels imply a failure of these metabolic processes; while inappropriately high levels of ketones indicate organic acidaemias.

Amino acids, acyl carnitine and urine organic acids: abnormal profiles of any of these indicate specific metabolic conditions which would of course require discussion with specialist teams.

Summary

Neonatal hypoglycaemia is the most common metabolic problem in newborns.

BG <2.6mmol/L requires action and monitoring.

The majority of neonatal hypoglycaemia is transient.

Severe hypoglycaemia <1.5mmol/L and sustained >72 hours and/or with a GIR >10mg/kg/min requires further investigation and management.

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