Amandas NICU Ed

We check blood sugars all the time in the NICU... but do you ever think about *why* newborns are so vulnerable to glucose instability?

Before birth, babies receive a continuous supply of glucose from the placenta. Then, with a single cord clamp, that disappears. Suddenly, the newborn must regulate glucose independently by breaking down glycogen, producing new glucose, mobilizing fat stores, and even creating ketones as an alternative fuel source.

It's one of the most important metabolic transitions of life!

Understanding glucose homeostasis helps us move beyond treating numbers and start understanding the physiology behind them. Why are premature infants at higher risk? Why do infants of diabetic mothers become hypoglycemic? Why does stress or illness affect glucose regulation?

These are the questions that help us anticipate problems, recognize risk factors, and provide better care at the bedside.

👉 This week's blog dives deeper into glucose homeostasis, hypoglycemia, hyperglycemia, ketones, and the physiology every NICU nurse should understand.

Follow for more NICU education, certification tips, and physiology made simple for bedside nurses.

NEC is one of those diagnoses in the NICU that every nurse remembers... abdominal distention, feeding intolerance, bloody stools, and x-rays. Baby's that can become critically ill very quickly.

Understanding the *why* behind NEC matters.

Why premature babies are at higher risk.
Why the immature gut is vulnerable.
Why perfusion, inflammation, bacteria, and feeding practices all play a role.
Why early recognition from the bedside nurse can make such a huge difference.

In this week’s newsletter, I’m breaking down:
• The pathophysiology of NEC
• Risk factors and early warning signs
• What nurses should monitor closely
• Prevention strategies
• High-yield concepts for the RNC-NIC and CCRN-N exams

If you want the full breakdown, make sure you’re signed up for my newsletter through the link in my bio ✨

𝗡𝗲𝗰𝗿𝗼𝘁𝗶𝘇𝗶𝗻𝗴 𝗘𝗻𝘁𝗲𝗿𝗼𝗰𝗼𝗹𝗶𝘁𝗶𝘀 (𝗡𝗘𝗖) is a devastating ischemic and inflammatory necrosis of the bowel. ⚡️

👶 NEC primarily affects premature and medically fragile newborns after the initiation of enteral feedings. 🍼

🔍 The exact cause of NEC isn’t fully understood: it’s believed to be multifactorial, with several risk factors increasing susceptibility.

📅 May 17 is NEC Awareness Day
If you’re not already following , now’s the time. Let’s work together to build a world without NEC 💙🫶

🌸 Happy Mother’s Day to all the incredible moms out there and a very special shoutout to our NICU moms 💕

To the moms who have learned to love through monitors, tubes, wires, and daily rounds…

To the moms who celebrate the smallest milestones; a successful feeding, a gained gram, a tiny diaper change or a full blown blowout 💩

To the moms who have faced uncertainty with strength, who have whispered words of comfort through isolette walls, and who have shown up every single day with love that knows no bounds 💓

Your courage, your patience, your tears, and your triumphs do not go unnoticed.

💗 You are your baby’s safe place.
💗 You are their advocate, their protector, their home.
💗 You are a NICU mom and that is a title of unmatched strength.

Wishing you a day filled with love, light, and the recognition you so deeply deserve. 💐

Congenital Adrenal Hyperplasia
Have you every taken care of a baby with CAH? CAH is an autosomal recessive disorder that causes an enzyme deficiency disrupting the production of cortisol and aldosterone. Cortisol and aldosterone are essential hormones for glucose control, stress response blood pressure homeostasis, and overall fluid balance.
21-dehyroxylase is the most common enzyme deficiency (though there are others). The deficiency of 21-OHD prevents synthesis of cortisol and aldosterone which causes and overproduction of ACTH and 17-OHD (the precurser to cortisol). This causes many issues....

The accumulation of 17-OHD causes and overproduction of androgens (like testosterone) and causes virilization of genetically female infants.
The lack of cortisol disrupts glucose and blood pressure homeostasis resulting in hypoglycemia and hypotension.
The lack of aldosterone prevents the tubules from reabsorption sodium. This results in salt wasting, potassium accumulation, hypovolemia, hypotension and shock.

The state newborn screening helps us identify CAH early, but must be confirmed because false positives can occur. False negatives are rare, but can occur after prenatal exposure to steroids which suppress the HPA axis. Many states perform re-screening after 3-5 days. Confirmatory testing reveals high 17-OHP levels.

Lifelong treatment and follow up is required for the infant with CAH and NICU nurses are essential in helping families understand the diagnosis, and learn how to administer medications. It is especially important families are trained how to provide stress dosing, including IM injection in cases when the infant is unable to take the medication by mouth.

Have you taken care of a baby with CAH? 💙
Does your state repeat newborn screening? 🩸



Reference:
Allis K. A Broken Pathway: Understanding Congenital Adrenal Hyperplasia in the Newborn. Neonatal Netw. 2021;40(5):286-294. doi:10.1891/11-T-694
Verklan, et al., Core Curriculum for Neonatal Intensive Care Nursing, Elsevier, 2021
Merke (2022).Treatment of classic congenital adrenal

Galactosemia is an inborn error of carbohydrate metabolism where the infant cannot properly convert galactose to glucose due to deficiency of the enzyme galactose-1-phosphate uridyltransferase (GALT). As galactose accumulates, it becomes toxic—particularly to the liver, brain, and kidneys.

What makes this condition especially important in the NICU is how quickly symptoms can develop once feeding begins.

These infants may present with poor feeding, vomiting, lethargy, hypoglycemia, and jaundice that can progress to liver dysfunction. One of the most concerning complications is E. coli sepsis, which is seen in approximately 10% of newborns with galactosemia.

Unlike some metabolic disorders that are silent early on, galactosemia often declares itself clinically, sometimes before newborn screening results return.

As NICU nurses, it’s important to understand:
• Why symptoms begin after exposure to milk (lactose → galactose)
• When to escalate concern for metabolic disease
• The urgency of stopping galactose intake
• Teaching families how early dietary management can be lifesaving

With prompt recognition and removal of galactose from the diet, outcomes improve significantly. Delays in treatment can lead to serious complications.

If you’re studying for your RNC-NIC or CCRN-N, this is a high-yield concept to understand—not just memorize.

Follow along for NICU education that helps you connect physiology to practice and feel more confident at the bedside.

Phenylketonuria (PKU) is a metabolic disorder where the body cannot break down phenylalanine, an essential amino acid found in protein. When phenylalanine builds up, it becomes toxic to the developing brain.

The challenge is that early on, there are little to no clinical signs. These babies won’t show you what’s happening until the damage has already begun.

That’s why newborn screening is critical.

As NICU nurses, it’s not just about knowing that PKU is on the screen. It’s understanding:
• Why protein intake is required for accurate testing
• Why delayed feeds or TPN can affect results
• When repeat screening may be needed
• And how early dietary management prevents long-term harm

Because with early detection and proper treatment, these babies can have normal growth and development.

This is one of those diagnoses where timing, awareness, and follow-through make all the difference.

If you’re preparing for your RNC-NIC or CCRN-N, this is a high-yield concept worth truly understanding.

Follow along for NICU education that helps you connect the physiology to your practice and feel more confident at the bedside.

Congenital Hypothyroidism is the most common endocrine disorder in the newborn period and, if undetected, can lead to intellectual disability. Most newborns are asymptomatic immediately after birth which makes newborn screening so important for identifying these babies.
There is a normal surge is TSH immediately after birth due to exposure to the cold temperature and the stress of delivery. This surge of TSH peaks in the first hour of life and gradually declines within the first few days of life. Subsequently increased hormone levels will peak around 24-36 hours of life. This is important to understand because when the newborn screen is sent within the first 24 hours of life, a false positive may occur.
Confirmatory testing includes measuring thyroid function to identify the type of hypothyroidism.
Infants with congenital hypothyroidism require treatment with thyroid replacement therapy (Levothyroxine). Levothyroxine should be administered 30 minutes prior to feeding. Pills are crushed and mixed with breast milk, formula, or water. Do not mix levothyroxine with drugs known to alter absorption such as iron and calcium. Soy formulas should also be avoided as they can alter absorption of levythyroxine.
Nurses are essential in providing excellent care to newborns with hypothyroidism and education to families. Levothyroxine administration must be thoroughly review and to watch for signs of thyrotoxicosis. Signs include tachycardia, irritability, and poor weight gain.
Newborns with hypothyroidism require follow up to monitor thyroid function and ensure adequate dosing of levothyroxine