Henry, day of life #2, with pulse oximeter around his foot
What I have finally figured out in trying to write about Henry’s newborn illness is that there is no possible way to cram the details into a few blog entries. And, as it turns out, it isn’t necessary. I mean, do you really need to read about each hourly crisis a whole year later, especially when you already know the happy ending? I didn’t think so.
For me, writing about Henry’s medical misadventures means picking out the moments that defined the experience for us, all those moments leading up to the best outcome we could have imagined: a thriving baby boy. And in fact, the only way I CAN write about it today is because of how it all ended. My heart aches for the families of preemies without a happy outcome, and I will never take for granted that we weren’t one of them.
Writing about it now is also an opportunity for the science writer in me to learn a little more about Henry’s illness, now that I can actually stand to read medical web pages about newborn respiratory disease just PEPPERED with stats on infant mortality. Medical types and longtime viewers of ER, you’ll dig the jargon and medical links here; my sincere apologies to the rest of you. There is just no way to talk about this stuff in English. And medical professionals, if I got something wrong, please be sure to let me know. Henry’s medical team taught us well, but it’s entirely possible I lost a little something in the translation.
So, as I was saying in Part 1…
Henry arrived at 11:15 p.m. on Sunday, June 11—blue and one month ahead of schedule, but perfect, as far as we could tell. Since Will had languished in my arms for what felt like hours after his birth, I was frustrated that Henry was kept across the room from me in the minutes after his birth—I was too dazed to understand the nurses huddled around him were giving him oxygen and becoming concerned with his desperate efforts at breathing.
Henry, 10-minutes old, June 11, 2006
Before long, one of the practitioners from the Newborn Intensive Care Unit arrived to evaluate his increasing respiratory struggle. To my secret relief, Baby Boy (as he was known then) was transferred to the NICU about 45 minutes later—his terrible, labored sounds were scaring me, and I was starting to understand he wasn’t ready to be with us.
Our nurse came by with a Polaroid of Henry on the unit, and I was shocked at the change. Instead of the sweetly swaddled newborn I had held briefly just an hour ago, he was laid out bare and exposed on a radiant warmer, with what looked like a snorkle covering the little face I had hardly seen. He was draped in wires and tubes, and the baby that had seemed so large and robust for a 36-weeker now looked painfully small.
Henry at six hours of life, measuring 18 inches and weighing 5 pounds, 14 ounces on arrival at the NICU.
(Scale is everything—that’s a preemie-size diaper.)
In the morning, we called surprised family and friends, telling them about his arrival, and what we believed to be true—that this was a minor setback, maybe a little fluid in the lungs, and he ought to be just fine in a day or two. I had no idea then Henry wouldn’t be coming home with us at the end of my 48-hour hospital stay.
So what was wrong with him?
As one of his practitioners explained to us, “Newborns have a fairly limited repertoire. This (“this” being rapid breathing, grunting, retracting and low and/or unstable levels of oxygen saturation) is pretty much what they do when they are in trouble, and it is up to us to figure out what is causing it.”
She went on to explain that when a near-term, seemingly healthy baby with Henry’s symptoms arrives in the NICU, the one of the first things considered is transient tachypnea of the newborn (TTN), also known as wet lungs. It is usually just a mild respiratory problem, characterized by rapid breathing, that begins after birth and lasts about three days. It can be more common in babies delivered via c-section or in a very rapid delivery like Henry’s, because, well, they just don’t get all that fluid squeeeeeezed out.
His medical team hoped to pin TTN, the least complicated of newborn respiratory problems, on him, but Henry’s increasing need for breathing support and increased episodes of oxygen desaturations (“desats”) quickly trampled the benign idea of a little extra fluid in his lungs. At the same time he was started on a ten-day course of IV antibiotics for presumed pneumonia and sepsis.
Henry’s neonatologist, a truly extraordinary doctor that spent hours with us, patiently spoke with us time after time in those first 40 hours as Henry’s condition worsened. As each update session ended, he would always ask, “Do you have any other questions for me?” Our biggest questions were the most basic: “What does he have? What is wrong with him and why are we here?”
Just hanging out
The answer was surprisingly unclear. We learned there is really no easy way to rule out pneumonia in a newborn with Henry’s symptoms, so he was treated for it whether he had it or not. Equally as likely, he showed up at the party with respiratory distress syndrome or RDS, the more baby-friendly term for respiratory failure of the newborn or the really old-fashioned moniker, hyaline membrane disease. Whatever you call it, it is a general term for the breathing difficulties endured by lungs too immature to produce adequate surfactant, an important substance produced in the lungs that helps the air sacs stay open. A developing baby naturally produces this necessary substance, BUT not until the last few weeks of pregnancy.
So how do you fix it?
When Henry first arrived in the NICU, he was started on supplemental oxygen delivered via nasal canula, but with a few significant desats and “dusky” episodes (a nice way to say your baby turned blue), he was switched to the snorkle, N-CPAP, which stands for nasal continuous positive airway pressure. We learned that CPAP is still a fairly mild form of respiratory support—a baby on CPAP will initiate every breath himself, while the pressure of the machine keeps his airways open as he exhales. The respiratory support is provided to keep the baby breathing while the lungs heal (if it is pneumonia) or start producing surfactant (if it is RDS).
But despite the support of CPAP, Henry continued having more desats. (As you sit reading this, you are probably “satting” near or at 100% oxygen saturation in your blood. The goal for Henry’s plan of care was to keep him between 90-100%. His desaturations, or “desats” were dipping into the 80s and 70s.)
We had learned to change his diaper around his tubes and leads and check some of his basic vitals during “hands-on” care, the scheduled time for changing, examining and handling babies in the NICU so they can get uninterrupted rest at other times, but he had become so fragile that even the stimulation of a diaper change sent his sats plummeting downward. Our physical contact with him was now limited to laying a hand gently against his skin without patting, rubbing or moving. The thing we wanted to do most, to hold him and touch him, was one of the most devastating things for his survival.
Careful monitoring by his team, plus more chest x-rays than I can count confirmed that Henry had a whole new layer of complications threatening his ability to breathe: on his second day of life, he developed both a pneumothorax, (an air leak into the space between the chest wall and the lungs) and a pneumomediastinum, an air leak into another part of the chest. The pressure of the air leak collapses the lung and affects the ability to breathe, so at 10:15 p.m. on June 12, at 23 hours of life, Henry’s doctor put in a chest tube (which is just what it sounds like) to drain the air leak while the lung healed.
Henry’s chest tube is attached to that giant hose on the right, evacuating the leaked air so his lung can reinflate.
After that, it was clear that Henry wasn’t heading home any time soon, so his team celebrated his 24th hour of life by placing an umbilical arterial line, which sounds terrible, but is really a kind way to draw blood, administer meds and give nutrition to babies in it for the long haul.
The next morning, just before dawn, Henry’s nurse practioner flew into our room to advise us of his recent crisis. We were catching a few hours of sleep, our first since his birth. She pushed the door open so hard it slammed against the wall, and in those seconds before she spoke, I tried to will her to say words that I could bear to hear.
Despite the chest tube and the support from CPAP, his sick little lungs just couldn’t do their work, and the effort became too great for him to breathe on his own. At 30 hours of life, after a significant desaturation event (sats below 40% for approximately two minutes) Henry stopped breathing, and didn’t respond to tactile stimulation and blow-by oxygen, so he was intubated and put on a mechanical ventilator. We are forever grateful that Torie was at his bedside before this pre-dawn event, and responded instantly to this emergency, lessening the amount of time his brain was without precious oxygen.
Henry on the mechanical ventilator, 32 hours of life.
Probably the most famous baby ever to succumb to respiratory distress syndrome, as many people told us once Henry was on the mend, was Patrick Bouvier Kennedy, the newborn son of President John F. Kennedy and his wife Jackie Kennedy. Young Patrick, born in 1963, was a near-term baby like Henry, but his tiny, critically-ill body became overwhelmed with respiratory distress, and he died at just 39 hours of life.
Therapies that Henry received, including CPAP, mechanical ventilation and exogenous surfactant might have saved Patrick Kennedy, but they either did not exist or were unavailable in 1963, even for the child of the President of the United States. Since the development of surfactant, survival rates for premature babies with RDS have increased dramatically and these days, most babies with RDS survive. I join legions of parents in thanking my fellow Wheaton alumna, Dr. Mary Ellen Avery, for discovering and advancing the use of surfactants in newborns with RDS. I can hardly imagine how many babies her work has saved.
Henry all rigged up with UA line, pulse ox, IV, chest tube, endotracheal tube & vent, nasogastric tube and monitor leads. And a partridge in a pear tree.
Despite the chest tube and the full breathing support of the ventilator, Henry’s condition, already critical, continued to deteriorate on Tuesday, June 13. He was given his first dose of surfactant, but his episodes of desaturations continued and his now hourly chest x-rays were suggesting the beginning of another complication, pulmonary interstitial emphysema, and the possibility of two additional pneumothoraces (which I am pretty sure is the plural of pneumothorax. May you never need to know.).
His doctor, who had been managing Henry’s care since his arrival on the unit, came into our room, sat down and said words that are seared into my soul: “We are at the edge of what we can do for Henry here. He needs to be transported to a hospital that can offer the two remaining therapies available.”
It’s odd what you process about times like this. When his doctor inquired if we preferred New York or Boston as options for treatment for Henry, I remember thinking how thoughtful it was for him to ask which city we might like to go live in for a while, and I wondered exactly what criteria we should use to choose. And later, I remember making polite conversation with the EMTs as they waited for their precious cargo to be loaded into the mobile isolette and readied for his ambulance ride. I think I actually asked them about traffic.
But we didn’t have to choose after all, because their first choice, the acute-care NICU in our state, just an hour’s drive away, had a warmer ready for him. Henry’s doctor cautioned us that Yale-New Haven Children’s Hospital would be quite different from the intimate, 12-bed NICU at our local hospital, with constant access to the now-familiar medical team. But despite the sophisticated care he had been receiving, Henry needed a hospital offering a specialized high-frequency ventilator, called an oscillator, to allow his damaged lungs to heal. He needed the experience of a nursing staff used to caring for critically ill babies like Henry and there was the real possibility that he would need an invasive, last resort treatment for sick lungs: ECMO (extra corporeal membrane oxygenation), a heart-lung bypass treatment that takes over for diseased lungs so they can heal.
Preparing Henry for transport
A transport team arrived, comprised of a neonatal nurse, a neonatal fellow and two EMTs. I don’t know that they wanted us there as they did the delicate work of preparing him for transport, but no one asked us to leave, even while his monitors blared warnings of his increasingly unstable blood pressure and sats. Henry’s nurse put a comforting arm around me and handed me tissue after tissue as I wept, watching the tightly choreographed movements of the transport team.
40 hours of life—all plugged into his mobile isolette and ready to roll.
It took nearly an hour and a half to prepare his equipment and stabilize him enough to move him from the warmer to the mobile isolette—each time they were about to move him, his sats would plunge. My heart sank when he held a stable reading for about 60 seconds and his doctor said, “Go, go! Get him moving now!” I’m sure he never meant for me to hear the stark urgency in his voice, but the words are etched forever on my heart. I just kept thinking, like a mantra, they would TELL US if this baby is too sick to survive transport. They would TELL US.
Finally, after administering a paralytic medication to help him through the transport, they plugged him in and started to move. But before they left the unit the transport nurse said, “Wait! He needs a kiss from mom before he goes.” They aren’t big on kissing in the NICU (infection is one of the most deadly complications a preemie can face), so this encouragement was a gift. After a quick kiss, they closed the hatch, and rolled him towards his waiting ambulance.
(continued in Part 3)