It appears that the H1N1 influenza’s debut in Minnesota may be winding down. Depending on one’s experience, the H1N1 pandemic might feel like the war in Afghanistan — a distant battle played out on television. To some, it’s just more media fear-mongering.
Standing at the bedside of a patient critically ill with the H1N1 virus can change all that. A few weeks ago I took care of a nearly middle-aged adult who’d been quite healthy prior to becoming infected with the pandemic virus. He had none of the established risk factors for a bad case of H1N1: pregnancy, obesity, asthma, a chronic medical condition, etc.
As his spouse described it, he’s the kind of person who had always seemed impervious to even the common cold. But not so with H1N1. The web of tubing, IV lines, and monitor wires strung across the patient and his bed could tell the most uninformed bystander that H1N1 appeared to be winning.
By the time I began caring for him, the patient’s breathing had deteriorated to the point where he needed the assistance of a ventilator machine and supplementation with very high levels of oxygen. In the tiny airspaces of a normal lung, oxygen quickly diffuses from inhaled air into the blood stream. In a lung congested with debris of a viral war (consider your nose two days into a cold — red-hot and plugged), blood oxygen levels fall. That’s because either some of the small tubes (bronchioles) of the lungs are too plugged to get air to the air sacs (alveoli), or because the air that does get to the alveoli is met by an impenetrable wall of mucus.
For this patient, a week or more into the infection, the battle just raged on — despite Tamiflu and aggressive supportive care that included an array of antibiotics aimed at killing off the bacterial infections that can arise in an H1N1-weakened body. His fever remained high, and he was requiring almost 100 percent oxygen (normal air concentrations of oxygen being 21 percent) just to keep his blood oxygen levels in the acceptable range. ICU and lung specialists were busy tweaking the myriad settings on the ventilator machine, trying to find a winning combination that would allow for a weaning down of the inhaled oxygen concentrations. Paradoxically, the high levels of oxygen that patients sometimes require are themselves caustic and injurious to the lung, so time is of the essence.
‘The kind of patient that follows you home’
For health-care providers, this is the kind of patient that follows you home. On a chilly Halloween night, I was wearing a Darth Vader mask and chaperoning my kids around the neighborhood — but I was thinking about this patient and how we were ventilating him. This is the kind of case that makes you nervous and angst-filled; it involves repeated review of all the details of care, asking, “Are we missing anything?” and “What more can be done?”
There were, in this case, a few more things that could be done. One was spurred on by the spouse, who, on an evening where the situation looked particularly dark, handed me a copy of a New York Times article. The Centers for Disease Control and Prevention (CDC) had just released a drug called peramivir for experimental use in patients just like this, those who were seriously ill despite treatment with standard anti-viral drugs. This patient had been getting the now-familiar Tamiflu through a feeding tube, but one can never be certain how well a drug is absorbed through the GI system of a very sick patient. Peramivir is essentially an intravenous form of Tamiflu, so once it’s infused, there’s no doubt as to how much of the drug the patient is absorbing. Early studies suggested peramivir would be safe, but it hadn’t been used in enough patients to know that for sure.
I, along with a colleague specializing in infectious diseases, grabbed a computer and read through the details of the CDC’s peramivir website. Our patient definitely qualified. We clicked through a series of questions, verifying that we understood the drug; the family understood the drug; and that we promised to report any side effects or problems. I provided our hospital’s contact information, hit the “send” button, and got a confirmation number.
Requests at rate of one per minute
In a matter of minutes, our hospital’s pharmacy heard from the CDC, which reported fielding requests for peramivir at the rate of one per minute. Our allotment would arrive at 10:30 the following morning. As all of this transpired, the patient’s blood pressure dipped, his heart rate went up and he became more unstable. 10:30 a.m. was just 16 hours away, but it felt longer than that for all of us, particularly his family.
The patient stabilized overnight, which is to say he returned to his critically ill baseline. The peramivir arrived right on schedule. We infused it. I felt that I should have been at the bedside to witness the infusion, seeing as I’ve never ordered an “experimental use only” drug. But the hospital was busy and I had other responsibilities.
As it happened, a front-page article in that day’s edition of the Star Tribune chronicled a 17-year-old patient who had been deathly ill with H1N1 in early September. Though peramivir hadn’t been released for experimental use at that time, the care team managed to get access to the drug, and the teen recovered. The article flatly claimed the unknowable as a certainty — peramivir had “saved his life.” The family read it, and I read it too. I cautioned them about seeing it as a miracle drug, though for the patient’s sake and for all of us, a miracle would be just fine.
Nothing really changed much, not that day or the next. How long does it take for a miracle drug, or any drug, to work? No one knows. We knew we had infused it, and that it was in his bloodstream. If the persistent fever was from actively replicating virus, something ought to have changed. But it hadn’t, yet.
The question of steroids
A conversation began about adding steroids to his medication regimen. Not the Barry Bonds kind of muscle-building steroids, but the kind of steroids that are potent inhibitors of the immune system. Why in the world would we want to give anyone who is fighting an infection a drug that would suppress his or her immune system? The explanation is complicated, but the answer is simple: Sometimes it appears that it’s our own overzealous immune response that ends up making us so sick. The term that’s used to describe the phenomenon is “cytokine storm.” It’s a Caddy Shack immune response, the dynamiting of the entire golf course to try to rid ourselves of a few pesky gophers. It makes for interesting cinema, but it can have a horrific effect on the golf course. Or the human body.
The use of steroids in patients who’ve become critically ill from an infection remains an area of debate in the medical literature, which is to say no one knows for sure. Because of our patient’s persistent fever, and because a lab test showed the patient’s own stress-related steroid level to be inappropriately low, we added steroids to his regimen and waited.
About four hours after his first dose of steroids, the patient’s fever broke, and we were finally able to begin weaning down the concentration of oxygen that the ventilator was delivering to him. The patient seemed to be coming out of his dark hole. Was it the peramivir finally kicking in? Was it the steroids? Was it both? Neither? The scientist in me really wanted to know, but personally I didn’t really care what turned things around: The patient was better. The family, of course, didn’t care either. Their loved one seemed to be tearing loose from the clutches of H1N1.
Sometimes we let our individual experiences bias our perceptions too much. A bad swimming episode as a child and we never go back into the water. The H1N1 virus is no more lethal, no more virulent, than it was a few weeks ago, before I took care of this patient. But it’s whole lot more real to me now.