Tom, the other doctor working in the emergency room, listens to the medical-control radio, then barks, "Proceed with rapid sequence intubation."
"How bad?" I ask.
"Sixteen-year-old, asthmaticus. And he's cyanotic."
"How far out?"
It's a common nightmare: A child wakes up suddenly. He feels as though he is drawing breath through a single, slowly collapsing straw. The muscles around his bronchi, the two slender airways that lead into the lungs, are tightening like boas. Frantically, the parents administer misted medication to force the muscles to slacken. But the boy collapses. They bustle him outside and wait for the ambulance. The paramedics find him turning blue on the front lawn. They slap on a high-flow oxygen mask and inject epinephrine—a potent bronchial muscle relaxer. It fails. Now the medics must pass a breathing tube down his throat or he'll be dead before he gets to the hospital.
Meanwhile, nature protects access to airways to the bitter end. Even as the brain winks out, jaw muscles clench, tongues writhe, and vocal cords spasm. To combat this resistance, the medics must sedate and paralyze the boy by giving specific drugs in rapid sequence. They establish an intravenous line and push the drugs, but they fail to thread the breathing tube down his throat. Desperate, they try to punch a hole in the boy's windpipe but somehow miss the best entry point—the cricothyroid membrane, which lies just below the Adam's apple. Close to losing him, they use an ambu-bag to pump oxygen through the mask held over his nose and mouth. By then his airways are so narrowed that only wisps of gas go in.
The radio in the emergency room crackles again. It's been twenty minutes since the first call. I pick up. A staticky voice: "Failed intubation. Request oxygen tank at ambulance bay."
"No. Don't stop at the entrance," I snap. Grabbing a laryngoscope and a breathing tube, I straddle the entry doors to the resuscitation room. Four medics charge in with the teenager. He is handsome, muscular, and dying.
Asthma kills 5,000 people a year in the United States.
"Over here," I say.
They throw him on a stretcher. I push the boy's teeth apart and slide in the curved laryngoscope blade. The breathing tube slides in beneath the droopy epiglottis. Home free, I think, pushing. But then it clicks—as if it has hit laryngeal cartilage and bounced away from the windpipe into the esophagus.
"Call Tom! Get a cric set!" I shout. Mark, a physician's assistant, dashes off to get the instruments for cutting a hole in the trachea.
"Wait. Look," the respiratory tech says. She releases the ambu-bag for exhalation. The transparent tube mists up. I listen to the stomach as she squeezes again: There is none of the gurgling that would signal entry into the esophagus. Over the chest the breath sounds are faint and choked by wheezing, but they're there. The pulse oximeter, which detects the light frequency of oxygen-saturated hemoglobin in the blood, slowly starts climbing. He is getting oxygen. Tom bursts into the room, loaded for bear.
"We're OK," I tell him. "Tube's in. Thanks."
One in 20 Americans has asthma. The roots of the epidemic remain tangled. Researchers debate whether it is aggravated by air pollution, dust mites, cigarette smoke, or new industrial allergens. Nor are there clear-cut genetic clues. The number of asthma-related deaths a year has increased about 50 percent since 1980, and the overall prevalence by 75 percent, but no one can explain why. The old way of thinking about asthma blamed overreaction of the muscles surrounding the airways. Newer evidence suggests that asthma has less to do with twitchy muscles than with the swelling that results from bronchial inflammation. As it happens, asthmatics' airways are packed with eosinophils—the quintessential allergic-response immune cells. Loaded with molecular bomblets, they served eons ago to knock off worms and other pathogens (a lot of intestinal parasites find their way into the lungs). In some people it doesn't seem to take much—a change of season, some specks of pollen, maybe a cold virus—to work these microscopic pit bulls into a froth.
Whatever the cause, the ultimate problem in asthma is getting air out, not in. The architecture of the lungs is the problem. You can push air in mechanically through intubation when patients grow too exhausted to inhale. But you can't mechanically help them exhale. And the danger is that if you force more air in than can seep out, pressure builds until blood return to the heart is blocked. The cure is pharmacological.
"Alice, epi zero-point-five IM, magnesium two grams IV, and Solumedrol 125 IV," I call across the room.
"Two of mag?" Alice asks.
"Yes," I affirm.
Magnesium is our secret weapon. Used for decades to suppress uterine contractions in premature labor, it has shown promise for relieving severe airway constriction. Epinephrine at 0.5 milligrams is a higher dose than the medics gave—and I will inject more if I have to. The Solumedrol, a steroid, is key to suppressing the inflammation, but it won't kick in for hours.
The hole in the boy's neck, luckily, is small and off to the side. I shine a light into his pupils. They shrink to pinpoints. At the very least, some of his brain lives.
Out in the hallway, the sight of me jolts the family.
"Doctor, oh, please! Help my son, Lord," the father cries. He squats, rocking on his heels, too terror-stricken to stand. The mother's tear-streaked face implores. But giving them false hope would be betrayal.
"He's stable," I say tentatively. "He's paralyzed and sedated, so it's impossible to tell how well his brain is doing. His oxygen level is holding. We really can't be sure at this point. . . . I think he has a good chance."
"Oh, God," an uncle shouts, "save this boy!" The father can only keen, "C'mon, c'mon, baby."
Sadly, their son is typical: African American children are 50 percent more likely than Caucasians to have asthma, and four times more likely to die from it. Asthma's caprice, however, knows no boundaries. I know of a doctor who died at home before she could reach the phone; the mother of a close friend succumbed while her husband rushed to a pharmacy.
For years, doctors have treated asthma with steroid drugs or epinephrinelike beta-agonists. Now there is a completely new class of drugs to draw upon: leukotriene modifiers. By blocking a key actor in the eosinophil arsenal, they seem to head off trouble before it starts.
The new eosinophil-inflammation model is compelling, but clinical medicine is unkind to models. Many asthma deaths stem not from days of inflammatory buildup but from so-called sudden asphyxic asthma, which, as in this teenager's case, can shut the lungs down within hours. The immune response is different: neutrophils—bacteria-fighting immune cells—greatly outnumber eosinophils.
The results of the boy's arterial blood gas analysis show that his oxygen level is good, but the carbon dioxide level is sky-high, indicating that he had been failing to exhale fully. I listen again to his chest. His breath sounds seem louder now—hisses, not tight squeaks.
"How about another gram of mag and another epi," I tell Alice.
"More mag?" she asks skeptically.
"I think it's working."
She draws up the magnesium.
The respiratory tech rechecks the ventilator: 10 breaths a minute, low volume per breath. The lung pressures, to my relief, are not climbing. Bronchodilator mists are running down the breathing tube. The paralytics should be wearing off. But the boy is still inert. Alice brings the parents to the bedside.
"Hey, it's your dad. I'm here, boy," the father says. The mother, her eyes brimming, beholds her son, a plastic tube looping out of his mouth.
Forty-five minutes later, Alice calls me over with a question. "He's trying to pull the tube out. Can we sedate him?" She is smiling.
"You bet," I tell her and then go in and give the family a big thumbs-up.
Next morning, our patient wakes up and yanks out the breathing tube. He remembers nothing of the night before. But he remembers everything else that matters.