We get a call for a girl having a “sickle cell crisis” in the projects on Osborn Street, in the East New York section of Brooklyn.

My partner Bronson’s brow wrinkles as he scans the computer screen mounted between our seats for more information. “I have no idea what to do for that,” he says, and turns on the lights and sirens.

“That’s why you’ve got me,” I say. I’ve dealt with a sickle cell patient before, and Bronson hasn’t, so I let him know there’s really not much we can do except give her oxygen and transport. Apparently, according to the 911 dispatcher, the girl came home from school about an hour ago in severe pain. Her mother called the pediatrician, who said to get her to the ER pronto.

We get to the apartment, up two flights of dimly lit, filthy cement stairs, to find a 16-year-old girl whimpering on the couch, her body quivering in spasms of pain. Her mother, hovering protectively over her, tells us her name is Charlotte.

“Charlotte,” I say, “how long ago did this start?”

She gasps through the pain. “An hour ago. In gym class.”

We get Charlotte into the wheeled stair-chair as quickly as we can, bump her down the steps, and hoist her into the ambulance. She’s small for her age, a common side effect in those with sickle cell disease. We lay her on the stretcher and give her oxygen.

Sickle cell disease, a recessive genetic disorder affecting about 72,000 Americans of African and Hispanic descent, is caused by an abnormality in the red blood cells. Malfunctioning hemoglobin causes the cells to take on a C, or sickle, shape in times of stress, flu, or infection. Normal red blood cells are soft, round, and doughnut shaped. They glide through small blood vessels easily. Sickle cells are hard, pointed, and “sticky.” They jam up and get stuck in the vessels, blocking the flow of blood (and vital oxygen) to tissues and organs, causing damage and the accompanying severe pain associated with a sickle cell crisis.

Since sickle-shaped cells live for only 10 to 12 days, as opposed to the 120-day life cycle of a normal red blood cell, the most common effect of the disease is anemia, characterized by pale skin, fatigue, and a wasted appearance. Our girl on the stretcher looks like she’s 12, rather than 16.

The disease is considered a recessive genetic disorder since the trait is needed from both parents to cause the actual disease. If both parents carry the gene, chances are 1 in 4 that the child will have normal hemoglobin, 2 in 4 that he will carry the sickle cell trait (be “a carrier”), and 1 in 4 that he will have active sickle cell disease. Oddly, the sickle cell trait seems to offer protection against the mosquito-borne malaria parasite, which could explain why people of African and South American descent carry the gene. A simple inexpensive blood test can determine the presence of the disease or the trait in newborns, and parents can opt for the test to be performed along with other routine newborn-screening tests. Couples wishing to have children can also undergo screening to determine whether they are carriers.

Although a sickle cell crisis presents with severe musculoskeletal pain, abdominal pain, and pulmonary problems, sickle cell crises are usually self-limiting, meaning they pass on their own, either in hours, days, or weeks. But until they do, the patient suffers, and tissue damage can lead to chronic pain conditions in the future. If brain tissues are deprived of oxygen, a stroke can result. I make sure the oxygen is flowing well to Charlotte’s mask, then take out my paperwork and a pen and ask Charlotte’s mother, “What does she take for the pain?”

Her mother wipes away a tear. She’s been dealing with this since Charlotte was born, and parents of sickle cell children often feel guilty for imparting such a painful disease to their kids.

“Motrin,” she says, “then Tylenol-with-codeine, then morphine pills if it gets too bad. But she doesn’t like taking those.”

This discrepancy is one we see every day. There’s 10 guys on Charlotte’s street corner who would commit crimes for those morphine pills. But this young, beautiful girl, who should be full of energy and life, resists taking drugs that zombify her for the pain of a disease with no cure. Most patients would gladly throw away their pain-relief medicines, if only they could also throw away their pain.

“When was the last time she was hospitalized?” I ask.

Charlotte’s mother thinks back. “September 8,” she says. “But her last crisis was mid-October. That one we handled with the Tylenol. It passed in about three days.”

A sickle cell cure lies in either bone-marrow transplant or stem-cell transplant from the cord blood of infant donors. In both, a successful transplant means the patient’s blood-making factory is completely replaced with healthy donor cells. In the less radical “mixed-blood partial chimerism” transplant, resulting in half a patient’s cells being healthy and half sickled, the painful crises are also virtually eliminated. Eighty-five percent of all transplant patients live symptom-free. Though bone-marrow transplants are no longer experimental, the 15% risk of marrow rejection, with fatal consequences, means such transplants are rarely performed. Few parents are willing to take the risk. A child’s disease must be critical, and even then, only 7% of patients meet the criteria necessary for transplant. Cord blood stem-cell transplants, which are less risky and can come from unrelated donors, seem to be the best hope for the future.

Less invasive treatments for sickle cell disease include lifelong monthly blood transfusions to increase the number of red blood cells in a person’s circulation, using penicillin as a prophylactic against the minor infections that can bring on a crisis, and administration of the cancer drug hydroxyurea, which reduces the frequency of painful crises. Although it’s impossible to prevent all crises from arising in the first place, good health maintenance and regular doctor’s visits are vital in preventing at least some of them.

I ask Charlotte’s mother what treatments her daughter undergoes. She says none.

“I’m thinking we’ll do the transfusions, but it seems like such a big procedure.” She sighs. “I just don’t know.”

I tell her to talk to the doctor about treatment options, and to see whether Charlotte is a good candidate for any of them.

We arrive at the hospital. I tuck a portable oxygen tank beside Charlotte’s legs and hook her up to it, so that her supply won’t be interrupted as we wheel her into the ER. Her legs are twitching in spasms, and she’s crying, but trying to hold it in. An hour ago she was in school. Now she’s on her way to the hospital. Again.

Ms. Klopsis is an emergency medical technician for the FDNY. This column details her observations and experiences on the job. Some names and identifying details have been changed to protect the privacy of patients.