A monitor in the intensive care unit at Cook County Hospital in Chicago continuously beeped and flashed alarms as the young woman's pulse rose above 140 beats per minute and her blood pressure fell. Her skin was ashen and clammy, her muscles slack, her lips cracked, her eyes rolled up under limp lids. It was clear she was dying. What wasn't clear was whether she could withstand the extreme measures required to save her.
The patient was in her late twenties and had begun experiencing severe pelvic pain following her last menstrual period two weeks before. By the time her mother brought her to the emergency room, she couldn't stand up straight because of swelling from an anaerobic bacterial infection in her belly. A DNA probe identified the original infection as Neisseria gonorrhoeae, which attaches to cells in the reproductive tract that nourish sperm. Although cervical mucus contains antibacterial compounds, menstrual blood can wash the mucus out, making it easier for Neisseria and other microbes to migrate up the reproductive tract and into the fallopian tubes. Her gynecologists put her on intravenous antibiotics and waited for her to heal. Instead, after four days, her infection had only grown worse.
A century ago, pelvic infections from gonorrhea were a major source of disability and one of the causes of the "female complaint" many patent medicines were marketed to relieve. In that preantibiotic era, many women suffered from lingering infections that could sometimes kill. Even today, about 150 women in the United States die each year from complications of pelvic inflammatory disease. This patient was about to become one of them.
As gonococcal bacteria multiply in the fallopian tubes, components in the bacterial cell walls rouse the immune system defenses. Antibodies bind to the cells, marking them for engulfment and destruction by white blood cells. Substances in the blood called complement proteins punch lethal holes in the bacteria. There is also a structural barrier: Loops of bowel and a membrane called the omentum stick together, shielding the abdominal cavity from bacterial infiltration.
But in a few cases, bacteria get through. The fallopian tubes fill with pus, an acidic soup of toxic enzymes and exhausted immune cells. As the pus collects, the body walls it off in a capsule formed of a blood component called fibrin. That pocket, or abscess, contains the infection. An abscess lacks blood vessels, so white blood cells, substances secreted by immune cells, and antibiotics have difficulty reaching the infection.
The body tries to make up for the lack of blood flow: Small blood vessels grow leaky to permit immune defenses to seep out into infected tissue. But the leakiness also allows bacterial products into the bloodstream, which can further ignite an inflammatory response. Eventually, the body cannot keep the arteries filled, and blood pressure falls. Heart function falters. Deprived of blood flow, the major organs fail, and the patient dies.
The only cure is to operate—drain the pus and remove the dead tissue. But inducing anesthesia in a critically ill patient is risky. The drugs that bring on sleep can depress the function of an already compromised heart, and anesthesia-induced paralysis curtails the function of the lungs. And if the clotting factors in the blood have been used up, the patient can bleed to death. So doctors often put off surgery until the crisis is unmistakable: The abdomen is rigid, the fever uncontrollable, the patient delirious and writhing in pain.
I am a gynecologic surgeon, and when this young woman was clearly in crisis, her doctors called me. The staff loaded her with enough fresh-frozen plasma to replace lost clotting factors. Then, after we moved to the surgical theater and the anesthesiologist completed the sedation, I quickly made an incision from navel to pubic bone. The pus spilled out. We suctioned the abdominal cavity and looked for the source of the infection.
The wall of one fallopian tube was dead, ruptured, the yellow-brown pus escaping under pressure through a red-black hole. The other tube, scarlet from inflammation instead of a healthy pink, was minimally involved. We removed the damaged fallopian tube. Then we cut the abscess away from the places where its fibrin walls clung to the fallopian tubes, to the colon and small bowel, to arteries and veins, and to the uterus. More pockets of pus lay hidden in the cavity between the cervix and the rectum, in the trough along the descending colon, and under the ovary.
We broke the pockets of pus open and cleaned the area. A generation ago, it was the custom to remove the uterus once an infection had advanced into the fallopian tubes. Now newer intravenous antibiotics can sterilize moderate infections after the abscess is drained. Finally, we peeled the remaining walls of the abscesses away from the peritoneum, the membrane that lines the abdomen and pelvis. It was like removing the rind from an orange. We sent samples to the lab to make sure the infecting microbes were sensitive to the antibiotic treatment. We checked for bleeding, washed the abdominal cavity with warm saline solution, and closed the incision.
The day after the operation was touch and go. The patient needed a tremendous amount of fluid to keep her kidneys, brain, and heart working. She required blood transfusions to deliver oxygen to these organs and to the site of the infection. She lay sedated on a ventilator in the intensive care unit all that day and all the next, and then she rallied. Her blood pressure and urine output rose, her pulse fell to normal, and her fever began to subside. The staff tapered her off sedatives, and she woke up. After a terrible vigil in a tiny waiting room, her mother went home. After a week, the young woman followed.
Each year about a million American women are treated for pelvic inflammatory disease, and sexually transmitted infections are usually the cause. The longer the infection remains untreated, the greater the risk of infertility. This patient's infection had advanced, and only time will tell whether she will be able to conceive. If scar tissue does not obstruct her unaffected fallopian tube, she might one day have children.
Stewart Massad is an associate professor of gynecology and obstetrics at the Southern Illinois University School of Medicine in Springfield.
