The patient’s sister pointed to the form lying on the stretcher. “It’s pouring out of him, doctor.” Then she lifted the sheet. “We even had to put these on.”
The young man, looking gaunt and miserable, reflexively pulled up his knees for cover. But there they were, diapers as puffy as pantaloons. I stared, trying to remember if I’d ever seen Pampers on a 22-year-old.
“How often?” I asked.
“All the time,” the sister said. “It never stops.”
I restudied the chart: His blood pressure was normal at 120/76. He didn’t have a fever, but his heart rate was 150. His lips were cracked, his eyes sunken, his skin shriveled—this patient was as dry as the Mojave.
“When did it start?” I asked.
“Two days ago, doctor,” the patient rasped.
“Have you traveled?”
“Anybody else sick at home? Any pets?”
“Have you had pain?”
I felt his belly. No hot spot of tenderness—just soreness all over. “And which came first?” I continued. “The vomiting or the cramping?”
He pulled the sheet a little higher. “The vomiting. Then the water coming out.” He winced. “Then so much pain.”
The diagnostic beads clacked together: vomiting first (appendicitis usually causes pain first) plus soft belly plus lots of diarrhea plus no fever. The answer: gastroenteritis (gastro = stomach, enter = intestine, itis = inflammation, a doctor’s job being, of course, to tell you in Latin what you just told him in English).
The emergency room nurse asked if I wanted to get more blood tests.
I was about to decline—the average stomach flu rarely throws an otherwise healthy young man’s electrolytes out of whack. But then I remembered his 150 heart rate. And the Pampers. “Sure. Thanks,” I said.
Gastroenteritis, stomach flu, food poisoning. Few maladies beget more misery, put the kibosh on more vacations, or make the food industry jump through more hoops than intestinal infections. In ascending order of size, the culprits include viruses, bacteria, and protozoa. A viral infection, for instance, set off cruise ship outbreaks in 2002; in 1993 a protozoan that spread through the water filtration system sickened 400,000 people in Milwaukee—almost two-thirds of the city’s population.
Bacteria, for their part, can provoke loss of lunch or loosening of bowel from the toxins they produce or by direct invasion or both. Staphylococcus, for example, is almost ubiquitous on people’s skin. Spread onto food at room temperature, one strain of the bacterium, Staphylococcusaureus, can multiply and secrete a heat-resistant, vomiting-inducing toxin. Other pathogens, such as cholera-causing Vibrio cholerae and Escherichia coli, must first get into the intestine before they can do their damage. Once in the gut, V. cholerae secretes a toxin that provokes the human intestine to shed up to one liter of fluid per hour, thus facilitating the pathogen’s spread to other hosts. The invasive E. coli takes a different tack: It attaches to cells in the intestine, then secretes a toxin that provokes cramping and diarrhea. The immune response to the infection provokes a bacteria-killing fever. One sign of the widespread inflammatory response is white blood cells in the stool.
Areas with poor water sanitation—mostly in the developing world—are at greatest risk for these bacterial infections. But the United States is hardly exempt: The Salmonella family alone—proud sponsor of over 2,400 disease-producing strains—is estimated to have caused 2 million cases of bacterial gastroenteritis last year. Although the infection rarely progresses very far, it can be lethal in those with compromised immunity: the very young, the old, or the debilitated.
Two hours later, the young man’s lab results surprised me—and renewed my respect for these germs. His white blood cell count was normal, but the level of urea nitrogen, a measure of dehydration, was sky-high. Even more worrisome, the creatinine level—a measure of kidney function—was twice as high as it should have been.
“Wow, he’s even drier than I thought,” I said to the nurse.
“On his third liter,” she replied. “That should be helping. But I just retook his temp. It’s 101.8.”
“I don’t have the white-cell stool smear back yet,” I said. “But he’s sick enough to deserve antibiotics. This must be an invasive enteritis.”
“What do you want?”
“Cipro, 500 milligrams.” Ciprofloxacin acts against a broad spectrum of bacteria.
When I went in to check on the patient, his heart rate was down to 105, but he still looked like a rag doll.
“I have no energy, doctor.”
I pointed to the IV bag. “This will help you.” His sister joined me at his bedside. “He needs to be admitted,” I told her. “We’re going to keep up the fluids and start some antibiotics.”
She caressed her brother’s forehead. “He has been so sick.”
The most likely culprit was Salmonella, which prospers in the conditions of modern food processing. Most other bacteria that cause foodborne illnesses stick to a preferred niche: lesser-known Campylobacter is common in chickens, and Aeromonas often crops up in milk; Shigella trots around via the water supply or dirty toilets; Yersinia enterocolitica prefers pigs; Vibrio parahaemolyticus infests uncooked shellfish, especially oysters. Salmonella, on the other hand, is promiscuous. It inhabits chickens, ducks, turkeys, dogs, and unpasteurized milk; turtles, iguanas, and even rattlesnake meat have caused outbreaks. By some estimates, 80 percent of Salmonella infections come from raw or undercooked eggs. Chickens not only spread it to each other but also contract it from inexhaustible reservoirs of rodent feces and farm waste. In 1994 one outbreak of 224,000 cases was tied to an ice-cream mix hauled in a container truck whose previous cargo had been unpasteurized eggs.
The good news is that thorough cooking (no runny yolks) destroys Salmonella, and continuous refrigeration thwarts it. The bad news: You can’t cook your dog. Moreover, the overuse of antibiotics on farms, along with injudicious use of prescription antibiotics among people, leads to more and more drug-resistant bacteria.
Using antibiotics against Salmonella is tricky because drugs can prolong bacterial shedding from the GI tract and increase the chance of spreading the infection. A mild infection can be left to run its course, but severe cases must be treated. The difficulty is that stool cultures can take 48 hours or more to confirm the diagnosis, leading to unhappy shoot-first, answer-questions-later situations.
After two hours, the nurse grabbed me. “His belly pain is worse.”
I walked over. The patient was clutching his middle. “Where does it hurt?”
“Here,” he groaned, waving a hand across his lower abdomen.
I pressed all around. He seemed most tender on the right: Appendicitis. “I’ve been sitting on an appie,” I muttered to the nurse. “He needs a CT scan.”
This curveball shouldn’t have surprised me. Some invasive bacteria, like Y. enterocolitica, mimic appendicitis so perfectly that outbreaks come to light only after doctors notice a spate of negative appendectomies. And more than 100 years ago, physician William Osler singled out typhoid fever—caused by Salmonella typhi—as one of the most protean and deceptive of diseases; before his students could call themselves doctors, he made them master its diagnosis.
The CT scan would take a while—an hour for the patient to drink the oral contrast, well over an hour for it to percolate down, and a half hour for the scan.
A seeming eternity later, the radiologist called: “Intussusception.”
“You’re kidding,” I blurted out, then kicked myself for the hours I’d wasted. Intussusception can be a surgical emergency; it meant that one part of the patient’s intestine had telescoped into another.
The surgical resident on the case was equally surprised. “No way,” he said, after examining the patient. “I’m going to talk to the radiologist.”
Twenty minutes later he was back with a revised diagnosis. “Colitis,” he declared. “Actually, pancolitis. Inflammation all over the colon. You really have to stare at the scan.”
Later that evening, the stool smear result came back: “sheets of white cells seen.” Although white blood cells can be a sign of a noninfectious condition such as ulcerative colitis, they were more likely a sign of widespread infection.
When I saw the patient two days later, he looked much better. I ran into the surgical resident in the hallway. “Looks like the stool culture is growing Salmonella,” he said. “Still don’t know the strain.”
“No pets, no travel, no turtles,” I pointed out. “Where did it come from?”
“Beats me,” he said. “But I did tell him, ‘Wash your hands, keep food in the fridge, and make sure you really fry those eggs.’ ”
Tony Dajer is assistant director of the emergency medicine department at New York University Downtown Hospital in Manhattan. The cases described in Vital Signs are true stories, but the authors have changed some details about the patients to protect their privacy.