A stroke of luck – Vital Signs
Heat was cutting through Manhattan like a scythe. Dehydrated and demented, our patients came in as limp as candles left in the sun. Sweltering ambulance crews gently laid them on stretchers, paused for a caress of air-conditioning, then marched out for more. Nurses could predict patients’ thermometer readings by the heat rising, as from embers, off the bodies. The week’s record stood at 108. The patient had not survived. That memory drove us again and again to jump into action. We prepared intravenous lines and liters of fluids, inserted catheters to monitor kidney function, and bathed the feverish bodies with ice water. * “Dr. Dajer, over here!” * I hurried to the farthest cubicle. On the stretcher lay a thin young Asian man, absolutely inert.
Deirdre, a nurse who had recently begun premed studies, stood by the bedside. She had already stripped the patient and inserted a rectal thermometer.
“Another heatstroke?” I asked as I helped her hold our patient steady on his side. The assault on his private parts generated not a twitch of response.
“Yes. The medics found him in a ratty walk-up apartment with all the windows closed,” she said. “Told me it was the hottest place they’d been in all week.”
While we waited for the thermometer to confirm the obvious, Deirdre flicked her head at me.
“What do you think of his chest? Looks like he walked into a baseball bat.”
Gently, I rolled the patient back a bit. Sure enough, faint blue and green splotches, oddly reminiscent of the hues in Monet’s Water Lilies, lay across his lower right chest.
“Can anyone tell us what happened?”
“Nobody,” Deirdre answered. “The medics don’t even know who called 911. I’m afraid you’re on your own.”
I gingerly probed along our patient’s rib cage. “Ribs are intact. Old bruising. Maybe five or six days old. I wonder if he fell off a chair when the heat finally got to him.”
Deirdre pursed her lips. “The medics found him in bed.”
“Well, maybe he got himself into bed after he fell, then passed out for good.”
Deirdre looked unconvinced. But then the temperature probe beeped.
“Look at this,” she said. The digital gray numbers flashed 100.2.
“Only 100.2? You can’t have heatstroke with a temp of 100.2,” I said. “Is your thermometer working?”
“Yes. Feel him – he’s not that hot.” I pressed both hands against his back.
“You’re right,” I admitted. “He’s not.”
“So now what?” I looked down at the young man. “Now what? Well, we have a comatose patient – with no history and, for the moment, not a clue as to what’s going on. First let’s get him into a monitored bed. Then start an IV line and round up the usual lab tests.”
We wheeled our mystery patient over to a bay equipped with a monitor that records heart rhythm, blood pressure, and breathing. After taking a minute or so to connect all the wires, Deirdre stood up and said, “Here’s another piece of bad news. His blood pressure’s 75 over 50 – pretty low even for a skinny young guy.”
“Why don’t you give him fluids? Saline. Wide open.”
She nodded and turned away.
Mr. X’s physical exam, except for the chest bruising, was completely normal. His head showed no signs of trauma, his eyes reacted to light, and he flinched when I pressed deeply into the nail beds of his fingers and toes. These were all signs that his brain was intact. But something – and there were dozens of potential culprits – was keeping it from waking up. As for diagnostic clues, we would have nothing more until our lab results came back in a few hours.
I stopped for a moment at the foot of the stretcher. Deirdre was inserting another IV line. I watched Mr. X’s chest move up and down. The breathing came fast. Fast and deep. A hunch took shape.
“Deirdre, how about a finger-stick glucose?”
“Coming right up.”
She pricked a finger, placed a drop of blood on the glucose reagent strip, wiped the strip clean, then inserted it into the reader. Her face lit up.
“Over 500. Sky-high. Good call.”
Normal glucose levels range from 110 to 140, depending on when the person last ate. The combination of extremely high glucose, deep rapid breathing, and coma pointed to one diagnosis: diabetic ketoacidosis, or DKA.
Instantly we went from crawling in the dark to sprinting in sunshine.
DKA is what used to kill young diabetics before 1926, the year insulin was first purified. Seventy years later we have unraveled the complex relationship between insulin and sugar metabolism. Now, with the availability of intravenous fluids and synthetic insulin, treatment of DKA is swift, sure, and very gratifying.
Diabetes mellitus comes in two forms, and the form that tends to afflict young people can be much more deadly than the other. Young diabetics usually can’t make insulin, the hormone we depend on for food metabolism; those who get the disease in middle age often can’t properly use the insulin they make. In young diabetics, the lack of insulin can turn a normal metabolic process into a devastating molecular stampede. If I was right, that was what had put Mr. X in a coma.
Humans must bum glucose – or simple sugar – for fuel, and we rely on two hormones, insulin and glucagon, to keep blood glucose levels from becoming dangerously high or low. After a meal, when blood glucose levels are high, clumps of cells in the pancreas – called islets of Langerhans – release insulin to bring glucose levels down. Insulin helps the body’s cells soak up more glucose from the blood; it also prompts the liver to convert glucose into glycogen, a form of glucose that can be temporarily stored in the liver. But when blood glucose levels are low, the islet cells in the pancreas release glucagon, which spurs the liver to break down its glycogen stores and release glucose into the blood.
If we don’t eat for 24 hours, however, our supply of glycogen runs low and the body begins breaking down fat to get glucose. But there is a problem with burning fat: it must first be broken down into smaller units called ketone bodies, which are weak acids. If too many ketone bodies are released, the blood becomes too acidic, upsetting the delicate chemical balance that cells need to function.
Insulin is what keeps ketone production under control. The islet cells in the pancreas that secrete insulin to regulate high blood glucose also keep a tight rein on ketones in the blood. When the ketone level in the blood climbs dangerously high, these cells secrete just enough insulin to keep ketone production at a safe level.
In young insulin-dependent diabetics, however, a self-destructive immune reaction has destroyed these insulin-secreting cells. Eliminate insulin and not only do glucose levels rocket up but the ketone “factory” goes berserk and rapidly acidifies the blood. The body desperately tries to shift the balance back. The lungs speed up breathing to shed carbon dioxide, which will reduce acidity in the blood. The kidneys, burdened with abnormally high levels of glucose and ketone bodies, filter the excess into the urine. The body pays a price for the spillover, though, in the loss of enormous amounts of water. The combination of dehydration and acidosis leads to coma and ultimately death.
A test of Mr. X’s arterial blood confirmed our suspicion of profound acidosis. I had no idea where Mr. X was from originally, but given where he was found (in Chinatown, which is right next to the hospital) and the absence of relatives, I could guess he was a recent arrival from China. Whatever had brought him to his dreary, dream-denying tenement in Manhattan, he had at last reached a safe harbor. We would beat death back with scientific exactness.
“Deirdre, how about 10 units of insulin IV now, then 7 in the saline bag over the next hour. And let’s crank up those fluids, starting with half a liter.”
Forty-five minutes later, Mr. X woke up. His real name, he told the interpreter, was Mr. Chen. He had never been diagnosed with diabetes, and the last thing he remembered was lying down for a nap. Yes, it had been hot, but he had felt more tired than thirsty. The bruises? He passed a hand over his chest and winced. Some people had hit him four days ago. What people? Silence. I looked up at Deirdre.
“You mean what are the odds a young man found alone and beaten up in Chinatown is here illegally? “
“He probably thinks we’re going to turn him in.”
Gaunt and wary, Mr. Chen’s face betrayed only physical pain. If he feared deportation after his long journey, he showed no sign.
“No more questions for now. You call the admitting office and I’ll get the residents down. He needs to stay in intensive care at least overnight.”
Sophia, the unit resident, called right back.
“Good case for you,” I announced. “Young Chinese man with DKA. Came in comatose, but he’s talking now. At first we thought it was heatstroke. But his temp was only 100.2. On a hunch we got a finger-stick glucose. It was really high – over 500. Blood pressure’s still a bit low, but we’re bringing that up with fluids. The labs are still cooking. Completely straightforward.”
“Sounds good. I’ll be right down.”
Good call, good case. For the first time in probably a long while, Mr. Chen was safe.
I went back to my other patients.
An hour later I checked in on Mr. Chen.
“You know, his pressure’s only up to 85 systolic,” Sophia said.
“Well, he was pretty dry when he came in, you know.”
“And did you see his hematocrit? Only 26. And what about that bruising over his chest?”
Blood has two components: A watery fluid called plasma and the blood cells it transports. The hematocrit measures the fraction of the blood that is solely blood cells, and a healthy young man’s is usually about 40 to 45 percent. I had figured that Mr. Chen’s hematocrit was low because he suffered from chronic anemia, a condition common among many recent immigrants from China. But when a patient is suffering from DKA and dehydration, the hematocrit (or blood cell count) should increase because the other portion of the blood – the plasma, which contains water – has decreased. So Mr. Chen’s real number of blood cells was probably far below what the already low hematocrit suggested. If he wasn’t chronically anemic, then he had recently lost at least one-third of his blood cells. But how? And where?
“And did you feel his belly?” Sophia persisted.
“Well, yes, when he came in,” I muttered as a whole new set of alarm bells started going off in my head.
“Right. Now he’s awake, and when I press on it, especially over the liver, he moans.”
“Well, DKA can cause intense abdominal pain,” I said, backpedaling.
I pressed my hand into the upper right part of Mr. Chen’s abdomen. He winced and tried to push my hand away.
I started thinking out loud. “But he says he got beaten up four days ago. Are you trying to tell me that on top of his DKA he’s also bleeding into the abdomen from an injury four days ago, even though ruptured livers aren’t supposed to survive anywhere near that long?”
I glanced at Deirdre. “I think that’s what she’s trying to tell you,” she said, pressing her lips together.
The clock on the wall told me it had been two and a half hours since Mr. Chen had come in. If Sophia’s theory of abdominal bleeding was correct, Mr. Chen was two hours overdue in the operating room.
Deirdre followed my gaze. “Should I page the surgeons?”
I felt a sudden need to kick myself. Of course, the first question the surgeons asked after they’d examined Mr. Chen was “Why has he been down in the emergency room so long? Looks like blood in that belly.”
The surgeon nodded sympathetically. He and I had collaborated on many cases before. “Heck, he’ll be in the OR in ten minutes.” He patted me on the shoulder. “Besides, if you hadn’t gotten his brain working again so fast, he couldn’t have told us about the belly pain, and then where would we be, right? “
“Right,” I agreed, not enthusiastically.
Three hours later the surgeon came back down.
“Boy, this guy was full of surprises. Remember how the pain was on the right? And we were figuring ruptured liver? Well, it was his spleen that was a mess. So he should’ve hurt on the left, not the right. Not only that, but we found old clot plus active bleeding. He must have opened up an old injury today, starting up bleeding that had stopped a few days ago. I’ve never seen a patient do that before.” He paused and smiled. “Best of all, though, is that we patched his spleen and he’ll be just fine.”
Deirdre plopped down next to me.
“So how do you put it all together?”
How indeed do you reconstruct a collision between man-made and molecular violence?
“It sounds crazy, but tell me if this makes sense,” I began. “He gets beaten up and starts bleeding from a ruptured spleen. Then it’s hot, and he’s dehydrated and too weak to get help. Maybe he’s had borderline diabetes before, but now he can’t drink to replace the water he’s losing. That’s when the sugar and ketones rocket up, and he goes into a coma.”
Deirdre jumped in. “And because of the dehydration, his blood volume drops, so there’s less pumping force in the blood vessels. So his blood pressure bottoms out.”
“Right, and that puts him into something like suspended animation. The bleeding stops, and a clot forms.”
“Then when we tank him up with fluids,” adds Deirdre, “we push up the pressure, and his nicely clotted off spleen opens up all over again.”
“That’s right. In the end, though, we were able to patch him up all right,” I said. “But it wasn’t what we did that saved him. When it counted, it was his diabetes that saved Mr. Chen from bleeding to death.”
COPYRIGHT 1995 Discover
COPYRIGHT 2004 Gale Group