Sarita Vendetta

She went home with that thrombus ready to break loose. Some time Christmas morning, her left ventricle pumped it into her aorta.

Was This My Fault?

“I THINK SHE HAS PNEUMONIA.”

Anne, a nurse-practitioner student to whom I’m teaching outpatient medicine, was right. Flo, a proud, stubborn, wiry, 72-year-old African-American had called me earlier that day hoping I would figure out the cause of her abdominal pain over the phone. I told her she would have to come into my office, where we found the problem in her left lower chest, not her abdomen.

Lying on our exam table, she looked quite ill. She moved when necessary, usually to cough up some thick, green sputum. She had a temperature of 101 degrees, and her heart raced at 120 beats per minute. I percussed her chest, tapping my left middle finger with my right middle finger, as I moved the left one down the left side of her back. The left lung’s hollow resonance changed to a dull thud at the base, indicating fluid’s presence where there should have been air. When I listened with my stethoscope to the lung base, I did not hear the normal smooth sound of air flowing without obstruction into the lung but instead encountered the dense crackles (“rales”) that the alveolar sacs make when air expands a lung bathed in pus.

The common bacteria that cause pneumonia prey most often on susceptible hosts. Flo’s 55 years of cigarette smoking have destroyed the cilia (hairs lining the airways) that propel the conveyor belt of mucus that traps inhaled foreign particles, including bacteria, before they reach the lungs and transports them up to the oropharynx to be swallowed. Smoking, drinking, and several decades of high blood pressure have made her heart’s chambers floppy and large and have clogged her arteries. The result: the blood that carries nutrients to keep her organs functioning and sends immune-system elements to fight her infections has difficulty getting where it needs to go.

“I want you to go to the hospital,” I told her, expecting her to refuse, and she did. Instead, she chose to get an antibiotic injection in both gluteus maximus muscles and to return the next day for the same treatment. After that, she started taking an oral antibiotic. Cefuroxime, the medicine I wanted her to take, cost too much for her to afford, so I gave her the last samples we had.

By Friday, she felt a bit stronger, but when I listened to her heart, I noted that her regular lub-dub, lub-dub sounds had given way to the random, irregular cadence of atrial fibrillation, the heart arrhythmia that former president George Bush made famous. The left atrium collects the oxygenated blood from the pulmonary veins and is supposed to contract just before the left ventricle does, giving the ventricle a little extra blood to eject through the aorta into the general circulation. Atrial fibrillation represents a breakdown in the heart’s electrical-conduction system. Instead of responding to a single electrical signal originating at the sinoatrial (SA) node, the left atrium finds itself under the influence of a disorganized mess of electrical activity and therefore quivers and does not contract. The atrioventricular (AV) node then receives about five times the normal 70 or so signals per minute to conduct to the ventricle, but it protects the ventricle from lapsing into the fatal rhythm of ventricular fibrillation because the node has a maximum rate at which it can conduct impulses. In Flo’s case, that rate was about 110 beats per minute, her pulse rate in my office that day.

After confirming her atrial fibrillation with an electrocardiogram, I told her again that she needed to be in the hospital. Her blood pressure had fallen from her usual 150s over 80s down to 110 over 70, which suggested that the absence of her “atrial kick” (the extra blood the atrium sends to the ventricle just before “systole,” the ventricular contraction) diminished the ejected blood volume enough to decrease the heart’s total blood output despite the increased heart rate. Her already diseased heart was working hard, demanding more oxygen from her diseased lungs, but supplying less blood and therefore moving closer to the mismatch between supply and demand for oxygen in the heart that creates heart attacks.

A fibrilating atrium also provides a place where blood can stand still and form clots. Once clots develop, the heart can send them into the circulation, where they go forward until they lodge in an artery whose diameter is too narrow to accommodate them, thereby cutting off the blood flow and killing the organ that depends on the blocked artery for blood.

So one potentially fatal disease, pneumonia, made me nervous enough. Now Flo had developed a serious complication, and I wasn’t feeling lucky. But after listening to my arguments, Flo just flashed her elegant smile and, in that low, husky voice that identifies veteran cigarette users, refused to go to the hospital. I did the only things I could do, which were to start her on warfarin to prevent clot formation and diltiazem to control her heart rate. Knowing that the hospital (one block away) and lab (across the street) would close in less than 45 minutes, I sent her for a chest X-ray and bloodwork, but she only had time to get the X-ray, which confirmed that her left lower lobe was socked in with pus, some of which was also present in the right lower lobe. She and Gladys, the neighbor who drove her to each of her appointments during her illness, had waited for me at the hospital, so I showed them the X-ray, after which they went back to Gladys’s car while I headed in the other direction, back toward my office, into the cold and wet fall evening. Before reaching my door, I remembered I would need her consent to have a visiting nurse see her at home over the weekend, so I retraced my steps back to the hospital, found a security guard who had seen the direction they had taken, and caught up with them. Flo agreed, with great reluctance, to allow the nurse to come.

Three days later, as I turned my green 1994 Nissan Altima into the narrow driveway between the converted house that serves as my office and the house next door, Flo was approaching the five brick stairs to our front door, holding Gladys’s right arm. 1 drove past and noted that Flo still moved at a cautious pace, normal for someone recovering from pneumonia, I thought, so this did not trouble me. I did not become troubled until I saw, when I examined her 15 minutes later, her cold, pale right leg and could not find either of the two pulses one usually finds in the foot.

“I was awake between one and four o’clock this morning because I felt numb and dead in my leg,” she explained. As the alarms exploded in my brain, she continued in the same tone she might have used to tell me how she had cooked her breakfast. “This morning it felt better, but about an hour ago it started again.”

Within a few minutes, I had John, one of the local vascular surgeons, on the phone, and he arranged for an immediate evaluation in the hospital vascular lab, where a technician validated that Flo’s right leg did not have a blood pressure below the knee because there wasn’t any blood flowing past the clot that had lodged in her popliteal artery behind the knee.

The dead lower leg convinced Flo to allow us to put her in the hospital, and that evening Tom, another vascular surgeon, removed the clot, restoring life to her right lower leg and foot. One has between four and six hours to restore blood flow to an unperfused limb, and Flo had her operation in time.

Christmas Eve came three days later, by which time Flo was walking with minimal pain and feeling better than she had in two weeks. Her pneumonia was resolving, her heart had converted the previous day back to normal sinus rhythm, and she wasn’t missing the cigarettes she had stopped using the day she entered the hospital. The vascular surgeon and I agreed that she was fit to go home, so I discharged her that afternoon before heading home myself, happy that she had won her gamble and would get to spend Christmas with her family, although she had told me in the hospital, “Christmas is just another day to me. Every day is Christmas.” That wouldn't be true in 1998.

I had the call duty for our group over the Christmas weekend, so I got the page from Neil, one of the emergency-room doctors, just before my wife Terry began serving her chocolate cheesecake as the sumptuous conclusion to our evening feast. My baby daughter's first Christmas had brought more fun, laughter, relaxation, and great food than any holiday I could remember. That all changed in a hurry.

“Dr. Eichel,” said Neil through my voice mail, “I need to speak to you about Flo..."

Damn, I thought. Pneumonia, atrial fibrillation, thromboembolism. All of which could have killed her but didn’t. Now what was going on?

“She’s had a big stroke” was Neil’s news. “She’s completely aphasic (she can’t speak), and she has a dense right hemiparesis [she can’t move the right side of her body].”

A predictable complication, but that didn’t make it any less devastating. Merry bleeping Christmas. I finished my conversation with Neil and went back to my family, but I wasn’t there anymore, and Terry noticed the change as soon as I reappeared. We were alone in the kitchen.

“What happened?”

“She’s had a big stroke." I made a small effort to hide my hurt, but I could feel my body’s emotional gates gape open so that anyone could see inside.

Terry allowed me a few quiet seconds, then gave me an affectionate squeeze behind my shoulders. “Are you okay?"

My response, couched in quiet, hitter, adult tones, was childlike. “Not really. It’s not fair. It’s Christmas. She’s a really nice lady."

I was in that helpless, wounded sadness that makes one burst into tears if one is prone to do that, but I was a “crybaby” until age 12, at which time my brain matured enough to allow me to suppress that urge with such power that for years I didn't cry at all, and I am just now recovering the ability to do so. I find unfairness in my work all the time, but Christmas with my daughter had brought it, in this instance, to another level. I took about a minute alone to compose myself and then sat down to cheesecake with the family. It’s not unlike me to be quiet, so I’m not sure my mother, my two sisters, or my brother was aware of my inner pains. Shortly thereafter, I told everyone I had to leave and said goodnight.

As always happens when I’m on my way to the hospital, my mind began reviewing everything I knew about the case. During her surgery three nights before, the anesthesiologist had placed an ultrasound probe down Flo’s esophagus and performed what has become the diagnostic procedure of choice for detecting dots on the heart’s valves and in its chambers: a transesophageal echocardiogram. He and the vascular surgeon looked at the images and thought they saw a clot in her left atrium. At that time, her rhythm had changed from the atrial fibrillation I had noted in my office three days earlier to atrial flutter. In atrial flutter, the atrium heats as it does in sinus rhythm, except that it beats very fast, about 300 times per minute. Again, the AV node acts as a gate to prevent all of the atrial heats from being conducted to the left ventricle. Instead, most often one signal for every two (“one-to-one block”) or one for every four (“three-to-one block") goes through to the ventricle. Diltiazem, one of the medicines I had given Flo in my office, slows conduction through the AV node, so Flo was in three-to-one block until her heart converted to sinus rhythm two days later, the day before Christmas Eve.

Sinus rhythm is a good thing, unless one happens to have a loose clot in one’s left atrium. Each coordinated atrial heat can send that clot forward into the left ventricle. Most of the time, blood thinners prevent new clot formation and help stabilize existing clots at their current site and size, but blood thinners do not dissolve large clots. So Flo’s timing was terrible. She converted into sinus rhythm when she had a fresh large clot, or thrombus, which was either loosely attached to the heart or was floating in the left atrium.

So she went home with that thrombus ready to break loose. Some time Christmas morning, her left ventricle pumped it into her aorta, where it traveled up to the aortic arch, followed the arch as far as the left carotid artery, turned left into that artery, and lodged in her left middle cerebral artery (MCA). The left MCA supplies a large cerebral cortical chunk, including Broca’s area, where our speech originates, and the motor cortex that drives the voluntary muscles on the body’s right side. Flo awoke unable to speak or move her right side. She tried to get to her phone but ended up on the floor next to her bed, where she stayed until her granddaughter, who had been trying to call her all morning, found her in the early afternoon and called 9-1-1.

Again, I thought, bad timing. If Flo had still been in the hospital when stroke occurred, she would have been a candidate for enrollment in the clinical trials going on at many U.S. medical centers to determine if treatment with clotbusting drugs (such as tissue plasminogen activator, or tPA) improves the outcome in nonhemorrhagic (no bleeding in the brain) thromboembolic strokes. Beginning about ten years ago, these drugs changed our approach to heart attacks by showing that you can “rescue" dying heart muscle if you can restore blood flow soon enough. The same now appears to be true, to some extent, with the brain, although nerve tissue dies more quickly, and the potential for catastrophic bleeding into the brain is much higher when you use a clotbuster in the setting of an acute stroke than during a heart attack. If the stroke victim gets to our hospital less than three hours after the onset of symptoms, the emergency room calls in an interventional radiologist. Under fluoroscopic (X-ray) guidance, the radiologist can thread a catheter through the neck and inject dye into the cerebral circulation, creating a picture (“arteriogram”) of the brain’s major arteries. If the arteriogram shows the expected blockage, the radiologist can advance the catheter to the occluded area and inject the clotbusting drug where it is needed and see the result. Flo arrived at the hospital about four hours too late for this intervention. Her CT scan proved this; some affected areas in her brain showed up dark, meaning that their destruction was already advanced enough to render them less dense than normal brain matter.

So, had I sent her home too soon? Was this my fault? When I arrived at the hospital, I was still debating this. I found Neil in the emergency room, but Flo had gone up to her room. As we looked over her CT scan, I shared my frustration with him. Six days earlier, I had anticipated these clots, started her on warfarin, and watched her toss emboli to her leg and head anyway. Neil said what I thought I knew but needed to hear: “It’s not your fault, )im. Don’t blame yourself for this.”

I nodded to him in appreciative acknowledgment and turned to walk out of the ER. “Merry Christmas, Jim,” he added. That softened me a bit; I turned and gave him half a smile. “Merry Christmas, Neil."

Upstairs, Flo was waiting for me with a cold left leg. Neil had asked me over the phone if her right leg, which was now paralyzed from the stroke, had become warmer than her left after the surgery on the right. I had told him no and that if he suspected a problem with the left leg, someone should get a “doppler” (a small ultrasound stethoscope) to listen for pulses in her left foot. When I arrived at Flo's bedside, her nurse had a doppler, which told me that the issue had not been resolved. The nurse began listening while I attempted to communicate with my hemiparalyzed and aphasic friend, whose withdrawn, tight-lipped expression and tired eyes told me almost everything. She wasn’t in pain, but she could not have been more annoyed. And now she felt the same absence of life in her left leg that she had felt in “her right just three days before. Her left leg was now cold and quiet, even to the doppler, below the knee. I paged the vascular surgeon.

“Merry Christmas, John,” I began, with as much sincerity as 1 could summon.

“That depends,” he replied, “on what you’re about to tell me.” I told him the story he didn’t want to hear.

Before he arrived, I had to make one more phone call. Neil had called Heidi, the neurologist on call, to see Flo in the emergency room to decide whether the patient should be given additional blood thinners, and Heidi had said no, there was too much risk of converting her embolic stroke into a hemorrhagic one. Heidi hadn’t known about the left leg. John was going to want to start heparin, an immediate-acting intravenous anticoagulant, and continue it until 48 hours after we reached Flo’s therapeutic level of warfarin. When I told Heidi about the leg, she agreed that we had to treat what was there and hope that she didn’t bleed into her head.

Thirty minutes later, John was making arrangements to take Flo to the operating room again. I asked him if he would have managed this case any differently, emphasizing the fact that her coumadin level was just below therapeutic when she left the hospital.

He thought for a moment and shook his head. “You had a stable patient. You could not have predicted that her INR [the index we use to measure how well the warfarin is anticoagulating the blood] would go down two days after you increased the dosage. We don’t get twice-daily INRs. We do them once a day while we’re adjusting the warfarin; a change in the dose changes the INR two days later.”

I went home not knowing what the outcome of her operation would be, but when I went to see her the next morning, she had two warm legs, hadn’t thrown any more large clots, and hadn’t bled into her head. Her dense hemiparesis and aphasia remained unchanged until I left for Florida with my family to visit my mother-in-law on Monday, three days after Flo’s Christmas stroke and leg embolus. If all goes well, she’ll undergo about three weeks of inpatient stroke rehabilitation to help her maximize the function she still has before she goes to what will likely be some kind of assisted-living situation, not to her home. This was not what this proud retired caterer had in mind. Right now, she can’t say anything except “Geez!” She can eat only purled food and thin liquids, and she can't move her right arm and leg. Given that this all started with a lobar pneumonia and that her blood seems to be hypercoagulable, I can’t help wondering if her body isn’t hiding another land mine waiting to go off: cancer in her lung. I won’t know until we do the follow-up chest X-ray next week.