“So why did you give her a 500ml bolus?” he asked with a smirk. “I’m just going to take her upstairs and diurese her.” I paused for a second to recall exactly why I had given crystalloid, but struggled remembering. Now we were admitting for heart failure, so in retrospect giving a crystalloid bolus was probably not the wisest. I regurgitated something about being total body fluid overloaded but intravascularly depleted, but was met with another smirk. It had been three hours since I wrote that order and I was currently distracted with the care of the other ten patients I had seen since then. “Well, I guess you could go either way. I see your concern, sorry brother.” He turned and strode arrogantly out of the ER, his bodily language whispering “Amateurs, pissants.” I cringed, “Well, crap.”
An hour later, the constant onslaught of patients slowed briefly, just long enough for me to review her labs and imaging and write my note. The scenario replayed in my mind. The radio crackled from triage, “We need a room.” This generally meant the patient was semi-acute and should be seen sooner rather than later. A triage nurse wheeled the patient around the corner heading for the only open bed and briefed me quickly as I met her en route. She was a 65 year old female with altered mental status and weakness concerning for a stroke. During the short transit I briefly assessed, “Hey ma’am, how are you doing? What’s going on today?” She looked up at me and answered, “I’m OK.” With that brief interaction I knew that her airway was intact, her breathing was at least temporarily ok, and her circulation was grossly adequate – well at least she was perfusing her brain. Further conversation revealed slightly delayed mentation, but no dysarthria or aphasia. I quickly transitioned to the NIH Stroke Scale after asking for a fingerstick glucose and a set of vitals. She was oriented, no obvious facial droop, her eyes were tracking in all directions. But when I asked her to raise her arms and hold them in the air, she could not lift her right arm. She was hemiplegic. She could not raise her right leg either. I turned to her husband who had just entered the room, “Sir, has she had a stroke before?” “Yes, she had stroke with residual deficits on the right, but this seems worse.” “And what about her mental status? Is she acting differently than usual?” “Yes, she seems different from her baseline.” “And what is this scar on her chest?” “She had a triple bypass.” “Is this a pacer/defibrillator?” pointing to a lump under her skin on her left upper chest. “Yes.” “And when did these symptoms start?” The symptoms had started insidiously two days previously.
“Alright guys, we are still working this up as a stroke, but we are not calling a stroke alert.” Calling a stroke alert activates a plethora of resources rapidly with the end goal of potentially giving a medication that may help lyse the clot causing an ischemic stroke. But there are certain criteria that must be met, including symptom onset within the last three to four and a half hours. If the symptoms started prior to that, then the medication is contraindicated due to significantly worsening risk of intracranial bleed. “As soon as we get blood and vitals, we can get a head CT.” The head CT differentiates between a hemorrhagic stroke and an ischemic stroke, two entities that are treated very differently.
“Let’s add cardiac enzymes, a BNP, and an EKG too. Make it a point of care troponin and electrolytes please.” Nurses perform point of care tests at the bedside providing vital information quickly, rather than waiting for results from the lab. “Sir, her blood glucose is 226.” I reminded myself, “Never miss hypoglycemia masquerading as a stroke.” Her vitals were grossly normal – not hypertensive, not hypotensive, normal heart rate. Hypertensive encephalopathy can cause a similar picture, also strokes frequently present with hypertension. “Let’s also get a urine and a chest x-ray, and get me a temperature please.” Urinary tract infection, pneumonia, and sepsis were all still on the differential diagnosis, often the elderly manifest these infectious processes with confusion. “Let’s also get a set of cultures and a lactate.” Her abdominal exam showed mild distention, and she squirmed when I pressed on her belly.” Maybe an intra-abdominal process? Bowel obstruction? She was also incontinent of urine. A mass on her spine or epidural abscess? Her husband mentioned that she was complaining of low back pain recently. “Let’s add an abdominal CT as well.” That will get her belly and grossly examine her spine.
“Let’s give her a 500ml bolus of normal saline.” There it was! There were a multitude of diagnoses on the differential at this point, but an intra-abdominal process and sepsis need early fluid resuscitation. And a 500ml bolus is a nice compromise between giving some fluid and giving no fluid. Initial fluid bolusing for a septic patient is 30ml/kg, so for a 70-100kg patient, that is easily two to three liters. Half a liter was like pissing in the wind. Moments later the lactate – a marker of poor perfusion, shock, and tissue hypoxia – resulted elevated at three, confirming the reasoning.
After initial verbal orders, determining hemodynamic stability, and figuring out a preliminary plan, I returned to the computer to formally place each order and review any available medical history. After attending to a few other patients, the results began to trickle in. Her creatinine was elevated significantly compared to the previous value indicating an acute kidney injury, but her electrolytes were grossly normal. Her EKG showed no ischemic changes and was unchanged from previous. Her troponin resulted next, it was elevated. Was this a Type 1 or Type 2 NSTEMI? Was this her primary process or a result of another stressor? Her CXR was read as stable cardiomegaly, but no acute cardiopulmonary process. Her head CT showed no acute bleed or interval change from the prior CT.
As the labs and studies intermittently resulted, the picture gradually became clearer. Her urinalysis showed no urinary tract infection. The abdominal CT was negative for acute abdominal processes but did show findings consistent with heart failure at the base of the lungs. Her BNP returned greater than fifty thousand, double her BNP from the previous month, indicating worsening cardiac function and likely heart failure. While perusing her imaging studies in our imaging software, I found a cardiac nuclear stress test from a few days prior that the family failed to disclose. It showed abysmal cardiac function with a severely depressed ejection fraction. After ruling out many other etiologies, it seemed that heart failure was likely the driving force of her symptoms. The pump failure decreased perfusion to her brain causing slowed mentation, decreased perfusion to her kidneys causing an acute kidney injury, and decreased myocardial perfusion further stressing a weak heart causing myocardial necrosis and troponin leakage. After gathering enough data to establish a definitive diagnosis, I consulted the hospitalist for admission and further management.
Maybe I should have run into the room and discontinued the 500cc bolus immediately upon discovering the likely heart failure, but unfortunately, it had already been given. In retrospect, with a BUN more than twenty times greater than the elevated creatinine, she was likely truly intravascularly depleted and the fluid bolus probably augmented her organ perfusion temporarily. And on exam, she was not in florid heart failure. Her lungs were dry, no crackles with auscultation, her legs were not grossly edematous. I may have missed the diagnosis if not for the scar on her chest and the cardiac history reported by her husband.
But this is the arena in which we ER physicians practice. We work in an undifferentiated and gray world of uncertainty. There are few absolutes. We create order out of chaos with a regimented and regularized approach to each patient. This is our forte, our niche. But when you live and work in the gray, there is potential for error. And later, upon scrutiny of each case with all the data and without time constraints, we are often criticized by our consultant colleagues for decisions made in those initial undifferentiated moments.
As ER physicians, we must be adaptive in our practice and dynamic in our thinking. We cannot major on the minutiae, we cannot be paralyzed by the atypical. We must act, and act quickly with minimal information. Few feel comfortable with this approach, but this is where we excel. And as our consultants roll their eyes and sigh at the 500ml bolus that muddies their nicely tidied chart and expertly narrowed tightly packaged diagnosis and treatment plan, we must forge on and discharge the next ten patients. And we must do that with a smile on our face, and a “thank you brother,” because we will consult them again for admission later that day.
This condescension causes significant frustration in our world. We can deal with belligerent and malignant patients all day, but it is the scorn of our colleagues that irritates us. For me, this dynamic in an ER physician’s practice is vividly described by my favorite Teddy Roosevelt quote: “It is not the critic who counts; not the man who points out how the strong man stumbles, or where the doer of deeds could have done them better. The credit belongs to the man who is actually in the arena, whose face is marred by dust and sweat and blood; who strives valiantly; who errs, who comes short again and again, because there is no effort without error and shortcoming; but who does actually strive to do the deeds; who knows great enthusiasms, the great devotions; who spends himself in a worthy cause; who at the best knows in the end the triumph of high achievement, and who at the worst, if he fails, at least fails while daring greatly, so that his place shall never be with those cold and timid souls who neither know victory nor defeat.”
So keep crushing it ER physicians, despite the negativity and pessimism. You are truly my heroes and heroines.