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Clinical Clarity from Hot Dogs on the Fourth of July

2010; Lippincott Williams & Wilkins; Volume: 32; Linguagem: Inglês

10.1097/01.eem.0000383987.04523.5a

1552-3624

Ravi Morchi,

Empathy and Medical Education

ImageIn 1916 four immigrants got together at Nathan's Famous in Coney Island, Brooklyn, NY. They debated who among them was the most patriotic, who was the most American. They decided to settle this debate with a competition, and in an American fashion, they declared it had to be an eating competition. So on the Fourth of July 1916, legend states that James Mullen consumed 13 hot dogs and buns to become Nathan's first hot dog eating champion. And so was born an American tradition. Over the years, the contest drew the best this country had to offer. Very large men struggled and strained against their own vagus nerve, which sent impulses to their brainstem about supranormal gastric distension, the desire to vomit, and the wise advice to put the hot dogs down and step away from the table. Yet they fought past the diaphoresis and the impending sense of doom to put away 20 or 25 hot dogs, and raise the coveted Mustard Belt over their head. Odd? Yes. But this behavior and these accomplishments were still believable. Believable, that is, until the Fourth of July 2001 when something very strange happened at Nathan's Famous Hot Dog Eating Contest. The ED, 2001. Paramedics stated the patient was a 56-year-old woman found lethargic on her toilet. Her sister called EMS. The patient was drowsy, but responsive to voice. Placed on the gurney with a monitor and face mask with reservoir bag, she was deemed stable, and transported to the hospital. Upon arrival, I saw a middle-aged African-American woman slouched over in a seated position. With transport from the EMS gurney to our stretcher, she briefly opened her eyes to take in the scene, and then let them drop closed again. Her temperature was 37°C, heart rate was 86 bpm, blood pressure was 140/80 mm Hg, respirations were 36 bpm, and pulse ox was 100% on 15L by face mask. I found her responsive to voice, and able to follow commands but slow. The main abnormality was that she seemed to prefer her eyes closed. “Are you in any pain?” I asked. She opened her eyes, looked up at me. “No,” she said. Then she closed her eyes, and dropped her head down. “Trouble breathing?” “No.”Image“Headache or chest pain?” “No.” “Vomiting or abdominal pain?” “No.” “Do you feel weak or tired?” With each question, she replied in the same manner: by lifting her head, opening her eyes, looking directly in mine, and answering “no,” and then promptly resuming her slumber. “Is there anything bothering you? Anything at all?” “You,” she said. She was in there. Her brain was working, and gears were turning. But she had no chief complaint. The Physical. Already having worn out my welcome, I decided to abandon the history till later, and proceed with the physical exam. Her pertinent findings were that she was a slightly overweight woman with an effaced left nasolabial fold, weak grip strength in her left hand, and a weak left foot to dorsiflexion. Although she was tachypneic, her breath sounds were clear and equal, her expiratory phase was not prolonged, and she demonstrated no increased work of breathing. It looks like she had a stroke, I told the nurse. He nodded. My thoughts turned to a head CT and the thrombolytic window. Fortunately, the family showed up before I could do much harm. Her head CT was significant for chronic white matter changes and small lacunar infarcts. The labs were pending when the sister came into the resuscitation room claiming that our patient had had a stroke four years earlier, and hobbled around the house with a paretic limb since that time. She was generally of good nature, alert, interactive, always on the go. So this was a significant departure from baseline. Her daughter added that everything was fine this morning. She heard her mother make her way into the bathroom, and then noticed it was a long while, and she had not come out. “She always takes a long time to go,” said the daughter. “Usually she strains a lot to get anything out.” When the daughter entered the bathroom, she found her mother on the toilet slouched over, apparently unconscious. She had not soiled herself. Family could not get her up, so they called the ambulance immediately. The answer must be in the urine. Like any older woman with baseline chronic brain disease, the UTI is our favorite culprit for all changes in mentation. We wait anxiously for the urine to declare itself guilty and relieve us of having to think much more about our patients' altered level of alertness. But unfortunately the catheterized urine specimen we obtained was entirely normal. I was at a loss for what could have happened to her. Her ECG was sinus rhythm with nonspecific T-wave abnormalities, but nothing more. The labs returned: CBC, chemistry, and troponin were all normal. I was preparing to perform a lumbar puncture. What am I missing? Some component of the history that I have yet to unearth? So I asked more questions, an extensive review of systems to the patient and her family. Nothing striking was turning up. I had to change my approach. The subjective was clearly getting me nowhere, but what about the objective? Could the clues to her disease come, not as words from her or her family but in the observable signs at the bedside? Tachypnea. Generally we think of pulmonary edema, pneumonia, bronchiolar collapse, or some other static or dynamic pathology involving the alveolar lumen or small airways. Occasionally we are dealing with a proximal or upper airway abnormality. Whatever the precise anatomic locale, tachypnea leads us to focus on the respiratory tree and pulmonary compliance. But this woman had no increased work of breathing. She was breathing fast and deep, but there was no evidence by physical exam that she had trouble inflating her pulmonary parenchyma. I even placed her in the supine position to see if she became more short of breath, and that was not the case. Her upright, portable chest x-ray was normal. Tachypnea without any corroborating lung findings must be a metabolic acidosis, I thought. Even without an anion gap by chemistry profile, I felt inclined to pursue a metabolic cause to this abnormal vital sign. So I took her off the face mask in preparation for an ABG. Hypoxemia. Immediately her arterial saturation trended down and leveled off somewhere around 80% on room air. “Wow, she's hypoxic,” the nurse mentioned. “What do you make of that?” But this overweight patient, who was quite lethargic and slumped over with her neck flexed, most likely had a component of hypoventilation contributing to the hypoxia. If I sat her up straight and had her take deep, full breaths, she would reconstitute to above 92%. So I did just that to show my nursing colleague what I meant. Our patient's arterial hypoxemia was simply the result of hypoventilation from her depressed mentation. Stimulating her enough to comply, we had our patient maintain an upright posture, and take several deep breaths. We watched the monitor, and cheered her oxygen saturation on as it began to climb: 82%, 84%, 86% … 86% … 86%. It rose no further. I was in disbelief. What's more, I was beginning to get frustrated with the course of things, history and physical. “The waveform looks good,” said our nurse. “It's probably real.” And there we have it. It was real. It was an observation made at the bedside, a physical finding that could not be debated, one that didn't entirely make sense, but nonetheless had to be managed, a tangible derangement, like tachypnea, to which I must submit my full attention. An abnormality to the most vital of signs that immediately trumped any historical fact or presumption I had about this case. You see, up until this moment, our patient was a case of “sudden onset depressed mentation with secondary hypoventilation and hypoxemia.” In that vein, investigations were aimed at determining a cause of rapid change in level of consciousness. Head CT and lumbar puncture for subarachnoid blood would be considered critical in this respect. Once our patient demonstrates that her hypoxemia is not from hypoventilation, either by failed bedside maneuvers or by an ABG that reveals an A-a gradient, then the game changes. Hypoxemia becomes a separate abnormality. No longer a sequela of hypoventilation from depressed mentation, it is now a primary derangement. In fact, it is likely to be the cause rather than the effect of the altered mental status in our cerebrovasculopath. The course of the case takes a sharp turn away from cerebral investigations focused on sudden onset lethargy, and turns toward a physiologic deconstruction of sudden onset arterial hypoxemia. Physiology. All causes of arterial hypoxemia, regardless of the patients' chief complaint (or lack of complaint), must come down to only a few known physiologic principles: hypoventilation of the alveolar lumen, a V/Q mismatch in favor of perfusion over ventilation (the extreme version of such a mismatch being an intrapulmonary or intracardiac shunt), or a problem with the alveolar-capillary membrane impairing the diffusion of oxygen. Whatever our patient or family claimed, whatever symptoms the patient had, whatever course of events occurred this morning, her hypoxemia had to be explained by one of these principles. I already knew hypoventilation was not the primary problem because I watched her chest rise with concerted effort in an upright position, and so doing could see that she wasn't simply partaking in shallow breaths with airflow limited to her trachea and bronchi (anatomic dead space ventilation unable to participate in gas exchange). With meaningful chest rise, she must be moving air into and out of her respiratory bronchioles and alveolar lumen. Intracardiac or intrapulmonary shunt is less likely because the patient did reconstitute to 100% on a face mask with reservoir bag. Impairment of diffusion across the alveolar membrane secondary to an inflammatory or infectious process unseen by x-ray and unheard by auscultation was possible, but her presentation seemed to be rapid onset this morning, not something that slowly progressed over the past few days. So I am left with V/Q mismatch. Air entry into the alveolar lumen would have to be impaired by something other than generalized hypoventilation, maybe alveolar edema, blood, pus, or gastric aspiration that was not seen on x-ray or heard by stethoscope. On the other hand, maybe ventilation was normal, but her perfusion was increased beyond the capability of the alveolus to deliver oxygen in certain areas of her lung, resulting in red cells streaming past pulmonary parenchyma without the opportunity to be oxygenated. This is difficult to imagine because our system exists in such a way that it allows complete saturation of RBCs early in their course across a particular alveolar membrane. Whatever the precise etiology of mismatch, it had to be rapid in onset to produce such a hyperacute alteration in mentation in this cerebrovasculopath. A vasculopath that had tenuous baseline blood flow and a tendency to peter out when that flow was complicated by low oxygen content, a rapid imbalance between ventilation and pulmonary perfusion producing sudden onset tachypnea and hypoxemia? I must consider pulmonary embolus. But she has no risk factors. As far as I knew, she had a paretic limb, but was mobile and never really stationary for any length of time. Her family swore that she was always on the go. No recent trauma to the limb. No recent surgery. Nothing. What is more, her HPI and ROS were entirely flat. She had no chest pain, shortness of breath, weakness, or anything that could have been remotely attributed to PE. She had no symptoms at all. Her chief complaint did not exist. How can she have a PE with a CC, HPI, ROS, PMHx, and risk factor analysis that were all benign? When every component of the subjective half of this case was reiterating neutrality, how can I say she had any positive corroborating symptoms for PE? How can I justify pursuing the diagnosis? Nathan's Famous, July 4, 2001. That year Takeru Kobayashi shattered the world record by consuming 50 hot dogs and buns in 12 minutes. Doubling what anyone else in history was ever able to accomplish, he would become known as the “Tsunami” Kobayashi. Statistics say he weighed 140 pounds and had a 30-inch waist. I remember watching the event with a grotesque curiosity that kept me from changing the channel. As I sat there in disbelief, he made dog after dog disappear into his mouth. I thought to myself, “He has no risk factors for being able to eat 50 hot dogs and buns.” This can't be happening, I thought. How can you fit such a large amount of physical matter into such a small space? After all, there are physical laws to this world. To my mind, it was an anatomic and physiologic impossibility. Except for the fact that he did it. The 50 hot dogs and buns had to be in his gastrointestinal system. They could be nowhere else. As much as every risk factor, chief complaint, or review of systems would have me believe, the Tsunami had presented with a glaring, striking, objective, physical abnormality that could not be argued with. A tangible truth made by measurement and observation. No component of the subjective, no expectation of mine could ever make this untrue. I could not rationalize it away or talk it out of existence. It would not disappear just because I thought it was not possible or because it didn't make sense. I had to respect it. I had to accept it had happened, and all my logic and all my clinical approach had to bend for it. It would never bend for me. For this physical truth, for the objective in all its miraculous and warped glory, I had to concede that Mr. Kobayashi harbored in him pathology that was not the hallmark of a normal man. It didn't matter how unlikely such pathology would be in the general population of 140-pound, 30-inch-waist Japanese men. Our individual patient either had a 100% chance of having the disease or a 100% chance of not having it. When he raises the Mustard Belt in victory, you know he is in the former group. He declares himself separate from the statistical analysis that applies to our general population. The asymptomatic PE. I had never heard of a PE presenting without chest pain or shortness of breath or weakness or, well, any symptom at all. But it didn't matter. Nothing else mattered at that moment except for the objective truth in front of my eyes: She presented with tachypnea unrelated to a loss of pulmonary compliance and hypoxemia unexplained by hypoventilation, lung auscultation, or chest x-ray. Those findings alone meant she could eat 50 hot dogs, and as unwilling as I was to accept the idea of an asymptomatic PE, I had to. Markedly abnormal objective findings can enslave us in this way. They demanded an explanation, and they owned my next clinical move. Her CT pulmonary angiogram was positive for diffuse thromboemboli. Diffuse. She must have harbored a deep venous thrombus in her paretic limb. Straining to move her bowels as she normally does, the cessation of her valsalva maneuver is characterized by a sudden drop in intrathoracic pressure, and the DVT siphoned right into the pulmonary circuit. The pathophysiology of arterial hypoxemia in PE is not entirely straightforward. The emboli themselves produce areas that are underperfused while still being ventilated. That is, they produce physiologic dead space ventilation, rather than the kind of V/Q mismatch in favor of perfusion that we normally associate with low arterial oxygen saturation. We know that the absence of hypoxemia should not rule out PE for this very reason. But we also know that a large, diffuse, clot burden can result in hypoxemia, maybe from shunting blood into a smaller area of viable, nonembolized, functioning lung that quickly becomes overwhelmed and complicated by the fact that nonembolized portions of the pulmonary parenchyma may collapse or fill with inflammatory exudate during the process of thromboembolization to its neighbors. If at play, these processes make it difficult for nonembolized areas to adequately oxygenate the increasing numbers of RBCs that are shunted their way from other embolized segments. The result would be a V/Q imbalance with excess perfusion and resultant arterial hypoxemia. Whatever the case, the objective derangement must be explained. The measured abnormalities of marked hypoxemia and tachypnea, with no hypoventilation, increased work of breathing, or orthopnea, must be explained. To avoid clinical error and make the diagnosis of typical diseases presenting atypically, we must concede that disease need not present the way we expect. That clinical logic and physiologic reasoning are limited precisely because the known principles of human organic function are incomplete, that what seems unlikely by history is still possible, that observable signs may declare it probable. We must put aside our expectations and presumptions based on the subjective, and pursue the objective truth with an open mind. We are bound to these physical measurements. After all, we made them. About Harbor Pearls This column features interesting cases treated by the faculty and residents of the department of emergency medicine at Harbor-UCLA Medical Center. The department was established in 1978, its emergency medicine residency program one of the nation's first. The program has delivered care to the underserved communities of Los Angeles County for more than 30 years in a high-volume, high-acuity Level I trauma, pediatric trauma, critical care, and disaster resource center. Its mission is to deliver the highest level of care and promote a sense of service. Return to EM-News.com