Two Hours - Case 6 | Episode 1

A 70-year-old man develops dizziness and difficulty walking. He sees his primary care physician. He's sent to the emergency department. Two hours pass between when the symptoms began and when stroke is finally on the differential.   By then, the tPA window is closing. The clinical story — and the way a posterior circulation stroke can hide in plain sight on a busy day in a busy office.  

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SPEAKER_01 1:28

The content of this podcast is intended for educational purposes only and does not constitute legal or medical advice. Laws vary by jurisdiction. Medical standards evolve. The case details presented are derived from publicly available court records, appellate opinions, and published reporting. Listeners should consult qualified professionals for advice specific to their circumstances. A stressful phone call on a summer afternoon. The kind that raises your blood pressure before anything clinical does. A 70-year-old man starts feeling headaches, dizziness, nausea. Over the next two hours, the symptoms build. Marked unsteadiness, weakness, a sense that something is wrong. He decides to go to his primary care physician's office. He takes a taxi and arrives unannounced. No phone call ahead, no appointment. His physician later testified that this was highly unusual for the patient. It is summer in the year 2015. What follows over the next several hours from a primary care office to a hospital emergency department raises questions about clinical decision making under diagnostic uncertainty, the design of triage systems, and the documentation that connects one clinical encounter to the next. This is on the record case six. The patient was a 70-year-old man with a history of hypertension, hyperlipidemia, coronary artery disease, a remote traumatic brain injury, and intracranial bleed requiring craniotomy from 1985 and a seizure disorder. He had been prescribed phenytoin, brand name Delantin, but was not taking it consistently. He lived independently. Late that morning, he received a distressing phone call. Within an hour, headaches, dizziness, and nausea began. By roughly two o'clock in the afternoon, the symptoms had progressed to include marked unsteadiness and weakness. That time, approximately 2 p.m., would later be reported to the hospital as the symptom onset. The last known well time. He took a taxi to his primary care physician's office. He arrived for an unscheduled visit and had not called ahead. His physician later testified this was highly unusual for the patient. The patient sat in the waiting room for approximately an hour before being seen.

SPEAKER_02 4:31

I want to pause here because this is a presentation that deserves some analytical attention before we go further. A 70-year-old man with hypertension, coronary artery disease, and a history of a prior intracranial bleed and craniotomy develops sudden onset headaches, dizziness, nausea, and unsteady gait after a stressful event. And he is symptomatic enough that he takes a taxi to his primary care physician without calling ahead. That is unusual behavior for a patient, his physician described as someone who at least gives the courtesy of a phone call. Something about his symptoms was significant enough to change his routine. The symptom cluster, headache, dizziness, nausea, unsteadiness, has a wide differential in this age group. Hypertensive emergency, medication effect, vestibular pathology, intracranial pathology. Any of those could explain this presentation. And his history, the prior craniotomy, the seizure disorder, the noncompliance with phenytoin, adds complexity to whichever direction the workup goes. This is a patient who needs a careful evaluation. And that evaluation is about to happen in a primary care office.

SPEAKER_01 5:51

The PCP examined the patient at approximately 5 p.m. He recorded a blood pressure of 200 over 120. His documented physical exam noted normal eyes, pupils equal and reactive, normal neck, normal cardiovascular exam, normal abdomen, no extremity edema, and one additional finding. Gate, unsteady. His chart listed the chief complaint as dizziness. The history noted that the patient had consumed coffee made with old milk and had taken a medication from South America. Something the PCP wrote phonetically as EPAIN with a question mark. He did not recognize the drug. He suspected it might be a stimulant that had caused the blood pressure spike.

SPEAKER_02 6:47

The EPEN mystery is worth a moment here. It was later identified as Epimen, a common South American brand name for phenytoin, the seizure medication the patient was already prescribed, but not taken consistently as alleged in the records. The PCP did not make that connection during the visit. It factored into his differential, he considered a metabolic reaction to an unknown foreign medication as one explanation for the presentation. I think it is also important to note the physical exam findings in context. The patient was noted to have an abnormal gait, but an otherwise normal exam, including normal neurological findings on the documented portions. In combination with a blood pressure of 200 over 120, an unsteady gait is not just a footnote. It could be a clue that something acute is evolving. It could also be explained by the blood pressure itself, but it deserves attention.

SPEAKER_01 7:52

The PCP's differential diagnosis included three possibilities. First, hypertensive encephalopathy. Second, an intracranial lesion, such as a brain tumor, which he noted could explain the headaches and dizziness. Third, a metabolic reaction to the unknown medication. When later asked directly whether he believed the patient was having a stroke, the PCP testified. No, I did not. He testified the thought crossed his mind, but he rolled it out. There was no focalization, no lateralization at that period of time. He did not have a stroke. He also testified that he screened for weakness, facial droop, slurred speech, confusion, blurred vision, nausea, and one-sided weakness, and found none. This screening was not documented in the chart.

SPEAKER_00 8:59

The chart documents gate, unsteady, and a standard systems exam, but it contains no record of a neurological screening. The PCP testified under oath that he performed one and found no focal signs. But the chart written at the time of care does not reflect that screening. In a malpractice proceeding, the chart is the primary evidence of what occurred during a clinical encounter. Testimony about what a physician remembers doing can support the record, but it cannot replace it. When the chart is silent on a clinical assessment, the legal analysis proceeds from that silence.

SPEAKER_02 9:43

The exam documents an unsteady gait and the blood pressure is significantly elevated, but we do not see objective evidence in the record that explicitly documents the findings of a full neurological exam. If a patient comes to your office with primary symptoms that are neurological in nature, we should make sure we document a thorough neurological exam while documenting the broader physical exam that may be more focused in nature. Documenting a full neurological exam would only help this physician, as we will see later in this case.

SPEAKER_01 10:25

Nebevilol, brand name Bistolic, 5 milligrams, and Amlodopine slash Ulmisartan. Brand name Azor, 5 slash 40. Both were given by mouth at approximately 5 p.m. The patient was instructed to lie down. After about 20 minutes, the blood pressure dropped from 200 over 120 to 180 over 100.

SPEAKER_02 10:51

I want to talk about this briefly because it will come up again once we know more about what is evolving with this patient. He was given oral blood pressure medications in the office, and in many cases that would be a reasonable decision. But it could also potentially be an issue for a patient experiencing certain acute neurological events. I'm not saying this is a bad decision for this physician to make, but I would want us to pause when seeing a patient like this and make sure we have identified what we are treating and why we are treating with this specific medication combination. If the patient is thought to have hypertensive urgency, then this is not unreasonable. If the thought is that the patient took a medication that produced a stimulant effect and raised his blood pressure, again, not necessarily unreasonable. The pharmacokinetics here become clinically important later in the evening. Nebivalol is a beta blocker with a peak effect at 1.5 to 4 hours and a half-life of approximately 12 hours. Olmusartin, the ARB component of azor, peaks at 1 to 2 hours with a 13-hour half-life. Amylotopene, the calcium channel blocker component, peaks at 6 to 12 hours with a half-life of approximately 45 hours. These are chronic outpatient medications. Their prescribing information frames full antihypertensive effect at within two weeks of treatment. They are not acute interventions, but again, it is not unreasonable to give a first dose in the office if you plan to start these medications and you are not thinking this is an evolving emergency. The PCP's clinical reasoning was that this was hypertensive urgency. And he treated the diagnosis he had made. I want to be clear about that. He was not treating a stroke, he was treating what he believed was a dangerously elevated blood pressure. And in that framing, oral antihypertensives are a standard tool. The issue is the pharmacokinetic profile in the context of diagnostic uncertainty. These medications, once given, continue lowering blood pressure for hours. They are not titratable, they cannot be stopped or reversed once administered. The EAN slash ESO prehospital stroke consensus is explicit. Prehospital treatment of high blood pressure in patients suspected of having an acute stroke is not recommended. The AHA slash ASA guidelines list only titratable IV agents, libetilolol, nicardipine, clevidipene for blood pressure management in the setting of acute stroke treatment. The reason is precisely what I just described. You need minute-to-minute control over blood pressure when the diagnosis includes the possibility of an acute ischemic event, because the ischemic penumbra, the brain tissue at risk, depends on perfusion pressure to survive. Now, the PCP did not believe this was a stroke. So in his clinical framework, these medications were appropriate. The teaching point is not that he made the wrong call in the moment. The teaching point is that the pharmacokinetic timeline of these drugs means their effects will continue for hours after the patient leaves the office. And if the working diagnosis turns out to be wrong, those effects cannot be reliably undone.

SPEAKER_01 14:30

He did not call 911, he did not call an ambulance. He later testified that in his clinical judgment, the situation was urgent but not life-threatening. He stated his headache lessened, his blood pressure became better, lessened 180 over 100, and it wasn't life-threatening. He was able to ambulate pretty well, and according to my judgment, an ambulance was not warranted.

SPEAKER_02 15:01

A quick note here: the patient had a reassuring response to the medications, which would further strengthen the physician's belief that this was likely hypertensive urgency. That improvement could provide some confirmation bias, and the response to treatment seems to validate the working diagnosis, which could make it easier to let the patient travel to the emergency room by taxi rather than calling an ambulance.

SPEAKER_01 15:23

The PCP wrote a prescription note for the patient to carry to the hospital. The note read History, seizure disorder, hypertension. 70-year-old patient has severe hypertension. Blood pressure 200 over 120. Given by Stolic, 5 milligrams, and Azore, 5 over 40 at 5 p.m. not taking BP pills, and Delantin 500BID, sent to ER. The note did not include the patients presenting symptoms, the headache, dizziness, and unsteady gait that had prompted the visit. It did not include the discharge blood pressure of 180 over 100.

SPEAKER_02 16:11

There are two separate issues here, and they both matter for every physician who manages acute presentations in an office setting. The first is transport mode. We have discussed in previous episodes how patients move from one clinical setting to another and why the method of transport matters. EMS pre-notification is not just about getting there faster, it activates the entire stroke architecture before the patient arrives. The AHA slash ASA pre-hospital chain, stroke recognition by EMS, hospital pre-notification, rapid transport to a stroke-capable facility, is the system designed to support the 60-minute door-to-needle target. When a patient arrives by taxi, unaccompanied, carrying a handwritten note, they enter through the standard registration pathway. They sit in a waiting room. The stroke team does not know they exist, especially in the setting of a subtle presentation that is not immediately apparent when the patient arrives. The second issue is the prescription note itself. That note was the only clinical communication between the PCP encounter and the emergency department. It conveyed blood pressure and medications. Important information. But it did not convey the clinical question. BP 200 over 120 gave Bstalek and Azor, sent to ER, is a medication list. Presenting with headache, dizziness, and unsteady gait, rule out stroke versus hypertensive encephalopathy, though please evaluate urgently is a clinical handoff. When you cannot be on the phone with the receiving team, the note is the communication link. And the information in that note shapes how the receiving team prioritizes the patient. We are looking at this in hindsight, and I want to acknowledge that. The presentation and the note are consistent with the working theory that the physician did not believe this to be an emergency. I would think a reasonable physician who believed this could be a stroke would have called an ambulance and called the emergency room ahead of time. The physician's care is internally consistent thus far, and he treated what he believed he was seeing.

SPEAKER_01 18:27

The patient arrived at the hospital's emergency department at approximately 6 p.m. He was ambulatory and unaccompanied, carrying the PCP's prescription note. He was officially registered at the front desk at 6.19 p.m. At 6.21 p.m., the electronic medical record logged his acuity as zero acuity unassigned. The chart reflects that at 6.26 p.m., the patient was noted to be with triage. At 6.53 p.m., a registered nurse, the sorter nurse, transported the patient from the initial waiting area to what the chart describes as a staging area for urgent triage. This was an intermediate zone before formal internal triage. The physical layout of this staging area is not described in the record. Between 6.19 p.m. and 6.53 p.m., 34 minutes, the record reflects that no chief complaint was entered into the EMR. No vital signs were taken, and no assessment note was handed to the registration clerk. The system showed the patient as awaiting triage with no clinical data.

SPEAKER_02 20:08

WIC high risk. The ESI handbook is explicit. Sudden speech deficits, motor weakness, facial droop, new confusion, all qualify for ESI-2. ESI-2 patients should be seen rapidly and moved out of the waiting room. The AHA slash ASA benchmarks set door-to-physician contact at 10 minutes or less, door-to-stroke team activation at 15 minutes or less. This hospital used what is called a sorter nurse model. The sorter nurse performs an initial assessment, often verbal, and writes the patient's complaints on paper, which is then handed to the registration clerk to initiate the chart. The clinical data enters the EMR through that manual handoff. When the handoff does not occur, when the paper is not passed or the complaints are not written down, the downstream clinical team has no information to act on. The attending physicians in the ED are looking at the EMR. If the EMR shows a waiting triage with no chief complaint and no vitals, those physicians have no awareness that the patient is even there, much less what they presented with. That is a systems design vulnerability. The entire information pathway depended on a single manual handoff, one person writing on paper and handing it to another person. When that step did not happen, the system produced a two hour gap between arrival and physician contact.

SPEAKER_01 21:49

At 7 p.m., seven minutes after being transported to the staging area. He stated he had walked into something. The record does not address what occurred during those seven minutes. At 7.05 p.m., an emergency room physician encountered the patient. The chart contains a single line entered by the sorter nurse. The patient was examined by the physician. No clinical findings. No vital signs. No separate physician note. No stroke screening. This is the entirety of the documentation from that encounter. This physician was not deposed during litigation. There is no discovery record of a specific attempt to depose them. We do not know what this physician observed during that encounter. Another emergency room physician working that day later testified he only knew this physician's first name and did not know what their specific area or duties were that day.

SPEAKER_02 23:02

Let me put a clinical frame on this. At 7.05 p.m., a physician was physically present at the side of a patient who had just been found on the floor. The chart reflects that an encounter occurred. But it contains no findings, no notation of the patient's neurological status, no vital signs, no assessment. We do not know what that physician observed because they did not create a record and were never asked. It is also possible, based on the deposition of the attending emergency room physician, that this physician was not assigned to that area, and may have been passing through, able to check on the patient quickly and confirm they were not in immediate distress, with the expectation that the patient would be triaged appropriately next. That is my speculation based on the available testimony, but we simply do not know. The teaching point, regardless, is straightforward. Any patient encounter, foo, even an informal one, even a brief one, uh benefits from documentation of findings. A chart entry that says examined by a physician without any clinical findings does not create a usable record for anyone downstream. If that physician had noted ataxia, facial asymmetry, altered speech, or even alert ambulatory, no acute distress, any documented observation, the clinical picture at 7.05 p.m. would be part of the record rather than a gap in it. Close the communication loop on any encounter, even if it's just in passing.

SPEAKER_01 24:46

At 7.38 p.m., 33 minutes after the undocumented encounter, a triage nurse called the patient's name for formal triage. The chart entry reads, Patient called to triage. No response. The nurse did not physically walk to the waiting area to check on the patient. The patient later testified about what was happening on his end. He said he had attempted to stand but didn't have energy and could not move his legs, arms, or fingers. His son later corroborated that when he arrived, his father was kind of blacked out and fell over.

SPEAKER_02 25:27

A patient who was referred from a PCP with a blood pressure of 200 over 120 does not respond when his name is called. The chart documents no response. And no one physically walks to where the patient is sitting to find out why. I raise this as a systems design question. Should triage protocols include a physical check step when a referred patient does not respond to their name? Particularly when the referral note, make if it had been entered into the system horizontal indicated an urgent presentation. This is the kind of protocol question that system safety analysis is designed to address. The question is not whether one nurse should have done something differently. The question is whether the process itself should have a built-in step that catches this situation. And let's remember, um, this case was from more than 10 years ago. Processes that may have been the standard of care at the time of an event may not represent the current standard of care.

SPEAKER_01 26:32

At 8.03 p.m., a stroke team was activated. The E.D. attending, a different physician from the one who had encountered the patient at 7.05, made his first contact with the patient at 8.04 p.m. He later testified this was his very first awareness of the patient. There is no evidence he or the resident working with him had been notified about the patient found on the floor at 7 p.m. or the unanswered triage call at 7.38 p.m. The timeline from this point moved rapidly. At 8.09 p.m., the first vital signs of the entire ED visit were recorded. Temperature 97.6, pulse 79, respirations 20, blood pressure 119 over 94, oxygen saturation 98%, glucose 105. At 8.10 p.m., the neurology team performed a National Institutes of Health Stroke Scale assessment. The score was 4, classified as a minor stroke. The patient was awake and alert but confused about the month. He had mild dysarthria, mild right-sided facial flattening, mild horizontal nystagmus on right gaze, significant right-sided dysmetria, and a wide-based ataxic gait veering to the right. He could not tandem walk. Motor strength was five out of five. At 8.14 p.m., five minutes after the 119 over 94 reading, the blood pressure spiked to 202 over 92. A head CT at 8.40 p.m. showed no acute hemorrhage, but confirmed evidence of a prior right-sided craniotomy with encephalomalacia.

SPEAKER_02 28:32

I want to draw attention to the blood pressure readings because they tell a pharmacokinetic story. At 5 p.m., the PCP recorded 200 over 120 and administered nebivolol and the mlodopine slash ulmazartin combination. By 8.09 p.m., so approximately three hours later, the blood pressure was 119 over 94. That is pharmacokinetically consistent with peak nebivelol and ulmasartin effect. Five minutes later, it rebounded to 202 over 92, likely a stress response during the stroke team evaluation or medication effect fluctuation. Here is the clinical contrast that matters. The neurology team immediately implemented permissive hypertension, ordering a target of 200 over 100. They wanted the blood pressure high. That is standard stroke management. Maintain perfusion pressure to the ischemic penumbra. At the same moment, the oral medications administered three hours earlier were producing their peak blood pressure lowering effect. The 119 over 94 reading occurred during an active ischemic stroke. The neurology team was trying to push the blood pressure up while those medications were pulling it down.

SPEAKER_01 29:47

The stroke team's decision on thrombolytic therapy, TPA, was documented as follows. Reason 4. TPA not administered. Stroke symptoms onset more than three hours before treatment. A separate note read, TPA administered no out of window greater than six hours, given unclear last-known well time. The stroke team noted the patient's history of prior brain injury and seizure disorder as risk factors, but did not formally cite them as TPA exclusion reasons. The documented basis for withholding TPA was the time window.

SPEAKER_02 30:32

The TPA decision involves a scientific question that we will examine in detail in episode two. Specifically, um the time window debate and the prior intracranial hemorrhage contraindication. For now, I will note this. The patient arrived at the hospital at 6 p.m. Symptom onset was reported as approximately 2 p.m. The 4.5 hour TPA window, Fuku, which was a class 1 recommendation in the 2013 AHA slash SA guideline, would have closed at approximately 6.30 p.m. The stroke team's first contact with the patient was at 8.04 p.m. Um, well outside any window. The recorded door to physician time was 124 minutes. The AHA slash ASA benchmark is 10 minutes or less. The question that episode two will explore is what would have happened if the patient had been triaged promptly at 6.19 p.m. He would have been within the 4.5 hour window. The stroke team could have been activated at that time, and then they would have confronted a different question, whether the prior craniotomy and cerebral hemorrhage from 1985 constituted an absolute contraindication to TPA. That question was never reached because the time window expired in the waiting room. That stepwise worsening, it's four to six over three hours, is consistent with the stroke mechanism the defense experts later described. This was a small vessel disease stroke in the pons, not a large vessel embolism. In embolic strokes, deficits typically appear all at once. In small vessel brainstem strokes, deficits can appear and then gradually worsen over 24 to 48 hours in a stepwise pattern. That distinction matters for the TPA debate. If the mechanism was small vessel disease rather than a clot in a large artery, the clinical benefit of a clot dissolving drug is less clear.

SPEAKER_01 32:59

The following morning, an MRI confirmed a moderate-sized acute left pontine infarct. The patient was discharged five days later to inpatient rehabilitation. His permanent injuries included right-sided hemiparesis, cognitive impairment, right-sided facial droop, dysarthria, and loss of independence. He required ongoing assistance with daily activities, bathing, cooking, cleaning, and mobility. He could not write.

SPEAKER_02 33:58

Those are anterior circulation findings. Posterior circulation strokes, strokes affecting the brainstem, cerebellum, or occipital lobes, present differently. Dizziness is the most common symptom. Vertigo, ataxia, visual disturbances, nausea, vomiting, headache. These symptoms overlap significantly with benign conditions. Vestibular, neuritis, migraine, hypertensive episodes, medication effects, the diagnostic challenge is real and well documented. Posterior circulation strokes are more likely to be misdiagnosed than anterior strokes precisely because the early symptoms are nonspecific. They can fluctuate, they can progress over hours to days. A patient can present with nothing more than dizziness and unsteadiness. And the same presentation in the same patient could be a dozen different things. The more specific posterior findings, crossed cranial nerve deficits, Horner syndrome, dysmetria, may not be present early or may not be present at all if the lesion is small. I'm not standing here saying this PCP should have diagnosed a posterior circulation stroke from a presentation of headache, dizziness, and unsteady gait in a hypertensive patient. That is a genuinely difficult diagnostic call. What I am saying is if you evaluate a patient with those symptoms and you decide it is not a stroke, write down exactly why. Pronator drift negative, cranial nerves intact, speech clear, gait a tax sick but symmetric, no lateralizing findings. That documented negative neurological screen, even a brief one, creates a defensible record regardless of the outcome. Without it, you are asking a jury to take your word for what you did years after the fact.

SPEAKER_01 35:46

The clinical timeline is established. A patient with an evolving posterior circulation stroke moved from a PCP's office to a hospital emergency department, where he remained for over two hours before a physician evaluation. In episode two, we examine how the legal system evaluated these events, what was alleged, what was defended, and how the case was resolved through settlement and directed verdict. The content of this podcast is intended for educational purposes only, and does not constitute legal or medical advice. Laws vary by jurisdiction. Medical standards evolve. The case details presented are derived from publicly available court records, appellate opinions, and published reporting. Listeners should consult qualified professionals for advice specific to their circumstances.