Grand Rounds Recap 3.9.22
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DR. GIBLER ANNUAL VISITING PROFESSOR LECTURE WITH DR. CHRIS MILLER
Part I: Leadership development in Emergency Medicine
Leaders need to focus on culture and process with the aim at producing outcomes that benefit patients.
The COVID-19 pandemic has unveiled new dimensions of service towards our patients and towards each other.
Do not lose sight of patient care at the center of our mission
Approach leadership, teamwork with appreciation and respect for individual strengths (ie. the “Iron Hexagon” if any side crumbles, the structure collapses)
Leaders need to be cognizant of diversity and equity when recruiting and supporting individuals in leadership positions.
Leadership development and growth in residency
“Never mistake a clear view for a long distance.” While our expectations are often linear, leadership transformation is typically not.
Lessons for development and growth by year
R1s: Know yourself; Seek self-improvement; Follow-through: ensure tasks are prioritized, understood, and accomplished
R2s: Decisiveness; Seek responsibility. Take it; Be tactically and technically proficient; Make mistakes. Fail fast. Move forward.
R3s: Train together as a team; Keep our team consistently informed; Set the example; Get comfortable in the uncomfortable.
R4s: Develop a sense of responsibility among our team; Know our team and look out for their welfare; Those you lead are there to do a job. Let them.
Fractals are complex patterns that are similar across different scales and repeat a simple process over and over. The above leadership lessons can be perceived as the building blocks of small unit leadership that allow you to succeed in a fractal way.
Part II: Emergency medicine leadership in healthcare development, evolution
Healthcare is at a point where we must think differently due to healthcare workforce issues, changing expectations of patients for engagement at home and in the office, and healthcare costs, fragmentation, and complexity.
As we innovate, we need to think and act faster, we need to fail and then evolve to the next step.
Emergency medicine physicians can lead in this space given our unique role and traits.
As one, systems must integrate and rationalize.
We must scale impacts, but scalability is irrelevant without matched performance outcomes.
Goal is to drive high quality at lower cost, which is encouraged and renumerated by the government. In order to facilitate this, we can look for fractals and support, expand those small units that contribute to success.
We must treat patient progression and capacity like a time-sensitive disease and bring the same degree of focus and rigor to these issues.
Lecture Summary points:
Unity of purpose will banish fear.
Risk is the tariff we pay to leave the shores of predictable misery.
Accountability - what we permit, we promote.
Take care of your humans.
QI/KT: HYPERTENSION WITH DRS. TILLOTSON AND YATES
Hypertension defined: SBP ≥ 140 or DBP ≥ 90.
Caveats to above definitions are if your patient is pregnant when they enter into a different paradigm depending on gestational age and blood pressure.
Hypertensive emergency defined by hypertension and evidence of end organ damage
Important to ask about symptoms suggestive of cardiac manifestations (ACS, dissection, microvascular disease), neurologic manifestations (hemorrhagic v. ischemic stroke), ophthalmologic manifestations (retinopathy), pulmonary edema, or renal failure.
Additional questions important to investigate “zebra etiologies” include symptoms suggestive of pheochromocytoma, thyroid, or cushingoid features, OSA, sexual function, diet, substance use disorder, supplements, and over the counter medications.
Zebra etiologies
Endocrine: Pheochromocytoma, Cushing’s, primary hyperaldosteronism, thyroid abnormalities
Congenital: aortic coarctation, renovascular abnormalities
OSA
Hypertensive urgency is defined by some as hypertension (≥ 180/110) without symptoms or evidence of acute target organ injury, but with significant risk factors.
High risk comorbidities: personal/family history, CKD, HLD, diabetes, smoking, substance use, obesity, OSA, adrenal/thyroid disorders, medication, or relevant symptoms
Patients are still often referred to the ED by PCPs for evaluation of potential hypertensive urgency because their guidelines still recommend that they do so.
But is it real and do you need to treat it? No, most blood pressures resolve on reassessment, and risk of antihypertensive is often greater than the risk of transient blood pressure elevation. Ultimately, evaluate and treat the patient in front of you.
Testing in asymptomatic hypertension
Options are vast for what you could order; however, there are no RCTs to suggest benefit in any specific tests, though organizational guidelines may suggest certain tests.
Most common tests that are ordered are a renal panel or BMP and cardiac screening, which could include a troponin or EKG. These two tests are supported by guidelines published in the American Family Physician.
Our protocol: BMP and EKG
Why should we care about asymptomatic hypertension?
Increased risk of cerebrovascular and cardiovascular disease with every 20 mmHg SBP and every 10 mmHg DBP. This is most notable among those aged 30-60 yo.
Also, question whether the blood pressure readings are actually secured correctly (prepare the patient and get them as comfortable as possible, use appropriate cuff and apply to appropriate area, document averages)
Initiating antihypertensives in the ED
If patients have 2 or more recorded BPs > 140/90 mmHg, consider starting an anti-hypertensive, especially in select patient populations with poor follow-up or markedly elevated BPs.
Which antihypertensive do you start?
ALLHAT Trial evaluated thiazide diuretics, CCBs, ACEis, and alpha blockers and found that CCBs were favored in all cause mortality reduction and stroke prevention, but worse at preventing HF. CCB and ACEi lowered BP and decreased all cause mortality, but ACEi worse at preventing stroke.
Two metanalyses also evaluated this question, but somewhat mixed results between the two.
Ultimately, AHA and JNC guidelines (and our protocol) suggests thiazide diuretics (HCTZ 12.5 mg qD starting dose) or CCBs (Amlodipine 2.5 mg qD starting dose). These are also reasonable options with respect to cost and have supplemental financial support via GoodRx, Walmart/Target $4 lists, etc.
Special populations
CKD - In patients 18 yo or older with CKD and HTN, antihypertensive treatment should include an ACEi or ARB to improve renal outcomes. Also recommended that these patients have close follow up.
Race - Race is a social construct. Choose the best medication for the patient in front of you.
Follow-up for patients
AHA recommends monthly follow up until BP control is maintained. This is supported by three different trials (SPRINT, ACCORD)
PCP follow up at UC - can include ED DC community clinics and referral to CHW.
Our protocol recommends follow up within 1-2 weeks with PCP after starting antihypertensives and follow up with a PCP at the next scheduled appointment for asymptomatic hypertension.
R1 CLINICAL KNOWLEDGE: PRES & RCVS WITH DR. SOBOCINSKI
Posterior Reversible Encephalopathy Syndrome (PRES) remains poorly understood, the key features of this syndrome are that it classically affects posterior cerebrum, is reversible, and is notable for edema secondary to hypoperfusion and capillary leak secondary to hypertension.
Risk factors for PRES include those related to: (1) hypertensive states (primary hypertension, secondary hypertension, renal disease (55%), autoimmune disorders (45%)) and (2) endothelial dysfunction (immunosuppression, cytotoxic agent use, infection/bacteremia/sepsis, eclampsia, autoimmune disorders like SLE, RA)
How does PRES present? Most common signs/symptoms include encephalopathy (28-92%) decreased level of consciousness (67-90%), acute hypertension or labile BP (61-80%), seizures (70-74%), visual disturbances (20-67%), headache (26-53%), and focal neurologic findings (5-15%).
Imaging in PRES: CT non-contrast may demonstrate vasogenic edema. MRI T2 Flair will similarly demonstrate vasogenic edema in affected areas.
PRES Management:
Blood pressure reduction with a goal 10-25% decrease using an easily titratable gtt such as Nicardipine.
Consider anti-epileptics in consultation with Neurology
Will likely require ICU level of care
Reversible cerebral vasoconstriction syndrome (RCVS) likely results from endothelial dysfunction and vasomotor dysregulation. Risk factors for RCVS include female predominance (2-10:1 predominance), substance use or use of vasoactive medications (triptans, sympathomimetics, estrogen), pregnancy, pheochromocytoma, surgery, and chiropractic neck adjustments.
How does RCVS present?
Severe, hyperacute headaches (94-100%), no evidence of aneurysmal SAH (but SAH okay), normal CSF, multifocal segmental cerebral artery vasoconstriction on CTA, MRA, or catheter-based angiography, potential focal neurologic deficits (visual, hemiplegia, dysarthria, numbness) depending on area affected, reversibility within 3 months.
RCVS2 Score on MDCALC includes following criteria: Recurrent or single thunderclap headache, intracranial carotid artery involvement, vasoconstrictive trigger identified, sex, SAH present on imaging.
Score > 5 has a 96% PPV, 96% NPV with 99% specificity and 90% sensitivity.
Score < 2 has 100% PPV, 71% NPV with 100% specificity and 85% sensitivity
Imaging may demonstrate evidence of SAH on CTA or could be normal. Cerebral angiography could demonstrate diffuse irregularity and narrowing (beading) or be normal if vasospasm resolves.
RCVS Management:
Broad blood pressure goals (SBP 90-180 mmHg) with permissive hypertension. May give Nicardipine or Labetalol for elevated BPs and fluids for hypotension.
Address pain with opiates or NSAIDS. Avoid triggers such as triptans and vasoconstrictive agents.
No seizure ppx necessary, but can treat seizures as normally would with BZDs.
Avoid steroids as they have been noted to increase mortality in RCVS
Most vasoconstriction (~90%) resolves without further medical intervention.
Counseling on trigger avoidance
R4 CAPTSONE: BIAS IN MEDICINE WITH DR. WOLOCHATIUK
There are many types of bias, and the focus of this lecture will be cognitive bias, but cannot discuss bias without thinking about implicit and explicit racial bias.
Bias is a strong inclination of the mind or a preconceived opinion about something or someone. Cognitive bias refers to systematic errors in thinking due to human processing limitations or inappropriate mental models.
There are over 100 types of cognitive bias, and we are all at risk with potential to affect our clinical decision making.
EM is ripe for cognitive biases given the environment that prizes efficiency and may push care providers to rely more on heuristics.
Some common cognitive biases include:
Availability bias - informed by recent diagnoses or exposures
Base rate neglect bias - base rate of a pathology is low, but pursue that diagnosis despite the low probability.
Search satisfying - Cease looking further for information when first plausible solution is found.
Diagnostic momentum - Continue treatment plan or adopt thought process initiated by others without independently evaluating the situation.
Dual process thinking is one way to address cognitive biases
Type 1 thinking - classically, fast, intuitive, pattern recognition - is where the majority of us spend 95% of time; however, it is also most prone to cognitive errors.
Type 2 thinking - classically, analytic, slower, more methodical - can still be marred by bias.
Ideally, need Type 1 and Type 2 thinking to facilitate optimal clinical performance.
Racial bias in medicine
Race is a persistent cause of healthcare disparities and a powerful determinant of a patient’s health, along with their sex, age, insurance status and socio-economic status, and these factors work additively from a risk standpoint
It impacts treatment decisions, treatment adherence, and patient health outcomes
Check out the book, Seeing Patients, by Dr. Augustus White III for further discussion on disparities in medicine.
Examples born out in several studies:
The time it takes for EMTs to transport women to a hospital after a heart attack is longer than it is for men
Hispanics receive fewer bypass surgeries for heart disease than other patients and fewer basic health-care measures such as flu vaccines
Similarly, African Americans receive fewer kidney and liver transplants than other patients, and more castrations when they have prostate cancer.
African American diabetics undergo more amputations than other groups
Adults from underrepresented racial groups whos have CAD and arrest receive fewer early interventions (angiography, PCI), had longer hospital stays, and higher death rates - not just blacks! Asians, pacific islanders, and native americans
Why is it difficult to discuss this? It can be uncomfortable and is often unconscious. But important for all of us to examine personally and to be activists and advocates for given implications for our patients.
How to combat bias?
Bias-specific teaching
Metacognition
“Slowing down”
Checklists
