Grand Rounds Recap 01.20.2021
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Leadership Curriculum
Pitching an Idea
Identify your audience
Know yourself
Set your goals
Define current standards
Outline needs and resource costs
Sell it
Audience:
Power dynamics - know the dynamics, if you have to do it in stages to build support
Personal relationships - do not bring this into the negotiations if avoidable as can change them
Culture differences - age, background, training, etc
Know what style your audience uses - see below
Know why should we do this and why shouldn’t we do this?
What is your style?
Avoidance
Will eventually get there whether you want to get there or not
May back out early and may need another facilitator to push you
Compromising
Goals are set but willing to compromise and know what they will compromise on
When they give something up and expect you to as well
Accommodating
Doesn’t want to make anyone mad
Values personal relationships and keeping everyone happy more than getting what they want
Competitive
If I don’t win I don’t win, wants everything
Goals
What is the ideal outcome
What is the settle point
What point do you walk away
Start on the same page
Define standards, an argument is only valid if both sides think so
Get as much objective data as you can
Weave in your audience’s own language as best you can
Real world implementation
Money and people are the things we need to know
What is it going to cost, what kind of people are needed
Thinking through all of the steps of implementation
Getting others to care - this is the real pitch!
The person pitching is always more important than the pitch itself
PRACTICE
Be excited and positive, read the room along the way
Keep it objective: don’t assign blame
Utilize any leverage you can
Knowing people along the way or knowing that the idea will fit the mission
Sometimes no is not right now: this takes reading the room
More research, follow-up!
Final pitches included:
Knowing the key stakeholders and who you are pitching too
Pertinent data to support your idea
Understanding the counter-arguments, benefits, drawbacks, what are the settle points, and cut points
Come up with possible solutions
qi/kt: TIa WITH drs. chuko and goff
Stroke: Acute neurologic injury that occurs due to cerebral, spinal, or retinal infarction or brain hemorrhage
Minor stroke: ongoing debate
Generally cited as NIHSS <5 or mRS 0-1
Others have adopted the description of “non-disabling”
TIA: time-based sudden onset of a focal neurologic symptom and/or sing lasting less than 24 hours and caused by reversible cerebral ischemia
Became a tissue dx - caused by focal ischemia without acute infarction
Epidemiology
TIA=0.3% of all ED visits in the US
240K per year
20-25% of strokes are preceded by TIA
Risk factors:
HTN is #1
DM
HLD
A fib
Age
Smoking/ETOH
Pathophysiology
Embolic: discrete, prolonged (hrs), extracranial vs cardiac origin
Thrombotic: atherothrombotic based lesions
Low flow/stenosis: short-lived (minutes) and often recurrent
Cryptogenic: often a cortical pattern of ischemia w/o identifiable source
Localization
Consider the vascular territory and consider the etiology based on the imaging
Multiple lesions, consider more embolic with showering
Dense lesions in a vascular territory
Deeper brain structures - can be embolic or thrombotic but more unique (less likely to be these causes)
Morbidity
JAMA 2000
90 days 10.5% returned to the ED w/ stroke, ⅕ within the first 2 days
JAMA 2020
2.4% develop strokes within 2 days
2.8% develop strokes within 7 days
4.1% develop strokes within 30 days
Change is from:
Better at treating cardiovascular risk factors
Change in definition
TIA Mimics
Migraine
Syncope
Peripheral vestibular process
Seizure, etc
Most common mimics:
Migraine
Syncope
Peripheral vestibular disturbance,
Seizure
This was done after a full workup and final dx by a neurologist
History:
Need to know LKN, duration, activity at onset
Symptoms: full neurological symptoms w/ severity and course
Other associated: headache, nausea, vomiting, LOC, chest pain
PMH: risk factors, personal stoke history
Family history: hypercoagulable disorders, stroke TIA
Collateral history: EMS report and family members
Positive sx
Excess of central nervous system
More likelihood of a mimic (visual, motor (jerking), flashing lights, pain, paresthesia)
Negative sx
Loss or reduction of central nervous system neuron function
Physical Exam:
Diligent and full exam - visual fields, dysphagia, and inability to walk are very important to document
Lab evaluation:
CBC
BMP: metabolic abnormalities
Coags: PT/INR, PTT
Lipid Panel:
SPARCL Study - For LDL range 100-190
High dose atorvastatin vs placebo
ARR 2.2%
NNT to prevent 1 stroke at one year - 258 and at 5 years 45
AHA guideline is that statins are recommended for patients with:
History of TIA
LDL >100.
Target >50% reduction or less than 70
Cardiac evaluation
Cardiac disease is the most common cause of death in TIA diseases in long term follow up
LVH, A fib, and AV conduction abnormalities double the risk or cardiac events at 90 days
10% of TIA patients showed A fib
25% of these showed new onset
Additional 2% on 24 hour monitoring
25% of ischemic strokes are classified as cryptogenic
Maybe indicate undetected paroxysmal AF likely accounts for a proportion of these events
High Sensitivity troponin
TRELAS study
24% stroke patients w/ coronary culprit lesion found vs 79% in NSTEMI-ACS patients
50% stroke patients had no angiographic evidence of CAD
Mechanism: likely type 2 MI or neurogenic heart syndrome
Echocardiogram
10-18% with Cardiac source of embolism
10-11% change in management
Actionable findings:
PFO
Akinetic apical segment
Complex aortic arch atherosclerosis
LV thrombus (surgical management or AC changes)
Imaging:
Non-con Head CT initially - looking for bleeds or intracranial mimics
CTA: looking for high grade stenosis as a cause
Similar recs from the AHA.
MRI imaging as soon as possible
MRI DWI: get changes within minutes - hyperintense signals due to cytotoxic edema within minutes.
Sensitive 83-97% for early ischemia.
DWI + 2-3x greater risk of stroke following TIA
MRI DWI: 32.5% showed acute infarction
MRI DWI: 35.2% showed ischemic lesions
Vascular imaging sensitivities:
CTA: 77-90%
MRA: 82-94%
Carotid US 70-90%
High Risk Criteria:
Crescendo TIAs (very serious and should have the stroke team involved)
Symptomatic internal carotid stenosis >50%
Known/suspected cardiac source of embolism
Known hypercoagulable state including pregnancy, ABCD2 score >=3
Benefits of admission
Expedited diagnostic investigations
Ready access to thrombolysis
Early CEA
Greater opportunity for risk factor modification
ABCD2 score:
The Canadians: prospective validation: >5 high risk (31% sensitivity, 87% specificity at 7 days for a stroke)
>2, 94% sensitivity 12% specificity at 7 days
Annals in 2013: adequate risk start in the ED? NO - does not perform well
Treatment
DAPT- CHANCE and POINT trials
Starting ASA + clopidogrel within 12 hours of symptom onset reduces the 90 day stroke incidence at the cost of increasing bleeding rates when compared to ASA alone
THALES: Ticagrelor and ASA
Reduced risk of stroke after TIA (5 vs 6.3%)
Reduces risk at 30 days
taming the sru WITH dr. gawron
Combined Trauma and Medical Resuscitation
1.3% from the NHTSA medical emergencies precipitate MVCs (survey data)
29% ‘black out’, 35% seizure, 11% Heart attack, 20% Diabetic reaction
Neuro emergencies as cause of accident
MVCs suspicious for medical cause (110 patients):
49% had seizure
6.3% stroke
1.8% ICH
Found down trauma:
2017 - 66% had acute medical condition alone, 7% major trauma, 10% both
Preparation
Keep in mind that the trauma team is a specialist - they are at risk for narrowing their focus
It is important for us to consider the big picture and understand the other etiologies
Recognition:
Mechanism - single vehicle, “found down”, falls (esp elderly)
Risk factors: advanced age, medical conditions
Clinical clues: abnormal telemetry, pumps/line/tubes, neuro deficits, findings that doesn't match the mechanism
Performance under pressure
Stressors:
Primary-those which arise from the demands on the task in front of us
Secondary - aspects of the situation that are unrelated to the challenge itself
Secondary are more likely to impair you performance
Selective attention - allows us to focus on the task but can lead to worse performance if there are multiple inputs of information
Thinking under pressure - Dual-process theory
System 1: intuitive, unconscious reasoning that relies on heuristics
System 2: conscious, analytics
Clinical knowledge: cyanotic congenital heart lesions WITH dr. kein
Cyanosis
Peripheral: distal extremities, vasoconstriction, diminished peripheral blood flow
Central - blue discoloration around lips, tongue and sublingual, +/- peripheral
Low SaO2, abnormal hemoglobin
CHD, sepsis, respiratory disorders, hemoglobinopathies
Historical clues to cyanosis
Feeding: diaphoresis, crying, decreased intake, increased time and decreased weight gain
Activity: irritability, decreased activity
Breathing: fast or irregular
Physical exam findings: tachypnea, tachycardia, hepatomegaly , lethargy
Cyanotic Congenital Heart Diseases
Truncus Arteriosus:
Single truncal valve that leads to an artery that splits to the aorta and PA w/ a large VSD
Equal pressures in the pulmonary and systemic - leads to early pulmonary HTN
Presents: birth to 2 months
Heart failure, exam findings (bounding pulses)
CXR: cardiomegaly, right sided arch
EKG: Normal/RVH or LVH
Transposition of the Great Vessels
Aorta off RV and PA off LV
Presents at birth with severe cyanosis
92% are diagnosed within the first day of life
Loud single S2
CXR: egg-on-a-string
EKG: RAD, RVH
Tricuspid atresia
No connection between RA and RV
Entirely dependent of the ductus for pulmonary perfusion
Presents: birth to 2 weeks (when the ductus closes)
Single S2
CXR: +/- small heart
EKG: LVH, R/L Atrial enlarge
TAPVA
All 4 pulmonary veins don’t drain where they are supposed to
Most common is supra-cardiac
Presentation: obstruction dependent
CHF, shock
No specific exam findings
CXR: snowman or figure 8
EKG: RAD, RVH, RAE
Tetralogy of Fallot
Large VSD, RVO tract obstruction, overriding aorta, RVH
R and L sided pressures are equal
Cyanosis is dependent on the degree of obstruction
Presents: Birth to 2 weeks
Symptoms: tet spell - hypercyanotic spell that resolves with increased SVR / decrease preload (knee to chest)
Murmur
CXR: boot shaped heart
EKG: RAD, RVH
Ebstein’s Anomoly
Leaky and displaced tricuspid valve, with ductal dependent pulmonary blood flow
AV septal defect
Total mixing lesion
Frequently with Trisomy 21
50% of kids with Trisomy 21 will have cardiac defect
Double outlet RV
Both the pulm and systemic arise from the RV, VSD dependent
Pulmonic atresia
Will present similarly to Tetralogy of Fallot
HLHS
Underdeveloped LV and small Aorta
Frequently present in shock
Initial management of blue baby:
Hyperoxia test: give 100% for 10 minutes - if ABG <100, then cardiac in origin
Modified Hyperoxia test: put them on O2 in ED and put on pulse ox and see if up trends
STAT echo
Ductal Dependent (transposition, tetrology, epstein, critical pulm atresia) -prostaglandin E1
0.05mc/kg/min
Watch for APNEA, hypotension
Be prepared to intubated
Maintain O2 sat 75-85% (higher can increase pulmonary circulation too much)
Judicious fluid management (nothing >10cc/kkg)
Early inotropic support
Cardiology and cardiac surgery consultants
Tet Spell Management: TOF, other RV outflow tract obstruction lesions (pulmonic stenosis)
Hyperpnea, tachypnea, agitation ->AMS, LOC, death
Stepwise treatment approach:
Knees to chest (with parental comfort)
100% O2
Morphine (to calm agitation)
5-10 IV fluid bolus (increase preload)
Phenylephrine infusion
Propranolol (to decreased HR and allow adequate filling)
Surgical Repair
General postop complications
Postpericardiotomy syndrome (echo for effusion/tamponade, salicylates)
Pleural effusions - may be chronic
Infectious complications (2% will end up septic)
Modified Blalock-Taussig Shunt: Goal saturation of 70%
Shunt obstruction - should have a murmur
If suspect, start fluids and heparin
Arterial switch for Transposition lesions
When they are switched the coronary arteries are re-implanted.
ED visits in children with CHD: many other reasons that are not cardiac related
Important to remember that they have decreased reserves
Adults w/ CHD: arrhythmias, endocarditis, bleeding and thromboembolic risk
Concomitant renal/lung/liver disease
Pre-existing EKG abnormalities (bundle branch)
Baseline O2 saturations
Chest pain consideration
Much lower frequency of the pain being due to ischemia or ASC
wellness grand rounds WITH dr. shewakramani
Maslow’s Hierarchy of needs: people are at different stages and at different stages people need different things
This can make it hard to figure out what is important and what your passion is
In residency often living in the physiological needs area
How wellness is approached in healthcare: do a lot of activities, yoga, massage
These take time, we only have so much
You can do all of this and feel great into the shift - what about during the shift?
Your day can easily be ruined by patients and moments
Bayleaf: 7 steps to a happy life/job/sucky day
First know when: recognize what your trigger is
The steps work sequentially but are interconnected/interdependent
B: Breathe
Fight the natural desire to respond back to angry people/patients
Focus on the air entering and let it out
This creates space to choose the most appropriate response, better response
A: Accept
What it isn't: ignoring the issues and pretending everything is ok
What it is: it just is - you can’t change the problems, but now what?
There is no purpose in resisting
Serenity prayer: things we can control, things we can influence, and things we have to accept/adapt.
Realizing that the only thing we have complete control over is you
Influence: we can share ideas but people may not accept this
Accept: elements of the issues you can neither control nor influence
Y: ask whY
Socrates: he got smarter by asking questions
The one thing that I know is that I know nothing
Why are you here? But asking in the way of kindness not bitterness
Patients will pick up on the bitterness
L: Listen
It is more than just hearing, it is paying attention to the people and how they move/react
It is not waiting our turn to talk or leave the room
The best communication is when you can listen well and turn it around
Who is coming into who’s life?
People trust the person, not the degree
Nobody cares how much you know, until they know how much you care
Teddy Roosevelt
Seek first to understand then to be be understood
Steve Covey
Echoing: using someone else's words, it allows you to enter their world
E: Empathize
Understanding feelings and be there with them
Walk a mile in their shoes, or walk a mile in your shoes in a relevant situation
A: Appreciate
What it isn't: being sarcastic about it, sarcasm spreads
Finding something to learn from
What is this teaching me?
Feel grateful for things that you have, in the negatives things you can learn
F: Forgive
This is a tough one, but all the prior steps have brought us here
You can’t just forgive, otherwise you will feel like a doormat
We can not expect our patients to be perfect and kind, they are uncomfortable
