Grand Rounds Recap 9.2.2020
/
history of stroke and reperfusion WITH Dr. kreitzer
The story of how it all happened...
Epidemiology of Stroke
800K people are effected per year
87% are ischemic strokes
5th leading cause of death, and 3rd leading cause in women
Annual cost is $34 billion
Complications from stroke
Infections
Depression
Limb contractures and pain
DVT/PE
Costs to the family and society
Approximately 2400 years ago Hippocrates:
Described Apoplexy
A disease “to strike down with violence, a swift and terrible act by the gods”
Thought to be due to a plethora of body humors
1600-1800
1600:
William Harvey described the circulation of the brain
Stroke was thought to be due to obstruction due to “blood lacking animal spirits”
1700s:
Stroke was accepted as a vascular disease
1800s:
Crude CEAs were performed
No real stroke treatments, not treated differently than a psychiatric disease
1800s and Beyond
Still called apoplexy: when a patient falls to the ground and the person is struck instantaneously as if struck by lightning.
1928: blood vessel syndromes are recognized
1929: first cerebral angiogram
1950: NINDS as part of the NIH to treat neurologic and psychiatric casualties of WWII was created
Lytic therapy
1933: first recognized that lytics could dissolve fibrin clots
1946: tPA was described by danish researchers
1958: first use of lytic in stroke patients
1970s: animal models for breaking up clots
1986: lytics for MI were approved by the FDA
Lytics fell out of favor due to early studies that used a slow perfusion long after the onset of the stroke
1972: head CT was available which lead to the next advancements
Modern Stroke research:
1981 was the seminal research in primates:
Closed the MCA and reopened it
Measured cerebral blood flow
Defined the concept of “penumbra”
That some neurons can be saved
Stroke Care in the 1980s:
Focus was on rehabilitation
No concept of a “window” of time
There was still a need for a tool for reporting clinical exams in research
The NIHSS - was created as a tool to communicate findings
1983: Posterior strokes with streptokinase infused
After this more work was done to evaluate and characterize lytics
NINDS Phase 3
Many animal studies coming out about acute ischemic stroke and tPA
1988 was the perfect time:
Cell phones
Pilot tPA study was completed
NIHSS was developed
Model of the Rapid Stroke team was developed in Cincinnati
Regional and multi-disciplinary
Used early cell phones
Enrolled the patients in the NINDS phase III study
Used a trauma model where every minute counts
Part 1
Enrolled patients within 90 mins
Part 2
Enrolled patients within 91-180 minutes
All to look at different doses and ability to enroll
December 1995 trial was published
FDA gave tPA approval
624 patients
No significant difference in improvement at 24 hours
Significant improvement at 3 months based on 4 outcome measures
NIHSS
Barthel index
Modified Rankin
GCS
No significant different in death
NNT of 7
Shorter time to treatment showed more favorable outcomes
Criticisms of this study:
Subjects in the later time frames had less severe strokes in the tPA group
This was due to patient recruitment
Funding by the people who created tPA
Lack of 24 hour benefit
Up to ⅕ may have not had a stroke
Hard to blind tPA as it looks different that saline
Many other studies that do not show the same benefits
Though a lot of them used different agents and different inclusion/exclusion
Policy and Controversy
“Brain Attack” campaign was immediately launched
AHA rapidly incorporated tPA
AHA was getting funding from Genentech
Some on the panel did not disclose relationships for speaking
Stroke care is nuanced:
Changes have been made in future studies due to the criticisms
Some critiques are not valid
Any hemorrhage is a bad outcome: not true
Neurons die within 3-6 mins after they lost blood: penumbra exists
Hurdles that were still to overcome:
Policy change and reimbursement
For 10 years after the FDA approval only 1-1.5% were treated
No infrastructure was in place
Big change for neurologists
No money for stroke infrastructure
Guidelines to improve care were made
Stroke care is better when care is delineated by what hospitals are capable of
How to make us better:
Devices started coming out
IMS III: Endovascular Therapy (EVT) vs tPA alone?
Neutral study and was stopped early
Devices started coming out and getting better
Sept 2014: MR. CLEAN was presented
Showed benefit for LVO in the anterior circulation on CTA getting EVT
After this many studies came out
Pooled data showed:
Patients do better neurologically and life saving
Extend time to treatment
DAWN (6-24 hrs) and DEFUSE (6-16 hrs)
CTP and MRI were used and looking at imaging mismatch
Immediately practice changing
CTP guided endovascular therapy
Penumbra and core is calculated with a mismatch ratio
Core infarct <70ml
Mismatch is >1.8
Mismatch volume is >15ml
No upper age limit
RESILIENT trial
Same study was replicated in Brazil with less availability
Extended window lytics:
Wake-up protocol
Acute stroke MRI with DWI and FLAIR sequences
MRI timing within 3.5 hours of symptom recognition
To enable treatment within 4.5 hours
Patient must meet all other inclusion/exclusion criteria for tPA
These are rare patients
Shortening the time to treatment
Mobile Stroke units
Ongoing trial at this time about outcomes and cost effectiveness
tPA vs TNK
TNK is less likely to be deactivated
It is more fibrin specific than tPA
A one time bolus
No major difference in first few studies, some studies may show it helps
MOST
Augmenting the tPA treatment with anti-platelet agents
Lytic + EVT vs EVT alone
SKIP - recent trial showed non-inferiority of EVT alone
2 other are in process
Can reperfusion save lives?
Extend the people out to 10 years and a clear benefit is seen
Will see a survival benefit over time in years
R4 case follow-up WITH dr. gottula
Aortic Stenosis
Pathophysiology
3rd most common cardiac disease (after CAD and HTN)
>85 years old: 48% of patients have AS
Symptomatic AS has a 25% / year mortality
Preload dependent state
Decreased stroke volume
Leads to LVH
Then to diastolic dysfunction
In AS: LVP is significantly higher than the aortic pressure
Diagnosis
Physical Exam Findings:
Loud of S2
Systolic crescendo-decrease murmur
Likelihood ratios are not great on PE findings
Ultrasound is used to grade AS
3 things to measure:
Functional valve area
Peak velocity
Gradient across the valve
AV continuous wave doppler to measure the AV VTI
Will give a peak velocity ( >2.5m/s is diagnostic of AS)
Mean gradient (>10 is mild)
Pulse Wave on the LVOT
Get the VTI
Ned the LVOT diameter to calculate the area (machine will do this)
Treatment
Symptomatic patients
Surgical
Medical management
Afterload reduction and modify risk factors
HTN
Must be cautious when modifying the blood pressure
Diuretics are not typically sufficient
CCB and BB have inotropy on an already overloaded ventricle
Vasodilators are dangerous in AS
Nitroprusside
Arteriodilator with an immediate onset and offset
Agent of choice
Vasodilators used only in:
Severe HTN and decompensated heart failure
Need invasive monitoring
Helps CI and stroke volume
Hypotension
Vasopressor of choice
Phenylephrine
Increased the diastolic pressure which helps coronary perfusion
Reflex bradycardia
No epinephrine
Increases myocardial oxygen demand
Reflex tachycardia
r1 clinical treatment WITH dr. gillespie
See Dr. Gillespie’s full post here
Acute Low Back Pain
Between 3-6 weeks and less, below rib cage and above gluteal folds
Nonspecific low back: no identifiable pathologic cause
Epidemiology
2.4% of ED visits are back pain
50-80% of adults will have a clinically significant back pain event
Treatment goals:
Reduction of pain and disability
Setting expectations
Reassurance and Education
Pharmacotherapy
Treatment options:
NSAIDS
Evidence from 2020 Cochrane review
Slightly increased improvement and reduction of pain
Disability reduction, high quality evidence
No difference in adverse events, low quality
Return to work time interval
No clear difference vs placebo, very low quality evidence
Combination therapy:
2015: Cyclobenzaprine or percocet
One week follow up no improvement with the addition of percocet or flexeril
Acetaminophen
no improvement after one week with the addition of acetaminophen
Lidocaine patches: 2005 pilot study
Follow up pain scores
Statistically significant
Showed improvement in life
Insufficient evidence but strong safety profile may provide significant benefit
Skeletal muscle relaxants:
Improvement in pain and physical outcomes when solo therapy
Moderate to high quality evidence
In combination therapy showed no improvement at one week
Significant side effect profiles
Dizziness, drowsiness, work impairment
2019 Annals of Emergency Medicine
Addition to ibuprofen did not improve functionality or pain more than ibuprofen alone at one week follow up
Acetaminophen
No therapeutic efficacy in acute low back pain
Cochrane database in 2016
No benefit
2019 in Pain
Ineffective and no therapeutic benefit
Steroids:
Non-radicular low back pain:
IV steroids showed not significant effect
Prednisone showed no therapeutic benefit
Opiates: very limited literature for acute low back pain
2015 JAMA did not show benefit when combined with ibuprofen
Yet frequently prescribed for the low back pain in the US ED’s
Minimal evidence but high potential for harm
Insufficient evidence
Injectables
Antidepressants
Anti-epileptics
Acupuncture
Mild to moderate benefit in the ED setting in Australia
Temperature therapy
2006 Cochrane:
Heat wrap shows some improvement in pain after 5 days
Patient education
2 studies show that validating pain and education do help the pain
Spinal manipulation
Maybe for acute low back pain in up to 6 weeks
Vertebral Artery Dissection is a real risk
Physical therapy and exercise therapy
May help in chronic pain but no real benefit for acute low back pain
Massage
Mild improvement in pain
r2 cpc WITH drs. ijaz and roche
Chronic Salicylate Toxicity
There are multiple medications with ASA in them
Acid-Base Imbalance
Normal pH with AG and low bicarb
Metabolic acidosis
pCO2 is low
Respiratory alkalosis
Epidemiology
15000 cases per year
>60% are intentional
Toxic dose
150mg/kg or 6.5g, whichever is less
Symptoms:
Tinnitus
Nausea and vomiting
Confusion
Tachypnea
Chronic Overdose
Mostly in older patients
Often due to therapeutic misadventures
Underlying disorders like chronic pain conditions play a role
Frequently unrecognized
Serum concentrations are intermediate elevation
Mortality
Is higher than acute OD due to delayed recognition
Pathophysiology
ASA stimulated the medulla causing hyperventilation
Causes increases lactate
Increased fatty acid metabolism leading to a wide AG
Increased renal bicarb excretion
Metabolic acidosis
Toxic effects:
Serum pH determines level of non-ionized salicylate
Non-ionized is the more toxic form
Lower pH causes more of the non-ionized form
Chronicity
Suggests much higher tissue levels of salicylate
Treatment
Activated charcoal if taken acutely
Bicarb bolus: 1-2mEq/kg
Infusion: D5W +150mEq @ 2x mIVF
Goal urine pH 7.5-8.0
Glucose
These patients have a neuroglycopenia
Need to supplement dextrose in the fluids and consider empiric D50 in AMS patients
Potassium repletion:
Goal K >4.0
Add 20-40 mEq to Bicarb gtt
Dialysis:
ASA >100, ASA >90 w/ renal dysfunction
If there is pulmonary or cerebral edema
Standard therapy fails
r4 capstone WITH dr. hughes
Words Matter
What
The words we choose
Sexualizing procedures
On a patient’s worst day we are sexualizing something that we are doing to them, there are other ways to represent ‘exciting’ procedures
Words that bias providers in the EMR
Negative interactions
Words like drug seeking and non-adherence were found to be used more in black patients in the EMR.
Instead of Substance abuser change to “having substance use disorder”
The word abuser biased the physician to think the patient was personally culpable and in need of punitive measures vs other words
Neutral vs stigmatizing language
In patients with sickle cell disease:
A positive attitude toward the patients and how aggressive with treatment was measured
Neutral chart lead to physicians being more aggressive with treatment and positive
Documentation in the ED has been shown to bias the care on the inpatient side
Instead of using “the patient states” just write what the patient is describing
“State” as a word could bias the future providers
Quotations
For pain description is appropriate
Though we often use them to use the patient’s words against them
How
How we deliver the words
Setting
If delivering feedback should be in person to help provide actionable feedback
Non-verbal cues
Men
Lean into the conversation
Nodding is agreeing with the statement
Women
Sit back and “remove from situation”
Nodding is listening
Be mindful of
How you stand
If you’re rushing
How much eye contact you make
Tone
Empathy and authority together while running a resuscitation are key
Nursing evaluations on the residents:
51% of female residents rated negatively in competency
Only 20% of male residents were rated negatively
Why
Using words to inspire action
As physicians we have a platform build into our profession
Don’t need to have a passion in policy to inspire change
We should use our platform to help people and the passions we have
Don’t be afraid to ruffle feathers
But...pick your battles and come with solutions
r3 small groups WITH drs. hunt, pulvino, and wolochatiuk
Admit, discharge, transfer w/ Dr. Wolochatiuk
32 yo F that is 32 weeks pregnant with sudden R sided facial paralysis LKW 2 hours ago
Physical Exam
Cant wrinkle forehead with flattened nasolabial fold
No other CN deficits
No other findings on exam
Bell’s Palsy
Bilateral facial palsy=Lyme until proven otherwise
Bell’s is very common in the 3rd trimester and first week postpartum
Important to work up HELLP syndrome in these patients
Taste is not equal on both sides of the tongue in Bell’s vs norma in stroke
House-Brackmann grading will help determine treatments
Disposition:
Discuss with the patient’s OB and discharge
65M with HTN on lisinopril coming in with dental pain
Physical Exam
Tongue and lip swelling started an hour ago
What else do you want to know?
Managing secretions?
Tongue space?
Voice muffled?
What to do?
NP Scope with a pre-loaded tube for possible intubation
Disposition:
No ENT
Transfer to a center for ENT evaluation
Angioedema: 2 types
Bradykinin
Histaminergic
Treatment:
H1 blockers
Steroids
Epinephrine
TXA:
Literature shows no help in the acute side, maybe in hereditary in prevention
2 yo M with a Fever x4 days
Physical exam:
AOM
Given antibiotics and discharged
Comes back in after 4 days on abx with swelling now
Physical exam:
Swelling and erythema behind the ear
Tender over the mastoid
Normal CN
Diagnosis
Mastoiditis
Disposition
Transfer for peds ENT
may need a tympanostomy or mastoidectomy
Mastoiditis
Suppurative infection of the mastoid air cells
Usually complication of the OAM
No change in incidence with rescue prescriptions for AOM
Clinical diagnosis
AOM on otoscopy
Inflamm changes over mastoid
Protudent mastoid
CT?
CT:
CNS involvement
CN involvement
Hx of cholesteatoma
Cover staph, strep, and H flu >>>Pseudomonas
Clinda
If MRSA concern:
Vanc+Ceftriaxone/unasyn
Vanc +zosyn in severe or chronic
55yoM with dental pain x 1 week hurts to chew
Physical Exam
Fluctuance over the buccal surface
Fluctuance over the L maxillary molar
What else do you want to know?
Trismus
CN Involvement
Submandibular or sublingual involvement
Disposition?
Discharge after drainage with dental follow up in 48 hours
Periapical Dental Abscess Drainage:
Poke the area and milk it out
Provides a lot of relief
Oral Boards Case w/ Dr. Pulvino
Pain and swelling in the mouth with associated SOB
Febrile, tachycardic, tachypneic
Physical Exam
Swelling under the chin, feels more prominent in then neck
Floor of mouth is edematous
Ludwig’s Angina
Severe and rapid cellulitis of the mouth and submandibular spaces
Swelling of soft tissue and displacement of the tongue posteriorly causing airway obstruction
Mortality is down to 8% due to antibiotics
Most are odontogenic in etiology, especially from the molars
Management
Antibiotics
Unasyn, Clindamycin, PCN +/- metronidazole
Airway
Glycopyrrolate for secretion control
Afrin and lidocaine to prepare for fiberoptic intubation
Test narew with a NP airway to see what will work for ETT size
Lube the NP with the lidocaine
Awake look with Ketamine and push paralytics once view is obtained
Prep the neck ahead of the intubation
ENT consult and airway management
Steroids may help avoid the need for airway management
Epistaxis with Dr. Hunt
Epidemiology
60% of adults will have one episode in their lifetime
10% will need medical attention
More likely in men than women
Thought that estrogen helps provide a healthy mucosa
Anatomy
Anterior is 90%
From Kiesselbach's plexus
Posterior is 10%
Significant morbidity
From sphenopalatine artery and branches of the carotid artery
Many different causes
Trauma (nose pickers)
Cocaine use
HTN
Coagulopathy
Lack of humidity
Chronic vasoconstrictor (afrin) use
Malignancy (esp in the Asian population)
Renal/liver insufficiency
Initial assessment
ABCs
Can have hemorrhagic shock from the nose bleed
Vitals, H&P
Medical problems
Any anti-coagulation
Exam
Use full PPE to protect your eyes and mouth
Patient positioned in sniffing position and not head tilted backwards
Nasal speculum
Allows better visualization on the area
Insert up to the nose and then back to the toes to avoid the turbinates
Fraser tip suction
allows better suction
Light source to see what your doing
Management
Vasoconstriction and direct pressure
Blow nose and apply Afrin (oxymetazoline)
Direct Pressure for 15 min
Hold the ala, not the bony portion
Nose clip to help with compliance
Cauterization
Silver nitrate
Avoid doing both nares
Small areas
Go from periphery to the center
TXA
RCT in 2019
135 TXA and compression vs nasal packing vs simple nasal compression
TXA as effective as anterior packing and decreases rebleeding rates
Anterior packing
Painful and uncomfortable
Patients may need anxiolysis for appropriate packing
Important to anesthetize the area
Will need 24-48 hours follow up with ENT
Merocel
Nasal tampon-flat fabric with strings
Dip in lubricant and wait until fully in the nares then inflate it
Gauze
Use bayonet forceps and shove in until no more can be added
Rapid rhino
5cm for anterior bleeds and 7.5cm for posterior bleeds
Dip in sterile water prior to insertion
Antibiotics
Reasonable to withhold abx though
Should be given to immunocompromised and those with valvular heart disease
2014 analysis of 3 studies
showed no TSS or otitis media
Uncontrolled bleeding
High likelihood of posterior bleed
ENT consult
Admission
