Grand Rounds Recap 10.28.20
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Morbidity and Mortality WITH Dr. Koehler
Case 1: Acute Upper GI Bleed
Risk factors
Prior bleeds
Anticoagulant use
Age 70-80
Steroid use
SSRI use
International Society for Thrombosis and Hemostasis defines major bleeding as fall in hemoglobin of 2 or more or need for 2 units of transfusion or more
Anticoagulation and antiplatelet medications lead to higher risk of GI bleeds
FOBT is meant for outpatient colon cancer screening
Sensitivity of 25% for UGIB in ED
Different medications and foods can affect the reagent
British Society of Gastroenterology and the American Gastroenterology Association say it should only be used for colorectal screening
Glasgow Blatchford Score
Disposition and risk stratification tool for GI bleeds
Case 2: Trauma Tertiary Exam
Tertiary Exam
Primary is ABCs
Secondary is complete head to toe evaluation
Tertiary is another complete exam (including labs and imaging) within 24 hours
Meant to find missed injuries
Literature quotes 15-22% of injuries were found with tertiary
Most common missed injuries are in upper and lower extremities
Case 3: Colitis
Bacterial
Shigella, salmonella, ecoli, cdiff
Viral
HSV, CMV
Inflammatory Bowel Disease
Ulcerative colitis, Crohn’s Disease
Diverticular disease
Typically left sided
Ischemic
Watershed areas
Splenic flexure
Sigmoid colon
Most patients will improve with antibiotics and bowel rest
When to operate?
Evidence of gross perforation
Profound sepsis without improvement with resuscitation
Rising lactate within 2 hrs
Observation of 6 hours without improvement
Increasing pressor requirements
Case 4: Atrial Fibrillation and Heart Failure
Pathophysiology
Atrial stretch, increased sympathetic tone, fibrosis, loss of atrial kick, worsening of heart failure
Spiraling of one pathology leads to worsening of the other
AHA ACC and HRS
Recommends no IV beta blockers or calcium channel blockers should not be given for patients with decompensated heart failure
Digoxin
Onset > 60 minutes, likely hours
Positive inotrope
Caution with renal impairment
May not work with high sympathetic tone
Amiodarone
Good s/p cardioversion to maintain the rhythm
Difficult to cardiovert afib patient who also has acute heart failure
Esmolol
Infusion, can be turned on and off
9 minute half life
Can monitor patient for worsening symptoms
Use bedside echo to evaluate your hypotensive patients
Case 5: Septic Arthritis
Septic Arthritis
Risk factors
Rheumatoid and osteoarthritis
Patients on dialysis, diabetes
Alcohol use disorder
IVDU
Synovial fluid analysis
<25k WBC, (-) LR 0.32
>25k (+) LR 3.2
>50k, (+) LR 7.7
>100k, (+) LR 28
CRP, synovial fluid, WBC <50k cannot exclude septic arthritis
IDSA recommends you cannot exclude if <50k WBC
Gram positive stain 29-65% sensitivity, negative 40-50%, positive in gonorrhea 25% of the time
Blood cultures positive in ⅓ patients
Hemarthrosis makes it difficult to interpret your synovial fluid analysis
Case 6: Pancreatitis
Pancreatitis:
Severity scoring
Ranson’s
BISAP
Requires less lab values
Perform similarly
Oral Intake
Previously NPO was the standard of care
Concern of pancreatic enzymes worsening symptoms
Monitor with pain and lipase levels
Now we encourage PO intake as tolerated
Immediate feeding group had shorter length of stay
No difference in symptoms or lipase
Canadian guidelines say patient should have regular diet on admission and self advance diet
For severe pancreatitis, nutrition should be started as soon as possible with NG or NJ
Case 6.5: Hypertriglyceridemia Pancreatitis
Higher need for ICU admission, SIRS response, persistent organ failure
Treatment: volume resuscitation, PO as tolerated, goal to decrease triglycerides to <500 with insulin
Insulin reduces production of triglycerides and increases their metabolism
Heparin and plasmapheresis are other treatments.
Monotherapy with heparin causes rebound hypertriglyceridemia
Plasmapheresis also falling out of favor due to lack of evidence of it being superior to insulin/heparin
QI/KT Cardiogenic Shock WITH Drs. Kimmel and Broadstock
Epidemiology
40-50k cases in the US per year
37% in hospital mortality, before PCI this was as high as 70-80%
50% 6 month mortality, unchanged in past two decades
Pathophysiology
Decreased cardiac output → decreased coronary perfusion → worsens cardiac ischemia through wall stress and increased myocardial demand
As you get more tachycardic, you spend less time in diastole so this decreases amount of time your coronaries are perfused
Increased peripheral vascular resistance is a compensatory mechanism, but this worsens the pressure the heart has to pump against
Assessing cardiac function:
TTE - available to us in the ED
EPSS
Assesses distance of mitral valve from septum
Parasternal long view
Other non-ED methods include: NiCOM, Flotrac-vigileo, RHC/PAC/Swan-ganz catheter
ED management:
Fluid management
If hypervolemic = diuretics
Do not fluid challenge
Iv lasix
Minimize afterload
Afterload reduction improves cardiac output
If SBP > 90, consider afterload reduction
Nitroglycerin drip
Oxygenation/ventilation
Supplemental O2
Maintain >90%
NIPPV showed may reduce hospital mortality and reduction of intubation rates in patients with pulmonary edema
Increases intrathoracic pressure, decreases venous return to right heart, be careful in RV failure
Vasopressors and ionotropes
Dopamine has increased mortality and arrhythmias
Vasopressin can decrease pulmonary vasoconstriction and is also a vasopressor
Dobutamine is a primarily B1 agonist with quick onset of action
May cause dysrhythmias
Milrinone PDE3 inhibitor with a longer onset of action
May cause initial hypotension
Epinephrine and norepinephrine are good agents in undifferentiated shock
Mechanical circulatory support
Intraaortic balloon pump
Inflates during diastole to help your coronary perfusion pressure
Deflates in systole to encourage forward flow
Impella
Encouraged forward flow in LV
VA ecmo
Heart and lung bypass
Potential bridge to LVAD or transplant
UC has ECMO capabilities
Formal QI/KT pathway to follow once it goes through peer review!
Visiting Professor Lecture: Ophthalmologic Emergencies WITH Dr. Glaucomflecken
How to Consult an Ophthalmologist
The phone call: don’t apologize
HIstory
Decreased vision
How bad, how fast, is there pain
Eye pain
Hows the vision
Quality?
Diplopia
Is it new?
Is there pain?
Is it binocular?
Flashes/floaters
History of retinal detachment
High myopia
curtain/vision loss
All patients
History of eye trauma
History of recent eye surgery
Exam
Visual acuity assessment, everyone scores somewhere on the list below
20/20
Big E? ~20/200
Count fingers
Hand motion
Light perception
No light perception
Use the pinhole if patient forgot their glasses
Optokinetic nystagmus can be helpful in patients who cannot cooperate with exam (at least 20/400 vision)
Pupils
Equal?
Afferent pupillary defect?
Sign of optic nerve problem
Pressure
Tonopen, tactile
<30 not concerned
30-40 start drops, see in AM
>40 concerning
Slit lamp
Helpful for all patients with eye pain, if you have it use it
If you cant see iris, something is wrong
Use fluorescein
Use tetracaine first
Fundus exam
Can be difficult exam, panoptic helpful
How to open swollen eyelids
Dry the skin and your glove
Get underneath the eyelash (tarsal plate)
Use a q-tip, roll eyelid up
The Red Eye - Pearls from Cases
Trauma Cases:
Subconjunctivae hemorrhage
if vision ok, lubrication drops prn
Hyphema
>50% and elevated pressure are concerning features
Page ophtho
Avoid blood thinners
Sickle cell screen if unclear cause
Limit activity
Cyclopentolate
Page ophtho again
Abrasion
Counseling and topical antibiotic if acuity intact and does not appear ulcerated
+/- nsaid and tetracaine
Topical nsaids are expensive and burns the eye, would avoid
Tetracaine: Dont give entire bottle to patient, it has 200 drops in it, can cause complications
Tetracaine on abrasion mimics could cause complications
Extraocular muscle entrapment
CT scan
Young patients more often have orbital floor fractures leading to entrapments given the ‘trap door’ resilience of the floor
Eyelid laceration
No deep sutures below the brow as to avoid the septum
Beware margin involving and canalicular lacerations
Don’t miss the open globe
Open globe
Trauma + no light perception = open globe until proven otherwise
Peaked pupil
Siedels sign
Call ophthalmology, IV moxifloxacin, tetanus, npo, zofran, eye shield, CT
Corneal foreign body
Carefully remove, do not cause an open globe
Topical antibiotic (small abrasion likely present)
Follow up within 24 hours
Orbital compartment syndrome
High pressure, nonreactive pupil, no light perception, no motility
Lateral canthotomy
Infection Cases
Corneal ulcer
Location, where is it (overlapping pupil?), how big is it
Look for hypopion
No contact lens
Topical antibiotic - moxifloxacin if contact lenses, erythromycin if not
Follow up within 24 hours
Endophthalmitis
Pus in eye
Ophthalmology to see immediately
Herpes
Oral antivirals
Topical antibiotic
Dendritic lesions hallmark of diagnosis
Avoid starting steroids as ED, consult with ophthalmology prior to initiation
Conjunctivitis - Bacterial
Topical antibiotic depends on allergies and risk factors
Ofloxacin
Polytrim
Erythromycin
Conjunctivitis - Viral
Reassurance
Start a topical and follow up if unsure
Infectious Keratitis vs Conjunctivitis
Keratitis can blind the patient - antibiotics such as ofloxacin or moxiflaxoacin
Must be seen within 24 hrs
Discharge/Admit/Consult/Transfer WITH Dr. LaFollette
Community Rhythms
Cases:
26 yo F with anxiety. EKG shows SVT.
Modified valsava
REVERT trial JAMA 2015
43 vs 16% success vs traditional valsalva as initial method
Adenosine. 6-12-12?
Be wary of 12 if going through a central line, otherwise likely more effective as initial dosing
35 yo M with weakness. EKG shows afib with RVR
RAFF2 Trial
Cardioversion vs procainamide followed by cardioversion (under 48h symptoms, acute onset afib)
both very effective. Medications more effective in younger, first time population.
Should we anticoagulate post cardioversion?
Let higher Chads2vasc (2+) guide post-cardioversion AC
No difference in PA vs lateral pad placement
Starting energy for synchronized cardioversion
max energy with increase first-shock success
86 yo M hx of CAD with palpitations. No chest pain or SOB. EKG shows frequent PVCs
In a patient with structural heart disease, PVCs can be concerning, if suspicion for it the patient needs an echo.
If totally asymptomatic, very unlikely to represent concerning pathology
If symptomatic, likely beneficial to ablate, even can cause a cardiomyopathy (rarely)
Assess for electrolyte and ischemic issues as predisposing factors
92 yo hx of CAD, DM, HTN, HLD with weakness. EKG shows bradycardia. BP stable
Electrolytes, medication and other reversible etiologies should be considered first
Can trial atropine to see if there is response
Consider Sinus Nodal Dysfunction (SND) especially if inappropriate non-response to stress / standing, almost all symptomatic SND require AICD
