Grand Rounds Recap 09.16.20
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EMS GRAND ROUNDS with DR. GRAY
Mobile Stroke Unit Updates
Staffed by: RN, paramedic, EMT (driver), CT tech
Wireless connection to stroke team
Interventions: tPA, reversal agents, BP control, hypertonic saline, RSI medications
Out-of-Hospital Cardiac Arrest (OHCA)
>300,000 adults per year in the US
Survival to hospital admission in EMS-treated, non-traumatic OHCA is 28% [Utstein et.al.]
Half of OHCA patients are treated on scene and not transported
Continuous, high-quality chest compressions are paramount to improve chance of ROSC in cardiac arrest patients [Cunningham]
EMS is a coordinated system of response and emergency medical care involving multiple people and agencies
Need to measure the effectiveness of an EMS system
Clinically meaningful problem with various factors contributing to success and efficiency
Cardiac Arrest Registry to Enhance Survival (CARES)
Started in 2004 to collect OHCA surveillance data and help communities increase survival rates
Now includes 26 state registries and community sites in 16 additional states
Secure, web-based system in which participating agencies enter local data
Can compare de-identified EMS data on a local, state, and national level
Telephone CPR is the standard of care
Providing guidance through OHCA CPR and other emergency situations while coordinating dispatch of police/fire
Rapid Dispatch
Address auto-populated into the computer aided dispatch (CAD)
Predefined response list
Medical director should have input into dispatch response
AED Program for other first responders (police, etc.) and public
AEDs are becoming more common in heavily-traveled areas (airports, malls, stadiums)
Many EMS systems keep an AED registry and notify 911 callers
Chance of bystander defibrillation tripled 30-day survival where AED was accessible [Denmark study]
EMS Physician Role
Medical director is responsible for the overall quality of medical care in the EMS system
More direct/active roles in some systems
Scene response, realtime QI, mass casualty incident
PAIN IN PEDIATRICS with DR. BRYANT
We underestimate and misunderstand pain in children
Untreated pain in pediatric patients can have impacts on future CNS pain processing, lead to avoidance of complications in future care, and induce fear and increased perception of pain in future care
Special needs patients can oftentimes have a variety of different presentations that are representative of pain - trust the caregiver
Non-pharmacological treatment
Give them a sense of choice as much as possible
Make them as comfortable as possible - keep them in parents’ arms, keep them in a calming environment for as long as possible, etc.
Distractions with toys/lights - plug for Child Life!
Pharmacological treatment
Neonatal
Use “sweeties”
Volume of distribution is smaller, brain-blood-barrier is more porous
Opiate medications can hit them quicker and more significantly than older patients - be cautious with dosing
Infants/Children
Very important to ask what medication is being given at home (acetaminophen, ibuprofen), how often, and how much
Intranasal medication can be used as a temporizer and/or bridge
Goal volume 0.3ml, max 1ml. Have them in sniffing position if possible
Midazolam
Fentanyl
Ketamine
Skin/soft tissue
Elamax has quicker onset than EMLA
LET for lacerations
Jet lidocaine
Medications to avoid
Codeine
AAP recommends no codeine to children under 12 or breast feeding mothers
FDA no codeine for those under 18 for pain or cough
Tramadol
Dextromethorphan (Robitussin)
R1 CLINICAL TREATMENTS: PERICARDITIS with DRS. STEVENS & JENSEN
Pericarditis involves inflammation of the pericardial sac and can cause pleuritic chest pain
Three EKG features that are consistent with pericarditis:
Diffuse ST segment elevation
PR depressions diffusely
Reciprocal ST depression in aVR and V1 only
Presentation
Prospective cohort study of 453 patients with acute pericarditis demonstrated that patients with fever, subacute course, large effusion, tamponade, and NSAID failure identifies higher risk of complications. Concurrent oral anticoagulation use does not increase risk of complications. [Imazio, 2007]
Prospective cohort of 274 patients with viral or idiopathic pericarditis noted arrhythmias, male gender, age <40 years, ST elevation, and recent febrile syndrome increased risk of concurrent myocarditis within 12 months [Imazio, 2008]
Diagnosis
High sensitivity CRP levels are elevated in ¾ of patients at presentation and identifies patients at higher risk for more severe symptoms in acute pericarditis [Imazio, 2011]
Treatment
NSAIDs
Mainstay of treatment for idiopathic and viral etiologies
Acute or recurrent pericarditis
Ibuprofen
600mg-800mg TID
10 days of ibuprofen and indomethacin are both safe and effective when compared to placebo in postpericardiotomy patients [Horneffer, 1990]
Aspirin
650mg-1000mg TID
In a case series of 254 low-risk patients with acute pericarditis, high-dose aspirin was efficacious in the majority of cases with decreased frequency of recurrences and pericardial constriction in aspirin-responders compared to non-responders [Imazio, 2004]
Systematic review of a retrospective study and a prospective, randomized, single blind study in 58 patients with postmyocardial infarction pericarditis, and noted that both aspirin and indomethacin are equally efficacious in providing pain relief [Berman, 1981]
Indomethacin
25mg-50mg TID
Requires tapering of medications at ~24 hours after symptom resolution
Consider GI PPx when prescribing NSAIDs depending upon patient age, comorbidities (peptic ulcer disease, concurrent steroid use), or on anticoagulation
Colchicine
Used as an adjunct to NSAIDs to reduce risk of treatment failure and recurrent pericarditis
Dosing <70kg - 0.6mg BID loading dose on day 1 + 0.6mg daily after
>70kg - 1.2mg BID loading dose on day 1 + 0.6mg BID
Prospective, randomized, open-label design trial of 120 patients with first episode of acute pericarditis found that colchicine with conventional therapy compared to conventional therapy decreased the recurrence rate of pericarditis of 18 months and symptom persistence at 72 hours with a NNT 5 [Imazio, 2005]
Multicenter, double-blind trial of 240 patients with acute pericarditis demonstrated that colchicine with aspirin or ibuprofen therapy significantly reduced the rate of incessant or recurrent pericarditis without significant change in adverse events [Imazio, 2013]
Systematic review of four RCTs involving 564 patients demonstrated that colchicine reduces the number of recurrences in patients with acute or recurrent pericarditis without significantly increasing adverse effects [Alabed, 2014]
Systematic review of 7 clinical trials of 1275 patients demonstrated that colchicine is well tolerated and efficacious for primary and secondary pericarditis without significant side effects or drug withdrawal [Imazio, 2014]
Colchicine has a very narrow therapeutic window and can cause GI side effects in overdose. Ensure the patient recognizes and understands these risks prior to prescribing.
Steroids
Dosing 0.2-0.5 mg/kg/day
Taper starts 2-4 weeks after symptoms resolution and CRP normalization
Stop taper if symptoms return or CRP becomes elevated again
Systematic review of 7 studies of 451 patients demonstrated that steroids, especially at high doses, had a detrimental risk-benefit profile as compared to NSAIDS + colchicine use in patients with pericarditis [Lotrionte, 2010]
Retrospective review of 100 patients demonstrated high doses of steroids (1mg/kg/day) for recurrent pericarditis has more side effects, recurrences, and hospitalizations than low-dose steroids (02-0.5mg/kg/day) [Imazio, 2008]
Surgical management
Retrospective cohort of 184 patients demonstrated that surgical pericardectomy is safe and effective method of relieving symptoms in patients with chronic relapsing pericarditis wiho failed medical management [Khandaker, 2012]
R2 CPC with DRS. CHUKO & LAFOLLETTE
Female in her 70s with a PMH of polymyalgia rheumatica who presents with epigastric abdominal pain x4 days that radiates to her left upper quadrant. She has not had a bowel movement in the last 5 days, whereas she normally has 2 bowel movements per day. She denies nausea, vomiting, diarrhea, dysuria, urgency, frequency. She denies recent travel or sick contacts. She also endorses intermittent chest pain that is left-sided without associated shortness of breath or cough. Denies exertional exacerbation. Reports word-finding difficulty and mental slowness which has been getting progressively worse.
Vital signs T 99.7, HR 93, BP 154/70, RR 27, SpO2 96% on RA. She appears mildly anxious in no acute distress. Breath sounds are diminished at the base in the left lung field. She has an obese abdomen that is soft and easily compressible throughout, diffusely tender to light palpation without guarding, rebound, or peritoneal signs. She is noted to have bilateral pitting edema. She has word finding difficulty without any other focal neurologic deficits.
Noted to have a leukocytosis of 16.9, a normal lactate and troponin. EKG with sinus tachycardia. CXR with a small left pleural effusion without other obvious abnormality.
And then a test was ordered…
CT abdomen/pelvis with IV contrast for (incidental finding of) pulmonary embolism
Pulmonary embolus
Epidemiology
VTE is the third most common type of cardiovascular disease
>90% of PEs originate from DVTs
If untreated, an acute PE has a mortality rate as high as 30%
The highest incidence of PE is among patients 60-80 years of age
Presenting symptoms:
78% have sudden onset dyspnea
38% have unilateral painful swelling of a lower extremity
34% have chest pain
22% have fainting or syncope
Pathophysiology
Increase in RV pressure
Decrease LV preload
Increase in pulmonary vascular resistance
Right heart failure
Decreased systemic arterial pressure
Diagnostics
Use Well’s criteria to risk stratify
Treatment
Assess for risk factors for risk/benefit of initiating anticoagulation
Anticoagulants reduce risk of recurrent VTE by 90-97%
HAS-BLED score
Provoked versus unprovoked
During the initial 6 months of treatment, cancer patients have a 7-8% risk of developing recurrent VTE
Disposition
Patient with PE in shock -> ICU
R1 CLINICAL KNOWLEDGE: MYASTHENIA GRAVIS with DR. MARTELLA
Pathophysiology
Disease of the neuromuscular junction where there are autoantibodies against the acetylcholine receptor
Clinical presentation
50-60% present with isolated ocular symptoms
Diplopia, unilateral/bilateral ptosis
Symptoms worsen with sustained vertical gaze
15-25% will have only isolated ocular symptoms
50-85% presents with ocular findings +/- generalized findings
Proximal muscle weakness with upper extremity >lower extremity involvement
15% with bulbar symptoms
Dysarthria, dysphagia, fatigable chewing, facial weakness
Differential diagnosis
Ophthalmic
Thyroid eye disease, Levator dehiscence
CNS
Multiple sclerosis, ALS, Parkinson’s, Wernicke’s encephalopathy
PNS
Nerve: CN palsies, Horner’s syndrome, Guillain Barre,
NMJ: Lambert-Eaton, botulism, organophosphate poisoning
Diagnosis
Ice Pack test
Addresses ptosis, put ice pack on eyelid for 2 minutes
If improves: positive result; 80% sensitivity
Quantitative myasthenia gravis test
Assesses for muscular fatigue
Breath count test - have the patient take a deep breath in and count to 20
Serologic testing: Anti-AChR is 99% specific, Anti-MuSK is 40% sensitive
Electrophysiologic: repetitive nerve stimulation, single-fiber EMG, routine nerve conduction studies and needle EMG
Can be associated with thymic hyperplasia or thymoma
Myasthenia Crisis evaluation
Definition: worsening muscle weakness, resulting in respiratory failure that may require intubation and mechanical ventilation
Crisis evaluation
20% of initial presentation of MG, 4% mortality rate
Measure vital capacity (<1L) or negative inspiratory force (<20cm H20)
Intubation considerations
Paralytics - depolarizing medications should be DOUBLED, non-depolarizing medications should be HALVED
Non-invasive ventilation
Retrospective study of 41 patients demonstrated shortened ICU stay and hospitalization, and prevention of intubation/sedation complications
Stressors: infection, surgery, pregnancy, medications
Treatment
Ventilatory support as needed
Plasma exchange, IVIG
Disposition
ICU for myasthenia crisis
Admission floor versus higher level of care for non-crisis myasthenia gravis
R3 TAMING THE SRU with DR. BERGER
In all comers with syncope, ~1% mortality at 10 days and 10% mortality at 2 years
Decreased survival in neurologic, cardiac, and unknown causes of syncope
We see ½ of all elderly patients within the month of their death
Cardiac arrest of unknown etiology has poor prognosis
Organ systems most often missed in cardiac arrest are respiratory, cardiac, and exsanguination
Post-ROSC pressors are up to your discretion
This is about the patient and taking care of them per their wishes
R4 CAPSTONE with DR. GOTTULA
Emergency medicine is a sacred vocation
Physicians are called to be set apart to take care of others
How to uphold this during the daily grind
Respect everyone
Actively participate
Be intentional
Do the little things right
Arterial pressure monitoring
Indirect and direct methods
Many factors affect accuracy
How to get an accurate blood pressure: correct cuff size, patient positioning, and rate of cuff deflation
Inaccuracies are magnified in critically ill patients: 33mmHg direct versus indirect blood pressure measurements [Cohn] that has been replicated in other literature [Bur]
Infection prevention strategies in ventilator-associated pneumonia
Elevate the head of the bed to 45 degrees in intubated patients
Suction subglottic secretions above ETT
Implement oral hygiene
Chlorhexidine solution to the oral cavity after intubation
Assess endotracheal cuff pressure (20-30cm H20)
Place orogastric tube
Sedation practices
Richmond Agitation-Sedation Scale (RASS) to reassess your patient after sedation has been started
Target light levels of sedation
Optimize pain with opiates first
Start light with sedation and titrate up as needed
Avoid benzodiazepines if possible
