Grand Rounds Recap 8.3.22
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CPC WITH Dr. Grisoli & Dr. Frederick
Patient with a history of a pulmonary vascular cancer presents with SOB, weakness, hypothermia, tachypneic, cachexia, and elevated JVD
Diagnosis: Purulent pericarditis leading to pericardial effusion and Cardiac Tamponade
Purulent Pericarditis
1-2% of cases of Pericarditis
Etiology:
contiguous spread intrathoracic infection (pneumonia, empyema) 40%
hematogenous 29%
myocardial extension (endocarditis, perivalvular abscess) 20%
direct infection (trauma, surgery, iatrogenic) 9%
other 2 (GI/esophageal extension)
Presentation
Fever is the most common clinical manifestation of purulent pericarditis, and chest pain does not always co-occur. Dyspnea associated with effusive-constrictive pericarditis is common, and pericardial effusions are present in most cases.
Instead, systemic symptoms and signs are common, such as cough (94%), dyspnea (88%), chest pain (76%), fever (70%), night sweats (56%), orthopnea (53%)
Diagnostic Findings
ECG
Typical findings
PR Depression and General ST elevations with PR elevation and ST depression in aVR
Spodic Sign
~30% pts with pericarditis; 5% pts OMI
II, lateral precordial leads
downsloping TP at least 1 mm in ≥ 2 leads
Tamponade
Becks triad(Hypotension, JVD and muffled heart sounds) or Hypotension alone are not common findings on initial presentation
Physiology
fluid accumulation – acute or chronic
intrapericardial pressure
transmitted to cardiac chambers and RA most vulnerable (thin walled, lowest intracardiac pressure, surrounded by pericardial effusion)
Decreased filling
Reduced inflow
Increased Intrapericardial pressure reduced systemic venous – RA pressure gradient to a level in which cardiac output can no longer maintain coronary artery and systemic perfusion so cardiovascular collapse occurs – often abruptly with a vagal component in a phenomenon referred to as the "last drop"
Ultrasound
Right atrial (RA) collapse during cardiac systole
Right ventricular (RV) collapse during cardiac diastole
Respiratory flow variation across the mitral valve
Inferior vena cava (IVC) >2cm and respiratory variability
Breast Feeding considerations in pregnant and Lactating patients and colleagues WITH Dr. Sabedra
Medicine categories
The Old
ABCDX categorization system was phased out in 2015
The New
Minimal fetal risk
Fetal risk cannot be ruled out
Fetal risk has been demonstrated
Pregnant
Medications we care about
Bupenorphine = safe in pregnancy and lactation
NSAIDs
1st trimester - Risk cannot be excluded but appears low
• 20-30 weeks - Small increased risk of oligohydramnios
>30 weeks - risk of premature closure of the ductus arteriosus
Opiates - increased association with defects; "start low and go slow”
Ketamine - little to no data; maybe safe, but not 1st line
Bupivacaine - lowest fetal-to-maternal ratio of intradermal anesthetics
Steroids - avoid in 1st trimester
Tetracyclines
Can cause accumulation in fetal bone and teeth
Doxycycline
Thionamides
1st trimester > PTU
Beyond 1st > Methimazole
Antiemetics
Vitamin B6, doxylamine, dimenhydrinate
Phenergan, Reglan, Thorazine safe for fetus
Zofran
Possible increased risk of cleft palate and VSD
Droperidol: no real data and not recommended
Tachydysrhythmias
Adenosine is safe
CCB are preferred to BB as BB should be avoided in 1st trimester(associated with IUGR)
Procainamide is safe and well tolerated
AVOID amiodarone as the fetal thyroid has high iodine content
Cardioversion is safe for baby and mother!
Diagnostics
D-Dimer
Pregnancy adapted Years algorithms
Radiology
Dose less than 50mGy is considered safe
Per the CDC
50-100mGy is inconclusive in terms of safety to the fetus
>100mGy especially doses above 150mGy are viewed as the teratogenic threshold
American college of radiology
Risk to fetus is small at modern radiation doses
CT abdomen is ~13mGy
Lead shielding to wrap the pelvis does not significantly alter radiation dose to the uterus
CTPA is generally safer than V/q for baby and offers more diagnostic accuracy
MRI and US are extremely safe
Risk benefit
20mGy 0.8% increase chance of cancers dx less then 40yrs
Fetal mortality in an apply is 1.7% and 6-37% in a ruptured appy
Lactation
Maternal infections
COVID
Encourage hand hygiene and mask wearing
Herpes
Active lesions on the breast should refrain from breastfeeding until lesions have resolved
May breast feed from unaffected breast when lesions on affected breast are covered completely
HBV and HCV
If cracked or bleeding nipples should refrain from breastfeeding or using expressed milk until lesion has healed
HIV
CDC and AAP recommend against breastfeeding in the US where there is access to clean water and affordable feeding replacement regardless of viral load and antiretroviral therapy
Untreated active TB
Should not direct feed but can give expressed milk
May resume feeding once treated for ~2 weeks and documented not to be contagious
Alcohol, Drugs, Nicotine
Alcohol
“If you can find your baby you can breast feed”
Breast milk BAC is equal to maternal blood BAC
Must attain BAC levels > 300mg/100ml before significant effects are reported in baby
Active use of illicit drugs means breast feeding should be avoided
THC and CBD data limited and unknown
Nicotine cessation products may be used
Meds
LactMed- most comprehensive source of information of maternal medication
Organization of Teratology Information Specialists
Infant risk center
Medication counseling and breastfeeding information
Contrast
Routine CT or MR contrast is not contraindicated
Mothers receiving contrast agents do not need to stop breastfeeding and/or to express and discard their milk
Mastitis
Inflammation of the mammary gland in segmental distribution
Risk factors hyperlactation, milk micro biome
Continue to breastfeed
Antibiotics may be indicated
~10% of cases progress to abscess which may require drainage
Inflammatory mastitis, bacterial mastitis
Management
ICE, NSAIDs, Acetaminophen
Screen for Perinatal Mood and Anxiety Disorders (PMAD)
Antibiotics
No MRSA risks
Dicloxacillin or cephalexin
MRSA risks
Bactrim
Clindamycin
Breast feeding
Recommended for the first 6mo exclusively then AAP supports up to 2 years or beyond as long as desired by mother
There are tons of barriers to successful breastfeeding and 60% of mothers do not breastfeed for as long as they intend to
Issues with lactation and latching
Concerns about infant nutrition and weight
Mother’s concern about taking medications while breastfeeding
Unsupportive work policies and lack of parental leave
Cultural norms and lack of family support
Unsupportive hospital practices and policies
How to be a good caregiver and coworker
Ask if they are breast feeding
Make sure they know they are free to feed or pump in the ED
Ask if they need a pump
For your colleagues
Acceptance and normalization
Encourage time to pump, eat and drink
Stop others from interrupting, Hold their phone
Understand that not only does pumping need to happen but that you can’t choose a convent time
All women are unique and may require different amounts of time to pump
EKG Quick Hits on Left ventricular Hypertrophy WITH Dr. Roche
Diagnostic Criteria
Voltage criteria
Soklov-Lyon
Depth of V1+the tallest r wave height in V5-6>35mm
Non-voltage Criteria
Increased R wave peak time > 50 ms in leads V5 or V6
ST segment depression and T wave inversion in the left-sided leads: AKA the left ventricular ‘strain’ pattern
Armstrong Criteria
Retrospective Paper trying to find criteria for ACO in patients with LVH
“In patients with STE in leads V1 to V3, an ST segment to R-S–wave magnitude 25% excluded the diagnosis of a STEMI. If the ST segment to R-S–wave magnitude was 25%, presence of STE in 3 contiguous leads or presence of T-wave inversions in the anterior leads classified patients as having a ‘true’ STEMI.
sensitivity of 77% and specificity of 91% (vs sensitivity of 73% and specificity of 58% for STEMI criteria)
From Dr. Smiths ECG blog” STE in LVH rarely exceeds 4 mm in height, the 25% criterion is likely far too insensitive. For example, in a patient with an S-wave 30 mm in depth, the STE would have to exceed almost 7 mm. “ Read more here
Typical LVH with strain pattern
increased R wave amplitude with asymmetric ST depression having a slow downslope, and a more rapid terminal rise
R4 Capstone: Against Medical Advice WITH Dr. Frankenfeld
Leaving AMA
Common reasons
Refusal of procedure
Symptomatic needs
Long wait times
Children at home
Pets
Risk factors
Younger age
Male
Diagnosis
Socioeconomic status
Medicaid
Substance use
Will leaving AMA affect insurance coverage
This is false. Insurance coverage of the ED visit does not change with leaving AMA.
Structured Approach
Patients leaving AMA are 10 times more likely to initiate a litigation process against the emergency physician and the hospital than a typical ED patient with a rate of around 1 lawsuit per 300 AMA cases
patients who leave AMA may be severely ill and at risk of experiencing adverse events. They are also more likely to return to the ED and be emergently hospitalized within a short time after the initial ED visit
What we should do
Seek to ensure the patient understand the plan of care we want to undertake
Try to find a middle ground with a medically acceptable alternative acceptable to all parties.
Ensure the patient has capacity to refuse care
If the patient has capacity, understands the risks and benefits, and compromise has been attempted then a patient may leave AMA.
It should always be made clear that a patient may return for care
R3 Taming the SRU WITH Dr. Ferreri
Patient presents with a syncopal episode with some preceding dizziness. They presented hypotensive and tachycardic. EKG was unchanged compared to prior with persistent ST depression and concerning ST elevations in II,III,aVF. Echo with substantial pericardial effusion with mitral valve inflow variation.
Patient taken to cath lab with Cardiology for LHC showing non-obstructive coronaries. A pericardial drain was placed with frank blood output and concern for large amount of clotted blood in the pericardium. CT surgery consulted for concern of LV free wall rupture.
Structural Complications of MI
3:1000 MIs, has become much more rare in the PCI era as compared to the fibrinolytic era
Ventricular Septal Rupture
Mitral Valve Regurgitation
LV free wall rupture
Rate of those with free wall rupture 0.01% of those with STEMI or NSTEMI
50% present within first 5 days, 90% within first 2 weeks
Mortality rate approaches 50% in those with LV rupture
Mortality rate as high as 81-100% in those with LV free wall rupture and cardiogenic shock
Acute rupture tends to be large and associated with anterior infarction sites
Complete Rupture:
Leads to hemopericardium and tamponade, often death
Often present in PEA arrest
Incomplete / Subacute Rupture
Organized thrombus and pericardium seal ventricular perforation Leads to: 1) rupture with tamponade, 2) formation of false aneurysm, 3) communication with LV through perforation, or 4) LV diverticulum
Cardiac Tamponade due to LV Freewall rupture
Presentation
Hemodynamic instability
Tachycardia
Hypotension
JVP
Muffled heart sounds
Narrow pulse pressure
Pathophysiology
The development of cardiac tamponade hinges on abnormalities related to 1) Systemic venous return 2) respiratory variation and 3) pericardial compliance
Pericardial compliance
Acute vs chronic accumulation leads to differences in pericardial compliance and thus the rapidity at which tamponade physiology develops
Chronic leads to increased pericardial compliance and thus increased volume threshold at which appropriate pressures are created to induce tamponade
Systemic Venous Return – typically venous return occurs in ventricular systole and early diastole
As the effusion worsens, leads to diminished ventricular filling during diastole
Eventually leads to decreased CO and BP reduction
Also have an elevation in the RA pressure to eventually equal that of the RV, decreasing RV diastolic filling and thus CO
Respiratory Variation
Intrathoracic pressure decreases with inspiration leading to increased systemic venous return (and decreased pulmonary venous return to the L heart)
Free wall expansion is limited in tamponade leading to constriction and septal bowing to the left with inspiration, decreasing LV compliance and leading to decreased LV filling
This relationship between the right and left ventricles is called ventricular interdependence, and as pericardial pressures increase, the relationship between the ventricles plays a more important role in maintaining cardiac output
Diagnostics
Pulsus paradoxus with arterial line
The main study on this was only done in ventilated icu patients
EKG
Electrical alternans
Low voltage QRS
Sinus tachycardia
CXR
Increased cardiac silhouette in the setting of >200cc fluid accumulation
Echocardiography
RA/RV collapse
Plethoric IVC
Tricuspid and mitral inflow variation
Goals of Echo
Characterize the effusion
Is it pericardial or pleural?
Pericardial will come anterior to the descending thoracic aorta
Is the effusion hyperechoic or hypoechoic, loculated, etc
How large is it? Volume?
Trivial – seen only in systole
Mild (<10 mm)
Moderate (10-20 mm)
Severe (>20 mm)
Evaluate for right sided atrial and ventricular collapse
Right atrial diastolic collapse is the earliest finding and one of the most sensitive finding associated with tamponade (50-100% Se, 33-100% Sp)
In order to interpret this appropriately, it is helpful to use the relationship of ventricular contraction to whether or not the atrioventricular valves are open or closed
when the atrioventricular valve is open, this is atrial systole and thus ventricular diastole, and when it is closed this is atrial diastole
Therefore if the atrioventricular valve is closed and there is associated collapse, this is right atrial diastolic collapse which is a finding of cardiac tamponade
Very useful to identify in the Parasternal long axis view because get RVOT in view with the mitral valve to evaluate cardiac cycle
Right ventricular diastolic collapse occurs at the opposite time, specifically when the atrioventricular (tricuspid) valve is open – this is ventricular diastole
Much more specific finding for tamponade 72-100% Sp
Note that you can use the mitral valve as a representation if the tricuspid is closed
Absence of chamber collapse carries a 90% NPV for tamponade
Important to note that in cases where there are increased right sided filling pressures (like in pulmonary hypertension) we may not see right sided collapse
Evaluate for mitral and tricuspid inflow variation (the echocardiographic equivalent of pulsus paradoxus)
Under normal circumstances, there will be a decrease in flow across the mitral valve of less than 25% with inspiration and an increase in tricuspid inflow with inspiration of less than 40%
In order to appropriately evaluate mitral and tricuspid inflow velocities, it works best to obtain an apical 4 chamber view. Then using pulse wave doppler place the indicator at the tip of the mitral or tricuspid valve leaflet as it enters the ventricle
you can then calculate the mitral or tricuspid inflow variation using a tool on the ultrasound. It is measured by taking the peak of the tallest E wave (rapid ventricular filling) and the peak of the lowest E wave (associated with respiration) and calculating the percent change
Note that the a wave is the atrial kick phase
You may have to decrease your sweep speed to get appropriate images (gives you more wave forms per time interval)
Mitral inflow – decrease in flow with inspiration exceeds 25%
Tricuspid inflow – increase in flow with inspiration (as systemic venous return increases) exceeds 35% per our taming the sru guidelines / booklet
Evaluate for a plethoric IVC
measure the IVC 2-3 cm from the IVC-RA junction
>2cm with minimal respiratory variation
