Dierential diagnosis of cavitary lung lesions:

Infection:
Bacterial:TB, NTM, Staph, Strep, Nocardia, Actinomyces, Rhodococcus
Fungal: Crypto, dimorphics, molds, PCP (rare)
Parasites: Strongyloides
Viral (rare):CMV, VZV
Malignancy:
Primary lung cancer, metastases, lymphoma, Kaposi sarcoma (rare)
Rheumatologic:
Vasculitis (GPA, rarely MPA), sarcoidosis
Emboli:
Bland or septic

Uncomplicated Staph aureus bacteremia (SAB)

Criteria for uncomplicated SAB:
Negative follow-up blood cultures at 2-4 days
Defervescence within 72 hours of therapy
No evidence of metastatic infection
No indwelling devices
Cather-related bloodstream infection or primary bacteremia without evidence of endocarditis on echo
Treatment duration
Depends on etiology!
If uncomplicated, 14 days from rst negative blood culture is recommended by IDSA
How well-studied is treatment duration?
Turns out, not that well
Prospective observational cohort in 2013 looked at treatment duration of patients with uncomplicated SAB, ~50% MRSA
(Chong et al 2013, Antimicrob Agents Chemother)
Compared short-course (<14 days) with intermediate-course (14 days)
Rates of treatment failure, crude mortality were not signicantly dierent
Short-course therapy was signicantly associated with relapse (7.9% vs 0%, p=0.036)
Notably, there was a trend toward more treatment failures (p=0.06) among patients with primary bacteremia
(unknown primary source of infection)

Protein gap
Whats a protein gap?
The dierence between the total serum protein and serum albumin (normal <4)
What causes an elevated gap?
Anything that causes an increase in non-albumin proteins
Immunoglobulins, carrier proteins, acute phase reactants
First step: polyclonal or monoclonal?
Protein electrophoresis
Polyclonal gammopathy: essentially anything that sustains a reactive or inammatory response (infections,
connective tissue diseases, liver disease, etc)
Monoclonal gammopathy: usually due to a clonal process that is potentially malignant (multiple myeloma, MGUS,
Waldenstroms, amyloid, etc)

Parapneumonic eusions
Brief reminder of what an exudate is:
Acute response to any pleural injury (infectious, immunologic, malignant) is attraction of neutrophils to the pleural space
 Around 72 hours after injury, mononuclear cells enter the pleural space and become the predominant cells
Macrophage predominance is replaced by lymphocytes after ~2 weeks
Neutrophil-predominance: think acute process (acute bacterial pneumonia, acute PE, acute pancreatitis)
Lymphocyte-predominance: think subacute or chronic process (TB, malignancy)
What is a parapneumonic eusion?
Pleural eusions that develops adjacent bacterial pneumonia due to increased pulmonary interstitial uid that traverses the
pleura to enter the pleural space and increased pleural capillary permeability
Three main types
Uncomplicated
Sterile collection of uid that forms when interstitial uid increases during pneumonia and moves across the pleural
membrane
pH: >7.2
Glucose: >60
WBC: <5,000
Gram stain, culture: negative
Complicated
Bacterial invasion of the pleural space
pH: often <7.2
Glucose: often <60
WBC: 5,000-50,000
Gram stain, culture: +/-
Empyema
Pus in the pleural uid
pH: <7.2
Glucose: <60
WBC: >50,000
Gram stain, culture: usually positive

Turner Syndrome and the Liver

Liver disease is common
20-80% prevalence of LFT abnormalities
Why does this happen?
Were not sure, but three main changes have been observed
Steatosis, fatty liver: thought to be due to metabolic syndrome associated with TS
Architectural changes:thought to be due to disruption in genes that regular vascular development, ultimately
causing local hepatic hypoxia and compensatory hyperplasia
Biliary involvement: thought to be due to alterations in genes that impact immune tolerance that create an
autoimmune diathesis seen in TS
LVH and repolarization changes
What is LVH again?
Left ventricle hypertrophies in response to pressure overload
Causes increased R wave amplitude in left-sided leads (1, aVL, V4-V6) and increased S wave depth in right-sided
leads (III, aVR, V1-V3)
Main causes: HTN (most common), AS, AR, MR, aortic coarctation, HCM
What arerepol changes? Arent ST changes always scary?
Thickened LV wall leads to prolonged depolarization (increased R wave peak time) and delayed repolarization (ST and T
wave changes in lateral leads)
Since LV is the dominant ventricle in LVH, all leads should reect this abnormality
Confers a doubled risk of death or stroke due to MI!
ST segment and T wave changes are in the opposite direction of the dominant QRS in all leads (except in the transitional
leads)

Atrial Fibrillation Management

Which is a better strategy: rate control or rhythm control?
In non-valvular Ab, there is no survival benet between rate and rhythm control strategies, but rhythm control trends
toward increased mortality (AFFIRM 2002, NEJM)
Largest RCT of rhythm vs rate control
4060 patients, age >65, without contraindication to Warfarin
 Specic medications were determined by physician (note lots of crossover)
Rate: beta blockers, calcium channel blockers, Digoxin
Rhythm: Amiodarone, Sotalol, Propafenone, Procainamide
All patients recommended to be on Warfarin
Primary end-point: death
25.9% in rate vs 26.7% in rhythm, p=0.08
Secondary end-points: composite death, disabling stroke, disabling anoxic encephalopathy, major bleeding, cardiac
arrest
32.7% in rate vs 32.0% in rhythm, p=0.33
Adverse events: large dierences with rhythm control strategy
Pulmonary event (1.7% in rate vs 7.3% in rhythm, p<0.001)
GI event(2.1% in rate vs 8.0% in rhythm, p<0.001)
Bradycardia(4.2% in rate vs 6.0% in rhythm, p=0.001)
Prolongation of QT(0.3% in rate vs 1.9% in rhythm, p<0.001)
Bottom line:
While the AFFIRM data showed no dierence between rate and rhythm control, there was a trend of more people
dying in rhythm control and clearly many more serious side eects
If rate control is used, what is adequate rate control?
Among patients with permanent Ab, lenient rate control is as eective as strict rate control in preventing cardiovascular
events (RACE II 2010, NEJM)
RCT on lenient (HR <110) vs strict (HR <80 at rest, <110 with exercise) rate control
Notably it was very dicult to get people to strict rate control:only 75% of pts got to strict resting control
based on criteria; 72% exercise HR control
614 patients, age <80, on oral anti-coagulation
Primary end-point: composite of CV mortality, CHF, stroke, VTE, major bleeding, arrhythmic events
12.9% in strict vs 14.9% in lenient, p<0.001
Secondary end-points:
CV mortality (2.9% in strict vs 3.9% in lenient)
CHF (3.8% in strict vs 4.1% in lenient)
Stroke (1.6% in strict vs 3.9% in lenient, CI 0.13-0.92)
VTE (0.3% in strict vs 0% in lenient)
Major bleeding (5.3% in strict vs 4.5% in lenient)
Syncope (1.0% in strict vs 1.0% in lenient)
All-cause mortality (5.6% in strict vs 6.6% in lenient)
Adverse events: no dierences in any, dizziness, fatigue, dyspnea
Bottom line:
No need to try to drive down heart rate below 110bpmif it is otherwise well-tolerated
If rhythm control is used, which is better: ablation or anti-arrhythmic therapy?
Overall, RF ablation results in a lower rate of recurrent atrialtachyarrhythmias than anti-arrhytmic therapy (RAAFT-2 2014,
JAMA)
RCT on RF ablation vs anti-arrhytmic threapy
127 patients, treatment-naive, paroxysmal Ab
Primary end-point: time to rst atrial tachyarrhythmia >30seconds
54.5% in ablation vs 72.1% in anti-arrhythmic, p=0.02
Adverse events:
9% of patients in the ablation group experiencespericardial eusion with tamponade: it comes at a cost
Bottom line:
It's really a coin-ip if a patient stays in Ab after ablation
Consider symptom-driven management of Ab (Prystowsky 2015, JAMA)