All posts by andersodav

GI Report & M@M Pearls 10/11/17 – Ileitis & Post Thrombotic Syndrome (PTS)

Thank you to Patrick for presenting a medical mystery case of an elderly woman w/ hx of anal squamous cell carcinoma and MDS presenting after recent antibiotics use with acute abdominal pain a/w bloody stools and diarrhea. Her labs were notable for a WBC count of 45 and CT imaging of her abdomen showed no perforation w/ small bowel wall enhancement c/f ileitis. We discussed the ddx of ileitis below w/ primary concern for Crohn’s disease vs infectious etiologies in this patient. She is improving on IV abx and has declined a scope by GI at this time.

Key Pearls

  • Ileitis may present acutely with right lower quadrant pain and/or diarrhea, or with chronic obstructive symptoms and bleeding. The tempo hints to causes per below.
  • Ileitis, defined as inflammation of the ileum, is classically caused by Crohn’s disease (CD) however, a wide variety of diseases may be associated with ileitis (see table below).
  • Do not prescribe opioids to patients with suspected IBD as they are associated with increased mortality (see paper below).


Causes of ileitis beyond Crohn’s disease and infections include systemic disorders -spondyloarthropathies, vasculitides, ischemia, and amyloidosis as well as medications may lead to ileal inflammation. See below for table with global categories of illnesses, specific examples associated with these and common illness scripts to refer back to. Here is a super helpful paper complements of our GI fellow Sara Lewin “Ileitis: When It Is Not Crohn’s Disease.”


***M@M Summary of Data Regarding Post-Thrombotic Syndrome and Correction***

  • Remember DVT ppx in all patients p/w IBD flares (even if bleeding) as they have a marked increased risk of DVTs

Incidence of Post thrombotic Syndrome (PTS) after Symptomatic DVT

Kahn S et al. Ann Intern Med 2008

    • Multicenter prospective study of PTS occurring over 2 years following acute symptomatic DVT in adults (n=387)
    • 43% incidence of PTS (modified Villalta scoring)
      • 30% mild (Villalta 5-9)
      • 10% moderate (10-14)
      • 3% severe (> 14 or ulcer)
    • Proximal DVT increases likelihood of PTS
      • 2.23 increase in MV score vs. distal, p < 0.001
    • Proximal DVT increases risk of recurrent ipsilateral DVT
      • HR 2.4, p = 0.036
      • Known data from CaVent Trial (2016)
    • N = 176 (84% of original 209 randomized)
      • 87 from CDT group, 89 from control group
      • Post Thrombotic Syndrome
    • ARR of 28% (43% CDT versus 71% control)
      • (2 year f/u had ARR of 14.4%)
    • BUT, still no difference between QOL scores…

Society for Vascular Surgery Practice GuidelinesLEVEL 2C – not level 1A as I stated in M@M

“We suggest a strategy of early thrombus removal in selected patient meeting the following criteria a) a first episode of acute iliofemoral DVT, b) symptoms < 14 days, c) a low bleeding risk and d) ambulatory with good functional capacity and acceptable life expectancy.” (level 2C)

Acute venous thrombosis: thrombus removal with adjunctive catheter-directed thrombolysis – ATTRACT (2017)

A multicenter open-label two armed RCT (n=692) comparing pharmacomechanical catheter-directed thrombolysis + standard therapy VS standard therapy w/ a primary outcome of development of post-thrombotic syndrome (PTS) at 2 years. Data is expected to be published this year in the NEJM, however the primary endpoint of reduction in any PTS was not met with associated increases in bleeding and quality of life metrics were not different between groups. However, data from subgroups and secondary analyses suggest that catheter-directed thrombolysis may have a benefit in patients who have acute iliofemoral deep vein thrombosis. The data also showed a trend towards greater treatment effect for catheter-based interventions with patients who present with more severe symptoms, however this was not the intent of the initial trial and should be viewed more as hypothesis generating. Feelings are this may push guidelines for management of early thrombus towards medical management. Until then we should follow guidelines per above.

Attract Trial


Moffitt Pearls 10.03.17 – Chest Pain in the Young , FFR & Myocardial Bridging

Thank you to Vaibhav for presenting the fascinating case of a young woman with a hx of myocardial bridging s/p unroofing p/w recurrent chest pain and elevated troponin to 1.8 of unknown cause. She has had an extensive prior work-up that has included abnormal MRI (initially thought to be Sarcoid, then reviewed normal), mild diastolic dysfunction and reduction in voltage c/f infiltrative disorder. She will get a repeated cardiac MRI (possibly PET), ANA, serum free light chains and ESR/CRP to help determine the cause.

Key Pearls

  1. Low voltage on the ECG is defined by < 5mm in limb leads and < 10mm in the precordial leads. Amyloid is the predominate infiltrative disease to consider with this finding as other diseases such as Sarcoid often does not present with low voltages.
  2. Myocardial bridging is present in up to 25% of people per autopsy/imaging reports AND it can be very difficult to determine if this is driving symptoms. 
  3. Medical management for myocardial bridging includes beta-blockers and calcium channel blockers to decrease inotropy. Nitrites are contraindicated as they increase contractility.

More on Myocardial Bridging

  • The major coronary arteries occasionally have a segmental intramyocardial course. During systole, this segment of the vessel is compressed, a condition referred to as milking or systolic “myocardial bridging.” On angiography, bridging is recognized as compression of a segment of a coronary artery during systole, resulting in narrowing that reverses during diastole. This occurs most often in the left anterior descending coronary artery or its septal perforator branches
  • Myocardial bridging, which causes coronary artery obstruction only during systole, would not be expected to reduce total myocardial perfusion significantly since almost two-thirds of blood flow in the left coronary system occurs in diastole.  

Differential Diagnosis of a young pt w/ Cardiac Chest Pain:

Always rule out MI first!

  • Atheromatous CAD
    1. Think of RF including hyperlipidemia, hyperhomocysteinaemia, lipoprotein a
  • Non-Atheromatous Coronary Artery anomalies
    1. Myocardial bridging – artery dives through myocardium instead to the epicardium (tx: with B-blockers and nondihydropurine calcium channel blockers)
    2. Coronary Dissection (surgical)
    3. Anomalous coronary (surgical)
    4. Embolism to the coronary arteries – septic or clot  (through PFO)
    5. Prizmental Angina – vasospam (tx amlodipine, nitrates)
  • Hypercoagulable States
    1. Antiphospholipid syndrome
    2. Nephrotic syndrome
    3. Factor V Leiden and Antithrombin III
  • HCOM w/ demand (tx maintain euvolumia, beta-blockers)
  • Microvascular d/o (treat as angina – risk factor reduction, beta-blockers, nitrates)
  • Pericarditis
Fraction Flow Reserve (FFR) is traditionally used to quantify the degree of coronary artery narrowing to evaluate for stenting during a catheterization. The FAME trial re-defined flow limiting lesions as < 0.8 which is used to decide which lesions to stent. Diastolic FFR has also been used in the evaluation of myocardial bridging with a flow rate < 0.76 do determine if a lesion should be stented or not. Interestingly enough, dobutamine is used in the cath lab and NOT adenosine (which is usually used) the determine whether myocardial bridging is causing flow limitation.

Moffitt Pearls 10.2.17 – Upper GI Bleed

Key Pearls for Upper GI Bleed Evaluation and Management

  • JAMA Rational Clinical Exam series: Does this patient have a severe upper GI bleed? A great resource for evaluation of a patient with suspected upper GI bleed attached below!
  • Bleeding sources proximal to the ligament of Treitz are considered Upper GI bleeds by definition

-> Top 3 causes include peptic ulcer bleed, gastritis and variceal bleed.

  • NG lavage with blood or coffee grounds has a positive LR of 9.6 for UGIB, but sensitivity is only 44%! If it’s there, you’re likely dealing with UGIB, but if it’s not, you still might be!
  • The other features that have solid likelihood ratios for UGIB are melena on exam (LR, 25) and BUN/Cr ratio >30 (LR, 7.5).
  • Blood clots in the stool make UGIB much less likely (LR 0.05).
  • The Blatchford prediction score efficiently identifies patients who do NOT need urgent scope. Score components are HR, BP, hgb, BUN, melena, syncope (as in our patient today), liver disease, and heart failure.
  • Remember: We usually use a transfusion threshold of hgb 7.0, but if someone is unstable and actively bleeding, transfuse regardless of hgb level!


Moffitt Pearls 9.29.17 – Fever in a Returning Traveler – Part 2

Moffitt Pearls 9.29.17 – Fever in a Returning Traveler – Part 2

Thank you to Kenny and Manoj for presenting the interesting case of a young man with tetralogy of fallot returning from Australia and Indonesia with a jaundice, fevers, sore throat and adenopathy initially treated for strep throat then admitted with atypical lymphocytes c/f EBV related mononucleosis. Once again we had to re-frame the patient in real time and prevent anchoring on travel history for diagnosis.

Key Pearls

  1. Thank you to HH for sharing the ddx for a mono-like illness (fevers, adenopathy, sore throat): HIV, CMV, EBV, toxoplasmosis and bartenella.
  2. The differential for peripheral lymphocytes includes acute viral infections such as EBV/CMV, bacterial infections such a pertussis, TB or brucellosis and malignancies such as lymphoma, CLL and ALL.
  3. See the NEJM article below for approach to fevers in a returning traveler from Feb 2017.

Intern Report Peals from yesterday (thank you Rabih for diagram!!)





Cardiology Report – Septemeber 19th

Cardiology Report Pearls 9/19/17 – Syncope & Aortic Stenosis

Thank you, Kelly, for presenting a case of an older male who presented with exertional syncope found to have severe, progressive aortic stenosis.


Key Pearls:

  1. Aortic stenosis with a tricuspid aortic valve is generally a disease of octogenarians. If presenting earlier, consider monocuspid (20-30s) or bicuspid valves (40s-60s).
  2. Remember that bicuspid aortic valves are also associated with aortic root dilatation – which increases the risk of both aortic insufficiency and aortic dissection.
  1. Severity of aortic stenosis is determined by valve area (< 1.1 cm), peak velocity (> across the valve, and gradient across the valve. These metrics have some caveats (e.g low EF and cirrhosis c/b portal HTN) and are very operator dependent.


Approach to Sudden Collapse:


  • Abnormal structural
    • HCM (35%) -> also remember ARVC or LV non-compaction
    • Anomalous origin of a coronary artery (17%)
    • Myocarditis (6%)
    • Valvular – mitral valve prolapse or aortic stenosis (~2%)
  • Structural normal
    • Long QtC
    • Channel defects such as Brugada syndrome
    • Catecholaminergic polymorphic VT
    • Electrolytes – Potassium, Magnesium, Calcium
    • Trauma – commotio cordis


  1. Heat Stroke
  2. Seizure or neurological – bleeds
  3. Dehydration
  4. Toxicology – supplements in athletes

Flashback to this previous post on syncope.

Schematic of the Continuity Equation to Calculate Velocity:



Survival in Aortic Stenosis



Remember the big 3 symptoms that portend significantly increased mortality in aortic stenosis: syncope, angina, and heart failure. Mortality remains low while patients are asymptomatic. After angina, syncope, or dyspnea related to heart failure develops, the prognosis worsens dramatically if severe aortic stenosis is left untreated. The epidemiology of untreated and treated aortic stenosis was first described in the 1960s by Ross and Braunwald.

Simplified Approach to Management of Aortic Stenosis:





Moffitt Pearls 8.29.17 – Cardiology Report

  1. Management of atrial fibrillation (AF) is broken down into rate control and rhythm control – see details on AFFRIM trial below. Use the CHaDsVasC score to determine anticoagulation.
  2. In patient’s with a reduced ejection fraction do not use calcium channel blockers for rate control (class iii, level C evidence).
  3. Amiodarone and dofedilide are two options for anti- arrhythmia therapy in patient’s with HFrEF.
  4. See below for flow sheet on cardioversion of patient’s with hemodynamically stable AF.


The Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) Trial (2002)

Bottom Line:  In patient’s with nonvalvular AF, there is no survival benefit between rate and rhythm control, but rhythm contol trends towards increased mortsality.

Major Points:

Multicenter, parallel group, RCT of > 4,000 patients w/ nonvalvular AF

Rate control (HR <80 at rest) was achieved with B-blockers, Ca++ channel blockers, and/or digoxin (n=2,027)

Rhythm control strategy varied considerably but included class 1a (procainamide), 1c (propafenone, flecanidie) and III (amiodarone, sotalol, dofetilide) (n=2,033)

Median follow-up: 3.5 years

Analysis: Intention to treat

Primary Outcome: All cause mortality at 5 years 25.9% vs 26.7% (HR 1.15, CI 0.99-1.34, P=0.08)

What if my patient cannot be anticoagulated??

Among patients with nonvalvular atrial fibrillation (AF), the majority of thrombi are located within or involve the left atrial appendage (LAA). The importance of the LAA in thromboembolic risk among patients with AF provides the rationale for ligation or occlusion of the LAA in patients who are candidates for but have either absolute or relative contraindications to long-term oral anticoagulation

Percutaneous approaches, referred to as LAA occlusion procedures, that mechanically prevent embolization of LAA thrombi have been developed and shown to be effective

The left artial appendage ligation or LARIAT procedure was developed here at UCSF and is used in such patients (video below)

Cardioversion of patient’s with hemodynamically stable AF.

**Remember unstable patients should be immediately cardioverted**

Cardioversion Flow.png Pearls

Moffitt Pearls 8.23.2017 – Morning Report – ILD

Thank you to James for presenting a fascinating case of middle aged woman with a questionable history of ILD presenting with acute worsening of a chronic cough concerning for an ILD flare vs. undiagnosed infection.


  1. In a patient presenting with an ILD ALWAYs rule out infection & look for an underlying cause.
  2. When BAL is negative x48h, then you can consider empiric steroids. Steroids are really only useful for acute idiopathic ILD (COP and AEP) and for some ILDs from known causes (see “approach to ILD” below)!
  3. Idiopathic pulmonary fibrosis (IPF) & nonspecific interstitial pneumonia (NSIP) p/w a restrictive PFT pattern, however hypersensitivity pneumonitis (HS) can present with air trapping and obstructive +/-restrictive PFTs
  4. Back to the Jen B rule – A patient is considered immunosuppressed if they take ~20 mg of Prednisone for 2-3 (remember PCP prophylaxis)

An Approach to ILD

Broken down into 4 categories

  1. Known Causes – drugs, RA or CTD,
  2. Idiopathic interstitial pneumonia
  3. Granulomatous disease (eg, Sarcoid)
  4. Other causes

And a few more pearls on ILD

  1. Try to find any underlying cause!
  2. Bronchial biopsy can be very useful if it can be obtained!
  3. Alphabet soup: What about UIP (usual interstitial pneumonia) This is pattern – that is characteristic of end-stage IPF (see chart below).
  4. Steroids are useful in acute idiopathic ILD and some forms of ILDs from known causes (eg connective tissue diseases). NOT useful in other forms. However, for critically ill patients in the ICU with respiratory failure from ILD flare, oftentimes our pulmonary experts will still recommend it

Table to better understand the alphabet soup!

Histological Pattern Clinical Syndrome Associated Diseases
Usual interstitial pneumonia Idiopathic pulmonary fibrosis (IPF) Connective tissue disease (CTD), drugs, asbestosis
Nonspecific interstitial pneumonia (NSIP) Idiopathic NSIP CTD, drugs, HP
Desquamative intestinal pneumonia (DIP) Idiopathic DIP Smoking, CTD, drugs, toxic inhalation
Organizing Pneumonia Cryptogenic OP  
Diffuse Alveolar Damage (DAD) Aute interstitial pneumonia Infection, aspiration, trauma, sepsis, pancreatitis