MR with Moyukh + Dr. Chitale: Stress Tests and Coronary Fistulas

A middle aged female with a vague history of “extra coronaries” who presents with worsening dyspnea on exertion. Her initial stress echo was negative, but when here symptoms progressed 2 years later she had an MRI which confirmed 2 extra coronary fistulas. Although she did not meet strict criteria for repair, the repair was ultimately done due to her persistent symptoms, and she is now symptom-free!
*When should we order a stress echo instead of the usual treadmill EKG stress test? 
The bottom line – for the most part, we should start with treadmill EKG tests, not exercise echoes!
-Hard indications: an uninterpretable EKG (LBBB, TWI, paced), evaluation of exercise-related LVOT, AS, and pulmonary hypertension
-Soft indications: as in this case, we sometimes order it when our pre-test probability for ACS so high that we aren’t going to believe a negative EKG treadmill
-Contraindications: baseline wall motion abnormalities, severe CHF (hard to see wall motion abnormalities) or poor images with prior echoes (as in morbid obesity), other contraindications to exercise (will need a nuclear test)
*Coronary Fistulas
What? Extra coronary arteries that connect with a) the RA/RV chamber or b) the PA, creating a L-> R shunt
Inline image 2
Why are these a problem, and how can they present?
a) they can cause ischemia by coronary steal -> angina or angina equivalent (in this patient, SOB)
b) overtime lead to pulmonary hypertension
How do you decide when to repair these?
There are certain criteria, including angina, evidence of pulmonary hypertension, and a high shunt fraction. This patient did not meet any of these strict criteria, but was still repaired because of refractory symptoms. As Nishant aptly pointed out, it is possible that shunt fractions worsen with exercise, so people with exercise-related symptoms may not meet the criteria even though they could benefit from the repair.

MR Night Float Interesting Case with The Kanch: Epidural abscess

An elderly patient with back pain called to ED for + blood cultures 2 weeks s/p treatment for Klebsiella UTI found to have epidural abscess.
-Initially, there was a high suspicion for endocarditis given the new murmur found on exam – prompting discussion of empiric therapy
   -For native valve endocarditis – common pathogens include S. aureus, Streptococci, Occasional gram negative rods and HACEK organisms – treatment of choice is Vancomycin + Ceftriaxone
   -For prosthetic valve endocarditis – common pathogens include S. aureus and S. epidermis; treatment of choice is Vancomycin + Rifampin + Gentamicin

MR with Jossy and Dr. Shlager: Acute Liver Failure in a patient on Azathioprine

A middle aged female with history of renal transplant (in 2013 2/2 ANCA vasculitis) on immunosuppression presents with one month of jaundice, light stools, and vague abdominal pain. Her initial labs showed a bilirubin of 16 with transaminases in the 80s-90s, INR of 1.3, and AKI on CKD without evidence of structural obstruction on imaging. Her initial workup included a liver biopsy, after which she became more encephalopathic with a rising INR, meeting criteria for ALF. UCSF was then contacted for potential transplant. The etiology of her ALF is still not clear, but thought most likely a result of azathioprine hepatotoxicity
*One confusing thing in this presentation were the relatively low AST/ALT. We discussed that the patient could have had an insult several weeks ago and her liver enzymes are now just ‘burnt out’; because of this, she should still be worked up for all of the usual causes of ALF (i.e. hepatitis, autoimmune disease, etc) that are usually associated with higher transaminases.
*Definition of Acute Liver Failure: INR > 1.5 + Encephalopathy in a patient without pre-existing liver disease (often defined as developing in <26w)
-While only INR + encephalopathy define ALF, we discussed the following signs of poor prognosis as ALF progresses: hypoglycemia, signs of HRS (creatinine rising or oliguria), hypotension
*My patient with had negative hepatitis serologies in the last 5 years and is low risk. Do we need to resend these? What should we send?
In the case ALF (or concern for progression towards ALF), repeat hepatitis serologies AND viral loads should almost always be sent. We often forget about hepatitis A, but this is common and the biggest risk factor for this progressing to liver failure is age.
-Would send: hep A IgM, hep A IgG, hepB surface Ab, hepB core Ab, hepB surface Ag, hepB DNA, hepC ab, hepC RNA
*What causes ALF?
Acute Liver Failure actually has a nice differential because it’s actually quite limited with a few big categories: Toxins, Viral, Vascular, Metabolic, Other
Inline image 1
And, random antibiotic pearls:
*For every antibiotic you choose, ask yourself what you are covering and what you are missing. It is the only way to learn the nuances of these drugs over time!

MR with The Kanch: Calciphylaxis

An older woman who presented with worsening shortness of breath and lower extremity rash found to be severely anemic and in renal failure.  She was later diagnosed with calciphylaxis and started on hemodialysis.
– Calciphylaxis or “calcific uremic arteriolopathy” is part of a continuum of the systemic vascular and soft-tissue calcification that is common in end-stage renal disease (ESRD) – clinical manifestations result from reductions in the arteriolar blood flow
-Calciphylaxis is a clinical diagnosis – this patient did have a biopsy which further supported – calciphylaxis is usually VERY painful – this case was unique in that the patient only had mild pain
Biopsy can be dangerous and can worsen the lesions, so take this into account when considering biopsy!
-Treatment of choice for post patients is IV sodium thiosulfate – which is given during dialysis

MR with Sonia: Ischemic stroke in a young patient

A youngJapanese female with a possible history of seizure presents with 3 days of R-sided facial droop and weakness. Initial CT head was negative; CTA was obtained for dissection but this was also normal. MRI ultimately revealed an ischemic infarct in the left putamen, consistent with the patient’s presenting symptoms. We discussed an approach to stroke in the young patient, including the high prevalence of dissection in this group and the importance of obtaining a CTA with initial imaging. 
1. When is a hypercoagulable workup appropriate in ischemic stroke?
There is really no good data to guide this, and all of the information I could find was based on expert opinion. Their recommendation is to send the workup if a) echo + vascular studies show no clear etiology in a young patient without other risk factors (such as ours), b) family or personal history of other systemic thromboses, or c) other clinical features of SLE or APLS
2. Causes of venous AND arterial thrombosis (as opposed to the long list of causes of only venous thromboses, which often do not require further workup)
-Causes of hyperviscosity: PCV, Waldenstrom’s Macrogloulinemia, SCD
Paradoxical emboli (VTE that pass through R->L cardiac shunt)

MR with Liezel + Dr. Meadows: Acute Aortic Insufficiency and Shone’s Syndrome

A young man w/ Shone’s syndrome (, asthma, and alcohol use presents with subacute SOB, lower extremity edema, and back pain. He has good functional status and no history of heart failure in the past. On initial presentation, he was found to have a low grade fever, new afib, and a wide pulse pressure; these vitals alone pointed towards the ultimate diagnosis of aortic endocarditis cause acute aortic insufficiency. 
1. The physical exam can be KEY in helping you diagnose new AI
The findings are not subtle and no special maneuvers are required – you just need to know what to look for.
-Wide pulse pressure (this patient’s was 147/47)
-Bounding pulses and PMI
-Decrescendo diastolic murmur at LSB (for me, this is not always as easy as the first two findings – sometimes it’s very loud and other times hard to hear)
2. Why is acute AI so different from chronic AI?
a) Cardiac output drops rapidly in acute AI: In chronic AI, the heart dilates to maintain cardiac output (though ejection fraction drops as regurgitation develops, the dilation allows the stroke volume to remain the same). In acute AI, this doesn’t happen, so both ejection fraction AND stroke volume rapidly drop off. This can cause cardiogenic shock.
b) Pulmonary congestion is much worse in acute AI: The dilated hearts of chronic AI can better accommodate the regurgitation and pressure increases only slightly. In acute AI, new regurgitation against stiff hearts cause rapid pressure increases, backing up into the lungs and causing pulmonary edema.
Inline image 1
3. How do you manage acute AI?
Valve replacement! Medical management is limited but includes maintaining a good HR (if you drop it too low, regurgitant volume increases and CO decreases), diuresis if needed, and possibly dobutamine (reduces afterload and improves inotropy).

MR with Shawn: Cryptogenic Stroke and Venous Sinus Thrombosis

An elderly gentleman with a pmh of ulcerative proctitis on mesalamine and azathioprine, HTN, HLD, and DM2, who presented with cryptogenic stroke found to have a grade V aortic atheroma on TEE.  He later presented with a venous sinus thrombosis – patient thought to potentially be hypercoagulable given history of ulcerative proctitis.  .
Management of aortic atheromas from the American Heart Association/American Stroke Association-> for patients with an ischemic stroke or TIA and evidence of aortic arch atheroma, antiplatelet therapy is recommended (Class 1; Level of Evidence A); statin therapy is also recommended (Class 1; Level of Evidence B); the effective of anticoagulation with warfarin compared with antiplatelet therapy is unknown and surgical endarterectomy of aortic arch plaque for purposes of secondary stroke prevention is NOT recommended.
Mechanisms of cryptogenic stroke -> 

1)  cardiac embolism 2/2 paroxysmal atrial fibrillation, aortic atheromatous disease, or other cardiac sources

2)  Paradoxical embolism

3)  Undefined thrombophilia -> the patient in this case was worked up for thrombophilia!

4)  Substenotic cerebrovascular disease (ie, intracranial and extracranial atherosclerotic disease causing less than 50% stenosis) and other vasculopathies (eg, dissection)
Workup of cryptogenic stroke -> the minimum workup for cryptogenic stroke includes:

-Noncontrast brain CT or brain MRI

-Blood glucose

-O2 sat

-Serum electrolytes/renal function tests

-CBC including platelet count

-Markers of cardiac ischemia



Great link regarding workup of cryptogenic stroke: