Category Archives: #Infectious Disease

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

A young man w/ Shone’s syndrome (https://en.wikipedia.org/wiki/Shone%27s_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.
 
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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).

Wednesday: MR with Alice and Dr. Harry Hollander: Leptospirosis

A middle aged man with fever, bone pain who presents after travel with thrombocytopenia, transaminitis, and AKI ultimately diagnosed with Leptospirosis.

*How do I factor in prophylaxis in a returning traveler?– know that malaria has A LOT of resistance – you need to know if the patient received appropriate prophylaxis for Falciparum in the region – Malarone (atovaquone and proguanil) is generally good for malaria prophylaxis.  The Yellow Fever is a good vaccine

*Know the DDx for fever in a returning traveler: Malaria, Dengue, Chikungunya, Rickettsia, Scrub Typhus, Leptospirosis, Influenza, and Acute HIV

*This case was a very classic presentation for leptospirosis known as Weil’s disease-> liver damage (causing jaundice), AKI (tends to be an interstitial nephritis); and bleeding

*Most ricketssial disease have a dramatic response to doxycycline – also the drug of choice for leptospirosis if the patient does not have meningeal disease

*Geosentinel is a global surveillance network of travel medicine clinics that collect data from ill international travels.

http://www.istm.org/geosentinel

Monday MR with Melissa Itsara: GNR bacteremia

 

A middle aged man with stage IV HCC of unknown etiology who presented 2 weeks after biliary stent placement with confusion found to have E. Coli bacteremia.

 

**Learning point for Gram-negative bacteremia

-Treat presumptively with Zosyn – consider 2nd gram negative agent if: immunocompromised; high risk for P. aeruginosa, or unit antibiogram shows drug resistance > 20-25% for GNR pathogens

Risk factors for P. aeruginosa

-Current hospitalization or admission to an intensive care unit

-Recent P. aeruginosa infection

-Recent hospitalization

-HD

-Admission from along-term care facility

-Recent IV abx

-Recent chemo

-Immunosuppression

 

MR with Moyukh: EBV hepatitis

A young female w/ history of Crohn’s (in remission) presented with RUQ and fever after a URI, found to have ALI + neutropenia and atypical lymphocytes on smear. She was initially treated for acute cholecystitis but imaging showed only splenomegaly; she was ultimately diagnosed with EBV as the cause!
What are the most common GI manifestations of EBV?
*NINETY PERCENT (90%!) of people with EBV get some LFT abnormalities – these can be predominantly hepatocellular (elevated transaminases) OR cholestatic (elevated alk phos and bili)
*Splenomegaly occurs in ~ 50% of individuals
How do you test for acute EBV?
*The first line test should be the heterophile antibody – it is highly specific in the right clinical setting (i.e. classic malaise, LAD, sore throat) but somewhat insensitive.
*In an atypical clinical setting, or if high suspicion for EBV but negative heterophile antibody, it is reasonable to test EBV-specific antibodies. +IgM with (-)IgG is consistent with acute infection.
When do you treat EBV with antivirals?
There is really not data that shows acyclovir has significant clinic benefit over placebo; treatment remains supportive. If you’re even thinking about treating, ID and (in this case) GI should be involved.
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MR with Jessica Duhe + Lyle Shlager: HCV management in the new treatment era

A middle aged woman presents for management of HCV. She has cirrhosis w/ portal hypertension; she was treated unsuccessfully 20 years ago with IFN + ribavirin, then again with addition of a third agent in 2012. With the advent of new therapies, she was re-treated and achieved SVR; however, she continued to require active management of decompensated cirrhosis and HCC screening.
*See this excellent NEJM take on updates in treatment of patients with cirrhosis: https://resident360.nejm.org/content_items/treatment-of-patients-with-cirrhosis
1. Who qualifies for HCV treatment?
-With the new therapies, EVERYONE! Asymptomatic patients, cirrhotics, AND decompensated cirrhotics can all be treated; if someone has decompensated cirrhosis, they should be listed for transplant in addition to being treated.
2. Who is at risk of treatment failure?
-Cirrhotics and patients on BID PPI. 
-Patients with HBV are at risk of HBV flare during HCV treatment; hence all patients must be tested for HBV prior to treatment initiation.
3. Once someone achieves SVR, are they cured for life?
-In short, yes (99% sustained cure for life) but they can always be re-infected (with same or different genotype)
4. When should beta blockers be used for varices in cirrhotics?
-Though BB used to be given to any cirrhotic with varices, new data shows a decline in survival when these are used in end stage cirrhotics, thought due to negative effects on already poor cardiac reserve. This has led to the “window hypothesis”, which essentially states that BB should be used during a specific period when someone has known medium to large varices but does not yet have refractory ascites or hypotension.
 
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MR with Nishant + Dr. Kim: Leukocytoclastic Vasculitis and Endocarditis

A middle aged man presents with 6 days of severe myalgias, low grade fevers, and rash. He initially underwent a broad work-up for his rash including infectious and autoimmune etiologies; his blood cultures ultimately grew staph aureus and TEE showed new severe AI and an aortic vegetation.
1. Endocarditis can present in very atypical ways – in an unknown inflammatory condition, it is on the differential!
2. Staph Aureus is BAD
– This patient subsequently found to have septic cerebral emboli
IE due to Staphylococcus aureus is associated with complications more frequently than other pathogens (stroke 21 versus 14 percent, systemic emboli 27 versus 18 percent, persistent bacteremia 17 versus 5 percent, and in-hospital mortality 22 versus 14 percent) [1].
-Staph aureus infection is itself a criteria for surgical repair of left-sided endocarditis. See this excellent algorithm to decide who gets surgery: https://www.uptodate.com/contents/image?imageKey=CARD%2F54251&topicKey=CARD%2F2148&rank=1~150&source=see_link&search=surgical%20indications%20for%20endocarditis
3. Leukocytoclastic vasculitis (i.e. the histologic correlate to ‘palpable purpura’) is classically associated with HSP but actually can result from many etiologies (in this case, the patient’s lesions may have been a combination of septic emboli and true immunologic complex lesions)
– think big categories of vasculitis, chronic infections, and medications
– one rheum attending uses complement levels for the initial branch point:
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