Thanks to Rachel Snyder for presenting the case of a young man with chest pain after a recent viral prodrome, who is thought to have a (likely viral) myopericarditis.
We talked about where troponins come from:
Harrison’s Principles of Internal Medicine: STEMI
We talked about the kinetics of cardiac biomarkers.
Harrison’s Principles of Internal Medicine: STEMI
- Remember that the diagnosis of ACS depends on the right clinical setting, with appropriate EKG changes, and a rise and fall in troponin with at least one value above the 99th percentile
- Note that CKMB rises within 4-6h of myocardial necrosis, but is far less sensitive and specific than troponin; it is no longer recommended in most situations, except possibly to diagnose reinfarction. It is released from both myocardial and skeletal muscle
- Troponin is most sensitive because there’s more of it per gram of myocardium; it also rises within 4-6h and can stay elevated for 7-10 days after injury
- An increase in troponin of >20% after a recent infarct suggests reinfarction
- A quick note on Troponin I (TnI) vs T (TnT)
- At Penn, TnI is used as a point-of-care (POC) test
- TnT is renally cleared (so is TnI, but less so than TnI), so patients with ESRD may have low grade elevations which may add to the challenge of diagnosing ACS
Remember that many things other than ACS can cause troponin elevation
Daubert et al 2010
Lastly- don’t forget the importance of the physical exam in ruling out tamponade, so make sure you do a pulsus if you’re worried about it! Here’s how to do it.
Late post from last week. Thanks to our excellent sub-I Juan Spinnato for presenting the case of an older man with subacute cough, dyspnea and polyarthralgias who was found to have a marked eosinophilia, and was ultimately diagnosed with a large intrahepatic mass, now favored to be cholangiocarcinoma 😦
- Polyarthralgias have a huge differential, so certain features can help narrow your differential
- Distribution: pattern (small vs large joints), symmetry, axial involvement
- Extra-articular manifestations (rash, eye symptoms, muscle weakness)
- Duration: <6 weeks is often viral, >6 weeks bears further investigation for other causes
- Periodicity: intermittent (crystalline arthritis) vs constant
- Demographics (gender, age, race, family hx)
We also talked about the utility of inflammatory markers!
- What can increase or decrease the ESR?
- Increase: infection, inflammation (duh), malignancy, trauma
- Decrease: abnormally shaped RBCs (SCD, spherocytosis, etc), heart failure, extreme leukocytosis
- There are underlying conditions that can ‘falsely‘ elevate the ESR more than expected
- Elevate: older age (correction formula: ULN of reference range = age/2 for men and (age + 10)/2 for women), female gender, ESRD, obesity
- Conditions that can cause a discrepancy between ESR and CRP
- Elevated ESR, normal CRP
- monoclonal immunoglobulins
- SLE (felt to be because type I IFNs produced in SLE inhibit CRP synthesis by liver)
- Elevated CRP in SLE should raise suspicion for underlying bacterial infection
Richie et al. Diagnostic Approach to Polyarticular Joint Pain. Am Fam Phys. 2003.
Thanks to everyone who chimed in for our first HUP intern intake report, and to Nilan Schnure for presenting the case of a 65 year old woman who presented with months of intermittent fevers, progressive pancytopenias and oral ulcers.
This was a difficult case and is still ongoing, but we decided to focus our differential around her oral ulcers.
- There are two flavors of DIC- acute and chronic. The latter is associated with vascular malformations (aneurysms, hemangiomas), liver disease and malignancies, while the former is more common and related to sepsis, acute leukemia, trauma, etc.
- Oral ulcers can stem from a variety of infectious (HIV, HSV, Coxsackie), inflammatory (SLE, Crohn’s, Behcet’s, Sjogren’s) and nutritional (Vit C deficiency) conditions (and don’t forget benign recurrent aphthous stomatitis).
- Basic labs like LDH, haptoglobin and especially a reticulocyte count can help you decide whether pancytopenia is peripheral or marrow-related in origin.
- Porter et al. Oral ulcers and their relevance to systemic disorders. Aliment Pharmacol Ther. 2005. PMID 15709981
Today we talked about a young woman with worsening dyspnea on exertion and a history of pneumothorax, with diffuse cystic lesions on chest CT and was ultimately diagnosed with LAM (lymphangioleiomyomatosis)!
- LAM can be either sporadic or associated with tuberous sclerosis
- LAM is mediated by LAM cells which are smooth muscle cells of unknown origin that infiltrate various organs/tissues, particularly lymphatic channels and capillary beds- they then lodge there and cause ‘frustrated lymphangiogenesis’, leading to cystic remodeling in the lung
- ~35% of patients who are ultimately diagnosed with LAM present with pneumothorax; almost without exception, they are female and tend to present in their 30s (pathogenesis thought to be driven by estrogen). They can also present with chylous effusions and chylous ascites.
- The 2011 MILES trial in NEJM showed that sirolimus stabilizes FVC and functional performance in LAM (see graph below) during the 1-year treatment phase.
- Ultimately the only treatment is lung transplant; LAM has been known to (rarely) recur in the transplanted lung
MILES trial, NEJM 2011
Lastly, remember that there are lots of cystic lung diseases (algorithm below), and knowing how to differentiate cysts vs cavities vs bullae can help you hone down your differential.
Gupta et al, AJRCCM
- Gupta et al. Diffuse cystic lung diseases, part I. AJRCCM. PMID 25906089. (there’s also a part II)