Shout out to our stellar resident Dr. Bryan Wilner! Here’s what our ICU nurses had to say:

Dr. Wilner was of great assistance to us this evening for some critically thinking time. We were perplexed about a specific cardiac issue with a patient. Unsure if it was cause for concern, we asked Dr. Wilner who was sitting in the CCU rounding room for time to pick his brain, he obliged.  We are thankful for his collaboration while we provided our patients with the safest proactive care.

What an amazing example of great teamwork and collaboration! Your patients are benefiting from it! 🙂


55yo hispanic gentleman with poorly controlled diabetes presents with substernal chest pain radiating to his jaw starting 3 days ago, in ED troponin 1.2 and initial EKG below.

Pericardial effusion?

Today at Morning Report, we had a case of recurrent pericardial effusion. The discussion lead to a broad differential. Here is a European Heart Journal article (2013) with a nice list of Infectious vs. Non-infectious causes of pericardial effusion:

Viral (most common: Echovirus and Coxsackievirus (usual), Influenza, EBV, CMV, Adenovirus, Varicella, Rubella, Mumps, HBV, HCV, HIV, Parvovirus B19 and Human Herpes Virus 6 (increasing reports)
Bacterial [most common: tuberculous (4–5%), Coxiella burnetii, other bacterial rare may include Pneumo-, Meningo-, Gonococcosis, Haemophilus, Staphylococci, Chlamydia, Mycoplasma, Legionella, Leptospira, and Listeria]
Fungal (rare: Histoplasma more likely in immunocompetent patients, Aspergillosis, Blastomycosis, Candida more likely in immunosuppressed host)
Parasitic (very rare: echinococcus, toxoplasma)
Autoimmune and autoinflammatory
Systemic inflammatory diseases (more common in systemic lupus erythematosus, Sjögren syndrome, rheumatoid arthritis, systemic sclerosis, systemic vasculitides, Behçet syndrome, Sarcoidosis, Familial Mediterranean Fever)
Pericardial injury syndromes (post-myocardial infarction, post-pericardiotomy syndrome, post-traumatic)
Primary tumours (rare, especially pericardial mesothelioma)
Secondary metastatic tumours (lung, breast cancer, lymphomas, and  melanoma)
Metabolic (Uraemia, Myxedema)
Direct injury (penetrating thoracic injury, oesophageal perforation, and iatrogenic)
Indirect injury (non-penetrating thoracic injury, and radiation injury)
Mediastinal radiation, recent, or remote
Drugs and toxins (rare): Procainamide, hydralazine, isoniazid, and phenytoin (lupus-like syndrome), Penicillins (hypersensitivity pericarditis with eosinophilia), Doxorubicin and daunorubicin (often associated with a cardiomyopathy, may cause a pericardiopathy). Minoxidil. Immunosuppressive therapies (e.g. methotrexate, cyclosporine)
Haemodynamic (heart failure, pulmonary hypertension, and hypoalbuminaemia)

Our conversation lead us to: Drug-induced lupus. Here are a few highlights:

Epidemiology: 15,000 to 30,000 cases per year.
–> 15 to 20 percent of those taking procainamide, and 7 to 13 percent of those taking  hydralazine, to as low as 2 per 1000 for those taking anti-tumor necrosis factor (TNF) agent, and 5 per 10,000 of those taking minocycline.

Pathogenesis: drug metabolism (eg, slow acetylators) and/or immunogenetic characteristics (drug acting as hapten/agonist to T cell, activating lymphocytes, abnormal thymus function)
–> especially patients with (HLA)-DR4, HLA-DR0301, and the complement C4 null allele, slow acetylators.
–> noted to be dose dependent (>100mg daily)

Causative drugs:
procainamide, hydralazine, minocycline, diltiazem, penicillamine, isoniazid (INH), quinidine, anti-tumor necrosis factor (TNF) alpha therapy (most commonly with infliximab and etanercept), interferon-alfa, methyldopa, chlorpromazine, and practolol. Several others probable+possible.

Diagnosis: history of taking one or more of known drugs for at least one month (often longer) and with the development of at least one clinical feature of SLE. Discontinuation of offending medication resolve symptoms within weeks but sometimes up to several months.

Asking one of our UTSW Rheumatology experts today, Dr. Guillermo Quiceno says that SLE features usually will show early, within the 1st month or months – not likely years. For those with persistent symptoms even after stopping the offending medication may require Plaquenil.

****and REMEMBER from a 2016 post:
Myocarditis: inflammation of the heart muscle
Pericarditis: the inflammation of the lining outside the heart.
Myopericarditis: elevated troponin in the setting of pericarditis without new onset of focal or diffuse depressed LV function by echo or MRI
Perimyocarditis: with new onset of focal or diffused depressed LV function

Remember: Acute pericarditis: dx by the presence of 2 or more: chest pain, pericardial friction rub, ECG changes (diffuse ST-segment elevation or PR depression) and pericardial effusion.

Typical ECG: initially diffuse ST elevation and PR depression, followed by normalization of ST and PR segments, and then diffuse T-wave inversions

#fridayimagechallenge (with answers)

This week’s CXR brought to us by Dr. Kondamudi

60yo Male with HFrEF and ED presents for device implantation, below is post- procedure CXR (click on image for full screen)


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Busy Week for UTSW IM!

Jeopardy Champions!

The 2017 Southern Regional Meeting of the Society of General Internal Medicine (SGIM) was held Feb 10-12 in New Orleans, LA. Our team of erudite residents – R3 Carlos Cardenas, R2s Nitin Kondamudi and Timothy Brown, and R1 Grace Liu – did UTSW proud by beating 7 other teams to clinch first place in the Jeopardy tournament!

After coming in a close second in 2016, the UTSW team returned to the stage with renewed thirst and took an early lead with rockstar-level answers including:

  • Southern Tick-Associated Rash Illness (STARI) and its Lone Star tick vector
  • Trousseau’s sign
  • Idarucizumab for Dabigatran reversal
  • Cheyne-Stokes respiration
  • The rare prion-mediated Kuru disease

With a runaway lead of 2800 points to 1000 going into final jeopardy, the team pulled out an effortless win after gambling 0 points in the final round.

The UTSW IM team are also this year’s Texas ACP jeopardy (Doctor’s Dilemma) champions and are headed to Nationals in 6 weeks. They are looking to build a bigger pool of players – interested candidates can reach out to Carlos, Tri or Arjun for further details.

Published in JAMA!

Our residents Christina Yek and Arjun Gupta teamed up with Dermatology faculty Dr Melissa Mauskar to publish a Parkland-strong Clinical Challenge case in JAMA this week. “A previously healthy man in his 40s presented with 4 days of fever and a rash…” Think you know the answer? View the case and take the challenge!

Ambulatory Report: Adrenal Incidentaloma

We had a great Ambulatory Report today with the help of our own Christian Ngo and Endocrinologist Dr. Abramowitz, teaching us how to workup/manage adrenal incidentalomas:


  • All patients:
    • cortisol (1mg dex suppression test: am cortisol <1.8 rules out and >5 rules in). 24 hour urine cortisol is only used in patients where suspicion for Cushings is high or in patients (ie on HRT or with liver disease) where binding globulins may interfere with the results.
    • metanephrines/catecholamines (24 hour urine: >4x ULN rules in). Free serum metanephrines are only useful in patients who you have a very high suspicion of a pheo.  Remember that TCAs and SNRIs can lead to falsely elevated metanephrines/catecholamines.  
  • Only patients with HTN (no matter how mild):
    • Renin/Aldo. Abramowitz recommends using the “Texas Two-Step” guidelines by Dr. Auchus.  The most important lesson to learn from this paper is that a suppressed renin is more important than an elevated aldosterone.  A renin <1 and aldosterone >15 gives you the diagnosis. Avoid using the ratio of >20 that we learned for Step 1. Remember that aldosterone antagonists (aldactone) will completely interfere with the test. ACE-I/ARBs do to a lesser extent so if their renin/aldo studies are +, then you have the diagnosis, however, if their studies are indeterminate/negative, either refer to Endocrine for assistance or, if it’s safe to do, change them to a CCB or BB for ~ 1 month and then repeat screening.  

Refer to Endocrinology if patient has:

  • Any worrisome features on imaging (>10HU, >4cm, irregular, >50% washout, calcifications, growth >1cm)
  • A functioning adenoma
  • Their tests are indeterminate (especially patients on SNRIs/TCAs whose metanephrine/catecholamine screen might be falsely + or a patient on ACE-I/ARB/aldactone that you feel might be interfering with the tests).

Long term monitoring: (there are no set guidelines)

  • Repeat imaging: 6mo, 12mo, then 24mo and if no changes, you can stop imaging.
  • Repeat labs (cortisol, metanephrines/catecholamines) yearly x 4 years (Dr. Abramowitz is confident you can stop after 2 years if imaging and hormonal studies are all negative/stable).

To Summarize (per Dr. William Young, NEJM):


#fridayimagechallenge (with answers)

You are on a radiology elective and come across this CXRsarcoidosis-2


Continue reading #fridayimagechallenge (with answers)

UTSW Internal Medicine

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