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)


Continue reading #fridayimagechallenge (with answers)

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)

CASE CHALLENGE (with answers)

Case Challenge

answer below the break, lots of correct answers, chocolate goes to the intern brando(e)ns

Hi all, welcome to a new blog format. The basics- an interesting case is presented once a month on the blog. Basic information will be provided, you can request additional testing and imaging via the survey link provided. Additional testing you request will be updated twice during the week. Answer and explanations will be posted the following week. When you feel comfortable making a diagnosis, provide it with your name in the same survey link (or if feeling confident comment on the blog itself) for a chance at reducing your EROC burden (kidding, but seriously chocolate for correct answers).

Without further ado

85yo white male with a history of prostate cancer (1990s, s/p radiation and chemo), CAD, HTN, HLD, CHF (NICM, previously reduced EF, now in 50s), AVR (5 years ago, bioprosthetic, not on AC) presents with severe back pain.

3 months prior to admission patient seen in OSF ED for new onset, severe left inguinal pain which was much worse with movement and hip flexion, the pain radiated towards the back with movement but not at rest. He described the pain as a muscle pull, he had not had similar pain previously. Workup for hernia was negative, patient unclear on what was performed but believes he received blood products. He was discharged from the ED with gradual resolution of the pain over 3 weeks.

From ED visit until 2 weeks ago he had no significant complaints other than mild fatigue. Starting 2 weeks prior to admission patient presented to a local ED 6 times for minor cuts on hands that would not stop. Bleeding was stopped with dermabond and he was discharged home each time.

2 days PTA he was feeling well and went for “a long walk”. on the morning of admission he awoke with significant pain in his right inguinal area, similar in quality and intensity to previous left inguinal pain. At this point he came into our ED for evaluation.

ROS notable for bleeding as described, easy bruising starting 4 months ago, mild fatigue, moderate nausea with pain, no NS/chills/v/d.

Past Medical Hx:

  1. Prostate CA- diagnosed in mid 1990s, s/p surgery radiaton and chemotherapy.
  2. CAD- s/p CABG 10 years ago
  3. CHF- apparently had reduced EF in past, now normalized. Per patient EF “in 50s” recently, AICD in place
  4. Aortic valve replacement- 5 years ago, bioprosthetic, no AC, followed closely
  5. HTN- controlled
  6. HLD
  7. Do not know if he has had c-scope

Past Surgical Hx:

  1. CABG- no issues with post-op bleeding
  2. SAVR
  3. prostatectomy

Family Hx:

  • Hypertension mom, DM2 dad

Social Hx:

  • Lives in abilene w/ wife, no bad habits

Outpatient Medications:

  • Lasix 20mg BID
  • Metformin 500mg BID
  • Metop XL 25mg qday
  • Methocarbamol prn
  • Diazepam 5mg prn
  • lyrica 75mg qhs

On arrival he was found to be tachycardic to the 120s, BP 95/65, RR 20, SaO2 98% on ambient air with T of 36.8 C. He appeared uncomfortable though not in significant distress. His HEENT exam was normal including no gingival/mucosal findings, he was tachycardic but regular w/o m/r/g. Lung exam was normal. Abdominal exam was notable for tenderness in the lower right quadrant that was referring to groin. GU revealed no hernia, no swelling, no erythema, no TTP. Extremities notable for 10cm resolving ecchymoses on RUE. Flexion of right hip caused significant pain in groin area. Palpation of lower right back caused moderate pain in right groin. No dermatologic changes were found other than ecchymoses previously descried and healing wounds on b/l hands which had previously been dermabonded. No petechiae seen.

  • BMP 145/3.4/106/25 (gap 16)/ 16/.88
  • CBC 10/6.1/18/151
  • INR 1.1
  • LDH 568
  • T bili 3.5 (no fractionation in ED). AST 25 ALT 45 alk phos 100
  • PTT 105
  • D dimer 6
  • Haptoglobin <10
  • Retic ct 8.2
  • fibrinogen 368
  • mixing study: PTT 85 pre, 65 after mixing (did not correct)
  • DAT negative
  • Factor VIII activity: <1
  • Factor VIII inhibitor: 58 (high titer identified) 
  • Factor IX activity: normal
  • Factor X activity: normal
  • vWF activity: normal
  • ANA 1:160 homogenous
  • RF negative
  • CCP negative
  • SSA/ SSB negative


  • CT head no abnormalities
  • CT abd/pelvis with contrast:  There is mild rotatory scoliosis of the lumbar spine, associated with multilevel degenerative changes of the endplates and facet joints. No worrisome lytic or blastic skeletal lesions are seen. Subcutaneous edema is present within the right flank.
  • The right psoas muscle is enlarged with ill-defined intramuscular hemorrhage. As the right psoas muscle measures approximately 6.2 x 7.2 cm in axial cross-section on axial image 38, and comparison to the left psoas muscle, which measures 2.4 x 4.3 cm at the same level.



Continue reading CASE CHALLENGE (with answers)

UTSW Internal Medicine

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