Chest xray and Chest CT: discrepancy?

Today at #MorningReport we had a case of a common diagnosis with an uncommon presentation.

A patient with recent cancer, s/p kidney transplant on immunosuppression but now with CKDIII came into the hospital for worsening shortness of breath and a dry cough. PA+lateral chest xray showed patchy RLL consolidation with very small bilateral effusions. He was started on antibiotics for community-acquired pneumonia and no JVD, rales and trace bilateral edema.

See the initial PA/lateral CXR:

Over the next 6 hours after lying in his bed, he came significantly more tachynpenic with an ABG of pH 7.42 and pCO2 24 and pO2 56. What do you think?

Repeat portable CXR at that time. Yikes!

Looks like worsening interstitial pattern! Differentials included: 

  • Bacterial: CAP, atypical, legionella, nocardia, actino, aspiration, MRSA
  • Fungal: PCP (“fluffed out”), crypto, histo, NTMB
  • Non-infectious: metastic cancer, pneumotoxicity – COP/BOOP/eos pneumonia 2/2 Tacro or Statin or pneumonitis, PF and DAD 2/2 chemo, DAD, DAH or sarcoid
  • Hypervolemia from CKD
  • Pulmonary embolism
  • ACS, heart failure

CT scan confirmed the diagnosis!

Cause of his SOB and acute worsening? Volume!

Patient recieved some diuretics and tachypnea improved dramatically.

Dr. Meredith Greer sent these notes over from our very own, Dr. Abbara, in the Radiology Department: look at the CT chest because there you can see the bilateral pleural effusions looking much bigger as the patient is laying supine and they are sort of layered out. When the pt is getting the PA/L CXR a lot of the effusion can hide in the gutters. It is possible that while the pt was laying down he developed atelectasis on top of his effusions and when he stood upright for the plain film that his effusions went down but the atelectasis didn’t have time to open back up yet.

https://radiopaedia.org/articles/pulmonary-pseudotumour

 

 

#TodayAtMorningReport

We had a fascinating case of anemia, thrombocytopenia and hemolysis – initially we had a broad differential but eventually focusing on MAHA vs transfusion reaction.

Take a look at the graphic below as well as some slides from Dr. Nagalla discussing a Clinical-Pathology-Case recently and his diagnostic reasoning around this topic.

From Wintrobe’s Clinical Hematology 13th edition:

 

 

 

 

#fridayimagechallenge(with answers)

45yo Buddhist monk with no past medical history presents to the parkland ED with 1 week mild chest pain on exertion and palpitations. Initial ECG is shown below.

 

Continue reading #fridayimagechallenge(with answers)

RESIDENT RECOGNITION!

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! 🙂

#fridayimagechallenge

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:

Infectious
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)
Non-infectious
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)
Autoreactive
Cancer
Primary tumours (rare, especially pericardial mesothelioma)
Secondary metastatic tumours (lung, breast cancer, lymphomas, and  melanoma)
Metabolic (Uraemia, Myxedema)
Trauma
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

UTSW Internal Medicine

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