WoW: Let's Curbside Dr. Kansagara

A special shout out to Dr. Devan Kansagara for his appearance on the famed podcast "The Curbsiders". Did you know that Dr. Kansagara was one of the co-authrors of the American College of Physicians guidlines on hemoglobin A1c targets in Type 2 Diabetes?


Faculty and soon to graduate PGY-3s, did you know that you can now receive free CME and MOC credits on select episodes of The Curbsiders? Check out for additional details.

ALS Presenting as Hypercarbic Respiratory Failure

Thanks to Dr. Mayo for her presentation today of hypercarbic respiratory failure in an elderly male who was later diagnosed with amyotrophic lateral sclerosis (ALS).

One way to think about the elimination of carbon dioxide is:

  • "won't breath" - CNS
  • "can't breath" - PNS, respiratory muscles, chest wall, pleura, upper airway
  • "can't breath enough" - lungs

This allowed us to think through some common causes.

  • Decreased central drive - sedative medications, stroke, OSA
  • Decreased respiratory or thoracic cage function - spinal cord injury, ALS, Guillain-Barre, phrenic nerve injury, Myasthenia Gravis, Lambert Eaton, tetanus, organophosphate poisoning, neuromuscular blockade, metabolic disorders (low Phos, Mg; hyper-hypothyroidism)
  • Increased dead space - PE, severe pulmonary vascular disease, dynamic hyperinflation (COPD, severe asthma), end stage interstitial lung disease
  • Increase CO2 production - fever, thyrotoxicosis, increased catabolism, metabolic acidosis
  • Multifactorial - vocal cord paralysis, severe laryngea/tracheal disorders, foreign body aspiration,obstructive goiter

In this instance, pulmonary function tests (PFTs) and maximal inspiratory/expiratory pressures (MIPs and MEPS respectively) were key. Remember that neuromuscular disorders such as ALS demonstrate a predominately restrictive pattern on PFTs which means that patients may have a normal FEV1 and FEV1/FVC ratio. After diagnosis, regular spirometry (generally accepted to be every 3 months after diagnosis) is important to monitor progression. A recent review article highlights that two large trials (EMPOWER, BENEFIT-ALS) and the ALS trial database (PRO-ACT) found that the rate of decline in FVC predicts the liklihood of death. Another recent study showed that twitch trans-diaphragmatic pressure is the most powerful biomarker for mortality. But, that sniff nasal inspiratory pressure (SNIP) is an excellent correlate. And that a VC within a normal range suggests a good prognosis. Ultimately, there is no one single test which predicts all.

WoW: Recognizing Stellar Faculty

In the past few weeks, OHSU Department of Medicine faculty have been recognized for their outstanding accomplishments as clinicians, educators, researchers and role models.


A special shout out to Dr. David Lieberman who has been selected as the incoming President of the American Gastroenterological Association (AGA). He has been at OHSU since 1982 and the Chief of the Division of Gastroenterology at OHSU since 1998. For more information about Dr. Lieberman and his accolades, please refer to the very nice article published in Gastroenterology announcing his new position.


And, a round of applause for Dr. Erin Bonura who was awarded the Faculty Senate's Teaching Award. She completed her post-graduate training in Infectious Disease at OHSU and later went on to obtain her Master's in Clinical Research. She is an Associate Program Director for the Internal Medicine Residency Program and has introduced Team Based Learning curriculum into the Residents' training.

Shock with Dr.s Ran and Bender

We were fortuante enough to have two guest presenters for Noon Report this week- Dr. Ran Ran with Critical Care and Dr. Aron Bender with Cardiology. They talked through a case from the MICU of undifferentiated shock found to have markedly troponinemia. The discussion not only involved urgent management of an unstable patient but also interpretation of EKG findings and troponin elevation. Below are a few key teaching points. For full details, please refer to the posted materials on MedHub.

EKGs require a lot of practice to maintain proficiency. And, proper interpretation for ischemia is a must as rapid mobilization of resources is necessary in the event of acute plaque rupture or thrombus driven MI. Dr.s Ran and Bender reviewed the Third Universal Definition of Myocardial Infarction and provided some of their own tips. 

1. Interpret the electrographic regionality 

ekg and heart.PNG

2. Look for reciprocal change

3. Don't forget Sgarbossa's criteria for LBBB

 Concordant ST elevation > 1mm in leads with a positive QRS complex (score 5)  Concordant ST depression > 1 mm in V1-V3 (score 3)  Excessively discordant ST elevation > 5 mm in leads with a -ve QRS complex (score 2)

Concordant ST elevation > 1mm in leads with a positive QRS complex (score 5)

Concordant ST depression > 1 mm in V1-V3 (score 3)

Excessively discordant ST elevation > 5 mm in leads with a -ve QRS complex (score 2)

Evidence-based cardiac exam, dyspnea triangle

Thanks Josh Liu for a great case! Also thanks to Peter Sullivan, physical diagnosis attending expert for his pearls. This is a patient with a history of heart failure and paroxysmal atrial fibrillation who presented with several weeks of progressive dyspnea with evidence of right sided failure, cardiac tamponade physiology from a likely hemorrhagic cardiac effusion from a supratherapeutic INR.


Main points:

  1. ) A pulsus paradoxus of >10-12 mmHg has a +LR of ~3.3 and -LR of 0.03 which is the best diagnostic test we have for tamponade physiology (a reflection of a greater than expected drop in stroke volume during inspiration in the setting of high wall pressures and increased bowing of the septum towards the left side). With such a strong negative LR, pulsus is a good maneuver worth learning to make you feel more reassured that a patient does not have tamponade. Here is a great Stanford 25 page to review how to perform a pulsus.
  2. ) Things to do immediately in a patient with tamponade physiology include considering the following: hemodynamic stability (consulting the ICU), IV access, coagulation status (reversal if indicated), fluids to support preload, other consultants (cardiology/ cardiothoracic surgery for definitive treatment)
  3. ) An approach to dyspnea is the dyspnea triangle (below) which is categorized by how often these diagnoses appear: pulmonary, cardiac, anemia and then more rare metabolic/ psych. Check out this great teaching script (especially for your medical student didactics!) by Jeff Wiese at Tulane on the approach to dyspnea. Starts on page 12.

Want to learn more?

Evidence-based cardiac exam

  • Here is a 2016 BMJ article that is a systematic review of the evidence for performing different aspects of the cardiac exam. Table 1 summarizes the evidence that exists for the various exam maneuvers. It is worth noting some high yield maneuvers include jugular venous waveform, pulsus paradoxus, aortic stenosis exam, and determining if the JVP is elevated or not.
  • Thanks Peter Sullivan for this additional pearl: a falsely elevated pulsus can be from anything that increases pressure around the heart such as asthma or obesity
  • In regards to the jugular venous waveform, check out this great Stanford 25 page on what the normal waveform is and how it changes depending on certain pathologies

Raynaud phenomenon

Thanks to Aaron for a great case! This was an elderly patient with a longstanding history of Raynaud phenomenon with acute onset of small purpura on the pads of this person’s toes who underwent a fairly comprehensive workup with likely primary Raynaud phenomenon.

Main points:

  1. ) Secondary Raynaud has a wide differential including rheum, hematologic/ vascular, drugs and other conditions. See below.
  2. ) The differential for secondary Raynaud should be suspected in a person who develops symptoms older, has abnormal nailbed capillaroscopy and/ or other systemic symptoms.
  3. ) Interestingly this patient had a low ESR which has a differential including clotting of the blood sample, hypofibrinogenemia, RBC membrane defects, CHF, amongother things (see this great paper from Adam Obley: Annals 1986; 104:515-523)

Want to learn more?

Raynaud phenomenon ddx


  • MCC systemic sclerosis, RA, SLE, Sjogren syndrome, Antisynthetase syndrome, MCTD


  • Cryoglobulinemia, Hypercoagulable state (eg APLA)
  • Vascular: embolic/ thrombotic, vasospasm


  • Cocaine, Sympathomimetics, Chemotherapy (eg cisplatin, bleomycin, vinca alkaloids, gemcitabine)


  • Hypothyroidism
  • Carpal tunnel syndrome
  • Frostbite

Here is a great NEJM and recommendation regarding how to approach Raynaud phenomenon.

Inflammatory markers for diagnosis

Thanks to Adam Obley here are two great papers one from the Journal of Pediatrics and another a systematic review of 9 studies that essentially concludes that there is no big increase in added utility in obtaining both ESR and CRP for inflammatory or infectious conditions and the over-testing adds up to significant amounts to the healthcare system

Cutaneous Polyarteriitis Nodosa

 The histologic classification of cutaneous vasculitis. Imaged referenced from  Carlson JA. The histological assessment of cutaneous vasculitis. Histopathology; 56:3-23.  

The histologic classification of cutaneous vasculitis. Imaged referenced from Carlson JA. The histological assessment of cutaneous vasculitis. Histopathology; 56:3-23. 

Thanks to Dr. Fleming for presenting an interesting case of cutaneous polyarteriitis nodosa which started as distal peripheral neuropathy.

Cutaneous PAN is a rare form of PAN. There is a slight female predominance (1:1.7) with an average age of diagnosis 43.5years. The etiology is generally unknown. However, it may reflect underlying disease, infection of medication use. Individuals with CPAN should be evaluated for: antecedent Group A beta hemolytic strep infection (check an ASO), hepatitis B, hepatitis C, parvovirus, mycobacterium TB, IBD, minocyline use.

Diagnosis requires pathologic correlation with clinical findings. Histologically there is small/medium artery vasculitis clinically presenting as tender subcutaneous nodules on the lower extremities, often with livedo reticularious and cutaneous ulceration. There are no specific serologic tests.

CPAN is described as a chronic, relapsing and remitting course. Treatment is less aggressive than PAN. Mild cases responds to NSAIDs and topical corticosteroids. More refractory cases require corticosteroids and immunomodulators indlucing hydroxychloroquine, azathioprine, dapsone, cyclophosphamide, methotrexate and IVIG. The prognosis is good without any known mortality for CPAN itself. However, there is a potential for progression to PAN. One study notes 2 out of 20 patients with CPAN developed PAN after 18 and 19 years of follow-up.

For additional reading, please refer to Morgan AJ Review: Cutaneous polyarteritis nodosa. Int J Dermatol. 2010 Jul; 49(7):750-6.

 Types of cutaneous vasculitis. Table created in reference to UpToDate resource entitiled "Types of cutaneous vasculitis" 

Types of cutaneous vasculitis. Table created in reference to UpToDate resource entitiled "Types of cutaneous vasculitis" 

WoW - Dr Jacobs to be OHSU President


This week, the OHSU board of directors unanimously named surgeon Danny Jacobs MD MPH FACS (current Executive VP, Provost, and Dean at UTMB) as the 5th President of OHSU. He will be assuming this new role on August 1 after Joe Robertson MD MBA. He trained at WashU, Penn and the Brigham, and has previously had faculty appointments at Penn, Harvard, Creighton and Duke. For more see this OHSU news announcement.