June 2016

Approach and Differential

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No me gusta!

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Lennard O. -

I'll have nightmares the whole month, worrying about poor Jimmy. I love the C3, awesome work!

Mizuho M. -

Haha! Yes poor jimmy!

Atheer Z. -

Good morning

Thank you for the great talk
I have had a 72 year old lady who presented to ED with SOB 2 weeks ago and history and exam I thought she would have PE. PMH: type II diabetes only, NOT on metformin
On gaining more details of history she was apparently started on new diabetes medicine FORXIGA which I didn't know what it was initially,
She was tachycardic at 115, sinus tachy on ECG with minor ST changes, normal BP, RR 25, SPO2 100% on room air
Normal CXR
I still thought she had a PE however no major risk factors and no signs of DVT
While waiting for blood I thought I should do Blood Gas which gave the diagnosis away
PH 7.07, PO2 normal, PCO2 in 20s, Bicarb 3.09, BE -20, lactate 1.8
High anion gap(30) metabolic acidosis with normal expected PCO2- compensating well
Hence diagnosis of HAGMA, blood sugar on 10, bedside ketones 7.4

Apperantly Forxiga is Dapagliflozin- SGLT2 inhibitor where there has been report that it can cause diabetic ketoacidosis picture

Admitted under endocrinology- given insulin infusion, dextrose, K, and monitoring
While in the ward developed hypotention and treated with sepsis but lactate normal, procalcitonin normal, then BP improved, discharged on day 5 doing well

I thought I should just point out that no all SOB are lung and heart causes

Thank you

Atheer Zaraga
ED specialist
Sydney Australia

Mizuho M. -

Thank you atheer for your interesting case! Precisely why we broke this topic up to 2 parts. Dyspnea part 1, we review the less common non-cardiac/pulmonary causes, & part 2- bread & butter cardio-pulmonary causes. Your case is case in point of keeping a broad ddx! Strong work! Thanks for listening!!!

Evan M. -

I Enjoy the program. Thank you for doing such a great job. I had one question on this last episode. You recommended heparin prior to CTA in some patients with high suspicion of PE. I have heard this previously and I have always found it curious. What do you think you might gain by giving heparin prior to a CTA (1 hour earlier perhaps) if you think a patient has a high likelihood of having a PE? Do you think the improvement in mortality you would get from correctly heparinizing a patient earlier who has a PE counteracts the harm you will do from inadvertently giving heparin to patients you incorrectly suspect PE in? It was my impression that heparinization would only very slowly help to reduce clot burden in a PE.

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