Metabolic Acidosis part I

Metabolic Acidosis (limited mostly to increased AG metabolic acidosis and delta-delta

Check anion gap
If anion gap increased --> suggests increased unmeasured anions: organic acids, phosphates, sulfates
If anion gap decreased --> suggests decreased albumin or increased unmeasured cations: Ca, Mg, K, Li, bromine, immunoglobulins

If increased AG, determine the delta-delta (or delta ratio) to assess for other concomitant metabolic abnormalities.

Delta-delta = (delta anion gap)/(delta HCO3)
Delta anion gap = Calculated anion gap - Expected anion gap
Calculated anion gap = Na - (Cl - HCO3)
Expected anion gap = Albumin x 2.5
Delta HCO3 = 24 - HCO3

If delta-delta value:
1-2 --> pure AG metabolic acidosis
<1 --> AG metabolic acidosis and concomitant non-gap metabolic acidosis
>2 --> AG metabolic acidosis and concomitant metabolic alkalosis

Aids for intuition:
If delta ratio > 2, this points to a relatively small delta HCO3 (as the denominator will be relatively small).
If delta ratio < 1, this points to a relatively large delta HCO3 (relative to delta AG).  Increased Cl can account for this.


Osmolal Gap = Measured osmolality - calculated osmolality
Calculated osmolality = (Na x 2) + (glucose/18) + (BUN/2.8)
If osmolal gap > 10, suggests ingestion

The New Building Blocks of Learning

Need to imbed the video, talking points, questions?

http://www.ted.com/talks/sugata_mitra_the_child_driven_education.html

1. Broadband

2. Collaboration

3. Encouragement

4. Challenge

Troponin Elevation DDx

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1860726/

Excellence in Medicine through Rescue from Failure- Gawande

Below you will find excerpts from a commencement address given by Gawande re: excellence in medicine, from a perspective I had never heard before. 

"... the best surgeons I saw involved the ability to handle complexity and uncertainty. They had developed judgment, mastery of teamwork, and willingness to accept responsibility for the consequences of their choices.  

...I thought that the best places simply did a better job at controlling and minimizing risks—that they did a better job of preventing things from going wrong. But, to my surprise, they didn’t. Their complication rates after surgery were almost the same as others. Instead, what they proved to be really great at was rescuing people when they had a complication, preventing failures from becoming a catastrophe. 

....When things go wrong, there seem to be three main pitfalls to avoid, three ways to fail to rescue. You could choose a wrong plan, an inadequate plan, or no plan at all.  

...But recognizing that your expectations are proving wrong—accepting that you need a new plan—is commonly the hardest thing to do. We have this problem called confidence. To take a risk, you must have confidence in yourself. In surgery, you learn early how essential that is. You are imperfect. Your knowledge is never complete. The science is never certain. Your skills are never infallible. Yet you must act. You cannot let yourself become paralyzed by fear.  

Yet you cannot blind yourself to failure, either. Indeed, you must prepare for it. For, strangely enough, only then is success possible.  

...[The attending surgeon had] never seen a serious belly problem [after carotid artery surgery]. But the surgeon was humble enough to understand that he could.  

...So you will take risks, and you will have failures. But it’s what happens afterward that is defining. A failure often does not have to be a failure at all. However, you have to be ready for it—will you admit when things go wrong? Will you take steps to set them right?—because the difference between triumph and defeat, you’ll find, isn’t about willingness to take risks. It’s about mastery of rescue."

Choose a high risk clinical scenario and describe No plan, Inadequate plan, and Wrong plan scenarios. Then describe the Right plan. Try this exercise regularly and your patients and your hospital will benefit greatly from your preparedness. 

This connects to point #9 from our post on Clinical Reasoning - Progressive Problem Solving. Review that post to reinforce principles in Clinical Excellence. 

put in an example high risk case and connect to EN

Sinus Transillumination

A simple and practical physical exam maneuver to aid in the detection of sinusitis and other sinus space-occupying lesions.

Review these notes from the FPnotebook and these videos on frontal (one and two) and maxillary (one and two) sinus transillumination and practice on a number of "normals", include in your routine examination, and of course use in your focused ENT exams.

Include the sinusitis scoring criteria (Sapira's).

Appropriate Hypercoagulable Testing

EFFECTS OF ANTICOAGULANT THERAPY ON HYPERCOAGULABLE TESTING
AND OTHER ISSUES AFFECTING RESULTS from Institute of Transfusion Medicine, by Irina Chibisov, MD. 2012.

SUMMARY
Many factors interfere with results and interpretation of hypercoagulable studies. When possible, hypercoagulable testing should be done outside of an acute event, including thrombosis, infection, inflammation, and most definitely prior to the initiation of anticoagulation therapy.

Factor V and prothrombin DNA testing is fairly definitive.  Test results for protein S, C, and antithrombin III deficiencies are more difficult to interpret as environmental factors can influence the results. Clinical and family history should always be used to aid in testing interpretation. It is important to rule out acquired protein S, C, and antithrombin III deficiency prior to establishing a diagnosis.

Treatment with Coumadin can interfere with protein C and S testing. Ideally, Coumadin use should be held for two weeks prior to undergoing these tests. Alternatively, heparin use can replace the Coumadin during that time frame. Acquired protein S deficiency is quite common, frequently caused by factors such as pregnancy, liver disease, inflammatory conditions, and thromboembolism.

Acquired antithrombin deficiency can result from mild liver disease, acute thrombosis, nephrotic syndrome, and heparin anticoagulant therapy. Protein S assays are not reliable during pregnancy and heparin therapy can result in a false positive antithrombin III test result; but, antithithrombin III can be checked on Coumadin.

It is always important to remember that protein C, S, and antithrombin III congenital deficiencies are rare and should be suspected in strongly thrombophilic patients: i.e., those with a venous thromboembolism prior to age 50, recurrent venous thromboembolism, or with an extensive family history of thrombosis. When results are borderline, repeat testing and comparative studies of other family members can be appropriate.

Finally, direct thrombin inhibitors cause significant interference with all functional coagulation assays and hypercoagulable testing should not be ordered inpatients on these agents.

INCOMPLETE - needs to be edited to be more blog-friendly & clinically applicable. Case?