1) Does this make sense to me?

2) Is this relevant to me?

Obviously you won’t be able to retain any of the information you learn if you don’t even understand it. And you’re even less likely to retain it if it has no relevance to your life.

I realized I needed to post something on Hyponatremia when I had to go back to my Mass Gen hyponatremia algorithm flow chart for the hundreth time that day all the while knowing that in 5 minutes I’d forget it again. So I sat down and decided to break it down so it made sense to me.

That having been said, I present to you a simplified understanding of the management of hyponatremia, the most common electrolyte abnormality…ever.

So why is this important to you? In other words what is the relevance?

1) It’s common. In fact it is the most common electrolyte abnormality with up to 30% of hospitalized patients developing it, mostly in elderly.

2) Its deadly dangerous. (Anytime you have death as a potential outcome there is something to look out for.) The risk of morbidity and mortality increases with the severity of hyponatremia in almost every known disease state.

3) Possible treatments vary greatly from each other. They vary so greatly that they are in fact opposites (i.e. giving fluids vs. restricting fluids) Choosing the wrong treatment option can lead to above mentioned “death” scenario.

Please make sure he never suffers at the hands of hyponatremia:

The Basics:
Definition: <135 mEq/L, severe if < 125 mEq/L
Normal range: 135-145 mEq/L

One key point to remember here: The extracellular sodium concentration is more indicative of water balance than it is of total body sodium content. Essentially, the serum sodium value says more about how much water is in blood vessels than it does about the actual sodium content. Think dilution.

Signs/Symptoms: It begins very nonspecific and mild with headaches and irritability and progresses to nausea and vomiting, some mental slowing, unstable gait/falls, confusion/delirium, and disorientation. Then to the more severe, what you don’t want to see in your patients: stupor/coma, convulsions, respiratory arrest and…I would put death here but at that point its not a very helpful symptom in terms of management. In general, the more severe the symptom the more quickly and aggressive you need to treat.

Here is what most med students, and very likely most interns think of when going through Hyponatremia (sorry for the blurred font)

Just so you’re not that intern. Here are the Big Picture Steps for understanding Hyponatremia:

Hyponatremia Management: The BIG Picture

OVUM (for those of you mnemonic freaks out there, I’m one too.)
Osmolality + Volume status + Urine = Management!

1) Check Serum Osmolality: Why? To rule out causes of “false” hyponatremia such as an increase in protein, lipids, glucose, mannitol, or glycine (secondary to urolgic or gynecologic procedures). Essentially we are asking, is this “true” or not?

Question: Why do lipids, glucose, protein, mannitol affect serum sodium values?
Non sodium solutes such as glucose cause fluid to shift into the vasculature essentially causing a dilution of serum sodium concentration. Osmotic pressure baby. What this does is give the appearance of a drop in sodium. Remember this formula?  Corrected Serum Osmolality = 2Na + Glucose/18 + BUN/2.8. Well, now you know why BUN and Glucose are in there. There are strong solutes.

2) Check Volume status: Why? Whether fluid is retained or not helps us tentatively approach the etiology (Is is due to cirrhosis, heart failure, nephrotic syndrome? Or is it due to diarrhea, vomiting,  diuretic use?) Then we can decide which treatment options to consider: To give water or not to give water, that is the question…

Whether ’tis nobler in the mind to suffer
The slings and arrows of outrageous fortune,
Or to take arms against a sea of troubles
And by opposing end them.

Take arms I say, take arms! Arms filled with bags of saline…unless of course the patient has SIADH.

Question: How do we determine volume status? This is done clinically. (ie. check for postural hypotension, JVP, tachycardia, skin turgor, signs of swelling/edema.)

3) Check Urine Osmolality and Urine Na: Why? To find out if the kidneys are the culprit. If Urine Na >20 → most likely yes.

4)Management/Treatment: Ultimately you either replace fluids or restrict them. The correct decision needs to be made to avoid unwanted outcomes. Additional info along the way can lead you to discovering the underlying pathology. An example would be finding out that the Urine Osmolality is >100 mOsm/kg suggesting an SIADH picture (ADH causes you to retain water by activating aquaporin channels in the collecting ducts so naturally the Urine Osmolality would be higher). Might there be a pulmonary or CNS lesion we are unaware of? This can lead to a crucial discovery for the patient’s care.

Question: Why are patients often euvolemic in SIADH while also excreting so much sodium?
In Syndrome of Inappropriate Antidiuretic hormone Hypersecretion, you have just that – hypersecretion of ADH, causing retention of water at the level of the collecting ducts. The thing is, the body’s Osmoregulatory systems are still working fine. It senses and increase in fluid and tries to get rid of the excess as best as it knows how: by getting rid of sodium, hoping that water will follow. Which of course it doesn’t. Hence patients tend to either be euvolemic or slightly hypervolemic and hyponatremic. Voila!

One last major point to consider during the initial workup is if this acute or chronic. An acute episode of hyponatremia is defined as being <48 hours and evidenced by neurological sequelae, since the brain has much less time to adapt to the osmotic differential.

The long and the short of it (The Review)

When being presented with a patient that is hyponatremic I realize that I first need to know whether this hyponatremia is “true” or not which is where serum osmolality comes in. Second, I need to know whether I should be preparing to give this guy fluids or restrict fluids. This is where knowing the volume status comes in. And finally, checking his Urine tells me whether I am dealing with something kidney related or not. Instead of relying on a blurred mental image of the hyponatremia algorithm I can actually think it through in a way that makes sense. Which is why it’ll stick this time around.

Train yourself to review

Did that make sense? Was it relevant to you? I hope you can answer yes to both questions. Try to get into the habit of reviewing material you’ve just read especially when studying for the boards or for exams. The review will help you to realize if there was something you didn’t really understand as well as help your brain file it away appropriately, having made the important connections and associations. It literally can take only 5 seconds for a big picture review.

Dive back into those physio and biochem books if you have to and make sure you get the basics. As a resident, these concepts are foundational and inform your decision making.

Enjoy your sodium!

Drinking too much water

One interesting phenomenon that I think we as clinicians will be seeing more of is hyponatremia secondary to drinking too much water. You’ll see this mainly in athletes training for a marathon, a triathlon, or just exercising really. The excess water intake essentially dilutes serum sodium before the body has time to excrete the excess. The treatment for water intoxication is just fluid restriction in mild cases, and in severe cases the use of diuretics and/or vasopressin receptor antagonists such as the Vaptans.

Helpful Algorithms
(Click on the images to make them bigger)

HEPARIN AND WARFARIN

We ended up spending the next few minutes discussing why it is so important to consider these other two proteins in our knee jerk response. If a patient needs to be anti-coagulated for any acute venous thromboemboli you should treat with heparin AND warfarin. Warfarin inhibits vitamin K dependent carboxylation of the factors mentioned above, and because Proteins C and S have anticoagulating properties and have relatively shorter half lives, they get affected by Warfarin first and create a temporary PROTHROMBOTIC state. The heparin given for the first 5-6 days of the treatment is to cover that brief window where Proteins C and S are out of commission, at least until the INR is therapeutic (2.0-3.0).

Interestingly enough, I found out that there is another anticoagulant that is Vitamin K dependent, Protein Z. It seems it works on inhibiting Xa…good to know. If this was all boring repetition for you then great, thats kind of the point. I thought I’d put this up here because I was surprised at how many had forgotten exactly the roles of Proteins C and S.

And here’s our lovely cascade for your reviewing pleasure:

BARRIERS TO LEARNING

David Sousa talks about several barriers we have when learning. Two major barriers mentioned can be summed up in the following two questions: 1) Do you understand the material? and 2) Is it meaningful?  Asking ourselves these two questions can revolutionize how we study and help us retain information better. Once you become more aware of these two points you’ll be amazed at how often you just continue reading without having fully understood what was just read. The same goes for whether the passage is meaningful.

Our brain is an incredible triage nurse constantly asking whats more pressing? whats more important? what needs to be done NOW? Therefore if you dont even get what you are reading, the brain throws it out. If its not meaningful in any way, if it doesn’t hold your attention, then your brain right clicks and ‘empties trash contents’. Done.

My suggestion: At the end of every section or subsection you read stop and ask yourself: Did I understand that material? Really? Was it meaningful? How so?

THE BARRIER OF SAFETY

Those two barriers of comprehension and meaning are dwarfed however by another more massive barrier. That of safety. Basically -

Do you feel safe?

This single insight has rocked my cognitive world. Essentially Sousa is saying that due to evolutionary reasons we homo sapiens place safety far far above anything else in regards to the brain’s time and energy investments. Naturally this makes sense. We would rather be alive first, an expert at tracing our hands on cave walls second.

Heres the rub though, the brain makes no distinction between externally perceived threats and internal ones. So your worrying about getting into a residency program could be as threatening as a pack of wolves might have been to our fore fore fore fathers (for some of us more so). In both instances the brain senses a threat (real or imaginary) and responds with a massive and often continuous flood of hormones, neurotransmitters, and electromagnetic changes that all but shut down our ability to learn, process, and retain any information not directly related to the threat.

For me, this meant I study better and infinitely more effectively when I’m safe and at peace, obviously externally but more importantly internally as well.

Why do you think children who go to schools with metal detectors or who live in generally more dangerous neighborhoods don’t do as well as their safer counterparts? Factoring out socioeconomic status and other similar reasons, its been shown that students who feel safer perform better. Period.

My question to you: DO YOU FEEL SAFE?

The sources I used to tackle this were 1) Kaplan’s Lecture Notes 2) High Yield Behavioral Science by Fadem (3rd ed.) and 3) UsmleWorld Qbank.

A quick note about the Kaplan notes: There are a series of rules for dealing with patients and with legal issues towards the end of Kaplan’s Behavioral notes that I found amazing. The reason they work so well is because they give you a few solid principles with which to apply to an infinite amount of scenarios. For example, one of the rules Kaplan created for the physician-patient relationship is “Never pass off your patient to someone else”. I can’t tell you how many times I saw a behavioral question on the test with this as one of the answer choices. An example of this would be to refer your patient to a specialist or offering to help your patient see a counselor for their specific issue, etc. I remember in the past I would seriously consider this as an option(making the question more difficult for me). After reading Kaplan’s “rules,” the behavioral questions are less grey and more black and white.

Risk and Odds just seemed the same to me for a long time. Since then, I have come to understand to important difference. Lets start with Relative Risk.

Relative Risk can be addressed by asking the following question: How many times more likely is an “exposed” group to develop a disease over a certain period of time as compared to a “non-exposed” group?

Here’s the key: Relative Risk looks to the future for the effect of a particular cause hence it is used in prospective studies say a cohort study.

Lets compare the above with Odds Ratio. The Odds Ratio can be addressed by asking te following question: How many times more likely is a diseased group to have been exposed to a risk factor as compared to a non-diseased group?

Here’s the key: Odds Ratio looks to the past for the cause of a particular effect hence it is used in retrospective studies such as a case-control study.

Lets go through some examples so we can get a better picture.

Using the table above as our 2×2 contingency table lets first consider the following case. A group of 70 individuals decide to begin a new therapeutic drug X, however the drug X has been known to cause cancer. They are compared to a control group of 60 individuals that takes a placebo instead. Question: What is the Relative Risk of developing cancer from Drug X compared to the control group? Here we need to consider whether we are looking at a case-control study or a cohort study. This is more of a cohort study, meaning the study is looking to the future to see if Drug X leads to cancer. Remember that a case-control study looks to the past.

TO CALCULATE THE RELATIVE RISK

Take the number of individuals who developed cancer (disease in the table) after having been exposed to the drug (40 or A in the table) and divide that number by the total of individuals exposed (70). Consider this value to be more of a percentage of the total exposed. We then divide this value (A/A+C) by the number of non-exposed who developed cancer over the total number of non-exposed (B/B+D). Therefore Relative Risk = the ratio (A/A+C)/(B/B+D).

To understand Odds Ratio now, lets go through another but similar example. A group of 60 individuals with cancer are being evaluated to see they were exposed to a particular toxin X. They are compared to a group of 70 individuals that do not have cancer and is similarly being evaluated for exposure to Toxin X. It is found that 40 of the 60 cancer individuals were indeed exposed and that 30 of the non-cancer individuals have also been exposed to Toxin X. Lets pause for a moment and realize that we are looking at a studying that is taking people who ALREADY have a disease and looking to the past to see if they were exposed to a Toxin thereby possibly drawing some association between the toxin and cancer.

TO CALCULATE THE ODDS RATIO

You could just memorize the shortcut AD/BC. For those of you who want to understand why this is the case read on. To calculate this lets first take the diseased group (with cancer) and compare the odds of having been exposed to not having been exposed. Not here that we are NOT dividing by the total amount in the group as we did in Relative Risk (ie. it is not a percentage of the total rather it is a comparison between two values in this case having been exposed and not having been exposed). In the table above it would be A/B. This new value is now divided by the odds of having been exposed versus not having been exposed in the non-diseased group (C/D). This comes out to (A/B)/(C/D). If we remember from basic math dividing two fractions by each other is the same as multiplying one fraction by the reciprocal of the other (A/B)*(D/C) and multiply across, which is now (AD/BC).

To recap:

Odds Ratio – Look to the past, Case-control study

Relative Risk – Look to the future, Cohort study

I hope this helps. Please leave a comment if there are any mistakes here or if you have any questions.

1. Kaplan Biostats Videos/YouTube Videos

2. HY Biostats

3. UsmleWorld Biostats Subject review

4. UsmleWorld Step 1 Qbank

The UW Biostat subject review was by far the one that brought it all home for me. Granted this was probably because I had gained some basic understanding already from the previous videos and Glaser’s book. The subject review is nicely organized by main sections and organized in order that builds on itself. I definitely recommend purchasing it. If you only pick one thing to do I suggest doing that, because honestly the Kaplan books and videos do not cover everything you need to know for potential Step 1 questions.

Here’s an example of a video that was helpful for me. Khan academy actually has several videos out on YouTube for Statistics. I would watch these during my breaks and found that the presenter clarified some things I never really understood. You might or might not like his style of teaching. Enjoy!

Here are some topics I feel are high yield for the Step 1 exam:

• Sensitivity (snout)
• Specificity (spin)
• Positive predictive value, PPV (remember this depends on prevalence)
• Negative predictive value, NPV (also depends on prevalence)
• Relative Risk (remember to use in cohort studies)
• Odds Ratio (remember to use in case-control studies)
• Confidence Intervals
• Setting a cutoff point on normal distributions (classic example is the fasting blood glucose cutoff for diabetes)
• Attributable Risk
• Number Needed to Treat
• P value (probability that the null hypothesis is correct)
• Correlation coefficient (describes a linear association does NOT necessarily imply causation)
• Variability or the percent of variability (remember to square the correlation coefficient)
• Which test to use chi-square? correlation? t-test? ANOVA?
• The biases: length-time, lead-time, confounding, selection, etc.

All that said, I am sure I left out some potential test question topics. What I left out however, I’m sure the UW subject review will cover. One thing I do want to cover is something I personally had difficulty understanding for the longest time and it was only recently that it became clear and that is the difference between relative risk and odds ratio. Risk and Odds, they always sounded like the same thing.

I want to say at the beginning that the exact details of eye muscle functioning are probably not the highest yield material for Step 1 studying. Also, explaining this in words is definitely not the most effective way of explaining the eye. Animation would be ideal here, alas. With that said lets get into this crazyness.

The first thing I want to point here is a foundational point. The eye muscles and the eye socket itself point outward at about a 20 degree angle away from the midline. Let me be clear: NOT the eyeball but rather the orbit and the majority of the muscles come out of the skull at a 20 degree angle away from the midline. You can see this from the picture. The eyeball itself however is pointed forward as you can see.

THE SUPERIOR RECTUS EXAMPLE

Lets look at the superior rectus (the central muscle in the image here) to get an idea of how this particular non-alignment plays out. If you look carefully at the insertion point of the superior rectus here we can see that if it were to contract not only would the eye turn upwards it would also intort. To visualize intorsion lets first imagine a point on the very top of the eyeball – the exact center of eye in the image (since it is a superior view). Intorsion would mean this point moves medially towards the midline causing the eye to essentially rotate about its own axis. Now we can better imagine the action of the superior rectus: eye elevation and slight intorsion. Intorsion, however, would give us a tilted view of the world and with each eye intorting if we wanted to look up, things would appear very confusing.

The question then arises: How can we look up without causing intorsion of the eye?

To prevent this intorsion nature ingeniously created another muscle (the inferior orbital in this case) to essentially cancel out the intorsion by causing extorsion (outward rotation of the eye about its axis). In addition to extorsion, the inferior orbital elevates the eye as well. So to recap we have two muscles working in concert with each other: one causing elevation and intorsion (superior rectus) and the other causing elevation and extorsion (the inferior orbital). The intorsion and extorsion cancel each other out and the eye can look up without tilting.

Look at the following image to get a better understanding of how the inferior orbital cause elevation and extorsion. To really see if you understand this concept try to work out for yourself using these images how the eye might handle looking down. To get you started, realize that in order to look down the eye would need to use both the inferior rectus as well as the superior orbital. Which one would cause the extorsion? Which one causes the intorsion? Do you see how this cancels out to produce leveled depression of the eye?

TESTING THE SUPERIOR AND INFERIOR ORBITAL MUSCLES

One last point I want to make has to do with how we test the superior and inferior orbital muscles. Lets use the superior orbital muscle as an example. In order to test whether it is working generally we ask the patient to turn the eye medially (adduct) and then look down. The reason we do this is to remove the depressing ability of the inferior rectus. If, after removing the inferior rectus’ depressing ability, the eye can look down then the superior orbital muscle is functioning.

To understand how turning the eye medially “removes” the inferior rectus’ depressing ability we need to revisit the idea that the major eye muscles are coming out of the skull at roughly 20 degrees from the midline (see image above). If, for example, the right eye turns medially then its central axis line would be roughly perpendicular to the line of the inferior rectus. At this point if it were the only muscle to contract it would cause the eye to extort or rotate outwardly about its own axis. In reality the other muscles would prevent this from happening.

Now that the depressing ability of the inferior rectus is removed by turning the eye medially would can test the superior orbital muscle ability to depress the eye and therefore its functioning. The Inferior Orbital muscle is essentially the same idea. We test it by  turning the eye medially and then looking up instead.

As always I am more than open to comments and discussion. Good luck with the studying!

The best way to approach the issue is by first understanding two important concepts: 1) The lumbricals and what they do. 2) Is the patient being asked to extend their fingers or make a fist?

The last point in particular might clear up a lot of confusion. We’ll see why later. First lets start with the Lumbricals. What you need to know is that the Lumbricals are responsible for flexing the MCP and extending the PIP and DIP joints. The Median nerve controls the lumbricals for digits 2 and 3. The ulnar nerve controls the lumbricals for digits 4 and 5. Here’s is how a hand would look with all lumbricals working (flexing the MCP joints and extending the PIP and DIPs):

A nice way to remember this is that L umbricals make an “L” shape. Therefore if the lumbricals don’t work then we have the opposite: extended MCP and flexed PIP and DIP. Here are two images (one my hand, the other I got from google images):

Consider this more of a dramatization since I don’t actually have Klumpke’s palsy.

Note: MCPs extended, PIP/DIPs flexed. Klumpke’s palsy has also been called “total claw hand”, because as a commenter wonderfully pointed out there are injuries to both the median AND ulnar nerves.

Ok, so how does all relate to the Pope’s Blessing sign? It really all comes down to which lumbricals aren’t working. Let’s look at a distal ulnar nerve lesion. In this scenario the ulnar lumbricals don’t work, meaning the 4th and 5th fingers have extended MCP and flexed PIP/DIP (remember non-functioning lumbricals). As a result the 4th and 5th fingers appear partially flexed. Now here’s the key: If you ask the patient to extend their fingers you accentuate the discrepancy between fingers. We end up with extended 1st, 2nd, and 3rd digits while the 4th and 5th digits remain partially flexed giving us the classic pope’s blessing sign.

The confusion, I found out, was when in the past the Pope’s blessing sign was considered a distal median nerve lesion. Let’s consider why this was the case and why it might also appear to be a pope’s blessing sign (and why I call it the crooked Pope’s blessing).

With a distal median nerve lesion we are knocking out the lumbricals of digits 2 and 3. Remember what we said about non-functioning lumbricals? We end up with extended MCP and flexed PIP and DIP. If, as before, we ask the patient to extend their fingers we end up with the classic claw hand of a median nerve injury (see below). But, this looks nothing like a pope’s blessing you might ask. That’s because we asked the patient to extend their fingers. Here’s the key, please read carefully: If we asked the patient to “make a fist” instead, we end up with fully flexed 4th and 5th digits with the dysfunctional partially flexed 2nd and 3rd digits. If you do this with your own hand right now…you can see that the 2nd/3rd digits are elevated above the 4th and 5th and might appear as a pope’s blessing, albeit crooked due to the flexed 2nd and 3rd digits, hence the “crooked” pope’s sign.

A picture of a distal median nerve injury with fingers extended:

Here is a chart I made that breaks all of this down in a clear format. I suggest you play with the different variations to see where the differences lie.

To recap, remember it really is about which lumbricals are working and which aren’t. As for the confusion regarding the pope’s blessing sign I hope that cleared things. The 2010 version of First Aid also has the same descriptions as above. The only problem I found was that it wasn’t clear whether the patient was being asked to flex their fingers or to extend them. Even so, I am still human and if you feel that something above is incorrect or unclear please leave a comment below and I will do my best to bring more clarity to the issue.

I hope this helped!

Oh, and don’t opt out of doing the surveys. They are just as beneficial for you as they are to the school. They give you a good sense of where you currently stand with your knowledge and when you retake it after the animation you’ll be surprised at how much you learned in a few minutes.

So why split it into quadrants? The beauty for me behind this is that each quadrant has a group of nerve roots associated with it that correspond nicely to the area of the arm we are dealing with. Again starting with the medial quadrant which we said was the ulnar nerve (C8-T1) and it runs down the medial side of your arm and hand. The anterior quadrant, the median nerve runs down the anterior part of your arm and hand. Another interesting note: because it runs slightly medial to your biceps it would have more of the “medial” quadrant nerve roots (C6, C7, C8, T1) as opposed to the radial nerve which we’ll see later. The lateral quadrant is the musculocutaneous and axillary nerves run for the most part on the outside or lateral portion of your arm (C5,C6). Finally the posterior quadrant is the radial nerve which runs posteriorly innervating the extensors of the arm and forearm. Since the redial nerve runs slightly postero-laterally it will have more of the “lateral” quadrant nerve roots (C5, C6, C7, C8).

If you have trouble with the above try to remember to visualize your arm as a tube with four quadrants.Each quadrant has a set of nerve roots to it. If you get this down I promise you the brachial plexus, the nerve roots, the nerves and the muscles they innervate will all slide into place.

Another interesting trick is to see how the dermatomes for the hand line up nicely with the nerve roots. See the image I drew alongside Kaplan’s Diagram below: