Friday, January 13, 2012

"Let's Boil Some Water and Make Coffee. . ."

Good morning from Warrior Camp where all the Warriors are working hard and preparing for a decisive Victory over Boards—Written, Oral, Pain, and MOCA. 
We take Board exams to realize our highest potential professionally, to be leaders, to be chiefs of services and department heads, goals many I’ve been honored to work with have achieved.  But we also endure this process to be fully free, even after all these years.  We’re here today to battle the Beast of Boards and I’d like to cover a difficult keyword from last year that I spent a considerable amount of time upon summarizing.  Realizing that many are too busy for Warrior runs, coffee breaks, the sharing of insights, weak attempts at humor, and the like, I’m going to cover the keyword first today.  However, further realizing that many write me at wits end and tell me the insights and words of encouragement are vital to their efforts, we won’t abandon, but only delay, the sharing of insights back and forth which may prove helpful to some.  But today we owe it to those who eat and drink anesthesia and desire no other distractions, racehorses with blinders on, if you will, the chance to listen in on the key word and then leave us to move on with their 24/7 efforts toward the finish line.   
One of the most difficult keywords in 2011 was cerebral salt wasting syndrome.  I noted it in almost every key word profile I looked at.  Let’s attack. 

Keyword Pillbox Alert
Cerebral Salt-Wasting Syndrome
1.  First described by Peters in 1950, cerebral salt wasting syndrome (CSWS), also known as renal salt wasting syndrome (RSW), is the most frequent mechanism for the hyponatremia observed in 30% to 40% of those afflicted by subarachnoid hemorrhage (SAH).  It’s also common in the setting of cerebral infarction.  In cerebral salt-wasting syndrome, sodium is actively excreted from the kidneys and the intravascular volume deficit becomes more and more severe despite ongoing hyponatremia.
a.  Adrenal and thyroid function are normal in CSWS/RSW.
b. The frequency of CSWS/RSW is disputed.  Some believe it’s responsible for hyponatremia as often as SIADH, especially in neurosurgical patients, and others believe it is much less common.  Irrespective of this dispute, what’s clear is the Board is interested in CSWS/RSW and believe knowing about it is important to us in our role as anesthesiologists.
c.  Hyponatremia is obviously important in its own right, but one should also recall that hyponatremia predicts the onset of vasospasm at around 24 hours, so it’s especially important in this context, too.

2.  CSWS/RSW is associated with the release of brain natriuretic peptide (BNP), both from the brain and also apparently from the stressed ventricle at the time of hemorrhage.  The release of BNP is associated with sympathetic discharge.

3.  The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is also thought to cause hyponatremia, but, again, cerebral salt-wasting syndrome seems important, if not dominant.
a.  The distinction between CSWS/RSW and SIADH is important, and quite possibly the point of the examination question. Specifically, what many fail to appreciate is that cerebral salt-wasting syndrome calls for isotonic fluid replacement, whereas SIADH calls for fluid restriction.
b.  The problem is one of diagnosis in that both CSWS and SIADH present with hyponatremia, a concentrated urine, and natriuresis. 

4.  A key point for the anesthesiologist in dealing with hyponatremia in the setting of brain injury is to ask, “What is the status of extracellular volume—depleted or normal?”  If extracellular volume is depleted, CSWS is more likely than SIADH.  If extracellular volume is more or less normal, the diagnosis of SIADH must be more strongly entertained. 
a.  Critically, realize that SIADH primarily occurs due to a euvolemic inappropriate rise in ADH secretion, whereas CSWS/RSW is associated with a cascade of events, leading to the release of BNP, the establishment of decreased extracellular fluid volume, and the eventual release of ADH leading to water conservation and attempts to return to equilibrium, namely euvolemia.
b.  The above realization about underlying volume status helps one remember management—CSWS/RSW should be treated with fluids to correct underlying hypovolemia and SIADH should be treated with fluid restriction.  (Again, if I were writing this question, this would be the point of attack:  having diagnosed hyponatremia, does the anesthesiologist reflexively assume SIADH and restrict fluids, or rather try to determine if hypovolemia exists and perhaps administer fluids.)  One author states: “Failure to distinguish cerebral salt-wasting syndrome from SIADH as the cause of hyponatremia could lead to improper therapy (i.e., fluid restriction), thereby exacerbating intravascular volume depletion and potentially jeopardizing cerebral perfusion.” 

5.   In the absence of central monitoring, which is far from perfect but nevertheless often provides a useful trend, determination of intravascular volume status to differentiate CSWS/RSW from SIADH is never easy.  “Thirst” and “weight loss” are suggested by one author, along with, “orthostatic tachycardia or hypotension, increased capillary refill time, increased skin turgor, dry mucous membranes, and sunken anterior fontanelles. These signs usually appear only when the degree of dehydration is moderate to severe. Central venous pressure (CVP) may be an unreliable determinant of ECV.”

6.  Besides SAH, CSWS/RSW occurs in the setting of head injury, tumors, intracranial surgery, stroke, and meningitis.  It must also be recognized that cerebral salt-wasting syndrome can also occur in the absence of cerebral disease.

7.  Laboratory caveats, possibly testable but seems esoteric, in my opinion:
a.  Obtain serum sodium concentration because, as noted, patients with untreated cerebral salt-wasting syndrome are often hyponatremic.
b.  Obtain serum osmolality, and if measured serum osmolality exceeds twice the serum sodium concentration and azotemia is not present, suspect hyperglycemia or mannitol as the cause of hyponatremia.
c.  Measure urine output, and recall that urine is relatively dilute, and the flow rate usually high in cerebral salt-wasting syndrome.  (Urine is usually very concentrated, and the flow rate low in SIADH.)
d.  Urine sodium concentration is typically elevated in both SIADH and cerebral salt-wasting syndrome (>40 mEq/L). However, urinary sodium excretion (urine sodium concentration [mEq/L] X urine volume [L/24 h]) is substantially higher than sodium intake in cerebral salt-wasting syndrome, but generally equals sodium intake in SIADH. Therefore, net sodium balance (intake minus output) is negative in cerebral salt-wasting syndrome.
e.  Patients with either cerebral salt-wasting syndrome or SIADH can have hypouricemia and elevated FEUA. However, after correction of hyponatremia, hypouricemia and elevated FEUA may normalize in SIADH, but persist in cerebral salt-wasting syndrome.
f.  Fractional excretion of phosphate (FEP) should be determined when evaluating patients with hyponatremia and hypouricemia. Elevated FEP suggests cerebral salt-wasting syndrome as opposed to SIADH.

8.  Management of CSWS/RSW centers on correction of intravascular volume depletion and hyponatremia as well as replacement of ongoing urinary sodium loss usually with intravenous hypertonic saline solutions.  Some clinicians have reported a favorable response to mineralocorticoid therapy in cerebral salt-wasting syndrome.  (Mineralocorticoids (i.e. Fludrocortisone (Florinef)) enhance sodium reabsorption in the kidney by direct action on distal tubule cells, resulting in expanded extracellular fluid volume. They increase renal excretion of potassium and hydrogen ion.)
So there you have it, a hopefully lucid summary for your auditory synapses to savor and retain.  Let the cement cure!  For those now leaving to carry on your fine and dedicated efforts, thanks for tuning and I hope to see you down the line at a course.  For those so inclined. . .
Hallelujah. . .
Good afternoon from Warrior Camp where all you wonderful battlers I work with, some struggling, are committing and re-committing to beating the Beast of Boards.  One of my all time favorite recitations, I thought of it just the other day while watching a resident allow a wound to heal by secondary intention, a recitation with great relevance for you, a line from Sophocles:  “We must wait until evening to see how splendid the day has been.”  Goodness gracious, it’s only early afternoon, many of the most contributory anesthesiologist in our field took a time or two or three to pass Boards, and I’m certain that by evening, in your case, the splendor of the day will be fully realized by all.  
I’d like to read and paraphrase and comment briefly upon chapter 1 in Little Red:  Recitations, Pearls, Perils, and Passages to Passing Boards.  Of everything I personally do in my day, these have stood the test of time in keeping me sane, and in making me more positive, more forward looking, and more striving in reaching my goals.
I see you as a potential future leader in our field.  You might feel down at times over this process but the fact is others likely depend upon you and are looking to you for guidance:  Therefore. . .
“Be a leader”
As we begin our daily Ranger Run today, work on these lines, this recitation, and if you derive anywhere near the comfort and joy I have over the years in having these cemented into my synapses, you will be greatly enriched and rewarded, and my coaching purposes will be well-served. 
The Legend of Horatius Cocles

Then out spake brave Horatius,
The Captain of the Gate:
“To every man upon this earth
Death cometh soon or late.
And how can man die better
Than facing fearful odds,
For the ashes of his fathers,
And the temples of his gods,

And for the tender mother
Who dandled him to rest,
And for the wife who nurses
His baby at her breast,
And for the holy maidens
Who feed the eternal flame,
To save them from false Sextus
That wrought the deed of shame?

“Haul down the bridge, Sir Consul,
With all the speed ye may;
I, with two more to help me,
Will hold the foe in play.
In yon strait path a thousand
May well be stopped by three.
Now who will stand on either hand,
And keep the bridge with me?”
(Roman Legend of Horatius Cocles, 6th century, BC)

Tuesday, December 6, 2011

Let's Boil Some Water and Make Coffee. . .II

“Let’s Boil Some Water and Make Coffee. . .”
(script for podcast I)
Hallelujah. . .
Good morning from Ranger Camp where all the Rangers are working hard and preparing for a decisive Victory over Boards—Written, Oral, Pain, and MOCA Boards. 
The top Ranger T-shirt today is easy to read as we begin our daily Ranger Run, a quote from Edward Anderson, a contactor who worked at the White House when President Truman lived there.  Truman was doing a personal inspection of work completed when he happened upon these lines.  For a President then fatigued by a very unpopular war in Korea, a bad economy, a myriad of problems, the prospect of returning home to his simple roots enticing.  This President was ready to go home.  Here the lines which spoke most to him, it’s Recitation #9 in Little fRed:  Recitations, Pearls, Perils, and Passages for Working
Harder and Smarter to Pass Boards:
"Every man's a would be sportsman, in the dreams of his intent,
A potential out-of-doors man when his thoughts are pleasure bent.
But he mostly puts the idea off, for the things that must be done,
And doesn't get his outing till his outing days are gone.
So in hurry, scurry, worry, work, his living days are spent,
And he does his final camping in a low green tent."  (Reuben Anderson)

Ranger Run here for Podcast. . .
I’d like to thank the nice people from Documentary recordings who have kindly given us permission to use brief snippets of our Ranger Runs.  The complete set can be found at their website, documentary 
Let’s now to an important Lock’nLoad topic of interest to passing Boards.  These topics are relevant for all Boards—Written, Oral, Pain, and MOCA as these are the selected topics the Board has identified which more than 50% miss on the primary Written examination.  The Boards wants us to shore up in these areas and sends these 10-12 topics each year to training programs.  They are not answered, I’ll do that here, they are sometimes distributed merely as statements by training programs, but often nothing much comes of them at all.  Then they appear again. . . and again. . . and again.  So topics missed by more than 50% become strike-out pitches.  Our job is to get our bats off our shoulders, see them early, and hit them hard.  In this way, these are not nightmare unhittable strike-out pitches, missed by more than 50%, but competitive advantages for our guys.  Along with Big Blue, and most Lock’nLoads are in Big Blue, this territory is at the very top of our priority list to command and control. 
Ranger Lock and Load!
From The Joint Council on In-Training Examinations
American Board of Anesthesiology-American Society of Anesthesiologists
"The following responses on the ITE suggested misconceptions in specific areas of the knowledge domain of Anesthesiology. . . based upon the performance of CA-3 residents taking the examination for ABA credit."
According to the Board:  The majority of either CA2 residents (in the case of the ITE) or graduating CA3 residents (in the case of the ABBA Part 1 exam) in the United States did not know that. . . myotonic dystrophy type 1 increases the likelihood of heart block.
1.  Recitation command of Big Blue is greatly beneficial here. “Besides muscle weakness (especially respiratory), the most important symptom s are cardiac abnormalities, including cardiomyopathy, cardiac dysrhythmias, and cardiac conduction abnormalities. . . Anesthesia can also worsen cardiac conduction defects.  It is not infrequent to encounter RBBB or even sudden third degree heart block.”  So there you have it.   
2.  Don’t panic when you encounter something like “Type 1,” or the like; the Board loves to distract with jargon.  Under fire, and this is a shortcoming I suffer, exercise your synapses and apply what you know!  Further, over and over it’s clear, it all starts with memorization and recitation learning.  As the Oracle of Omaha Richest Man Warren E. Buffett says, “It’s when the tide goes out that the skinny dippers get caught,” and the tide here is memorization of Big Blue. 
3.  Again, with regard to myotonic dystrophy, “Besides muscle weakness (especially respiratory), the most important symptom s are cardiac abnormalities, including cardiomyopathy, cardiac dysrhythmias, and cardiac conduction abnormalities. . . Anesthesia can also worsen cardiac conduction defects.  It is not infrequent to encounter RBBB or even sudden third degree heart block,”—exactly to the point of the Lock’nLoad.
If you liked this podcast and found it helpful, I hope you join the Band of Brothers, which is a monthly newsletter with a CD, longer and more detailed.  The cost is reasonable, I spend a lot of time focusing upon, summarizing, writing, and re-writing the information so it has maximal firepower for recall in your synapses, and you can sign up for that on the ordering page at 
Farewell now from Ranger Camp where all the Ranger Warriors are working hard and preparing for a decisive win.  We don’t know much at times, but we do know a few things in the marrow of our bones.  One is this:  “Victorious warriors win first, then go to war.  Defeated warriors go to war first and then seek to win.”  Onward now to Victory!
We are the champions. . .

Monday, November 7, 2011

Let's Boil Some Water and Make Coffee. . .

A favorite recitation from Little fFred:  Passing Boards--Recitations, Pearls, Parables, and Passages is this:  "Suspicion of prior atrocities drives men to surpass report in their own cruel innovations, either by subtlety of assault or extravagance of reprisal." (Thucydides) (Recitation #36)  BTW:  I awarded my first shirt for completion of the recitation trail last week.  It was fun!)

It sometimes seems that those writing questions for Boards, whether Written, Oral, or Pain, desire to make this process progressively more difficult, and way beyond what they themselves encountered and with all due respect.   

An example of this is a keyword I was working upon this morning, namely activated protein C.  To me, at least, it seems a bit esoteric for a Board exam--a definite, "How Many Nits on a Gnat's Nut. . ."  First a question, then some summarized content.

Single best
Activated protein C (APC) is which of the following:
a)  Thrombocytopenic
b)  Anti-fibrinolytic
c)  Anti-thrombotic
d)  Anti-thrombocytopenic
e)  Fibrinolytic

Activated protein C
1.  Activated protein C (APC) inhibits factors V and VIII in the coagulation cascade and in this way inhibits the conversion of prothrombin to thrombin which in turn inhibits the conversion of fibrinogen to fibrin and thus inhibits clot formation.  Therefore, since the conversion of thrombin leads to fibrin and clot formation, also known as thrombosis, APC could be described as being anti-thrombotic.  

2.  Fibrin is formed clot, resulting from fibrinogen activation, through the clotting pathway.
a.  Fibrinolysis is the breakdown of clot, and it results from the conversion of the fibrinolytic enzyme plasminogen being converted to plasmin.  “Fibrinolysis” is the breakdown of clot therefore the term “anti-fibrinolytic” refers to the preservation of clot.  

3.  Patients with severe sepsis have systemic inflammation resulting in coagulation abnormalities that range from thrombosis to DIC; initially there is often thrombosis and this ultimately leads to low factors, low platelets, and low fibrinogen—DIC. 

4.  One, of many, pathophysiologic factors involved with sepsis might be low APC levels, leading to the initial thrombosis mentioned.  Indeed, recognition of sepsis caused micro-thrombosis and the presence of low levels of circulating APC led questions about the possible need for APC supplementation in sepsis.
a.  Because of the crucial role that protein C plays as an anticoagulant, those with either deficiencies in protein C, or some kind of resistance to APC, suffer from a significantly increased risk of forming dangerous blood clots (thrombosis). On the other hand, medical research into protein C's clinical and pharmacological effects has demonstrated that patients with severe sepsis, ischemic stroke and other serious medical conditions may benefit from treatment with recombinant human activated protein C (rhAPC) in the form of drotrecogin alfa-activated (branded Xigris by Eli Lilly and Company).  However, studies since have questioned the drug's overall benefit, and its use is now controversial, given the risk of serious bleeding associated with treatment.  However, it should be noted, another reference through MD Consult stated:  “Recombinant human APC is the first pharmacological drug that has demonstrated efficacy in the treatment of severe sepsis.”  A third source states:  “APC is recommended in the setting of severe sepsis with reasonable life expectancy beyond sepsis.  The cost is high and use remains controversial. A new randomized placebo controlled trial is currently under way.”

5.  As can be imagined, the most severe adverse effect of APC is serious bleeding, hemorrhage, as would be expected due to its anticoagulant effect.

6.  In summary, APC is a naturally occurring anticoagulant that inactivates factors Va and VIIa and prevents the generation of thrombin (and is therefore anti-thrombotic).  Best answer C.
(Reference:  MD Consult)

I hope this was helpful and, as you know, I'm with General George Smith Patton:  "The highest honor I have ever attained is having my named linked to yours in these great events."  Passing Boards is a Great Event, and it's fun being on your team.  Thanks, Niels F. Jensen, M.D.