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)

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