Dangerous electrolytes – part 2

3

Category : Acid-Base & Lytes, Attending Rounds

Reviewing the patient thus far:

 

The patient, a 40-something year old woman, has a long history of alcohol abuse.  Recently she has had minimal oral intake with much vomiting.  BP 100/60, pulse 120

120 67 32 99
1.9 21 0.7  8.9

 

pH 7.6
pCO2 26
pO2 100
HCO3 21

 

Your job is to identify all the abnormalities in this panel, and suggest the sequence of events most likely to result in these numbers.  What other information do you want?  

Three respondents did a great job describing the acid-base disorder.  

  1. The anion gap equals 32, thereby by definition the patient has an increased anion gap metabolic acidosis.
  2. The delta gap equals 21, thereby the revealed bicarbonate is 42, supporting an underlying metabolic alkalosis. 
  3. These two metabolic problems fit the story perfectly.  The patient had both positive ketones and a mildly elevated lactic acid level.  We expected a metabolic alkalosis with persistent vomiting.  The hypokalemia fits the clinical picture perfectly.
  4. Using the Winter's equation, one also finds a respiratory alkalosis.  Clinically, we felt that the respiratory alkalosis resulted from the hypotension and alcohol withdrawal.  
  5. All the acid-base abnormalities resolved over the next few days.

Now the electrolytes are really the point of this presentation.  The patient has hyponatremia, likely secondary to volume contraction.  Her serum osm = 259 with urine osm = 411.

She had hypokalemia secondary to vomiting.  We confirmed that vomiting was the cause with urine electrolytes. Urine Na < 10, Cl < 10, K = 45

We also checked Mg, normal at 2.5 and PO4 – very low at 0.7.

What are the risks of the severe hypophosphatemia, and how would that abnormality impact your treatment plan?  Also speculate why her initial PO4 was so low.

 

Comments (3)

I' m going to say her phosphate was low because of chronic alcoholism and lack of dietary intake but someone may inform me of some esoteric reason it may also exist in this patient.
I would point out one thing – The patient has hyponatremia, likely secondary to volume contraction. 
Technically this is inaccurate. The patient is indeed volume contracted based on history, physical and discrepancy of serum and urine osmols (the patient is protecting volume at the expense of tonicity) and some component of this is probably due to ADH secretion as a means of protecting volume. But hyponatremia means intravascular free water is high and says nothing about total body sodium which is low here (from vomiting and lack of intake). Absent a primary ADH disorder, this patient is hyponatremic because whatever fluid she is taking in (and she is almost certainly taking some liquid of some sort- few volume contracted patients who can drink fail to do so), is hypotonic. In all likelihood she is thirsty and drinking water. Without adequate sodium replacement it is the equivalent of giving her D5 W, without the D of course. Beer and alcoholic beverages mixed with water are also hypotonic so that remains a possibility.
Hyponatremia says nothing about her volume state. It never tells you she is volume contracted by itself. IT simply means her intravascular free water is excessive. In most cases, the body's regulatory mechanisms will protect against volume or perceived volume deficit, to exacerbate tonicity problems -to a point ( at some point the body will begin to protect the brain). Had she been drinking a hypertonic solution , or drinking nothing at all, in all likelihood her sodium would have been normal or high, even though she was volume depleted. 
The take-home  point is serum sodium never tells you about volume status in the absence of other information. 

In the nephrology world it is much more common to have an elevated serum phosphate.  Given my lack of expertise on low phosphate I consulted a phosphorus guru, and here was his response: 
The two biggest risks of such a low serum phosphate are rhabdomyolysis and heart failure (occasionally respiratory failure as well, though I see she has an impressive respiratory alkalosis so I suspect she’s breathing fine).  It is very important that this gets repleted before the patient gets glucose-containing IV fluids since the surge in insulin will drive phosphate intracellularly and exacerbate the problem.  It’s quite likely that the low phosphorus is nutrition related.
In response to Cory regarding hyponatremia.  I agree that serum sodium cannot predict extracellular fluid volume.  However, while Cory focuses on the input, as a nephrology fellow I focus on the output.  If the patient takes in water and the kidney puts out water then the net water balance is unchanged.  In volume contraction the kidneys preserve water at the expense of osmolality.  Without pathology, give the kidneys enough volume and they keep the osmolality normal regardless of PO intake (within reason: >14L free water /day or <400ml water/day)

Eric:
I don't disagree, and without pathology the body will maintain tonicity. But pathology is an unusual thing- I am quite suspicious this English Marathoner may have died of exercise induced hyponatremia  -she drank more water than she should have but almost certainly not enough to cause her death without some "pathology", in this case probably hormonal changes brought on by a marathon.
If you give the kidneys too much hypertonic solution, they will maintain osmolality for a time but eventually the patient will become hypernatremic, even without pathology. You simply need a certain amount of water to replenish all the compartments. IF not the brain and tissues will protect with intravascular and interstitial water until that mechanism no longer works. We don't put out exactly the same amount of water we take in (we do within reason but not exactly) because the three compartments have different needs in different circumstances. As I used to teach the ICU fellows, the worst analogy in medicine is that the body is like a gas tank, i.e. a fixed volume box. IT is anything but.  There are different compartments, and vessels of varying distensibilities and capacities and fluid shifts going on continuously.   

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