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17 days at the VA – day 11
25 Nov2009
Day 11 involved discussing 5 new patients, and continuing plans on the remaining patients.
One patient brought out some important teaching points. The patient is in his 70s and came in for weakness. His routine labs made the diagnosis:
| Electrolyte panel | |||||
|---|---|---|---|---|---|
| Na | 132 | Cl | 85 | BUN | 73 |
| K | 2.8 | HCO3 | 37 | creat | 2.8 |
| Blood Sugar | 205 |
Two months ago his values were:
| Electrolyte panel | |||||
|---|---|---|---|---|---|
| Na | 137 | Cl | 103 | BUN | 18 |
| K | 3.4 | HCO3 | 27 | creat | 1 |
| Blood Sugar | 144 |
While I think this is an easy one, the students and interns did not yet have the lab interpretation instincts. So I will ask my readers to provide the explanation. I will give my thoughts tomorrow.
Related posts:
- 17 days at the VA – Day 8
- Another hyperkalemia – my explanation
- Part 2 of the acid-base problem
- An acidosis question
- Another acid base problem
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4 Responses to 17 days at the VA – day 11
Robyn
November 25th, 2009 at 1:10 pm
Kidney problems – caused by diabetes?
teresa
November 25th, 2009 at 5:05 pm
I am only a lowly MS4, but I would not expect diabetic nephropathy to progress so much in only two months, especially with glucose control that doesn't look optimal but isn't terrible either. My (slowly developing) lab interpretation instincts are telling me that the degeneration in renal function and electrolyte (and acid-base) abnormalities stem from a common cause rather than than the first causing the second. Specifically, the pattern smacks of contraction alkalosis to me, with associated pre-renal renal failure. With the increased bicarb, fairly marked hypokalemia, and milder hyponatremia, I wonder if the patient were recently started on lasix? Another diuretic (a thiazide for instance) could potentially produce the same pattern, but I think loop diuretics would be the most likely culprit with this degree of volume loss.
If the primary problem were renal failure, I would expect to see loss of bicarb and hyperkalemia as the downstream effect. Plus the high BUN:Cr ratio suggests volume loss, although a FeNa (or physical exam) would be more specific tests. I am curious as to what his ABG showed (I am assuming you got one to assess his true acid-base status) and whether his lytes normalized after gentle volume resuscitation?
Pro Nephros
November 25th, 2009 at 11:16 pm
Umm – you said this was an "easy one", but I would like a little more history.
but without it, here goes:
1) BUN elevated out of proportion to creatinine suggests pre-renal azotemia
2) Chloride depletion metabolic alkalosis. Chloride may have been lost either by vomiting/NG suction or overtreatment with diuretics.
3) Hypokalemia due to urinary losses driven by high aldosterone levels (from volume depletion) causing avid collecting duct sodium reabsorption (which obligates potassium and hydrogen ion secretion). Magnesium depletion may also be playing a role.
If this is all true, the patient should clinically appear volume depleted, should have a history of either vomiting or diuretic treatment, and the fractional excretion of sodium should be quite low (assuming diuretic treatment has ceased). Treatment consists of NaCl given as isotonic saline IV, KCl given orally and/or IV(total body deficit is probably greater than 120 mEq), and possibly intravenous magnesium sulfate.
Snipergirl
January 17th, 2010 at 4:27 am
I think the giveaway here is the severe hypokalaemia. When you put that with the increased creatinine you wonder about things that cause ARF- the most common being volume loss. What sort of volume losses cause profound hypokalaemia? Commonly, diuretic therapy and GI losses. The increased bicarb suggests that it is chronic fluid loss causing the derangement so vomiting is unlikely. Additionally loop diuretics cause hypokalaemia, hypovolaemia and metabolic alkalosis- and are the most likely answer.