Published Sep 13, 2016
CCU BSN RN
280 Posts
I work in CICU, and had a patient attended by Vascular whose primary presenting problem had initially been sepsis (both things I don't DIRECTLY deal with regularly. MSICU was full, and I ended up with this patient this week, and MD staff who were either dismissive of questions or not particularly concerned, so I didn't get the answers I was looking for there) Hoping you guys will help me understand a bit more about what was going on with this person so I can have a better grasp next time.
Significant pmh:
Hyperparathyroidism- on PO alendronate at home once a week
Diastolic CHF
Patient presents 2 weeks post femoral embolectomy with tachycardia, profound hypotension, abdominal pain. Found to have grossly infected surgical site. Taken emergently to the OR for exploration, washout, I&D, you get the picture. Postop remained hypotensive with low urine outputs, given innumerable fluid boluses over a few days and Vanc/Zosyn. Wound left open from OR, continues with copious purulent discharge.
POD 3 develops lethargy and failure to thrive, literally zero PO intake except water for days and poor PO PTA. BP seems to have leveled out with SBPs now running in the 150's-160's instead of 80. IVF stopped and aggressive diuresis initiated with loop diuretics. Ionized Calcium at this point begins to trend up from 1.3 and progressively up to 1.6 on POD 6. No serum calcium drawn during entire admission. Phos is trending down as Calcium trends up, obviously.
Now, this is a complicated case with many co-morbid conditions and a variety of things going on with the patient (please ask specific questions if omitted details would help), but the one thing I feel like I don't have a great grasp on is why she became acutely hypercalcemic over the course of a few days? Would missing ONE dose of Alendronate for hyperparathyroid really do that? At what point does a high ionized calcium become dangerous? I know at what point a serum calcium requires aggressive treatment, but can't find anything in the case of ical.
Is this due to lack of PO intake?
Of note, ical did not decrease at all despite 3 days of aggressive diuresis with loop diuretics (as in, losing 3kg a day diuresis), which I read can be used as treatment for hypercalcemia in the first place....
Obviously I would've killed for an endocrine c/s about 3-4 days ago for further testing and recommendations on the topic, but primary team wasn't interested, so instead of poring over consult notes, I'm begging internet forums to share their infinite wisdom.
I know the patient's lethargy, myalgias, twitching, poor appetite could have been caused by a lot of things, but shouldn't the fact that these are all hypercalcemia symptoms have at least been given consideration?
Thanks in advance for your insight, again feel free to ask questions re: the case if they'll help give a more clear picture.
REcap:
1. Why did this happen?
2. Is it clinically significant?
3. At what number does an ical actually become dangerous?
4. What would be the best next steps re: testing/treatment if it were up to you