Case study of sorts

[Nurse SMS, MSN, RN]

Patient is middle aged (early 60s), smokes a pack per day, calls EMS after falling off the toilet and being unable to get up secondary to left sided onset of weakness. Gets TPA after arriving in the E.R. after being found to have 90-100% occlusion to vessels I cannot now remember. Recovers some movement and function of left extremities, has significant left facial droop. Trauma during Foley attempt in ER leads to necessity of suprapubic cath. Admitted to Neuro ICU where patient goes into ETOH withdrawal, is vented and placed on Ativan GTT. Recovers from withdrawal after a few days, weaned from vent. Significant aphasia present, aspirating own secretions. Made strict NPO, NG tube placed for tube feeding and meds. Occasional need for oral suction.

Patient transferred to PCU. Left side nearly flaccid with minimal movement noted. Patient moans constantly, incomprehensible sounds, no sensible verbalizations. Follows commands unreliably. Not always responsive to voice. CXR shows aspiration pneumonia and patient is on Vanc and Merrem. On 4L NC, spo2 93%, SR in the 80s, SBP 130s. Elevated sodium with orders for 250 ml FW flushes q6h, returns even more elevated the following morning and FW flushes ordered q4h now. Patient moaning constantly, becomes diaphoretic. Gradually pulse increases to ST in the 110-120 range, patient becomes agitated, attempting to sit up. Follows no commands. Spo2 tanks to 89% on 4L NC after breathing treatment, BP increases to 164/101. Obvious labored with see-saw respirations and mild supraclavicular contractions. Nonrebreather placed and patient placed sitting up to 90 degrees, spo2 improves to 99%. MD notified and ABGs are ordered, demonstrating respiratory alkalosis and metabolic alkalosis. CTA negative for PE. CT head shows no changes from previous. CXR shows no changes from previous. Cardiac enzymes, blood and urine cultures, EKG all pending at the time of transfer to ICU.

Ideas on what may have been going on with this patient and other courses of action that might have been taken? This isn't homework, it was my patient yesterday. I felt glad to recognize a problem and avoid a rapid response situation but patient's overall condition baffled me. Patient had been eating, following commands and making some verbalizations prior to transfer to stepdown. Decline was gradual over a few days and then culminated in rapid decline on my shift.

ETA- TMax 103.0 axillary

[emtb2rn, BSN, RN, EMT-B]

Carotid doppler done?

[Nurse SMS, MSN, RN]

Not sure. Might have been done in the ICU prior to transfer to stepdown, but definitely not done at the time of sudden decline. Patient had some serious occlusions. I wish I could remember now which vessels.

[blondy2061h, MSN, RN]

Were any labs done to check electrolytes at the time she started deteriorating? What about cardiac enzymes/BNP? How were her long sounds during this? When you say she had been eating- she had passed her swallow eval and been approved to eat?

My thoughts:

1. Fluid overload/flash pulmonary edema

2. A cardiac event

3. Another aspiration event.

4. PE

Did us she have a central line or art line that would place her at risk for a rapid onset sepsis?

[Esme12, ASN, BSN, RN]

Sepsis/ARDS

Any other co morbidity? Liver OK? Renal OK? diabetic?

http://acutecaretesting.org/en/journal_scanner/journals/hypernatremia_acquired_during_critical_illness

[SwansonRN]

Seems like impending respiratory failure, I would anticipate this patient getting tubed if they were coming up to me. HR and BP elevated d/t catecholamines. Did you see the CXR?

[Nurse SMS, MSN, RN]

Not diabetic. I did not see the CXR itself but read the report. It stated it was unchanged. AST/ALT elevated but not alarmingly so given alcoholic status.

In terms of eating, anecdotally from the spouse patient had been able to swallow some food while still in ICU. Obviously at some point someone realized the patient was aspirating due to NPO status and NGT present when the patient was transferred to PCU.

Patient did have a PICC line. Blood cultures were neg at the 24 hour mark.

Two things really threw me - high sodium despite free water flushes done religiously and metabolic and respiratory alkalosis. I would have expected respiratory acidosis.

Love all the questions you guys are asking. Helps my thought process. The day before the event the patient had been on D5W at 50 ml/hr. A new hospitalist came on rotation and stated strokes should never be on D5 and stopped it. I had never heard that before. Could the D5 have played a role? And if so, what?

[Emergent, RN]

I'm taking a shot in the dark here. Wondering whether the TPA caused micro-hemorrhaging, maybe in the adrenals. This could cause imbalance on sodium, leading to high BP, changes in mental status. Perhaps micro-hemorrhaging in other systems as well, ETOHer might be more vulnerable to that.

I suspect that there is more than one problem contributing to the clinical decline.

[SwansonRN]

Not diabetic. I did not see the CXR itself but read the report. It stated it was unchanged. AST/ALT elevated but not alarmingly so given alcoholic status. In terms of eating anecdotally from the spouse patient had been able to swallow some food while still in ICU. Obviously at some point someone realized the patient was aspirating due to NPO status and NGT present when the patient was transferred to PCU. Patient did have a PICC line. Blood cultures were neg at the 24 hour mark. Two things really threw me - high sodium despite free water flushes done religiously and metabolic and respiratory alkalosis. I would have expected respiratory acidosis. Love all the questions you guys are asking. Helps my thought process. The day before the event the patient had been on D5W at 50 ml/hr. A new hospitalist came on rotation and stated strokes should never be on D5 and stopped it. I had never heard that before. Could the D5 have played a role? And if so, what?[/quote']

Once the sugar in D5W is metabolized it's just water, therefore a hypotonic solution. Water gets pulled into the cells worsening cerebral edema. Patients with brain injuries should steer clear. At least, that's my elementary understanding of it. Someone else could probably explain it in a more eloquent way

I am not a neuro person at all, but I think that worsening cerebral edema would have a slightly different presentation?

[KRVRN, BSN, RN]

Was there a UA?

[nurseprnRN, BSN, RN]

I agree with the neuro-- free water was a bad idea. You want post CVAs to have higher serum sodium, to keep down the edema in the head post infarct. Was this a unit that routinely sees post-CVA patients?

Aphasia is usually associated c left hemisphere infarct/right sided weakness. If he has left-sided weakness and aphasia, he's done something bad to his other hemisphere. Was he always aphasic? Remember, aphasia can have many components, receptive (not obeying commands?) and expressive. CT isn't the last word in head imaging.

Chest sounds like flash pulmonary edema (serum Na+ + lots of free water); remember that the lungs' first job is CO2 management, and CO2 can still be lost there even as O2 intake is falling.

He might be hyperventilating from alcohol withdrawal (time frame?), which will make him resp alkalotic; alcoholics are often metabolic alkalotic-- which was primary, which compensatory, can you tell? What were the ABGs? Liver enzymes, serum ammonia?

I like the micro-hemorrhage in the adrenals, too.

Great case study to show that you can have LOTS of things wrong at the same time. It's all SATA, :) .

[sapphire18]

My thoughts would be worsening aspiration pna and withdrawal. I wonder why his L side became weaker after initially improving?