As usual, details have been changed to protect privacy. This is an update on a case posted to twitter in the past.
A middle aged woman with past history of hypertension presented to the ED with dysuria, decreased urination, and malaise. She rapidly developed severe hypotension (MAP in the 40s) and was resuscitated with 4 liters of 0.9% saline. Initial work-up is notable for acute kidney injury (creatinine 5x higher than baseline, though no indications for renal replacement therapy) and urinalysis suggestive of urinary tract infection.
She is admitted to the ICU due to hypotension. A bedside echocardiography on admission reportedly shows normal LV and RV systolic function.
You are evaluating the patient on night rounds (about 10 hours after admission) as the nurse reports oliguria (< 10 ml/hour), and they note that the nephrology consultant recommended continued 0.9% saline at 150 ml/hr. Should they hang the bag?
Anyone knowing my biases can imagine my answer was a resounding NO. But let’s evaluate this patient further.
One of the challenging pieces of handoffs in medicine (whether it be ED to ICU, within your own team, etc) is making sure to evaluate with a fresh perspective.
Vitals are notable for a MAP of 66-68 (no pressors), HR 90s, RR 24.
This patient is encephalopathic and only awakens to noxious stimuli. Capillary refill time is 5-6 seconds, and was done as in the ANDROMEDA-SHOCK trial:
This patient is encephalopathic with oliguria and altered peripheral perfusion. This patient is in shock! Because the MAP was hovering above the cutoff of 65, shock was not diagnosed.
If we follow the ANDROMEDA-SHOCK approach, the next step would be to assess fluid responsiveness. However, we can also learn from the trial that fluid responsiveness at this point in her history is quite unlikely:
Further review of medical records revealed this patient was on four antihypertensives at home. We tested a higher MAP goal (75 in this case) with peripheral vasopressors. Within 2 hours, urine output rose to 50 ml/hr, and incrementally rose to 100 ml/hr over the course of the shift. Total duration of vasopressor therapy was about 48 hours.
By day 5 of hospitalization, creatinine was near baseline as she recovered from septic shock due to Klebsiella urinary tract infection.
There are several take-home points from this case:
- A comprehensive patient evaluation (beyond the MAP alone) is needed to diagnose shock. Think Brain, Urine, Skin (get on the BUS 🚌!) for a simple evaluation that requires no gadgets (except a microscope slide for cap refill if you’re like me).
- A common approach to many cases of acute kidney injury (or even oliguria) is to throw extra fluid at it and hope for the best. Indiscriminate fluid loading is among the least zentensivist things we can do. We wouldn’t give extra boluses of cefepime if the patient wasn’t responding to treatment, we would change our approach.
- Renal resuscitation requires hemodynamic assessment as one would do for the rest of the body. Unless that preload is raising the stroke volume, this is for naught.
- Going a step further, a fluid liberal strategy may be associated with worse outcomes in acute kidney injury, as shown by a recent feasibility trial.
- While higher MAP targets aren’t broadly supportable, there is a rationale for it in select cases for patients with chronic hypertension (moreso if you’re a fan of subgroup analyses), or to protect renal perfusion pressure.
- This patient was in overt shock with MAP at the traditional goal, so a trial was reasonable.
- Had it not helped, I would have reverted to the prior goal and performed further investigation to find out why. One could have subsequently considered an inodilator test, as was done in the ANDROMEDA-SHOCK protocol.
- Cover image by balik on pixabay