AKI and #COVID19
68 yo PMH obesity, HTN, CAD w stent, OSA, T2DM
ED w SOB + fever 39.9°C. Poor oral intake
RR 40, Sat 94% Room Air, BP 157/74 HR 124. Alert. Bibasilar crackles
Labs: Cr 1.3 (baseline 0.8), WBC 10, K 5.4, HCO3 17, CK 184. UA and CXR (case from @NEJM)
68 yo PMH obesity, HTN, CAD w stent, OSA, T2DM
ED w SOB + fever 39.9°C. Poor oral intake
RR 40, Sat 94% Room Air, BP 157/74 HR 124. Alert. Bibasilar crackles
Labs: Cr 1.3 (baseline 0.8), WBC 10, K 5.4, HCO3 17, CK 184. UA and CXR (case from @NEJM)
How would you manage this AKI initially? What is the likely cause of AKI in patients with #COVID19? (this last question discussed in thread )
No easy answer except to say that FENa is very unlikely to be useful. It is not unreasonable to try fluids for AKI in the setting of perceived hypovolemia. However, this gets complicated when the potential for worsening ARDS exists. I'll try to tackle the answers one by one
FENa: Hypovolemia + normal tubular function should lead to Na reabsorption and a FENa < 1%. Tubular injury inappropriate Na wasting FENa > 3%. Patchy tubular, glomerular and vascular disease can cause falsely low FENa thus is a poor predictor of fluid responsiveness.
Evaluation of "volume status" using traditional clinical exam is not reliable. Hx of poor oral intake makes an empiric fluid challenge tempting. However some concerns in this case: Pt age, BMI and PMH (CAD, HTN, OSH, DM) put him at increased risk of having preexisting HFpEF
Infusing 1 L of HES to patients with compensated HFpEF altered intra-renal venous flow and this induced diuretic resistance. Increased CVP and alterations of IRVF have been linked to worsening renal function (Renosarca). ARDS / Sepsis is already a sign of poor volume tolerance
Ideally you would want to know if patient will respond to fluids before giving them. This is hard to do on the ED. However, the reason to give fluids would be to increase stroke volume. If stroke volume is normal/high, fluids make no sense! This can be measured easily!
You should also want to asses venous congestion before giving fluids. Lung Ultrasound is going to be useless because of ARDS. #IVC can help a LOT if you ask the right questions. A plethoric IVC means pt is unlikely to respond to fluids https://thinkingcriticalcare.com/2019/03/13/my-friend-the-ivc-foamed-foamer-foamus-foamcc/
#POCUS evaluation of stroke volume (LVOT VTI) and volume tolerance (IVC) takes 1-2 minutes and can add a ton of valuable information before deciding to give fluids!
If pt is transferred to the ICU and advanced monitoring is available, CO monitoring with Passive leg rise (PLR) guided fluid resuscitation has been shown to decrease the need for dialysis and mechanical ventilation.
*Before performing PLR authors determined if SV was inadequate
*Before performing PLR authors determined if SV was inadequate
HCO3 drip can be useful for patients with AKI, especially to manage K. Increasing blood pH shifts potassium into cells and thereby improves hyperkalemia 4.2% HCO3 could be better than isotonic if volume tolerance is a concern. Read this by @PulmCrit https://emcrit.org/pulmcrit/bicar-icu/
Etiology of AKI in #COVID19 is likely to be complex. Definitely some patients can present with severe diarrhea and could have a component of volume depletion. However, it is likely that most AKI is not a volume problem https://twitter.com/VelezNephHepato/status/1250656930986680320?s=20
Reports from show incidence of hematuria and proteinuria (as in this patient). Autopsies show tubular necrosis, obstruction of peritubular capillary lumens and glomerular capillary loops. Today @NEJM published convincing evidence of #SARSCov2 directly involving the kidney!
This patient was actually given 2 L IV fluid with no improvement on kidney function. Eventually required RRT with CRRT. Given I know nothing about CRRT, I hope my good friend @galindozip can complement this thread with his awesome knowledge!
Thank you for reading! Here is a link to the full case: https://www.nejm.org/doi/full/10.1056/NEJMcpc2002418?query=featured_home