Case vignette
48yo M w/ NICM, IVDU, HIV, CKD p/w flank pain and dysuria, F gradually worsening in last few days. He also has chronic SOB with orthopnea. No N/V/D, hematochezia/melena, or abdominal pain.
HR 120, BP 90/60, T 38.4, RR 17, SpO2 94%
L CVA tenderness. BLE 3+ pitting edema, +JVD.
UA with bacteria, WBC, +nitrites, +LE. Labs with pre-renal AKI (with elevated BUN), leukocytosis.
What do you do next?
Suspecting pyelonephritis leading to sepsis, you obtain a full septic work up and initiate ceftriaxone, which is appropriate based on previous urinary cultures/sensitivities. You consider alternative diagnoses such as septic nephrolithiasis, however CT non con A/P 2mo ago showed no kidney stones or other abdominal pathology. At bedside, you perform renal/bladder US to ensure no hydronephrosis and no urinary retention, further solidifying your diagnosis.
Meanwhile, you question how much fluids to give the patient. He appears chronically hypervolemic in the setting of known cardiomyopathy (2/2 drug use). However, you note both soft blood pressures and AKI. You suspect his kidneys are poorly perfused, though you are not sure if sepsis/early distributive shock or cardiorenal syndrome drives this.
You think trialing gentle fluid boluses is appropriate but want additional information -- so, you turn your ultrasound to the heart and lungs.
What do you see?
CP10 PLA: globally reduced LV motion and poor MV anterior leaflet movement, suggesting severely reduced LVEF.
CP10 IVC: IVC <2cm, >50% respiratory variation. (Note should be rotated 180 degrees.)
Not shown: no B-lines in bilateral lungs.
What do you do next?
While the LVEF is poor, your IVC assessment suggests possible fluid tolerance. You give 500mL crystalloid to see if this improves intravascular volume status. You reassess the patient within 30 minutes. His BP has improved and he shows no pulmonary edema on repeat US; in fact, his LVEF has also mildly improved. You discuss his care with medicine , noting his complexity, and admit him to the ward in stable condition.
Teaching Points. Many factors are used to assess a patient's volume status, an ongoing source of controversy and confusion in medicine. While no single factor is determinative, your history and exam are paramount. Labs such as BUN, Cr, BNP, and other markers of organ dysfunction can assist. And, of course: don't forget POCUS!
US can rapidly assess LVEF as well as IVC dilation, pulmonary edema, and (if difficult to see on exam) JVP. More complex measurements such as hepatic vein reflux can further assist.
Try to answer two questions: does the patient need more fluids (fluid responsiveness), and can the patient handle more fluids (fluid tolerance)?
If the patient has evidence of a dilated IVC or right heart strain, additional fluids may worsen venous congestion and not get to systemic circulation. If the patient has poor LV function or pulmonary edema, additional fluids may get trapped in the lungs, worsening pulmonary edema.
As there is no perfect measurement, consider trialing gentle fluid boluses (or passive leg raise test) if you are unsure and assess the patient's response. Reassess frequently, as ultrasound findings may change. (Not only may IVC and pulmonary edema findings change, but LVEF may, too!) If fluids are ineffective, consider vasopressors to mobilize venous reserve, improve cardiac output, and/or improve vascular tone.
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This particular patient is more complex than meets the eye. He is septic with soft blood pressures and has an AKI; however, he also has signs of hypervolemia. It is unclear if his kidneys are well perfused, which should be corrected if possible. This could be from intravascular volume deletion due to vascular leak/vasodilation from sepsis, which might improve with fluids. However, it could also be from cardiorenal syndrome (e.g., poor LVEF/forward flow), which would require ionotropes or diuresis. In addition, his total body hypervolemia could be from cardiomyopathy -- but it could also be from hypoalbuminemia, venous insufficiency, drug exposure, or other correctable etiologies that should be elicited.
Attempting a gentle fluid bolus is reasonable, but if this fails or causes worsening pulmonary edema, ionotropes to improve cardiac output should be considered. Discussing this patient with medicine (or the ICU, if your concern increases) early is reasonable, as ideal management takes time and may be difficult to optimize in the ED.
Food for thought: if this same patient were not septic and hypotensive, diuresis would be the next logical step. Patients with a combination of AKI, adequate perfusion, and hypervolemia are often treated with a lasix challenge.
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In sum, there is no one answer to diagnosing and managing volume status. Gone are the days when invasive CVP monitoring ruled. Use all your clinical clues, including POCUS, reassess frequently, and remember to ask both whether the patient needs more fluid and whether they can handle more fluid.
Sources + Further Reading:
- Helman, A. Etchells, E. Tillmann, B. Episode AKI – ED Management. Emergency Medicine Cases. January, 2021. https://emergencymedicinecases.com/aki-ed-management. Accessed [date]
- Podcast 162: Assessing Fluid Responsiveness. Scott Weingart. EMCrit-RACC. Nov 29, 2015. https://emcrit.org/emcrit/assessing-fluid-responsiveness/. Accessed 4/15/21.
- The IVC for Fluid Assessment Roundup. Scott Weingart. EMCrit-RACC. Nov 23, 2013. https://emcrit.org/emcrit/ivc-roundup/. Accessed 4/15/21
- Fluid Responsiveness. Chris Nickson. LIFTL. https://litfl.com/fluid-responsiveness/. Accessed 4/15/21
Residents: Dr. Michael Triller
Fluid Status: Sepsis, CHF, and AKI
April 2020