It gets passed down to each generation of providers that when a patient has an increase in creatinine or a decrease in urine output they need fluids. The only time a provider will stop and consider an alternative cause is if the patient has known heart failure.
What if I said there is another etiology that needs to be considered, especially in the ICU?
Patients admitted to an intensive care unit are often resuscitated before arrival or have significant input in the first couple of days in the ICU leading to hypervolemia. Hypervolemia in the ICU worsens outcomes and organ function. It leads to worse mortality, ICU length of stay (LOS), and worsening renal function (1,2). We have to understand and appreciate volume overload as a cause of acute kidney injury (AKI) to appropriately identify and treat these patients.
How does hypervolemia cause AKI? It is multi-factorial as are many disease processes. The kidney is surrounded by a layer of fascia, Gerota’s fascia, that keeps the kidney from appropriately swelling if the parenchyma gets congested. If it cannot increase in size with the increased water content it gets compressed against the fascia leading to injury. Another factor is intra-abdominal pressure. When patients get volume overloaded it leads to intestinal swelling and third-spacing which causes an increase in intra-abdominal pressure. As the pressure rises, it leads to intra-abdominal hypertension (IAH) and potentially abdominal compartment syndrome. IAH causes pressure on the kidney leading to AKI.
The etiology that I want to focus on is renal venous congestion. Too often when I was a resident and fellow I had providers tell me the edematous patient was extravascular volume overloaded but intravascular volume deplete and the patient should get more fluids. Now, I will acknowledge that patients can have low oncotic pressure and be third-spacing leading to intra-vascular depletion as seen in cirrhotic patients. But, if a patient has normal oncotic pressure, I cannot figure out how this dogma has continued to survive. The patient will have diffuse pitting edema and pulmonary edema and they will be getting maintenance fluids or boluses because they have an AKI. How does giving a patient fluid fix their volume overload?
If a patient is hypervolemic and developing an AKI, it is usually due to volume overload and renal venous congestion instead of a lack of intravascular volume. By understanding and treating renal venous congestion patients will have fewer ICU days, fewer AKI, fewer ventilator days, and improved mortality (1,2).
Physiology:
Urine output relies on having a positive net filtration pressure (NFP). The NFP is what drives ultrafiltration into Bowman’s capsule and creates a glomerular filtration rate (GFR). Here is a basic drawing of the interaction between the glomerulus and Bowman’s capsule, which together is called the renal corpuscle (Figure 1).
Figure 1:
The net filtration pressure is made of pressures that are pushing and pulling fluid between the glomerular capillaries and Bowman’s capsule. These components include the intravascular osmotic and oncotic pressure which are drawing fluid into the intravascular space and the opposing intravascular hydrostatic pressure which is pushing fluid out. The is the opposite for Bowman’s capsule where the capsular osmotic and oncotic pressures are drawing fluid into the intracapsular space and the capsular hydrostatic pressure is pushing it back into the intravascular space. The main components that contribute to the NFP are the hydrostatic and oncotic pressure of the intravascular space, and the hydrostatic pressure on the capsular side. The NFP equation typically names these as the glomerular capillary hydrostatic pressure (GCHP), Blood colloidal osmotic pressure (BCOP), and capsular hydrostatic pressure (CHP).
Net Filtration Pressure = Glomerular Capillary Hydrostatic Pressure – (Capsular Hydrostatic Pressure + Blood Colloidal Osmotic Pressure)
NFP = GCHP – (CHP + BCOP)
The normal values are GCHP=55 mmHg, CHP=15 mmHg, BCOP= 30mmHg. Giving a positive net filtration pressure of 10 mmHg
NFP = 55 – (15 + 30) = 10 mmHg (Figure 2)
Figure 2:
The more positive the NFP the better the GFR, so trying to make changes that improve the NFP will improve the patient’s urine output. The CHP is not able to be manipulated to decrease the pressure. When a patient has a kidney stone or bladder outlet obstruction it will increase CHP from backpressure and worsen NFP (3). The Intravascular oncotic pressure, or BCOP, is more difficult to navigate. According to this equation the lower the oncotic pressure the higher the NFP and 75% of oncotic pressure is albumin. This would imply a lower serum albumin would be beneficial. But, a low oncotic pressure leads to spontaneous third-spacing and decreases the intravascular hydrostatic pressure. If the oncotic pressure is too high it increases BCOP and decreases NFP and if it is too low it decreases GCHP and decreases NFP. I usually ensure the patient has an albumin >2.5g/dL to prevent spontaneous third-spacing.
The main focus is on GCHP when manipulating the patient’s hemodynamics to improve urine output. The hydrostatic pressure is based on the flow from the afferent arteriole to the efferent arteriole. Using a variation of Ohm’s law, we correlate flow and pressure. Ohm’s law is for electricity, V = IR. Ohm’s law can be changed to look at fluids.
Ohm’s Law (Fluids): Change in Pressure (△P) = Flow (F)・Resistance (R)
This formula is usually seen in hemodynamics when calculating resistance; R = △P/F.
The simplified equation for glomerular capillary hydrostatic pressure looks at the change in pressure from afferent arteriole to efferent arteriole: Pa – Pe. This is the pressure gradient that will increase NFP (Figure 3). I often think of the pressure across a dialysis filter that is helping push the ultrafiltrate out.
Figure 3:
Differential:
Hypovolemic/Distributive:
When the UOP decreases or the creatinine increases many people assume the problem is due to a drop in afferent pressure. The assumption is that hypovolemia or hypotension drops afferent arteriole pressure which drops the pressure gradient. This decrease in the pressure gradient drops the NFP and decreases urine output leading to an AKI (Figure 4). This leads many providers to give fluids as I stated above. This is definitely a cause of AKI for patients in the hospital, but it is not the only cause.
Figure 4:
Hypervolemic:
There are other causes of a decreased pressure gradient dealing with fluids. Time should be taken to evaluate patients in the ICU to assess whether another etiology is present. If the patient appears hypervolemic, has an increase in weight from admission weight, or has a positive fluid balance, an alternative cause should be considered. When a patient is hypervolemic the venous blood volume is increased creating back pressure on the renal venous system known as renal venous congestion. Renal venous congestion increases the efferent arteriole pressure and decreases the pressure gradient (Figure 5). The result of a decreased pressure gradient is the same, but it is due to venous pressure problems.
Figure 5:
If this patient gets IV fluids it may increase gradient transiently but will only worsen the problem.
Example: A patient has renal venous congestion and volume overload with an AKI. They have decreased UOP at 30mL/hr and are given a 1L fluid bolus. This causes a transient mild increase in the afferent arteriole pressure and for 2 hours after the bolus, their UOP increased to 60mL/hr before dropping back down to 30mL/hr. People then say the patient responded to the fluid and try to order more. But the patient is already volume overloaded and had an extra 60mL of urine output, but it left an extra 940mL of the fluid bolus in an already overloaded patient. The problem was not fixed.
Additionally, if the patient receives multiple fluid boluses, the creatinine can be diluted down, just like hemoglobin, giving a false sense of success when actually the patient’s renal function is worsening.
Heart Failure/Cardiorenal:
The combination of the above explains why decompensated heart failure patients with AKI are so difficult to treat. These patients are in a low-flow state (low cardiac output) which decreases afferent arteriole pressure and they also have significant renal venous congestion which increases efferent arteriole pressure. This is a double insult and causes a larger decrease in the pressure gradient (Figure 6). In a study looking at decompensated heart failure patients, it was found that venous congestion played a bigger role than decreased flow (4).
Figure 6:
Diagnosis:
There is no best answer for how to determine intravascular volume status. It depends on the provider's skill level with physical exams, ultrasound, and hemodynamic monitoring devices. I like to use the ultrasound and get a quick look at the IVC. The extremes are very helpful. If the IVC collapses completely with normal work of breathing I can safely say it is not renal venous congestion. If the IVC is dilated and non-variable I can say they do not need more fluids, they need either diuresis or better hemodynamics.
This is why I find the VExUS criteria very helpful (Figure 7). If I can show that there is venous overload to the point of organ congestion, I feel very confident that the patient falls into the renal venous congestion category. The VExUS study showed that it reliably identified patients with venous congestion and outperformed central venous pressure (CVP) (5).
Figure 7: VExUS Ultrasound Score
Treatment:
Treating a decreased pressure gradient due to hypovolemia or distributive shock is still the same as it has been, IV fluids and vasopressors. This will ensure appropriate blood flow and pressure.
For a decreased pressure due to renal venous congestion, the treatment is to decrease the renal venous pressure. This can be done by decreasing absolute volume with diuresis or by decreasing the venous pressure with venodilators. Diuretics are first-line and decreasing the volume should be the top priority. This can be difficult if the renal venous pressures are extremely elevated. When diuretics are initiated there can be an increase in creatinine before the appropriate decrease. It is important to just hold steady and continue diuresis. If diuretics alone are not working, adding a venodilator like nitroglycerin can work really well. As long as the patient has enough blood pressure to tolerated a nitrate, there should be a significant increase in UOP.
Last, cardiorenal is the most difficult to treat. Both sides of the pressure equation have to be addressed to appropriately treat the patient. Often these patients are started on diuretics, which will help the venous congestion, but is not enough to increase the afferent arteriole pressure. These patients need an increase in blood flow to the kidney. If the patient has low blood pressure, inotropes should be initiated to help increase flow. If the patient is normotensive to hypertensive afterload reduction with hydralazine, ACE inhibitors, or even nitroprusside will help (Figures 8-10).
Figure 8:
Figure 9:
Figure 10:
It is important to keep renal venous congestion in mind when dealing with patients in the ICU. If they are volume overloaded and have venous congestion, diuresis will improve outcomes. Stay strong in your resolve even if there are bumps in the road with increased creatinine at times and increased sodium.
References:
1. Messmer AS, Zingg C, Müller M, Gerber JL, Schefold JC, Pfortmueller CA. Fluid Overload and Mortality in Adult Critical Care Patients-A Systematic Review and Meta-Analysis of Observational Studies. Crit Care Med. 2020 Dec;48(12):1862-1870. doi: 10.1097/CCM.0000000000004617. PMID: 33009098.
2. Wang N, Jiang L, Zhu B, Wen Y, Xi XM; Beijing Acute Kidney Injury Trial (BAKIT) Workgroup. Fluid balance and mortality in critically ill patients with acute kidney injury: a multicenter prospective epidemiological study. Crit Care. 2015 Oct 23;19:371. doi: 10.1186/s13054-015-1085-4. PMID: 26494153; PMCID: PMC4619072.
3. Austin Peay State University. https://www.apsubiology.org/anatomy/2020/2020_Exam_Reviews/Exam_4/CH25_Physiology_of_Glomerular_Filtration.htm, 2020, accessed 3/20/21.
4. Wilfried Mullens, Zuheir Abrahams, Gary S. Francis, George Sokos, David O. Taylor, Randall C. Starling, James B. Young, W.H. Wilson Tang. Importance of Venous Congestion for Worsening of Renal Function in Advanced Decompensated Heart Failure. Journal of the American College of Cardiology. 2009 53;7:589-596,
5. Beaubien-Souligny, W., Rola, P., Haycock, K. et al. Quantifying systemic congestion with Point-Of-Care ultrasound: development of the venous excess ultrasound grading system. Ultrasound J 12, 16 (2020). https://doi.org/10.1186/s13089-020-00163-w
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