The Pre-brief
Current practice guidelines and recent reviews seem too keen on recommending albumin infusion as a “volume expander” in patients with cirrhosis and AKI.Â
From the get-go, any blanket recommendation that does not take into account a patient’s underlying physiology or hemodynamic status makes me uncomfortable (to say the least), not only can ‘volume expansion for all’ not be beneficial, it can be harmful in some cases!
Albumin in chronic liver disease is the 30 cc/kg in sepsis resuscitation. Obviously there is no single treatment that applies to every single patient.
Should I care about volume status in these patients prior to making therapeutic decisions?
Yes, up to 50% of patients with the suspected hepato-renal syndrome (HRS) are either volume overloaded or volume repleted. We know all too well that there are adverse consequences to iatrogenic volume overload. Thus this definitely raises questions on the utility of IV albumin for all comers.
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How should I determine my patient’s volume status?
The presence of ascites or leg edema in this patient population is unlikely to help.
A good neck examination can reveal increased JVP (highly recommended lecture on clinical JVP examination from @AndreMansoor: https://echo360.org/media/9d934437-65db-4695-bdd3-3ead454c2f9a/public ) However, JVP assessment is hard and requires significant expertise (something we should all strive for), in the meantime POCUS can help
POCUS IVC diameter > 2 cm with little respiratory variation and discontinuous intra-renal venous Doppler* are signs of venous congestion. In a recent study, @VelezNephHepato used the IVC diameter and collapsibility index to show that many patients with suspected HRS are actually misclassified
*Given increased parenchymal stiffness in chronic liver disease, Doppler assessment of hepatic or portal veins might not be reliable
Focused cardiac examination (FOCUS) can reveal the presence of low left ventricular ejection fraction, dilated right ventricle, tricuspid regurgitation or increased pulmonary artery systolic pressure!
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Why would a patient with cirrhosis and AKI have venous congestion?
Several possibilities can explain this:
- Co-existence of chronic cardiomyopathy and cirrhosis
- Low vascular resistance leading to high output heart failure with volume overload
- Porto-pulmonary hypertension resulting in right ventricular dilation
Determining the presence of venous congestion is important because renal perfusion can be thought of as the gradient between MAP and CVP; if MAP falls or if CVP rises the renal perfusion pressure will fall, potentially leading to AKI. Thus, not only can empiric fluids fail to benefit they can actually exacerbate the problem!!!
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Clinical Example:
This was a patient with cirrhosis that I saw on the ED presenting with AKI (Cr 5.8 mg/dl)and oliguria
POCUS showed an IVC of 2.2 cm with no respiratory variation and a biphasic intra-renal venous Doppler:
FOCUS showed dilated RV and moderate/severe tricuspid regurgitation:
Given BP was 70/50, the patient was treated with vasopressors and NO Albumin. A good urine output was obtained, and after -5 L fluid balance serum creatinine returned to baseline (1.1 mg/dl). Repeat POCUS exam confirmed decongestion: Small collapsible IVC and continuous flow on intra-renal venous Doppler:
The Debrief
- Patients with Cirrhosis and AKI present heterogeneously, not every patient is volume depleted while some are volume overloaded
- A good physical examination augmented by POCUS can reveal volume overload in this population
- Empiric IV albumin infusion for volume overloaded patients makes no physiological sense and might lead to adverse consequences
- Appreciating that volume expansive treatment should be tailored to underlying physiology and hemodynamic status will be a long battle with constant pushback from some (for example, this was shared with me by Dr Gomez Johnson: https://twitter.com/vikouerMD/status/1308199931396722689?s=20 )
- But one must remain vocal in order to achieve change!
- In this regard the effort from @NephroP @NephroGuy and @medpedshosp should be commended (read their letter to the editor here: https://www.bmj.com/content/370/bmj.m2687/rapid-responsesÂ
References
- Simonetto Douglas A, Gines Pere, Kamath Patrick S. Hepatorenal syndrome: pathophysiology, diagnosis, and management BMJ 2020; 370 :m2687
- European Association for the Study of the Liver. Electronic address: [email protected]; European Association for the Study of the Liver. EASL Clinical Practice Guidelines for the management of patients with decompensated cirrhosis. J Hepatol. 2018 Aug;69(2):406-460. doi: 10.1016/j.jhep.2018.03.024. Epub 2018 Apr 10. Erratum in: J Hepatol. 2018 Nov;69(5):1207. PMID: 29653741.
- Velez JCQ, Petkovich B, Karakala N, Huggins JT. Point-of-Care Echocardiography Unveils Misclassification of Acute Kidney Injury as Hepatorenal Syndrome. Am J Nephrol. 2019;50(3):204-211. doi: 10.1159/000501299. Epub 2019 Aug 8. PMID: 31394538.
- Iida N, Seo Y, Sai S, Machino-Ohtsuka T, Yamamoto M, Ishizu T, Kawakami Y, Aonuma K. Clinical Implications of Intrarenal Hemodynamic Evaluation by Doppler Ultrasonography in Heart Failure. JACC Heart Fail. 2016 Aug;4(8):674-82. doi: 10.1016/j.jchf.2016.03.016. Epub 2016 May 11. PMID: 27179835.
- https://echo360.org/media/9d934437-65db-4695-bdd3-3ead454c2f9a/public
Question is, in a cirrhotic patient with AKI who is hypovolemic, would your first choic volume expander be albumin 5% or ringer lactate?