Osmotic shifts, cerebral edema, and neurologic deterioration in severe hepatic encephalopathy

Eric Michael Liotta; Anna L. Romanova; Bryan D. Lizza; Laura Jarmila Rasmussen-Torvik; Minjee Kim; Brandon Francis; Rajbeer Singh Sangha; Timothy J. Carroll; Daniel R Ganger; Daniela P Ladner; Andrew M Naidech; James J Paparello; Shyam Prabhakaran; Farzaneh A Sorond; Matthew Brandon Maas

doi:10.1097/CCM.0000000000002831

Osmotic shifts, cerebral edema, and neurologic deterioration in severe hepatic encephalopathy

Eric Michael Liotta^*, Anna L. Romanova, Bryan D. Lizza, Laura Jarmila Rasmussen-Torvik, Minjee Kim, Brandon Francis, Rajbeer Singh Sangha, Timothy J. Carroll, Daniel R Ganger, Daniela P Ladner, Andrew M Naidech, James J Paparello, Shyam Prabhakaran, Farzaneh A Sorond, Matthew Brandon Maas

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

30 Scopus citations

Abstract

Objectives: We sought to determine the effect of acute electrolyte and osmolar shifts on brain volume and neurologic function in patients with liver failure and severe hepatic encephalopathy. Design: Retrospective analysis of brain CT scans and clinical data. Setting: Tertiary care hospital ICUs. Patients: Patients with acute or acute-on-chronic liver failure and severe hepatic encephalopathy. Interventions: Clinically indicated CT scans and serum laboratory studies. Measurements and Main Results: Change in intracranial cerebrospinal fluid volume between sequential CT scans was measured as a biomarker of acute brain volume change. Corresponding changes in serum osmolality, chemistry measurements, and Glasgow Coma Scale were determined. Associations with cerebrospinal fluid volume change and Glasgow Coma Scale change for initial volume change assessments were identified by Spearman's correlations (rs) and regression models. Consistency of associations with repeated assessments was evaluated using generalized estimating equations. Forty patients were included. Median baseline osmolality was elevated (310 mOsm/Kg [296-321 mOsm/Kg]) whereas sodium was normal (137 mEq/L [134-142 mEq/L]). Median initial osmolality change was 9 mOsm/kg (5-17 mOsm/kg). Neuroimaging consistent with increased brain volume occurred in 27 initial assessments (68%). Cerebrospinal fluid volume change was more strongly correlated with osmolality (r = 0.70; p = 4 × 10-7) than sodium (r = 0.28; p = 0.08) change. Osmolality change was independently associated with Glasgow Coma Scale change (p = 1 × 10-5) and cerebrospinal fluid volume change (p = 2.7 × 10-5) in initial assessments and in generalized estimating equations using all 103 available assessments. Conclusions: Acute decline in osmolality was associated with brain swelling and neurologic deterioration in severe hepatic encephalopathy. Minimizing osmolality decline may avoid neurologic deterioration.

Original language	English (US)
Pages (from-to)	280-289
Number of pages	10
Journal	Critical care medicine
Volume	46
Issue number	2
DOIs	https://doi.org/10.1097/CCM.0000000000002831
State	Published - Feb 2018

Funding

Supported, in part, by the National Institutes of Health’s National Center for Advancing Translational Sciences, Grant Number KL2TR001424, and the National Institutes of Health, Grant Number L30 NS098427 and by departmental funding from the Ken & Ruth Davee Department of Neurology in the Northwestern University Feinberg School of Medicine. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. Drs. Liotta, Rasmussen-Torvik, Sorond, and Maas received support for article research from the National Institutes of Health (NIH). Dr. Liotta is supported by a KL2 career development grant awarded through the North-western University Clinical and Translational Sciences Institute. Dr. Liotta’s institution received funding from NIH’s National Center for Advancing Translational Sciences and the NIH’s National Center for Advancing Translational Sciences, Grant Number KL2TR001424; he received funding from the NIH, Northwestern University, and NIH Grant Number L30 NS098427; and he disclosed that his institution received grant support from Placement of AoRTic TraNscathetER Valves II Trial (Edwards Lifesciences), TranS-catheter Aortic Valve RepLacement System U.S. Feasibility Trial (Direct Flow Medical), and SAGE-547 Clinical Trial (SAGE therapeutics) for his work on those clinical trials. Dr. Ganger received funding from Abbvie, Gil-ead, and Merck. Dr. Naidech’s institution received funding from the Agency for Healthcare Research and Quality, K18 HS023437. Dr. Maas’ institution received funding from the NIH. The remaining authors have disclosed that they do not have any potential conflicts of interest. For information regarding this article, E-mail: [email protected]

Keywords

Cerebral edema
Coma
Hepatic encephalopathy
Liver failure
Renal replacement therapy

ASJC Scopus subject areas

Critical Care and Intensive Care Medicine

Access to Document

10.1097/CCM.0000000000002831

Cite this

Liotta, E. M., Romanova, A. L., Lizza, B. D., Rasmussen-Torvik, L. J., Kim, M., Francis, B., Sangha, R. S., Carroll, T. J., Ganger, D. R., Ladner, D. P., Naidech, A. M., Paparello, J. J., Prabhakaran, S., Sorond, F. A., & Maas, M. B. (2018). Osmotic shifts, cerebral edema, and neurologic deterioration in severe hepatic encephalopathy. Critical care medicine, 46(2), 280-289. https://doi.org/10.1097/CCM.0000000000002831

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title = "Osmotic shifts, cerebral edema, and neurologic deterioration in severe hepatic encephalopathy",

abstract = "Objectives: We sought to determine the effect of acute electrolyte and osmolar shifts on brain volume and neurologic function in patients with liver failure and severe hepatic encephalopathy. Design: Retrospective analysis of brain CT scans and clinical data. Setting: Tertiary care hospital ICUs. Patients: Patients with acute or acute-on-chronic liver failure and severe hepatic encephalopathy. Interventions: Clinically indicated CT scans and serum laboratory studies. Measurements and Main Results: Change in intracranial cerebrospinal fluid volume between sequential CT scans was measured as a biomarker of acute brain volume change. Corresponding changes in serum osmolality, chemistry measurements, and Glasgow Coma Scale were determined. Associations with cerebrospinal fluid volume change and Glasgow Coma Scale change for initial volume change assessments were identified by Spearman's correlations (rs) and regression models. Consistency of associations with repeated assessments was evaluated using generalized estimating equations. Forty patients were included. Median baseline osmolality was elevated (310 mOsm/Kg [296-321 mOsm/Kg]) whereas sodium was normal (137 mEq/L [134-142 mEq/L]). Median initial osmolality change was 9 mOsm/kg (5-17 mOsm/kg). Neuroimaging consistent with increased brain volume occurred in 27 initial assessments (68%). Cerebrospinal fluid volume change was more strongly correlated with osmolality (r = 0.70; p = 4 × 10-7) than sodium (r = 0.28; p = 0.08) change. Osmolality change was independently associated with Glasgow Coma Scale change (p = 1 × 10-5) and cerebrospinal fluid volume change (p = 2.7 × 10-5) in initial assessments and in generalized estimating equations using all 103 available assessments. Conclusions: Acute decline in osmolality was associated with brain swelling and neurologic deterioration in severe hepatic encephalopathy. Minimizing osmolality decline may avoid neurologic deterioration.",

keywords = "Cerebral edema, Coma, Hepatic encephalopathy, Liver failure, Renal replacement therapy",

author = "Liotta, {Eric Michael} and Romanova, {Anna L.} and Lizza, {Bryan D.} and Rasmussen-Torvik, {Laura Jarmila} and Minjee Kim and Brandon Francis and Sangha, {Rajbeer Singh} and Carroll, {Timothy J.} and Ganger, {Daniel R} and Ladner, {Daniela P} and Naidech, {Andrew M} and Paparello, {James J} and Shyam Prabhakaran and Sorond, {Farzaneh A} and Maas, {Matthew Brandon}",

note = "Funding Information: Supported, in part, by the National Institutes of Health{\textquoteright}s National Center for Advancing Translational Sciences, Grant Number KL2TR001424, and the National Institutes of Health, Grant Number L30 NS098427 and by departmental funding from the Ken & Ruth Davee Department of Neurology in the Northwestern University Feinberg School of Medicine. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. Drs. Liotta, Rasmussen-Torvik, Sorond, and Maas received support for article research from the National Institutes of Health (NIH). Dr. Liotta is supported by a KL2 career development grant awarded through the North-western University Clinical and Translational Sciences Institute. Dr. Liotta{\textquoteright}s institution received funding from NIH{\textquoteright}s National Center for Advancing Translational Sciences and the NIH{\textquoteright}s National Center for Advancing Translational Sciences, Grant Number KL2TR001424; he received funding from the NIH, Northwestern University, and NIH Grant Number L30 NS098427; and he disclosed that his institution received grant support from Placement of AoRTic TraNscathetER Valves II Trial (Edwards Lifesciences), TranS-catheter Aortic Valve RepLacement System U.S. Feasibility Trial (Direct Flow Medical), and SAGE-547 Clinical Trial (SAGE therapeutics) for his work on those clinical trials. Dr. Ganger received funding from Abbvie, Gil-ead, and Merck. Dr. Naidech{\textquoteright}s institution received funding from the Agency for Healthcare Research and Quality, K18 HS023437. Dr. Maas{\textquoteright} institution received funding from the NIH. The remaining authors have disclosed that they do not have any potential conflicts of interest. For information regarding this article, E-mail: [email protected] Publisher Copyright: Copyright {\textcopyright} 2017 by the Society of Critical Care Medicine and Wolters Kluwer Health, Inc. All Rights Reserved.",

year = "2018",

month = feb,

doi = "10.1097/CCM.0000000000002831",

language = "English (US)",

volume = "46",

pages = "280--289",

journal = "Critical care medicine",

issn = "0090-3493",

publisher = "Lippincott Williams and Wilkins",

number = "2",

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Liotta, EM, Romanova, AL, Lizza, BD, Rasmussen-Torvik, LJ , Kim, M, Francis, B, Sangha, RS, Carroll, TJ, Ganger, DR , Ladner, DP , Naidech, AM , Paparello, JJ, Prabhakaran, S, Sorond, FA & Maas, MB 2018, 'Osmotic shifts, cerebral edema, and neurologic deterioration in severe hepatic encephalopathy', Critical care medicine, vol. 46, no. 2, pp. 280-289. https://doi.org/10.1097/CCM.0000000000002831

TY - JOUR

T1 - Osmotic shifts, cerebral edema, and neurologic deterioration in severe hepatic encephalopathy

AU - Liotta, Eric Michael

AU - Romanova, Anna L.

AU - Lizza, Bryan D.

AU - Rasmussen-Torvik, Laura Jarmila

AU - Kim, Minjee

AU - Francis, Brandon

AU - Sangha, Rajbeer Singh

AU - Carroll, Timothy J.

AU - Ganger, Daniel R

AU - Ladner, Daniela P

AU - Naidech, Andrew M

AU - Paparello, James J

AU - Prabhakaran, Shyam

AU - Sorond, Farzaneh A

AU - Maas, Matthew Brandon

N1 - Funding Information: Supported, in part, by the National Institutes of Health’s National Center for Advancing Translational Sciences, Grant Number KL2TR001424, and the National Institutes of Health, Grant Number L30 NS098427 and by departmental funding from the Ken & Ruth Davee Department of Neurology in the Northwestern University Feinberg School of Medicine. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. Drs. Liotta, Rasmussen-Torvik, Sorond, and Maas received support for article research from the National Institutes of Health (NIH). Dr. Liotta is supported by a KL2 career development grant awarded through the North-western University Clinical and Translational Sciences Institute. Dr. Liotta’s institution received funding from NIH’s National Center for Advancing Translational Sciences and the NIH’s National Center for Advancing Translational Sciences, Grant Number KL2TR001424; he received funding from the NIH, Northwestern University, and NIH Grant Number L30 NS098427; and he disclosed that his institution received grant support from Placement of AoRTic TraNscathetER Valves II Trial (Edwards Lifesciences), TranS-catheter Aortic Valve RepLacement System U.S. Feasibility Trial (Direct Flow Medical), and SAGE-547 Clinical Trial (SAGE therapeutics) for his work on those clinical trials. Dr. Ganger received funding from Abbvie, Gil-ead, and Merck. Dr. Naidech’s institution received funding from the Agency for Healthcare Research and Quality, K18 HS023437. Dr. Maas’ institution received funding from the NIH. The remaining authors have disclosed that they do not have any potential conflicts of interest. For information regarding this article, E-mail: [email protected] Publisher Copyright: Copyright © 2017 by the Society of Critical Care Medicine and Wolters Kluwer Health, Inc. All Rights Reserved.

PY - 2018/2

Y1 - 2018/2

N2 - Objectives: We sought to determine the effect of acute electrolyte and osmolar shifts on brain volume and neurologic function in patients with liver failure and severe hepatic encephalopathy. Design: Retrospective analysis of brain CT scans and clinical data. Setting: Tertiary care hospital ICUs. Patients: Patients with acute or acute-on-chronic liver failure and severe hepatic encephalopathy. Interventions: Clinically indicated CT scans and serum laboratory studies. Measurements and Main Results: Change in intracranial cerebrospinal fluid volume between sequential CT scans was measured as a biomarker of acute brain volume change. Corresponding changes in serum osmolality, chemistry measurements, and Glasgow Coma Scale were determined. Associations with cerebrospinal fluid volume change and Glasgow Coma Scale change for initial volume change assessments were identified by Spearman's correlations (rs) and regression models. Consistency of associations with repeated assessments was evaluated using generalized estimating equations. Forty patients were included. Median baseline osmolality was elevated (310 mOsm/Kg [296-321 mOsm/Kg]) whereas sodium was normal (137 mEq/L [134-142 mEq/L]). Median initial osmolality change was 9 mOsm/kg (5-17 mOsm/kg). Neuroimaging consistent with increased brain volume occurred in 27 initial assessments (68%). Cerebrospinal fluid volume change was more strongly correlated with osmolality (r = 0.70; p = 4 × 10-7) than sodium (r = 0.28; p = 0.08) change. Osmolality change was independently associated with Glasgow Coma Scale change (p = 1 × 10-5) and cerebrospinal fluid volume change (p = 2.7 × 10-5) in initial assessments and in generalized estimating equations using all 103 available assessments. Conclusions: Acute decline in osmolality was associated with brain swelling and neurologic deterioration in severe hepatic encephalopathy. Minimizing osmolality decline may avoid neurologic deterioration.

AB - Objectives: We sought to determine the effect of acute electrolyte and osmolar shifts on brain volume and neurologic function in patients with liver failure and severe hepatic encephalopathy. Design: Retrospective analysis of brain CT scans and clinical data. Setting: Tertiary care hospital ICUs. Patients: Patients with acute or acute-on-chronic liver failure and severe hepatic encephalopathy. Interventions: Clinically indicated CT scans and serum laboratory studies. Measurements and Main Results: Change in intracranial cerebrospinal fluid volume between sequential CT scans was measured as a biomarker of acute brain volume change. Corresponding changes in serum osmolality, chemistry measurements, and Glasgow Coma Scale were determined. Associations with cerebrospinal fluid volume change and Glasgow Coma Scale change for initial volume change assessments were identified by Spearman's correlations (rs) and regression models. Consistency of associations with repeated assessments was evaluated using generalized estimating equations. Forty patients were included. Median baseline osmolality was elevated (310 mOsm/Kg [296-321 mOsm/Kg]) whereas sodium was normal (137 mEq/L [134-142 mEq/L]). Median initial osmolality change was 9 mOsm/kg (5-17 mOsm/kg). Neuroimaging consistent with increased brain volume occurred in 27 initial assessments (68%). Cerebrospinal fluid volume change was more strongly correlated with osmolality (r = 0.70; p = 4 × 10-7) than sodium (r = 0.28; p = 0.08) change. Osmolality change was independently associated with Glasgow Coma Scale change (p = 1 × 10-5) and cerebrospinal fluid volume change (p = 2.7 × 10-5) in initial assessments and in generalized estimating equations using all 103 available assessments. Conclusions: Acute decline in osmolality was associated with brain swelling and neurologic deterioration in severe hepatic encephalopathy. Minimizing osmolality decline may avoid neurologic deterioration.

KW - Cerebral edema

KW - Coma

KW - Hepatic encephalopathy

KW - Liver failure

KW - Renal replacement therapy

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JO - Critical care medicine

JF - Critical care medicine

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ER -

Osmotic shifts, cerebral edema, and neurologic deterioration in severe hepatic encephalopathy

Abstract

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