LETTER TO THE EDITOR


https://doi.org/10.5005/jp-journals-10071-24581
Indian Journal of Critical Care Medicine
Volume 28 | Issue 2 | Year 2024

Hemodynamics: Strangers to Lung-kidney Crosstalk in ARDS?


Rohan Magoon1https://orcid.org/0000-0003-4633-8851, Anupama Gill Sharma2https://orcid.org/0000-0002-5364-7348, Nidhi Yadav3https://orcid.org/0000-0003-3186-5712, Nang Sujali Choupoo4https://orcid.org/0000-0001-6270-3981

1–4Department of Anaesthesia, Atal Bihari Vajpayee Institute of Medical Sciences and Dr. Ram Manohar Lohia Hospital, New Delhi, India

Corresponding Author: Nang Sujali Choupoo, Department of Anaesthesia, Atal Bihari Vajpayee Institute of Medical Sciences and Dr. Ram Manohar Lohia Hospital, New Delhi, India, Phone: +91 9711128628, e-mail: sujalichoupoo@yahoo.com

How to cite this article: Magoon R, Sharma AG, Yadav N, Choupoo NS. Hemodynamics: Strangers to Lung-kidney Crosstalk in ARDS? Indian J Crit Care Med 2024;28(2):177–178.

Source of support: Nil

Conflict of interest: None

Keywords: Acute kidney injury, Acute respiratory distress syndrome, Hemodynamic, Lung-kidney crosstalk, Vasopressors.

Dear Editor,

Todur et al. are applauded for their prospective observational study outlining lung-kidney crosstalk as an important determinant of acute kidney injury (AKI) prognosis in a cohort of acute respiratory distress syndrome (ARDS) patients on invasive mechanical ventilation (IMV).1 The authors’ demonstration of the role of driving pressure, oxygenation, and nutritional evaluation (DRONE) score in predicting non-resolving (subphenotype 2) AKI is noteworthy, but there do exist other facets of the research subject necessitating deliberation.1

Talking of the extrapulmonary consequences of ARDS, poor lung compliance is expected to lead to a reduction in the cardiac output, primarily owing to elevated intrathoracic pressures. Hence, hemodynamics per se is far from being strangers to the lung-kidney crosstalk featured in the Todur et al. research.1 Appropriate to the context, one misses an account of the systemic blood pressure targets and/or vasopressor-inotropic management in the index study. After the assessment of the cumulative data from 31 diverse studies involving a total of 5,04,535 critically ill patients, Cartin-Ceba et al. associate vasopressor-inotrope use with an accentuated risk of AKI, on separate random-effects meta-analysis (odds ratio: 4.52; 95% confidence interval: 2.03, 10.05; I2 = 92%).2 Meanwhile the value of I2 for the parameter over 75% bespeaks the prevailing inter-study heterogeneity, specific literature on AKI in ARDS deserves concurrent mention.2,3 In a study including 57 patients with severe ARDS due to influenza A (H1N1) pdm09 virus (pH1N1), Tignanelli et al. link vasopresssor use and duration with the need for continuous renal replacement therapy (CRRT). Out of 77% (44/57) patients on vasopressor support in their setting, those on CRRT have received vasopressors more often than those not requiring CRRT (89% vs 53%, p = 0.008) and received vasopressors for a longer duration as well (mean ± standard deviation, 10 ± 10.2 vs 1.9 ± 2.4 days, p = 0.003).3

Moreover, the nature of the vasopressor regimen (catecholamine or catecholamine-sparing) is equally relevant. With recent primary and post-hoc analytical literature (VANISH, VANCS, and ATHOS-3 randomized controlled trials) focusing on differences between the potential renal impact of norepinephrine with vasopressin in septic shock, the importance of reporting the vasopressor practices in observational studies akin to Todur et al. can indeed not be undermined.1,4 Of further note, the authors utilized the respective highest and the lowest 48 hours values of driving pressure and PaO2/FiO2 on IMV, to compute the corresponding DRONE score while following up the serum creatinine trajectories of their patients till day 5 for AKI-subphenotype characterization, where the vasopressor-inotrope support would have also classified as a peculiarly dynamic parameter of prognostic importance.1 To that end, it is only for the acknowledgement of the upcoming role of vasopressor quantification employing scoring systems norepinephrine equivalents (NEE), vasoactive-inotropic score (VIS), and cumulative vasopressor index), that the novel models like the MAVIC (mechanical ventilation, acute physiology and chronic health evaluation-III, vasopressors, inotropes, Charlson comorbidity index) are captivating enhanced attention for risk stratification in critical care.5

ORCID

Rohan Magoon https://orcid.org/0000-0003-4633-8851

Anupama Gill Sharma https://orcid.org/0000-0002-5364-7348

Nidhi Yadav https://orcid.org/0000-0003-3186-5712

Nang Sujali Choupoo https://orcid.org/0000-0001-6270-3981

REFERENCES

1. Todur P, Nileshwar A, Chaudhuri S, Srinivas T. Incidence, outcomes, and predictors of subphenotypes of acute kidney injury among acute respiratory distress syndrome patients: A prospective observational study. Indian J Crit Care Med 2023;27(10):724–731. DOI: 10.5005/jp-journals-10071-24553.

2. Cartin-Ceba R, Kashiouris M, Plataki M, Kor DJ, Gajic O, Casey ET. Risk factors for development of acute kidney injury in critically ill patients: A systematic review and meta-analysis of observational studies. Crit Care Res Pract 2012;2012:691013. DOI: 10.1155/2012/691013.

3. Tignanelli CJ, Wiktor AJ, Vatsaas CJ, Sachdev G, Heung M, Park PK, et al. Outcomes of acute kidney injury in patients with severe ARDS due to influenza A(H1N1) pdm09 virus. Am J Crit Care 2018;27(1):67–73. DOI: 10.4037/ajcc2018901.

4. Pickkers P, Darmon M, Hoste E, Joannidis M, Legrand M, Ostermann M, et al. Acute kidney injury in the critically ill: An updated review on pathophysiology and management. Intensive Care Med 2021;47(8):835–850. DOI: 10.1007/s00134-021-06454-7.

5. Vallabhajosyula S, Jentzer JC, Kotecha AA, Murphree DH Jr, Barreto EF, Khanna AK, et al. Development and performance of a novel vasopressor-driven mortality prediction model in septic shock. Ann Intensive Care 2018;8(1):112. DOI: 10.1186/s13613-018-0459-6.

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