Danilo Cardim1, Donald E Griesdale2, Philip N Ainslie3, Chiara Robba4, Leanne Calviello5, Marek Czosnyka6, Peter Smielewski5, Mypinder S Sekhon7. 1. Department of Anesthesiology, Pharmacology and Therapeutics, Vancouver General Hospital, The University of British Columbia, Vancouver, BC, Canada,. Electronic address: danilo.cardim@gmail.com. 2. Department of Anesthesiology, Pharmacology and Therapeutics, Vancouver General Hospital, The University of British Columbia, Vancouver, BC, Canada,; Division of Critical Care Medicine, Department of Medicine, Vancouver General Hospital, The University of British Columbia, Vancouver, BC, Canada,; Centre for Clinical Epidemiology and Evaluation, Vancouver Coastal Health Research Institute, The University of British Columbia, Vancouver, BC, Canada. 3. Department of Health and Exercise Sciences, The University of British Columbia - Okanagan, Kelowna, BC, Canada. 4. Anaesthesia and Intensive Care, IRCCS San Martino, Genova, Italy. 5. Brain Physics Laboratory, Division of Neurosurgery, Department of Clinical Neurosciences, University of Cambridge, United Kingdom. 6. Brain Physics Laboratory, Division of Neurosurgery, Department of Clinical Neurosciences, University of Cambridge, United Kingdom; Institute of Electronic Systems, Warsaw University of Technology, Poland. 7. Division of Critical Care Medicine, Department of Medicine, Vancouver General Hospital, The University of British Columbia, Vancouver, BC, Canada.
Abstract
AIM: Increased intracranial pressure (ICP) in hypoxic ischaemic brain injury (HIBI) can cause secondary ischaemic brain injury and culminate in brain death. Invasive ICP monitoring is limited by associated risks in HIBI patients. We sought to evaluate the agreement between invasive ICP measurements and non-invasive estimators of ICP (nICP) in HIBI patients. METHODS: Eligible consecutive adult (age>18) cardiac arrest patients with HIBI were included as part of a single centre prospective interventional study. Invasive ICP monitoring and nICP measurements were undertaken using: a) transcranial Doppler ultrasonography (TCD), b) optic nerve sheet diameter ultrasound (ONSD) and c) jugular venous bulb pressure (JVP). Multiple measurements applied in linear mixed-effects models were considered to obtain the correlation coefficient between ICP and nICP as well as their predictive abilities to detect intracranial hypertension (ICP≥20mm Hg). RESULTS: Eleven patients were included (median age of 47 [range 20-71], 8 males and 3 females). There was a linear relationship between ICP and nICP with ONSD (R=0.53 [p<0.0001]), JVP (R=0.38 [p<0.001]) and TCD (R=0.30 [p<0.01]). The ability to predict intracranial hypertension was highest for ONSD and TCD (area under the receiver operating curve (AUC)=0.96 [95% CI: 0.90-1.00] and AUC=0.91 [95% CI: 0.83-1.00], respectively). JVP presented the weakest prediction ability (AUC=0.75 [95% CI: 0.56-0.94]). CONCLUSIONS: ONSD and TCD methods demonstrated agreement with invasively-monitored ICP, suggesting their potential roles in the detection of intracranial hypertension in HIBI after cardiac arrest.
AIM: Increased intracranial pressure (ICP) in hypoxic ischaemic brain injury (HIBI) can cause secondary ischaemic brain injury and culminate in brain death. Invasive ICP monitoring is limited by associated risks in HIBI patients. We sought to evaluate the agreement between invasive ICP measurements and non-invasive estimators of ICP (nICP) in HIBI patients. METHODS: Eligible consecutive adult (age>18) cardiac arrestpatients with HIBI were included as part of a single centre prospective interventional study. Invasive ICP monitoring and nICP measurements were undertaken using: a) transcranial Doppler ultrasonography (TCD), b) optic nerve sheet diameter ultrasound (ONSD) and c) jugular venous bulb pressure (JVP). Multiple measurements applied in linear mixed-effects models were considered to obtain the correlation coefficient between ICP and nICP as well as their predictive abilities to detect intracranial hypertension (ICP≥20mm Hg). RESULTS: Eleven patients were included (median age of 47 [range 20-71], 8 males and 3 females). There was a linear relationship between ICP and nICP with ONSD (R=0.53 [p<0.0001]), JVP (R=0.38 [p<0.001]) and TCD (R=0.30 [p<0.01]). The ability to predict intracranial hypertension was highest for ONSD and TCD (area under the receiver operating curve (AUC)=0.96 [95% CI: 0.90-1.00] and AUC=0.91 [95% CI: 0.83-1.00], respectively). JVP presented the weakest prediction ability (AUC=0.75 [95% CI: 0.56-0.94]). CONCLUSIONS: ONSD and TCD methods demonstrated agreement with invasively-monitored ICP, suggesting their potential roles in the detection of intracranial hypertension in HIBI after cardiac arrest.
Authors: Chiara Robba; Alberto Goffi; Thomas Geeraerts; Danilo Cardim; Gabriele Via; Marek Czosnyka; Soojin Park; Aarti Sarwal; Llewellyn Padayachy; Frank Rasulo; Giuseppe Citerio Journal: Intensive Care Med Date: 2019-04-25 Impact factor: 17.440
Authors: Jennifer C Laws; Lori C Jordan; Lindsay M Pagano; John C Wellons; Michael S Wolf Journal: Pediatr Neurol Date: 2022-02-02 Impact factor: 3.372
Authors: Chiara Robba; Antonio Messina; Denise Battaglini; Lorenzo Ball; Iole Brunetti; Matteo Bassetti; Daniele R Giacobbe; Antonio Vena; Nicolo' Patroniti; Maurizio Cecconi; Basil F Matta; Xiuyun Liu; Patricia R M Rocco; Marek Czosnyka; Paolo Pelosi Journal: Front Neurol Date: 2021-06-16 Impact factor: 4.003