Cerebral Hemodynamics and Intracranial Compliance Impairment in Critically Ill COVID-19 Patients: A Pilot Study

Abstract

Introduction: One of the possible mechanisms by which the new coronavirus (SARS-Cov2) could induce brain damage is the impairment of cerebrovascular hemodynamics (CVH) and intracranial compliance (ICC) due to the elevation of intracranial pressure (ICP). The main objective of this study was to assess the presence of CVH and ICC alterations in patients with COVID-19 and evaluate their association with short-term clinical outcomes. Methods: Fifty consecutive critically ill COVID-19 patients were studied with transcranial Doppler (TCD) and non-invasive monitoring of ICC. Subjects were included upon ICU admission; CVH was evaluated using mean flow velocities in the middle cerebral arteries (mCBFV), pulsatility index (PI), and estimated cerebral perfusion pressure (eCPP), while ICC was assessed by using the P2/P1 ratio of the non-invasive ICP curve. A CVH/ICC score was computed using all these variables. The primary composite outcome was unsuccessful in weaning from respiratory support or death on day 7 (defined as UO). Results: At the first assessment (n = 50), only the P2/P1 ratio (median 1.20 [IQRs 1.00–1.28] vs. 1.00 [0.88–1.16]; p = 0.03) and eICP (14 [11–25] vs. 11 [7–15] mmHg; p = 0.01) were significantly higher among patients with an unfavorable outcome (UO) than others. Patients with UO had a significantly higher CVH/ICC score (9 [8–12] vs. 6 [5–7]; p < 0.001) than those with a favorable outcome; the area under the receiver operating curve (AUROC) for CVH/ICC score to predict UO was 0.86 (95% CIs 0.75–0.97); a score > 8.5 had 63 (46–77)% sensitivity and 87 (62–97)% specificity to predict UO. For those patients undergoing a second assessment (n = 29), after a median of 11 (5–31) days, all measured variables were similar between the two time-points. No differences in the measured variables between ICU non-survivors (n = 30) and survivors were observed. Conclusions: ICC impairment and CVH disturbances are often present in COVID-19 severe illness and could accurately predict an early poor outcome.

Intracranial Compliance Assessed by Intracranial Pressure Pulse Waveform

“…Likewise, Asgari et al [33], with another dedicated software program (MOCAIP, University of California at Los Angeles, Los Angeles, CA, USA), performed automated ICP peak analysis during cerebrovascular changes. However, the opportunity of a non-invasive bedside observation of ICC has been recently developed (B4C, São Carlos, Brazil) and was validated in children with hydrocephalus [34] and severe COVID-19 cases [35,36]. This system provides the ICPW in real time, with automated P2/P1 ratio calculation.…”

Noninvasive intracranial pressure waveforms for estimation of intracranial hypertension and outcome prediction in acute brain-injured patients

“…Critically ill patients with primary brain injury or with cerebral damage secondary to extra-cerebral diseases (i.e. acute liver failure, drug intoxication) are at risk of developing intracranial hypertension (IHT) [1], a life-threatening condition that, unless an invasive catheter to measure intracranial pressure (ICP) is placed for monitoring, may elapse unnoticed [2,3]. Nevertheless, ICP management based exclusively on prede ned thresholds may ignore the complexity of intracranial compliance (ICC) [4,5], which is in uenced by several intracranial (i.e.…”

Non-Invasive Multimodal Neuromonitoring in Non-Critically Ill Hospitalized Adult Patients With COVID-19: A Systematic Review and Meta-Analysis

“…In case of cerebral vasospasm, shunt, or micro-emboli, TCD may help to evaluate the constriction and patency of cerebral vessels ( 69 ). Similar to critically ill patients with COVID-19 ( 5 , 70 , 71 ), altered cerebral blood flow velocities, and vasomotor reactivity were detected by TCD in two studies in non-critically ill patients ( 4 , 34 ). This can be explained by various mechanisms: (1) respiratory failure with altered oxygen and carbon dioxide exchange that may have altered the cerebral vessels' diameter and autoregulation ( 72 – 74 ) (2) the use of non-invasive respiratory devices that may have increased intraabdominal and intrathoracic pressures ( 75 ), both of which may impair cerebral hemodynamics ( 76 ), and ( 3 ) the potential of inflammation and cytokines to have induced sympathetic over activity with changes in systemic and cerebral hemodynamic and cerebral autoregulation via vasogenic edema with an altered permeability of the blood-brain barrier ( 55 , 56 ).…”