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Introduction Transcranial Doppler (TCD) is a bedside, low-cost, and non-invasive technique able to evaluate cerebral hemodynamics [1]; the implementation of transcranial color-coded duplex sonography (TCCS) aids in evaluating the brain anatomy and intracranial lesions [2], real-time monitoring of “basic” (flow velocity (FV) and pulsatility index (PI)) as well as “advanced” TCD-derived parameters (Table 1; Fig. 1). In practice, we use a 2-MHz probe, and most information is obtained by insonating the middle cerebral artery through the temporal window; other windows include the transorbital, occipital, and submandibular windows. TCCD has the advantage to provide a direct visualization of the cerebral anatomy vessels and allow angle correction to assess FV [2]. TCD/TCCD practice is part of the standard training in our institution, and examinations are routinely performed by the medical staff. Table 1 Common parameters derived from transcranial Doppler Full size table Fig. 1 figure1 Simplified algorithms on the use of TCD to assess intracranial hypertension, brain death, autoregulation, and cerebral vasospasm in clinical practice. PI, pulsatility index; Vd, diastolic flow velocity; Vm, mean flow velocity; Vs, systolic flow velocity; LR, Lindegaard ratio; CCA, cerebral circulatory arrest. *The three reported images represent reverberating flow (top), systolic pikes (middle), and no flow (bottom), respectively Full size image We discussed herein on how we use TCD in neuro-critically ill patients for hemodynamic indications; some of these proposals could also be used in non-brain injured critically ill patients at a high risk of cerebral complications.

Purpose To provide consensus, and a list of experts’ recommendations regarding the basic skills for head-to-toe ultrasonography in the intensive care setting. Methods The Executive Committee of the European Society of Intensive Care (ESICM) commissioned the project and supervised the methodology and structure of the consensus. We selected an international panel of 19 expert clinicians–researchers in intensive care unit (ICU) with expertise in critical care ultrasonography (US), plus a non-voting methodologist. The panel was divided into five subgroups (brain, lung, heart, abdomen and vascular ultrasound) which identified the domains and generated a list of questions to be addressed by the panel. A Delphi process based on an iterative approach was used to obtain the final consensus statements. Statements were classified as a strong recommendation (84% of agreement), weak recommendation (74% of agreement), and no recommendation (less than 74%), in favor or against. Results This consensus produced a total of 74 statements (7 for brain, 20 for lung, 20 for heart, 20 for abdomen, 7 for vascular Ultrasound). We obtained strong agreement in favor for 49 statements (66.2%), 8 weak in favor (10.8%), 3 weak against (4.1%), and no consensus in 14 cases (19.9%). In most cases when consensus was not obtained, it was felt that the skills were considered as too advanced. A research agenda and discussion on training programs were implemented from the results of the consensus. Conclusions This consensus provides guidance for the basic use of critical care US and paves the way for the development of training and research projects.

SummaryPurposeAlthough invasive intracranial devices (IIDs) are the gold standard for intracranial pressure (ICP) measurement, ultrasonography of the optic nerve sheath diameter (ONSD) has been suggested as a potential non-invasive ICP estimator. We performed a meta-analysis to evaluate the diagnostic accuracy of sonographic ONSD measurement for assessment of intracranial hypertension (IH) in adult patients.MethodsWe searched on electronic databases (MEDLINE/PubMed®, Scopus®, Web of Science®, ScienceDirect®, Cochrane Library®) until 31 May 2018 for comparative studies that evaluated the efficacy of sonographic ONSD vs. ICP measurement with IID. Data were extracted independently by two authors. We used the QUADAS-2 tool for assessing the risk of bias (RB) of each study. A diagnostic meta-analysis following the bivariate approach and random-effects model was performed.ResultsSeven prospective studies (320 patients) were evaluated for IH detection (assumed with ICP > 20 mmHg or > 25 cmH2O). The accuracy of included studies ranged from 0.811 (95% CI 0.678‒0.847) to 0.954 (95% CI 0.853‒0.983). Three studies were at high RB. No significant heterogeneity was found for the diagnostic odds ratio (DOR), positive likelihood ratio (PLR) and negative likelihood ratio (NLR), with I2 < 50% for each parameter. The pooled DOR, PLR and NLR were 67.5 (95% CI 29‒135), 5.35 (95% CI 3.76‒7.53) and 0.088 (95% CI 0.046‒0.152), respectively. The area under the hierarchical summary receiver-operating characteristic curve (AUHSROC) was 0.938. In the subset of five studies (275 patients) with IH defined for ICP > 20 mmHg, the pooled DOR, PLR and NLR were 68.10 (95% CI 26.8‒144), 5.18 (95% CI 3.59‒7.37) and 0.087 (95% CI 0.041‒0.158), respectively, while the AUHSROC was 0.932.ConclusionsAlthough the wide 95% CI in our pooled DOR suggests caution, ultrasonographic ONSD may be a potentially useful approach for assessing IH when IIDs are not indicated or available (CRD42018089137, PROSPERO).

Background Although placement of an intra-cerebral catheter remains the gold standard method for measuring intracranial pressure (ICP), several non-invasive techniques can provide useful estimates. The aim of this study was to compare the accuracy of four non-invasive methods to assess intracranial hypertension. Methods We reviewed prospectively collected data on adult intensive care unit (ICU) patients with traumatic brain injury (TBI), subarachnoid hemorrhage (SAH), or intracerebral hemorrhage (ICH) in whom invasive ICP monitoring had been initiated and estimates had been simultaneously collected from the following non-invasive indices: optic nerve sheath diameter (ONSD), pulsatility index (PI), estimated ICP (eICP) using transcranial Doppler, and the neurological pupil index (NPI) measured using automated pupillometry. Intracranial hypertension was defined as an invasively measured ICP > 20 mmHg. Results We studied 100 patients (TBI = 30; SAH = 47; ICH = 23) with a median age of 52 years. The median invasively measured ICP was 17 [12–25] mmHg and intracranial hypertension was present in 37 patients. Median values from the non-invasive techniques were ONSD 5.2 [4.8–5.8] mm, PI 1.1 [0.9–1.4], eICP 21 [14–29] mmHg, and NPI 4.2 [3.8–4.6]. There was a significant correlation between all the non-invasive techniques and invasive ICP (ONSD, r  = 0.54; PI, r  = 0.50; eICP, r  = 0.61; NPI, r  = − 0.41— p  < 0.001 for all). The area under the curve (AUC) to estimate intracranial hypertension was 0.78 [CIs = 0.68–0.88] for ONSD, 0.85 [95% CIs 0.77–0.93] for PI, 0.86 [95% CIs 0.77–0.93] for eICP, and 0.71 [95% CIs 0.60–0.82] for NPI. When the various techniques were combined, the highest AUC (0.91 [0.84–0.97]) was obtained with the combination of ONSD with eICP. Conclusions Non-invasive techniques are correlated with ICP and have an acceptable accuracy to estimate intracranial hypertension. The multimodal combination of ONSD and eICP may increase the accuracy to estimate the occurrence of intracranial hypertension.

Maintaining an adequate level of sedation and analgesia plays a key role in the management of traumatic brain injury (TBI). To date, it is unclear which drug or combination of drugs is most effective in achieving these goals. Ketamine is an agent with attractive pharmacological and pharmacokinetics characteristics. Current evidence shows that ketamine does not increase and may instead decrease intracranial pressure, and its safety profile makes it a reliable tool in the prehospital environment. In this point of view, we discuss different aspects of the use of ketamine in the acute phase of TBI, with its potential benefits and pitfalls.

Cardiac arrest (CA) is a major cause of morbidity and mortality frequently associated with neurological and systemic involvement. Supportive therapeutic strategies such as mechanical ventilation, hemodynamic settings, and temperature management have been implemented in the last decade in post-CA patients, aiming at protecting both the brain and the lungs and preventing systemic complications. A lung-protective ventilator strategy is currently the standard of care among critically ill patients since it demonstrated beneficial effects on mortality, ventilator-free days, and other clinical outcomes. The role of protective and personalized mechanical ventilation setting in patients without acute respiratory distress syndrome and after CA is becoming more evident. The individual effect of different parameters of lung-protective ventilation, including mechanical power as well as the optimal oxygen and carbon dioxide targets, on clinical outcomes is a matter of debate in post-CA patients. The management of hemodynamics and temperature in post-CA patients represents critical steps for obtaining clinical improvement. The aim of this review is to summarize and discuss current evidence on how to optimize mechanical ventilation in post-CA patients. We will provide ten tips and key insights to apply a lung-protective ventilator strategy in post-CA patients, considering the interplay between the lungs and other systems and organs, including the brain.

Early detection of cardiovascular dysfunctions directly caused by acute ischemic stroke (AIS) has become paramount. Researchers now generally agree on the existence of a bidirectional interaction between the brain and the heart. In support of this theory, AIS patients are extremely vulnerable to severe cardiac complications. Sympathetic hyperactivity, hypothalamic–pituitary–adrenal axis, the immune and inflammatory responses, and gut dysbiosis have been identified as the main pathological mechanisms involved in brain–heart axis dysregulation after AIS. Moreover, evidence has confirmed that the main causes of mortality after AIS include heart attack, congestive heart failure, hemodynamic instability, left ventricular systolic dysfunction, diastolic dysfunction, arrhythmias, electrocardiographic anomalies, and cardiac arrest, all of which are more or less associated with poor outcomes and death. Therefore, intensive care unit admission with continuous hemodynamic monitoring has been proposed as the standard of care for AIS patients at high risk for developing cardiovascular complications. Recent trials have also investigated possible therapies to prevent secondary cardiovascular accidents after AIS. Labetalol, nicardipine, and nitroprusside have been recommended for the control of hypertension during AIS, while beta blockers have been suggested both for preventing chronic remodeling and for treating arrhythmias. Additionally, electrolytic imbalances should be considered, and abnormal rhythms must be treated. Nevertheless, therapeutic targets remain challenging, and further investigations might be essential to complete this complex multi-disciplinary puzzle. This review aims to highlight the pathophysiological mechanisms implicated in the interaction between the brain and the heart and their clinical consequences in AIS patients, as well as to provide specific recommendations for cardiovascular management after AIS.

Most patients with ischaemic stroke are managed on the ward or in specialty stroke units, but a significant number requires higher-acuity care and, consequently, admission to the intensive care unit. Mechanical ventilation is frequently performed in these patients due to swallowing dysfunction and airway or respiratory system compromise. Experimental studies have focused on stroke-induced immunosuppression and brain-lung crosstalk, leading to increased pulmonary damage and inflammation, as well as reduced alveolar macrophage phagocytic capability, which may increase the risk of infection. Pulmonary complications, such as respiratory failure, pneumonia, pleural effusions, acute respiratory distress syndrome, lung oedema, and pulmonary embolism from venous thromboembolism, are common and found to be among the major causes of death in this group of patients. Furthermore, over the past two decades, tracheostomy use has increased among stroke patients, who can have unique indications for this procedure—depending on the location and type of stroke—when compared to the general population. However, the optimal mechanical ventilator strategy remains unclear in this population. Although a high tidal volume ( V T ) strategy has been used for many years, the latest evidence suggests that a protective ventilatory strategy ( V T  = 6–8 mL/kg predicted body weight, positive end-expiratory pressure and rescue recruitment manoeuvres) may also have a role in brain-damaged patients, including those with stroke. The aim of this narrative review is to explore the pathophysiology of brain-lung interactions after acute ischaemic stroke and the management of mechanical ventilation in these patients.