Prognostication after cardiac arrest

Sandroni et al. Critical Care (2018) 22:150 https://doi.org/10.1186/s13054-018-2060-7 REVIEW Open Access Prognostication after cardiac arrest Claudio Sandroni1* , Sonia D’Arrigo1 and Jerry P. Nolan2,3 Abstract Hypoxic–ischaemic brain injury (HIBI) is the main cause of death in patients who are comatose after resuscitation from cardiac arrest. A poor neurological outcome—defined as death from neurological cause, persistent vegetative state, or severe neurological disability—can be predicted in these patients by assessing the severity of HIBI. The most commonly used indicators of severe HIBI include bilateral absence of corneal and pupillary reflexes, bilateral absence of N2O waves of short-latency somatosensory evoked potentials, high blood concentrations of neuron specific enolase, unfavourable patterns on electroencephalogram, and signs of diffuse HIBI on computed tomography or magnetic resonance imaging of the brain. Current guidelines recommend performing prognostication no earlier than 72 h after return of spontaneous circulation in all comatose patients with an absent or extensor motor response to pain, after having excluded confounders such as residual sedation that may interfere with clinical examination. A multimodal approach combining multiple prognostication tests is recommended so that the risk of a falsely pessimistic prediction is minimised. Keywords: Cardiac arrest, Coma, Prognosis, Hypoxic brain damage Background About 80% of patients who are admitted to an intensive care unit (ICU) after resuscitation from out-of-hospital cardiac arrest (OHCA) are comatose [1] and two thirds of them will die because of hypoxic–ischaemic brain injury (HIBI) [2, 3]. Severe HIBI causes delayed neuronal death [4–6] and diffuse brain oedema [7, 8]. However, only a minority of these deaths occur as a direct consequence of massive neuronal injury (i.e. from brain death) [9]. In fact, * Correspondence: 1 Istituto Anestesiologia e Rianimazione Università Cattolica del Sacro Cuore, Fondazione Policlinico Universitario “Agostino Gemelli, Largo Francesco Vito 1, 00168 Rome, Italy Full list of author information is available at the end of the article most deaths caused by HIBI result from withdrawal of life-sustaining treatment (WLST) following prognostication of a poor neurological outcome [10, 11]. To avoid premature WLST in patients with a chance of neurological recovery, the risk of a falsely pessimistic prediction should be kept to a minimum. In other words, when predicting a poor neurological outcome, the false positive rate (FPR) (i.e. the ratio between the number of patients with a falsely pessimistic prediction divided by the number of patients with good neurological outcome) of the index used should ideally be zero, or their specificity should be 100%. However, even the most robust neurological predictors are not 100% specific; for this reason, the current guidelines [12, 13] recommend using a combination of predictors. These may include clinical neurological examination, electrophysiological investigations (electroencephalogram (EEG) and short-latency somatosensory evoked potentials (SSEP)), serum biomarkers, and neuroimaging. The characteristics of these categories of predictors are discussed in this article. The aims of the present review are to summarise the current knowledge on the prediction of neurological outcome in patients who are comatose after CA and to provide practical recommendations on how to perform an accurate neuroprognostication in these patients. What represents a poor neurological outcome? The most commonly used measure for reporting neurological outcome after CA is represented by Cerebral Performance Categories (CPCs) [14]. CPC 1 corresponds to the best possible outcome (no or minor disabilities) while CPC 5 corresponds to death (Table 1). The CPC was adapted from the Glasgow Outcome Scale (GOS) for traumatic head injury. The GOS scores correspond to those of the CPCs in inverse order; that is, GOS 1 corresponds to CPC 5 and vice versa. Despite its simplicity and widespread use, the CPC has been criticised for being too focused on mental function and less informative about body functions, activity, and participation [15], which may explain the reported lack of agreement between the CPC and subjective quality of life measures [16]. Alternatives to the CPC include the modified Rankin Scale (mRS) [17], which © The Author(s). 2018 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. Sandroni et al. Critical Care (2018) 22:150 Page 2 of 9 Table 1 Cerebral Performance Categories (CPCs) and Glasgow Outcome Scale (GOS) CPC GOS Disability Conscious Independent Features 1 5 No, or minor Yes Yes Able to work and lead a normal life. May have mild dysphasia, non-incapacitating hemiparesis, or minor cranial nerve abnormalities 2 4 Moderate Yes Yes Able to travel by public transport and work in sheltered environment Independent in activities of daily life. May have hemiplegia, seizures, ataxia, dysarthria, or memory changes 3 3 Severe Yes No Limited cognition, dementia, locked-in, minimally conscious. Usually in institution, but it may be looked after at home with exceptional family effort 4 2 Unconscious No No Persistent vegetative state 5 1 Dead – – Certified brain dead or dead by traditional criteria includes a 7-point scale ranging from 0 (no symptoms) to 6 (death), and the extended GOS (GOSE) [18]. The GOSE categories range from 1 (death) to 8 (upper good recovery) and include important information such as independence at home and outside home, work capacity, social activities, and return to normal life. All of these scales have limitations and none has been specifically designed to describe the outcome after global HIBI. For clarity and for statistical purposes, in neuroprognostication studies the neurological outcome is generally dichotomised as ‘good’ or ‘poor’. However, there is no definite consensus on what represents a poor neurological outcome. Up to 2006, the majority of neuroprognostication studies defined poor outcome as CPC 4–5 (vegetative state or death) and a good outcome as CPC 1–3 (good neurological outcome and moderate to severe neurological disability). In the last 10 years, however, most studies included severe neurological disability (CPC 3) among the poor outcomes [19] (Fig. 1). This reflects different values and preferences in relation to neurological status after CA (...truncated)