European Resuscitation Council Guidelines for Resuscitation ... - CPR

18 de 0ctubre de 2010 www.elsuapdetodos.com1240 J.P. Nolan et al. / Resuscitation 81 (2010) 1219–1276the use of induced hypothermia in comatose survivors of out-ofhospitalcardiac arrest caused by VF. One randomised trial 355 and apseudo-randomised trial 356 demonstrated improved neurologicaloutcome at hospital discharge or at 6 months in comatose patientsafter out-of-hospital VF cardiac arrest. Cooling was initiated withinminutes to hours after ROSC and a temperature range of 32–34 ◦ Cwas maintained for 12–24 h. Extrapolation of these data to othercardiac arrests (e.g., other initial rhythms, in-hospital arrests, paediatricpatients) seems reasonable but is supported by only lowerlevel data. 317,357–363The practical application of therapeutic hypothermia is dividedinto three phases: induction, maintenance, and rewarming. 364 Animaldata indicate that earlier cooling after ROSC produces betteroutcomes. 365 External and/or internal cooling techniques can beused to initiate cooling. An infusion of 30 ml kg −1 of 4 ◦ C saline orHartmann’s solution decreases core temperature by approximately1.5 ◦ C. Other methods of inducing and/or maintaining hypothermiainclude: simple ice packs and/or wet towels; cooling blankets orpads; water or air circulating blankets; water circulating gel-coatedpads; intravascular heat exchanger; and cardiopulmonary bypass.In the maintenance phase, a cooling method with effectivetemperature monitoring that avoids temperature fluctuations ispreferred. This is best achieved with external or internal coolingdevices that include continuous temperature feedback to achieve aset target temperature. Plasma electrolyte concentrations, effectiveintravascular volume and metabolic rate can change rapidly duringrewarming, as they do during cooling. Thus, rewarming must beachieved slowly: the optimal rate is not known, but the consensusis currently about 0.25–0.5 ◦ C of warming per hour. 362The well-recognised physiological effects of hypothermia needto be managed carefully. 364PrognosticationTwo-thirds of those dying after admission to ICU following outof-hospitalcardiac arrest die from neurological injury; this has beenshown both with 227 and without 305 therapeutic hypothermia. Aquarter of those dying after admission to ICU following in-hospitalcardiac arrest die from neurological injury. A means of predictingneurological outcome that can be applied to individual patientsimmediately after ROSC is required. Many studies have focused onprediction of poor long-term outcome (vegetative state or death),based on clinical or test findings that indicate irreversible braininjury, to enable clinicians to limit care or withdraw organ support.The implications of these prognostic tests are such that theyshould have 100% specificity or zero false positive rate (FPR), i.e.,proportion of individuals who eventually have a ‘good’ long-termoutcome despite the prediction of a poor outcome.Biochemical markersEvidence does not support the use of serum (e.g., neuronal specificenolase, S100 protein) or CSF biomarkers alone as predictorsof poor outcomes in comatose patients after cardiac arrest with orwithout treatment with therapeutic hypothermia (TH). Limitationsincluded small numbers of patients studied and/or inconsistency incut-off values for predicting poor outcome.Electrophysiological studiesNo electrophysiological study reliably predicts outcome of acomatose patient within the first 24 h after cardiac arrest. Ifsomatosensory evoked potentials (SSEP) are measured after 24 hin comatose cardiac arrest survivors not treated with therapeutichypothermia, bilateral absence of the N20 cortical response tomedian nerve stimulation predicts poor outcome (death or CPC 3or 4) with a FPR of 0.7% (95% CI: 0.1–3.7%). 376Imaging studiesMany imaging modalities (magnetic resonance imaging [MRI],computed tomography [CT], single photon emission computedtomography [SPECT], cerebral angiography, transcranialDoppler, nuclear medicine, near infra-red spectroscopy [NIRS])have been studied to determine their utility for predictionof outcome in adult cardiac arrest survivors. 15 There areno high-level studies that support the use of any imagingmodality to predict outcome of comatose cardiac arrest survivors.Impact of therapeutic hypothermia on prognosticationThere is inadequate evidence to recommend a specific approachto prognosticating poor outcome in post-cardiac arrest patientstreated with therapeutic hypothermia. There are no clinical neurologicalsigns, electrophysiological studies, biomarkers, or imagingmodalities that can reliably predict neurological outcome in thefirst 24 h after cardiac arrest. Based on limited available evidence,potentially reliable prognosticators of poor outcome in patientstreated with therapeutic hypothermia after cardiac arrest includebilateral absence of N20 peak on SSEP ≥24 h after cardiac arrest(FPR 0%, 95% CI 0–69%) and the absence of both corneal and pupillaryreflexes 3 or more days after cardiac arrest (FPR 0%, 95% CI0–48%). 368,377 Limited available evidence also suggests that a GlasgowMotor Score of 2 or less at 3 days post-ROSC (FPR 14% [95% CI3–44%]) 368 and the presence of status epilepticus (FPR of 7% [95%CI 1–25%] to 11.5% [95% CI 3–31%]) 378,379 are potentially unreliableprognosticators of poor outcome in post-cardiac arrest patientstreated with therapeutic hypothermia. Given the limited availableevidence, decisions to limit care should not be made based on theresults of a single prognostication tool.www.elsuapdetodos.comClinical examinationThere are no clinical neurological signs that predict poor outcome(Cerebral Performance Category [CPC] 3 or 4, or death)reliably less than 24 h after cardiac arrest. In adult patients whoare comatose after cardiac arrest, and who have not been treatedwith hypothermia and who do not have confounding factors (suchas hypotension, sedatives or muscle relaxants), the absence of bothpupillary light and corneal reflex at ≥72 h reliably predicts pooroutcome (FPR 0%; 95% CI 0–9%). 330 Absence of vestibulo-ocularreflexes at ≥24 h (FPR 0%; 95% CI 0–14%) 366,367 and a GCS motorscore of 2 or less at ≥72 h (FPR 5%; 95% CI 2–9%) 330 are less reliable.Other clinical signs, including myoclonus, are not recommendedfor predicting poor outcome. The presence of myoclonus status inadults is strongly associated with poor outcome, 329,330,368–370 butrare cases of good neurological recovery have been described andaccurate diagnosis is problematic. 371–375Organ donationSolid organs have been successfully transplanted after cardiacdeath. 380 This group of patients offers an untapped opportunityto increase the organ donor pool. Organ retrieval from non-heartbeating donors is classified as controlled or uncontrolled. 381 Controlleddonation occurs after planned withdrawal of treatmentfollowing non-survivable injuries/illnesses. Uncontrolled donationdescribes donation after a patient is brought in dead orwith on-going CPR that fails to restore a spontaneous circulation.Cardiac arrest centresThere is wide variability in survival among hospitals caringfor patients after resuscitation from cardiac arrest. 57–63 Thereis some low-level evidence that ICUs admitting more than 50