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Prognostication in Comatose Patients Treated With Hypothermic TTM

Question Type:
Prognostic
Full Question:
Among adults with ROSC who are treated with hypothermia  (P), does does any clinical variable when abnormal (eg, clinical exam, EEG, somatosensory evoked potentials [SSEPs], imaging, other)  (I), compared with compared with any clinical variable when normal  (C), change Survival with Favorable neurological/functional outcome at discharge, 30 days, 60 days, 180 days AND/OR 1 year, Survival only at discharge, 30 days, 60 days, 180 days AND/OR 1 year (O)?
Consensus on Science:
Clinical Examination No study on clinical examination reported blinding of the treating team to the results of the index test. For the critical outcome of survival with unfavorable neurologic status or death at discharge, we identified very-low-quality evidence (downgraded for very serious risk of bias and imprecision) from 4 studies on corneal reflex, pupillary reflex, motor response, GCS, or myoclonus (295 patients).(Schefold 2009, 658; Fugate 2010, 907; Okada 2012, 734; Crepeau 2013, 339) For the critical outcome of survival with unfavorable neurologic status or death at 90 days, we identified very-low-quality evidence (downgraded for very serious risk of bias and very serious imprecision) from 5 studies on corneal reflex, pupillary reflex, motor response, brainstem reflexes, or myoclonus (388 patients).(Al Thenayan 2008, 1535; Bisschops 2011, 696; Samaniego 2011, 113; Rossetti 2012, 796; Oddo 2014, 1340) For the critical outcome of survival with unfavorable neurologic status or death at 180 days, we identified low- or very-low-quality evidence (downgraded for very serious risk of bias and serious or very serious imprecision) from 4 studies on corneal reflex, pupillary reflex, motor response, brainstem reflexes, or myoclonus (642 patients).(Rossetti 2010, 301; Cronberg 2011, 623; Bouwes 2012, 206; Legriel 2013, 343) Corneal Reflex. In patients who are comatose after resuscitation from cardiac arrest and are treated with TTM, bilaterally absent corneal reflexes at 72 to 120 hours from ROSC predicted poor outcome, with 2 (0–7)% FPR and 25 (18–32)% sensitivity(Fugate 2010, 907-914; Cronberg 2011, 623; Samaniego 2011, 113; Bouwes 2012, 63) (301 subjects; very-low-quality evidence). Pupillary Reflex. Bilaterally absent pupillary light reflexes (PLR) on hospital admission predicted poor outcome, with 32 (19–48)% FPR and 86 (71–95)% sensitivity(Choi 2012, 116; Okada 2012, 734) (86 patients; very-low-quality evidence). Bilaterally absent PLR at 72 to 108 hours from ROSC predicted poor outcome, with 1 (0–3)% FPR and 19 (14–25)% sensitivity(Fugate 2010, 907-914; Cronberg 2011, 623-630; Samaniego 2011, 113; Bouwes 2012, 206; Choi 2012, 116) (5 studies, 383 subjects; low-quality evidence downgraded for very serious bias). Motor Response to Pain. On hospital admission, bilaterally absent or extensor motor responses, corresponding to a motor score 1 or 2 (M1–2) of the GCS, predicted a poor outcome, with 53 (36–68)% FPR and 92 (75–99)% sensitivity(Okada 2012, 734-739) (66 patients; very-low-quality evidence). At 36 to 108 hours from ROSC, an M1–2 predicted a poor outcome, with 70 (65–74)% sensitivity and 10 (7–15)% FPR(Rossetti 2010, 301; Bisschops 2011, 696; Cronberg 2011, 623; Samaniego 2011, 113; Bouwes 2012, 206; Rossetti 2012, 796) (635 subjects; very-low-quality evidence). One study(Samaniego 2011, 113) indicated that both absent corneal reflexes and motor response to pain at 72 hours predicted poor outcome (CPC 4–5) more accurately in patients who did not receive any sedative drugs 12 hours or less before neurologic assessment than in those who did. Combination of Clinical Signs. Bilateral absence of 1 or more brainstem reflexes (pupillary, corneal, or oculocephalic) at 36 to 72 hours from arrest predicted a poor outcome, with 8 (4–14)% FPR and 56 (48–63)% sensitivity (3 studies; 304 patients; very-low-quality evidence).(Rossetti 2010, R173; Rossetti 2012, 796; Oddo 2014, 1340) In 1 study (103 subjects; very-low-quality evidence), the combined absence of corneal reflex, PLR, and M1–2 at 72 hours from ROSC predicted poor outcome, with 0 (0–8)% FPR and 15 (7–26)% sensitivity.(Bisschops 2011, 696) In that study, the index test was used as a criterion for withdrawal of life-sustaining treatment. A GCS of 4 or less at 96 hours from ROSC predicted poor outcome, with 5 (1–15)% FPR and 46 (28–66)% sensitivity(Schefold 2009, 658) (72 subjects; very-low-quality evidence). Myoclonus and Status Myoclonus. Presence of myoclonus within 72 hours from ROSC predicted a poor outcome, with 5 (3–8)% FPR and 39 (35–44)% sensitivity (6 studies,(Rossetti 2010, 301; Bouwes 2012, 206; Rossetti 2012, 796; Crepeau 2013, 339; Legriel 2013, 343; Oddo 2014, 1340) 845 subjects; very-low-quality evidence). In 1 study(Bisschops 2011, 696) (103 subjects; very-low-quality evidence), presence of myoclonus within 7 days after ROSC predicted poor outcome, with 11 (3–26)% FPR and 54 (41–66)% sensitivity. In 3 studies(Fugate 2010, 907; Samaniego 2011, 113; Rittenberger 2012, 114) (215 patients; low-quality evidence) presence of status myoclonus (defined as a continuous prolonged and generalized myoclonus) within 72 to 120 hours from ROSC predicted poor outcome, with 0 (0–4)% FPR and 16 (11–22)% sensitivity. However, reports of good neurologic recovery despite an early-onset, prolonged, and generalized myoclonus have been published.(Lucas 2012, 265; Accardo 2013, 872127; Greer 2013, e81; Legriel 2013, 343) In some of these cases,(Accardo 2013, 872127; Legriel 2013, 343) myoclonus persisted after awakening and evolved into a chronic action myoclonus (Lance-Adams syndrome). Electrophysiology Short-Latency SSEPs. For the critical outcome of survival with unfavorable neurologic status or death at discharge, we identified very-low-quality evidence (downgraded for very serious bias and very serious imprecision) from 8 studies on short-latency SSEPs, EEG, or Bispectral Index (BIS; 571 subjects).(Fugate 2010, 907; Leary 2010, 1133; Leithner 2010, 965; Choi 2012, 116; Mani 2012, 840; Rittenberger 2012, 114; Crepeau 2013, 339) For the critical outcome of survival with unfavorable neurologic status or death at 30 days, we identified 1 study on SSEPs (77 subjects; very-low-quality evidence, downgraded for serious bias and very serious imprecision).(Bouwes 2009, 1457) For the critical outcome of survival with unfavorable neurologic status or death at 60 days, we identified 1 study on brainstem auditory evoked potentials (26 subjects; very-low-quality evidence downgraded for serious bias and very serious imprecision).(Sakurai 2006, 52) For the critical outcome of survival with unfavorable neurologic status or death at 90 days, we identified 5 studies on SSEPs or EEG (362 subjects; low- or very-low-quality evidence, downgraded for serious or very serious bias and/or very serious imprecision).(Bisschops 2011, 696; Samaniego 2011, 113; Rossetti 2012, 796; Zanatta 2012, 749; Oddo 2014, 1340) For the critical outcome of survival with unfavorable neurologic status or death at 180 days, we identified 10 studies on SSEPs, EEG, or BIS (566 subjects; moderate-, low-, or very-low-quality evidence downgraded for serious or very serious bias and/or very serious imprecision).(Tiainen 2005, 1736; Stammet 2009, 437; Wennervirta 2009, 2427; Rossetti 2010, 301; Rundgren 2010, 1838; Cronberg 2011, 623; Kawai 2011, 483; Bouwes 2012, 206; Cloostermans 2012, 2867; Stammet 2013, 851) For the critical outcome of survival with unfavorable neurologic status or death at 1 year, we identified 1 study on EEG (106 subjects; very-low-quality evidence).(Legriel 2013, 343) In most prognostication studies, absence of the N20 wave after rewarming has been used—alone or in combination—as a criterion for deciding on withdrawal of life-sustaining treatment, with a consequent risk of self-fulfilling prophecy. In patients who are comatose after resuscitation from cardiac arrest and who are treated with TTM, a bilaterally absent N20 SSEP wave during TTM predicted poor outcome, with 2 (0–4)% FPR and 28 (22–34)% sensitivity(Tiainen 2005, 1736; Bouwes 2009, 1457; Bouwes 2012, 206; Cloostermans 2012, 2867) (424 subjects; moderate-quality evidence, downgraded for serious bias). A bilaterally absent N20 SSEP wave after rewarming predicted poor outcome, with 1 (0–3)% FPR (9 studies,(Leithner 2010, 965; Rossetti 2010, 301; Bisschops 2011, 696; Cronberg 2011, 623; Samaniego 2011, 113; Bouwes 2012, 206; Choi 2012, 116; Rossetti 2012, 796; Zanatta 2012, 749; Oddo 2014, 1340) 629 subjects; very-low-quality evidence downgraded for very serious bias and serious inconsistency) and 45 (41–50)% sensitivity. SSEP recording is prone to electrical interference. In 1 study,(Bouwes 2012, 206) 3 subjects with a bilaterally absent N20 during TTM rapidly recovered consciousness after rewarming and ultimately had a good outcome. In a post hoc assessment, 2 experienced neurophysiologists reviewed blindly the original tracings and concluded that the SSEP recordings were undeterminable because of excessive noise. EEG. Definitions of burst suppression were inconsistent among studies. Definitions of epileptiform activity, electrographic seizures, and SE were inconsistent among studies. Absence of Background Reactivity. Absence of background reactivity on the EEG recorded during TTM predicted poor outcome, with 2 (1–7)% FPR and 63 (54–72)% sensitivity (3 studies,(Rossetti 2012, 796; Crepeau 2013, 339; Oddo 2014, 1340) 249 subjects; very-low-quality evidence downgraded for very serious bias and serious imprecision). Absence of background reactivity on the EEG recorded after rewarming predicted poor outcome, with 0 (0–3)% FPR and 62 (53–70)% sensitivity (3 studies,(Rossetti 2010, 301; Rossetti 2012, 796; Crepeau 2013, 339) 223 subjects; very-low-quality evidence downgraded for very serious bias and serious imprecision). One group of investigators provided 3 of the 4 prognostication studies on absent EEG reactivity after cardiac arrest. Burst Suppression. Presence of burst suppression on initial EEG immediately after induction of TTM predicted poor outcome, with 0 (0–5)% FPR and 31 (19–44)% sensitivity (2 studies,(Rundgren 2010, 1838; Kawai 2011, 483) 119 subjects; very-low-quality evidence downgraded for very serious bias and serious inconsistency). Presence of burst suppression on EEG during TTM predicted poor outcome, with 6 (1–15)% FPR and 70 (56–82)% sensitivity (2 studies,(Cloostermans 2012, 2867; Rossetti 2012, 796) 107 patients; very-low-quality evidence downgraded for very serious bias, serious inconsistency, and very serious imprecision). In 1 study(Rundgren 2010, 1838) (95 subjects; very-low-quality evidence) presence of burst suppression on EEG after rewarming predicted poor outcome, with 0 (0–5)% FPR and 18 (8–34)% sensitivity. Epileptiform Activity. Presence of epileptiform discharges on EEG during TTM(Mani 2012, 840) (38 subjects) or after rewarming(Rossetti 2010, 301) (108 patients) predicted poor outcome, with 8 (0–39)% and 12 (3–31)% FPR, respectively. Quality of evidence was very low in both studies, downgraded for very serious bias and very serious imprecision. Presence of electrographic seizures with nonreactive EEG background during TTM(Rossetti 2012, 796) (61 patients), electrographic seizures during TTM(Mani 2012, 840) (38 subjects), or electrographic seizures both during TTM and after rewarming(Crepeau 2013, 339) (54 subjects) predicted poor outcome, with 0% FPR (95% CIs, 0–10, 0–22, and 0–9, respectively; very-low-quality evidence downgraded for very serious bias and serious or very serious imprecision). Presence of SE during TTM(Legriel 2009, 338) (51 subjects) or after rewarming(Wennervirta 2009, 2427) (30 subjects) predicted poor outcome, with 0% FPR (95% CIs, 0–22 and 0–13, respectively). However, in another study,(Legriel 2013, 343) the presence of an SE within 72 hours from ROSC was associated with good outcome in 2 cases (FPR 6 [1–21]%). In both those patients, SE was first recorded at 40 hours or greater from ROSC (shortly after rewarming), and the EEG was reactive (very-low-quality evidence, downgraded for serious or very serious bias and very serious imprecision). In 1 study(Rundgren 2010, 1838) (95 subjects), presence of electrographic SE on a burst suppression pattern was associated with an invariably poor outcome (CPC 4–5; FPR 0 [0–5]%), while an electrographic SE on a continuous background was still compatible with recovery of consciousness (FPR 4 [0–12]%; very-low-quality evidence downgraded for very serious bias and very serious imprecision). Flat or Low-Amplitude EEG. In 1 study(Cloostermans 2012, 2867) (46 subjects), a flat or low-amplitude (less than 20 mcV) EEG during TTM at 24 hours from cardiac arrest predicted poor outcome, with 0 (0–11)% FPR and 40 (19–64)% sensitivity. In another study(Rundgren 2010, 1838-1844) (95 subjects), however, a flat (less than 10 mcV) EEG recorded during TTM at a median of 8 hours from cardiac arrest or immediately after rewarming was followed by recovery of consciousness (FPR 46 [32–59]% and 5 [1–15]%, respectively; very-low-quality evidence downgraded for serious or very serious bias and very serious imprecision). Bispectral Index. In 1 study(Stammet 2009, 437) (45 subjects), a lowest BIS value of 0 during TTM, corresponding to a flat or low-amplitude EEG, predicted a poor outcome, with 0 (0–6)% FPR and 50 (31–69)% sensitivity. However, in another study(Stammet 2013, 851-858) (75 subjects), a lowest BIS value of 0 during TTM predicted poor outcome, with 10 (3–23)% FPR. The quality of evidence was very low (downgraded for very serious bias and very serious imprecision). EEG Grades. In 1 study(Crepeau 2013, 339) (54 subjects; very-low-quality evidence), a grade 3 EEG, corresponding to 1 pattern among unreactive, burst suppression, focal or generalized seizures, generalized periodic epileptiform discharges, SE, low amplitude (10 mcV or less), or alpha-theta coma, predicted poor outcome, with 6 (1–20)% FPR during TH and 0 (0–9)% FPR after rewarming. Other Neurophysiological Tests. In 1 study(Sakurai 2006, 52) (26 subjects; very-low-quality evidence), absence of brainstem auditory evoked potentials wave V during induction of TTM predicted poor outcome, with 0 (0–31)% FPR and 56 (31–78)% sensitivity. In 1 pilot study(Zanatta 2012, 749) (17 subjects; very-low-quality evidence), the bilateral absence of pain-related middle-latency cortical evoked potentials predicted poor outcome, with 0 (0–53)% FPR and 85 (55–98)% sensitivity. Blood and Cerebrospinal Fluid Markers Blood marker thresholds vary because of heterogeneous measurement techniques,(Bloomfield 2007, 121; Stern 2007, 84; Rundgren 2014, 726) the presence of extraneuronal sources of biomarkers (hemolysis, non–central nervous system sources, and neuroendocrine tumors for neuron-specific enolase (NSE),(Johnsson 2000, 750) muscle and adipose tissue breakdown for S100B,(Anderson 2001, 1255) and the incomplete knowledge of the kinetics of their blood concentrations in the first few days after ROSC. For the critical outcome of survival with unfavorable neurologic status or death at discharge, we identified 4 studies on NSE (354 subjects; low- or very-low-quality evidence downgraded for serious or very serious bias and very serious imprecision).(Fugate 2010, 907; Steffen 2010, R69; Storm 2012, 6; Lee 2013, 1387) For the critical outcome of survival with unfavorable neurologic status or death at 60 days, we identified 1 study on NSE (73 subjects; very-low-quality evidence).(Huntgeburth 2014, 358) For the critical outcome of survival with unfavorable neurologic status or death at 90 days, we identified 3 studies on NSE (248 patients, very-low-quality evidence downgraded for serious or very serious bias and very serious imprecision).(Samaniego 2011, 113; Rossetti 2012, 796; Oddo 2014, 1340) For the critical outcome of survival with unfavorable neurologic status or death at 180 days, we identified 8 studies on NSE or S100B (810 patients; moderate-, low-, or very-low-quality evidence, downgraded for serious or very serious bias and/or serious or very serious imprecision).(Tiainen 2003, 2881; Oksanen 2009, 165; Wennervirta 2009, 2427; Cronberg 2011, 623; Mortberg 2011, 26; Bouwes 2012, 206; Stammet 2013, 851; Zellner 2013, 1382) NSE. In comatose resuscitated patients who are treated with TTM, the threshold for prediction of poor outcome with 0% FPR varied between 49.6 mcg/L and 151.4 mcg/L at 24 hours from ROSC(Tiainen 2003, 2881; Oksanen 2009, 165; Wennervirta 2009, 2427; Kim 2012, 412) (309 subjects; very-low-quality evidence, downgraded for serious or very serious bias and very serious imprecision), between 25 mcg/L and 151.5 mcg/L at 48 hours(Tiainen 2003, 2881; Oksanen 2009, 165; Wennervirta 2009, 2427; Cronberg 2011, 623; Kim 2012, 412; Storm 2012, 6; Lee 2013, 1387; Zellner 2013, 1382; Huntgeburth 2014, 358) (10 studies, 919 subjects; moderate- to very-low-quality evidence downgraded for serious or very serious bias and very serious imprecision), and between 57.2 mcg/L and 78.9 mcg/L at 72 hours(Steffen 2010, R69; Storm 2012, 6; Huntgeburth 2014, 358) (193 subjects; low- or very-low-quality evidence). Limited evidence(Oksanen 2009, 165; Rundgren 2009, 784; Huntgeburth 2014, 358) suggests that not only the NSE absolute concentrations but also their trends over time may have predictive value. Limited evidence(Oksanen 2009, 165-170; Rundgren 2009, 784-789) suggests that the discriminative value of NSE levels at 48 to 72 hours is higher than at 24 hours. S100B. For S100B, the documented thresholds for a 0% FPR were 0.18 and 0.21 mcg/L at 24 hours after ROSC(Tiainen 2003, 2881; Mortberg 2011, 26) (2 studies, total 66 subjects; very-low-quality evidence downgraded for serious or very serious bias and very serious imprecision) and 0.3 mcg/L at 48 hours (1 study, 75 subjects; very-low-quality evidence downgraded for serious or very serious bias and very serious imprecision). Imaging All studies on prognostication after cardiac arrest using imaging have a small sample size with a consequent low precision and are prone to selection bias, because the imaging studies were performed at discretion of treating physician, which may have caused a selection bias and overestimated their performance. Imaging studies depend partly on subjective human decision in identifying the region of interest to be studied and in the interpretation of results. For the critical outcome of survival with unfavorable neurologic status or death at discharge, we identified 3 studies on computed tomography (CT; 273 subjects; low- or very-low-quality evidence downgraded for serious or very serious bias and serious or very serious imprecision).(Fugate 2010, 907; Kim 2013, 57; Lee 2013, 1387) For the critical outcome of survival with unfavorable neurologic status or death at 180 days, we identified 6 studies on CT or magnetic resonance imaging (MRI; 246 subjects; very-low-quality evidence downgraded for serious or very serious bias and very serious imprecision).(Wijman 2009, 394; Inamasu 2010, 534; Mlynash 2010, 1665; Cronberg 2011, 623; Kim 2012, 412; Kim 2013, 1393) CT Scan. The main CT finding of global anoxic-ischemic cerebral insult after cardiac arrest is cerebral edema,(Morimoto 1993, 104) which appears as a reduction in the depth of cerebral sulci (sulcal effacement) and an attenuation of the gray matter/white matter (GM/WM) interface, due to a decreased density of the GM. This attenuation has been quantitatively measured as the ratio (GWR) between the GM and the WM densities. In 4 studies(Inamasu 2010, 534; Choi 2012, 116; Kim 2013, 57; Lee 2013, 1387) (total 276 subjects; low- or very-low-quality evidence downgraded for serious or very serious bias and very serious imprecision), a reduced GWR at the level of the basal ganglia on brain CT performed within 2 hours from ROSC predicted an almost invariably poor outcome (FPR from 0% to 8%). Measurement techniques and thresholds for GWR varied among studies. In 1 study(Fugate 2010, 907) (102 subjects; low-quality evidence downgraded for serious bias and serious imprecision), a global cerebral edema on brain CT at a median of 1 day after cardiac arrest predicted poor outcome, with 0 (0–5)% FPR. MRI. The main MRI finding of anoxic-ischemic cerebral injury is a hyperintensity in diffusion weighted imaging (DWI) sequences due to cytotoxic edema. Presence of DWI abnormalities in cortex or basal ganglia (1 study, 21 subjects; very-low-quality evidence) or both (2 studies, 30 subjects; very-low-quality evidence) between 2 and 6 days from ROSC was associated with poor outcome (FPR, 0%–9%). Precision of prediction, however, was very low, due to the small size of these studies. Postischemic DWI abnormalities can be quantified using apparent diffusion coefficient (ADC). ADC values between 700 and 800×10−6 mm2/s are considered normal. In 1 study(Wijman 2009, 394) (22 subjects; very-low-quality evidence downgraded for very serious bias and very serious imprecision), presence of more than 10% of brain volume with ADC less than 650×10−6 mm2/s predicted poor outcome, with 0 (0–28)% specificity. In another study,(Kim 2012, 412) a low ADC at the level of putamen, thalamus, or occipital cortex also predicted poor outcome, with 0% FPR (95% CIs, 0–24%). The ADC thresholds varied according to the brain area studied.
Treatment Recommendation:
We suggest against the use of clinical criteria alone before 72 hours after ROSC to estimate prognosis (weak recommendation, low-quality evidence). We suggest that multiple modalities of testing (clinical exam, neurophysiological measures, imaging, or blood markers) be used to estimate prognosis instead of relying on single tests or findings (weak recommendation, low-quality evidence). Clinical Examination We recommend using bilaterally absent PLRs or the combined absence of both pupillary and corneal reflexes at least 72 hours after ROSC to predict poor outcome in patients who are comatose after resuscitation from cardiac arrest and who are treated with TTM (strong recommendation, low-quality evidence). We suggest against using an absent (M1) or extensor motor response to pain (M2) alone to predict poor outcome, given its high FPR. However, due to its high sensitivity, this sign may be used to identify the population with poor neurologic status needing prognostication or to predict poor outcome in combination with other more robust predictors (weak recommendation, very low-quality evidence). We suggest against the use of myoclonus during the first 72 hours from ROSC as a predictor for prognosticating a poor neurologic outcome (weak recommendation, low-quality evidence). We suggest that the presence of a status myoclonus during the first 72 hours from ROSC be considered at 72 hours after ROSC (in combination with other factors) as a predictor for prognosticating a poor neurologic outcome (weak recommendation, low-quality evidence). We suggest prolonging the observation of clinical signs when interference from residual sedation or paralysis is suspected, so that the possibility of obtaining false-positive results is minimized. We recommend that the earliest time to prognosticate a poor neurologic outcome is 72 hours after ROSC, and should be extended longer if the residual effect of sedation and/or paralysis confounds the clinical examination (weak recommendation, low-quality evidence). Electrophysiology We recommend using bilateral absence of N20 SSEP wave measured at least 72 hours after ROSC to predict poor outcome in patients who are comatose after resuscitation from cardiac arrest and who are treated with TTM (strong recommendation, low-quality evidence). SSEP recording requires appropriate skills and experience, and utmost care should be taken to avoid electrical interference from muscle artifacts or from the ICU environment, as well as confounding drugs. This test is only ordered in the appropriate clinical context. We suggest using persistent absence of EEG reactivity to external stimuli at 72 hours or longer after ROSC (weak recommendation, low-quality evidence), presence of persistent burst suppression after rewarming, or intractable and persistent SE (weak recommendation, very-low-quality evidence) to predict poor outcome in patients who are comatose after resuscitation from cardiac arrest and who are treated with TTM. We recommend against using BIS to predict poor outcome during TTM in patients who are comatose after resuscitation from cardiac arrest and are treated with TTM (strong recommendation, very-low-quality evidence). Blood Markers We suggest using utmost care and preferably sampling at multiple serial time points (24–72 hours) when assessing NSE, to avoid false-positive results due to hemolysis (weak recommendation, very-low-quality evidence). We suggest using serial high-serum values of NSE at 48 to 72 hours from ROSC in combination with other predictors for predicting poor neurologic outcome in patients who are comatose after cardiac arrest and who are treated with TTM (weak recommendation, very-low-quality evidence). However, no threshold-enabling prediction with 0 FPR can be recommended, and NSE levels are insufficiently specific to be used alone for estimating prognosis. Imaging We suggest using brain imaging studies for prognostication only in centers where specific experience is available (weak recommendation, very-low-quality evidence). We suggest using the presence of a marked reduction of the GM/WM ratio on brain CT within 2 hours after ROSC or the presence of extensive diffusion restriction on brain MRI at 2 to 6 days after ROSC in combination with other predictors for prognosticating a poor neurologic outcome in patients who are comatose after cardiac arrest and who are treated with TTM (weak recommendation, very-low-quality evidence). Early imaging markers of poor prognosis should not prevent support for a sufficient period of time to observe other clinical features, although some extreme CT scan findings are consistent with herniation and brain death.
CoSTR Attachments:
COSTR Draft Prognostication in Hypothermia 2015-3.pdf    
Evidence Profile Table 3a TH.pdf    
Evidence Profiles Table 3b TH.pdf    
Evidence Profiles Table 3c TH.pdf    
Evidence Profiles Table 3d TH.pdf    
Sandroni Hypothermia TH plenary and TF.pdf    

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