THERAPEUTIC HYPOTHERMIA AND TEMPERATURE MANAGEMENT Volume 5, Number 1, 2015 ª Mary Ann Liebert, Inc. DOI: 10.1089/ther.2014.0026

Letter to the Editor

Reply to Target Temperature Management for Post-Cardiac Arrest Patients Hans Friberg, MD, PhD,1 Tobias Cronberg, MD, PhD,2 and Niklas Nielsen, MD, PhD 3

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trial, but other explanations, including baseline differences between the trials and random error, could be equally important. Thanks to active and contemporary critical care, including a high rate of early angiography (2 of 3 patients) and prolonged observation time, we reached a 47% good neurological outcome rate at 6 months even when patients with initial nonshockable rhythms were included. This is very much in line with registry outcome data in patients managed at 33C (Nielsen et al., 2009). In conclusion, according to the largest trial to date on temperature intervention after cardiac arrest, we could not detect any difference between targeting a temperature of 33C as compared to 36C, giving the clinician the option to choose either. The optimal temperature and duration of temperature management remain to be defined.

n a letter to the editor (Aibiki et al., 2014), potential bias in the Target Temperature Management after Out-ofHospital Cardiac Arrest Trial (TTM trial) is discussed (Nielsen et al., 2013). The authors suggest that imprecise temperature control, early withdrawal of therapy, and low rates of good neurological outcome have added major bias that could affect the interpretation of the results. We wish to address these issues one by one. First, a feedback-controlled cooling device (intravascular or surface) was mandatory in the TTM trial, and temperature was strictly and successfully controlled in both intervention arms (Wise et al., 2014). In the original article, we presented temperature data as mean – 2 standard deviations, which accounts for q95% of all measures observed (Nielsen et al., 2013), while median and interquartile range was used in the Hypothermia after Cardiac Arrest Study Group (HACA) trial (HACA, 2002). Second, unlike previous cardiac arrest trials, the TTM trial had a protocol for when and how assessment of neurological prognosis should be performed and a strict and transparent protocol for withdrawal of life-sustaining therapy (WLST) (Cronberg et al., 2013). To allow for delayed awakening, prognostication was postponed compared to current guidelines (Peberdy et al., 2010). Moreover, the clinician performing prognostication was blinded to temperature allocation to avoid bias. Assessment of neurological prognosis in comatose patients was performed at a median of 118 hours (5 days) after the arrest in the TTM trial. Importantly, assessment of neurological prognosis does not equal WLST as Aibiki and coauthors incorrectly assume. If the strict and predefined criteria for WLST were not fulfilled, active care continued. Assessment of neurological prognosis was performed in more patients in the 33C group, possibly due to lingering effects of sedation, but a recommendation to continue care was also more frequent in the 33C group (Nielsen et al., 2013). Recommendations on WLST were the same in both temperature arms. Last, regarding our outcome data, we believe that Figure 1 illustrates this best. Survival is presented from two previous trials (Bernard et al., 2002; HACA, 2002) and for the TTM trial (Nielsen et al., 2013), showing that outcome in the 33C group was the same in all three studies while the difference can be found in the ‘‘control arm.’’ This could possibly be because fever was avoided in the 36C group in the TTM

FIG. 1. Outcome (survival) in three trials (a–c) is presented with similar survival rates in the 33C group (lower bars) of all three trials. The difference is seen in the control arm (upper bars) with low survival rates in (a) the HACA trial (HACA, 2002) and (b) the Bernard et al.’s trial (Bernard et al., 2002), as compared to the ‘‘control arm’’ (36C group) of (c) the TTM trial (Nielsen et al., 2013). With permission from Dr. B.S. Abella.

Departments of 1Anesthesiology and Intensive Care and 2Neurology, Ska˚ne University Hospital, Lund University, Lund, Sweden. 3 Department of Anesthesiology and Intensive Care, Helsingborg Hospital, Lund University, Helsingborg, Sweden.

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LETTER TO THE EDITOR Author Disclosure Statement

No competing financial interests exist. References

Aibiki M, Iwata O, Nonogi H, Kinosita K, Nagao K, and the Board of Directors of the Japanese Association of Brain Hypothermia. Target temperature management for postcardiac arrest patients. Ther Hypothermia Temp Manag 2014;4:104. Bernard SA, Gray TW, Buist MD, et al. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med 2002;346:557–563. Cronberg T, Horn J, Kuiper MH, Friberg H, Nielsen N. A structured approach to neurologic prognostication in clinical cardiac arrest trials. Scand J Trauma Resusc Emerg Med 2013;21:45. Hypothermia after Cardiac Arrest Study Group (HACA). Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med 2002;346:549–556. Nielsen N, Hovdenes J, Rubertsson S, et al. Outcome, timing and adverse events in therapeutic hypothermia after out-of-

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hospital cardiac arrest—a report from the Hypothermia Network Registry. Acta Anaesthesiol Scand 2009;53:926–934. Nielsen N, Wetterslev J, Cronberg T, et al. Targeted temperature management at 33C versus 36C after cardiac arrest. N Engl J Med 2013;369:2197–2206. Peberdy MA, Callaway CW, Neumar RW, et al. Part 9: postcardiac arrest care: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation 2010;122:S768–S786. Wise M, Horn J, Aneman A, Nielsen N. Targeted temperature management after out-of-hospital cardiac arrest: certainties and uncertainties. Crit Care 2014;18:459.

Address correspondence to: Hans Friberg, MD, PhD Department of Anesthesiology and Intensive Care Ska˚ne University Hospital Lund University 221 85 Lund Sweden E-mail: [email protected]

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