We report our experience of therapeutic cooling in comatose survivors at our academically affiliated community-based Veterans Affairs medical center. We show that it is possible to implement such a cooling protocol in this setting where the majority of arrests occurred in hospital. Of the patients who completed the therapeutic hypothermia protocol, 63% (5 of 8) had a favorable neurologic outcome at the time of hospital discharge. Although this is a small sample size, this rate is similar to those reported in the original trials (49% and 55%) [11
] and in subsequent series [20
]. This percentage of favorable outcomes is also consistent with larger registries that have noted that 60 to 85% of patients who survive in-hospital arrests tend to have a favorable neurologic outcome [2
In terms of the initiation of the cooling protocol from time of ROSC, our average of 3.7 hours is comparable to another series from a community hospital [20
] and the average time to goal temperature of 8.8 hours was also comparable to previous reports, which ranged from 5.0 to 9.2 hours [15
]. Given that most of the arrests were in-hospital, it would be hoped that time to initiation would be even shorter. However, there was no association with time from ROSC to initiation of protocol or time to goal temperature and CPC score at discharge, although the small sample size likely contributed to the lack of statistical significance.
In comparing the survivors of cardiac arrest, there was a significantly faster ROSC in the cases where the survivor was not in a coma afterwards. Although this data was not available in all cases, faster return of circulating rhythm was also associated with higher probability for favorable CPC given that more patients who were not in a coma were neurologically intact at discharge and at six months compared to the patients who were comatose. Although these noncomatose survivors were similar in age and comorbidities, and had high rates of initial PEA or asystole during arrest compared to the comatose survivors, there was a trend towards a higher proportion of primary cardiac etiologies (P = 0.07). Similarly, only one patient out of 18 arrests in the noncooled comatose survivor group was treated with electrical cardioversion, compared to more than 25% of the arrests in the noncomatose and cooled comatose survivor groups, suggesting increased evolution of rhythm to ventricular fibrillation or tachycardia in these latter arrests. Thus, there were some differences in the baseline characteristics in these patient groups which likely affected the duration of arrest. This also meant that, as expected, patients with longer periods of impaired cerebral perfusion were more likely to become comatose.
We should also point out that, within this sample, 38 patients did not survive the arrest itself and overall 65 patients (65%) died before hospital discharge. This rate is higher than reported in previous registries of in-hospital cardiac arrest [1
] and may be related to the large majority of patients having an initial rhythm at time of arrest of PEA or asystole (94% overall), which is associated with poorer outcome and has been noted to be the predominant initial rhythm in other in-hospital arrest series as well [24
]. Among patients who received cooling, 2 died within the following six months (18%). These observations are also in line with a recent study that demonstrated decreased chances of good outcome from cooling in patients with such nonshockable rhythms [26
]. It is possible that patients in the latter category may have more severe disease, but this study did not suggest that such patients were harmed by cooling.
Of the 18 cases in which the survivor was comatose and therapeutic hypothermia was not initiated, these patients were not felt to be candidates for therapeutic hypothermia due to change in goals of care status, hemodynamic instability, or severe coagulopathy and hemorrhage. There were 2 cases where patients might have benefitted from cooling and neurology was not consulted initially. These cases occurred before a formal cooling protocol was adopted by our hospital and relevant staff were educated in its implementation. Since staff training occurred, no further cases were identified. Moving forward, one way to prevent this in the future would be to have every case in which the patient was comatose after cardiac arrest discussed with the on-call neurologist, even in cases where there is a clear contraindication. Other measures to improve our current protocol might include providing a dedicated neurology code pager in code blue protocols and staff training and reorientation at regular intervals.
At our institution, hypothermia was instituted using surface cooling methods and cooling blankets or suits. While our time to target temperature was comparable to previously published studies, it might be possible to further shorten the cooling time by induction with chilled intravenous saline solution. Further, there has also been some concern that surface cooling has been associated with overshooting of goal temperatures which could lead to higher complication rates. Studies have shown that endovascular catheter-assisted hypothermia allows for better control of temperature and faster cooling rates [27
]. As such, the incorporation of endovascular cooing catheters might help achieve cooling at a faster rate and prevent overshooting of mild hypothermia goals. However, placement of these catheters requires a trained physician and this can often delay the initiation of cooling if the physician is not readily available [28
]. Many community hospitals, including ours, do not always have such trained individuals on staff. Thus, our experience demonstrates that it is still possible to implement a cooling protocol where advanced technologies are not available. It should be noted that, in our series, there were two cases of overshooting beyond 32°C but both of these patients had a favorable CPC score at discharge.
Complications that were noted during the cooling phase and in the week after induction of hypothermia included pneumonia, cardiac arrhythmia requiring administration of medication, deep venous thrombosis, and, in one case, subsegmental pulmonary embolus. It is unclear whether these complications were necessarily related to cooling, as these are also common complications that occur in noncooled cardiac arrest patients. However, a recent study of therapeutic cooling in stroke patients did report a somewhat higher incidence of pneumonia that did not adversely affect eventual patient outcome [29
]. Our rates were similar to those described by Prior and colleagues in their series at a community-based hospital [20
]. There were no complications associated with rewarming, and although one patient was warmed faster than expected, this was likely related to underlying fever leading to rapid increase in temperature once therapeutic hypothermia was completed.
Limitations of this study are largely related to the retrospective nature of this analysis. Some data points were not recorded in each case, and determination of timing often involved estimates based on ICU nursing charting and by extrapolating from time of arrest indicated by treating physicians. The objective of this study was not to show evidence of the efficacy of therapeutic hypothermia which has been well established but the implementation of a cooling protocol in this particular hospital setting. The lack of a true control group makes it difficult to interpret the overall significance of therapeutic hypothermia beyond comparison of results with previous trials. Although there were patients who were comatose and not cooled, the baseline characteristics of these arrests and the fact that they were actively not cooled precludes direct comparison with the patients who were cooled.