Aline Bouwes

Prognosis of coma after therapeutic hypothermia: A prospective cohort study

This study was designed to establish the reliability of neurologic examination, neuron‐specific enolase (NSE), and median nerve somatosensory‐evoked potentials (SEPs) to predict poor outcome in patients treated with mild hypothermia after cardiopulmonary resuscitation (CPR).

Acute posthypoxic myoclonus after cardiopulmonary resuscitation

BackgroundAcute posthypoxic myoclonus (PHM) can occur in patients admitted after cardiopulmonary resuscitation (CPR) and is considered to have a poor prognosis. The origin can be cortical and/or subcortical and this might be an important determinant for treatment options and prognosis. The aim of the study was to investigate whether acute PHM originates from cortical or subcortical structures, using somatosensory evoked potential (SEP) and electroencephalogram (EEG).MethodsPatients with acute PHM (focal myoclonus or status myoclonus) within 72 hours after CPR were retrospectively selected from a multicenter cohort study. All patients were treated with hypothermia. Criteria for cortical origin of the myoclonus were: giant SEP potentials; or epileptic activity, status epilepticus, or generalized periodic discharges on the EEG (no back-averaging was used). Good outcome was defined as good recovery or moderate disability after 6 months.ResultsAcute PHM was reported in 79/391 patients (20%). SEPs were available in 51/79 patients and in 27 of them (53%) N20 potentials were present. Giant potentials were seen in 3 patients. EEGs were available in 36/79 patients with 23/36 (64%) patients fulfilling criteria for a cortical origin. Nine patients (12%) had a good outcome. A broad variety of drugs was used for treatment.ConclusionsThe results of this study show that acute PHM originates from subcortical, as well as cortical structures. Outcome of patients admitted after CPR who develop acute PHM in this cohort was better than previously reported in literature. The broad variety of drugs used for treatment shows the existing uncertainty about optimal treatment.

The influence of rewarming after therapeutic hypothermia on outcome after cardiac arrest.

INTRODUCTION Treatment with hypothermia has been shown to improve outcome after cardiac arrest (CA). Current consensus is to rewarm at 0.25-0.5 °C/h and avoid fever. The aim of this study was to investigate whether active rewarming, the rate of rewarming or development of fever after treatment with hypothermia after CA was correlated with poor outcome. METHODS This retrospective cohort study included adult patients treated with hypothermia after CA and admitted to the intensive care unit between January 2006 and January 2009. The average rewarming rate from end of hypothermia treatment (passive rewarming) or start active rewarming until 36 °C was dichotomized in a high (≥ 0.5 °C/h) or normal rate (<0.5 °C/h). Fever was defined as >38 °C within 72 h after admission. Poor outcome was defined as death, vegetative state, or severe disability after 6 months. RESULTS From 128 included patients, 56% had a poor outcome. Actively rewarmed patients (38%) had a higher risk for poor outcome, OR 2.14 (1.01-4.57), p<0.05. However, this effect disappeared after adjustment for the confounders age and initial rhythm, OR 1.51 (0.64-3.58). A poor outcome was found in 15/21 patients (71%) with a high rewarming rate, compared to 54/103 patients (52%) with a normal rewarming rate, OR 2.61 (0.88-7.73), p = 0.08. Fever was not associated with outcome, OR 0.64 (0.31-1.30), p = 0.22. CONCLUSIONS This study showed that patients who needed active rewarming after therapeutic hypothermia after CA did not have a higher risk for a poor outcome. In addition, neither speed of rewarming, nor development of fever had an effect on outcome.

Induced hypothermia and determination of neurological outcome after CPR in ICUs in the Netherlands: Results of a survey

INTRODUCTION Induction of hypothermia is generally accepted to increase survival of out-of-hospital cardiac arrest, but lack of initiation of this treatment has been frequently reported. When patients remain in coma after treatment with hypothermia, determination of prognosis is difficult. Furthermore, little is known about the methods used in clinical practice to predict outcome after cardiopulmonary resuscitation (CPR). The aim of the present survey was to evaluate self-reported implementation of hypothermia after CPR and the methods used to predict neurological outcome at Intensive Care Units (ICUs) in the Netherlands. METHODS Between April 2008 and July 2008 an e-mail-invitation for an anonymous web-based 22-question survey was sent to one physician of each ICU in the Netherlands. RESULTS Of the 97 physicians surveyed, 74 (76%) responded. Thirty-seven (50%) responders always treated patients with hypothermia after CPR, 31 (42%) only when CPR fulfilled several criteria. The most important reason for not using hypothermia (six ICUs) was lack of equipment. Haemodynamic instability was the most cited reason for discontinuing treatment. Neurological outcome was predicted by clinical neurological examination (92%), cortical N20 responses of median nerve somatosensory evoked potentials (SSEP) (94%), an electroencephalogram (56%) or serum levels of neuron-specific proteins (5%). CONCLUSIONS In the Netherlands, the use of therapeutic hypothermia after CPR is reported by 92% of ICUs which, compared to previous reports, is an exceedingly high percentage. Neurological outcome is reported to be predicted mainly by neurological examination and SSEP or a combination of these and other assessments. The method used varies substantially between ICUs.