Therapeutic Hypothermia for Traumatic Brain Injury

Experimental evidence demonstrates that therapeutic temperature modulation with the use of mild induced hypothermia (MIH, defined as the maintenance of body temperature at 32-35°C) exerts significant neuroprotection and attenuates secondary cerebral insults after traumatic brain injury (TBI). In adult TBI patients, MIH has been used during the acute "early” phase as prophylactic neuroprotectant and in the sub-acute "late” phase to control brain edema. When used to control brain edema, MIH is effective in reducing elevated intracranial pressure (ICP), and is a valid therapy of refractory intracranial hypertension in TBI patients. Based on the available evidence, we recommend: applying standardized algorithms for the management of induced cooling; paying attention to limit potential side effects (shivering, infections, electrolyte disorders, arrhythmias, reduced cardiac output); and using controlled, slow (0.1-0.2°C/h) rewarming, to avoid rebound ICP. The optimal temperature target should be titrated to maintain ICP <20mmHg and to avoid temperatures <35°C. The duration of cooling should be individualized until the resolution of brain edema, and may be longer than 48h. Patients with refractory elevated ICP following focal TBI (e.g. hemorrhagic contusions) may respond better to MIH than those with diffuse injury. Randomized controlled trials are underway to evaluate the impact of MIH on neurological outcome in adult TBI patients with elevated ICP. The use of MIH as prophylactic neuroprotectant in the early phase of adult TBI is not supported by clinical evidence and is not recommende

Too cold may not be so cool: spontaneous hypothermia as a marker of poor outcome after cardiac arrest

In a recent issue of Critical Care, den Hartog and colleagues show an association between spontaneous hypothermia, defined by an admission body temperature <35°C, and poor outcome in patients with coma after cardiac arrest (CA) treated with therapeutic hypothermia (TH). Given that TH alters neurological prognostication, studies aiming to identify early markers of injury severity and outcome are welcome, since they may contribute overall to optimize the management of comatose CA patients. This study provides an important message to clinicians involved in post-resuscitation care and raises important questions that need to be taken into account in future studies

Management of mechanical ventilation in acute severe asthma: practical aspects

Background: Acute severe asthma induces marked alterations in respiratory mechanics, characterized by acritical limitation of expiratory flow and aheterogeneous and reversible increase in airway resistance, resulting in premature airway closure, lung, and chest wall dynamic hyperinflation and high intrinsic PEEP. Discussion: These abnormalities increase the work of breathing and can lead to respiratory muscle fatigue and life-threatening respiratory failure, in which case mechanical ventilation is life-saving. When instituting mechanical ventilation in this setting, amajor concern is the risk of worsening lung hyperinflation (thereby provoking barotrauma) and inducing or aggravating hemodynamic instability. Guidelines for mechanical ventilation in acute severe asthma are not supported by strong clinical evidence. Controlled hypoventilation with permissive hypercapnia may reduce morbidity and mortality compared to conventional normocapnic ventilation. Profound pathological alterations in respiratory mechanics occur during acute severe asthma, which clinicians should keep in mind when caring for ventilated asthmatics. Conclusion: We focus on the practical management of controlled hypoventilation. Particular attention must be paid to ventilator settings, monitoring of lung hyperinflation, the role of extrinsic PEEP, and administering inhaled bronchodilators. We also underline the importance of deep sedation with respiratory drive-suppressing opioids to maintain patient-ventilator synchrony while avoiding as much as can be muscle paralysis and the ensuing risk of myopathy. Finally, the role of noninvasive positive pressure ventilation for the treatment of respiratory failure during severe asthma is discusse

Monitoring of Brain and Systemic Oxygenation in Neurocritical Care Patients

Maintenance of adequate oxygenation is a mainstay of intensive care, however, recommendations on the safety, accuracy, and the potential clinical utility of invasive and non-invasive tools to monitor brain and systemic oxygenation in neurocritical care are lacking. A literature search was conducted for English language articles describing bedside brain and systemic oxygen monitoring in neurocritical care patients from 1980 to August 2013. Imaging techniques e.g., PET are not considered. A total of 281 studies were included, the majority described patients with traumatic brain injury (TBI). All tools for oxygen monitoring are safe. Parenchymal brain oxygen (PbtO2) monitoring is accurate to detect brain hypoxia, and it is recommended to titrate individual targets of cerebral perfusion pressure (CPP), ventilator parameters (PaCO2, PaO2), and transfusion, and to manage intracranial hypertension, in combination with ICP monitoring. SjvO2 is less accurate than PbtO2. Given limited data, NIRS is not recommended at present for adult patients who require neurocritical care. Systemic monitoring of oxygen (PaO2, SaO2, SpO2) and CO2 (PaCO2, end-tidal CO2) is recommended in patients who require neurocritical care

Neural detection of complex sound sequences in the absence of consciousness

Neural responses to violations of global regularities are thought to require consciousness. However, Tzovara et al. show that some comatose patients can also detect deviations in sequences composed of repeated groups of sounds, suggesting that the unconscious brain has a greater capacity to track sensory inputs than previously believe

Clinical Outcome After a Reactive Hypothermic EEG Following Cardiac Arrest

Background: Reactive electroencephalography (EEG) background during therapeutic hypothermia (TH) is related to favorable prognosis after cardiac arrest (CA), but its predictive value is not 100%. The aim of this study was to investigate outcome predictors after a first reactive EEG recorded during TH after CA. Methods: We studied a cohort of consecutive comatose adults admitted between February 2008 and November 2012, after successful resuscitation from CA, selecting patients with reactive EEG during TH. Outcome was assessed at three months, and categorized as survivors and non-survivors (no patient was in vegetative state). Demographics, clinical variables, EEG features, serum neuron-specific enolase (NSE) and procalcitonin, were compared using uni- and multivariable analyses. Results: A total of 290 patients were treated with TH after cardiac arrest; 146 had an EEG during TH, which proved reactive in 90 of them; 77 (86%) survived and 13 (14%) died (without recovery from coma). The group of non-survivors had a higher occurrence of discontinuous EEG (p=0.006; multivariate analysis p=0.026), and a higher serum NSE peak (p=0.021; multivariate analysis p=0.014); conversely, demographics, and other clinical variables including serum procalcitonin did not differ. Conclusions: A discontinuous EEG and high serum NSE are associated with mortality after CA in patients with poor outcome despite a reactive hypothermic EEG. This suggests more severe cerebral damage, but not to higher extent of systemic diseas