Out-of-hospital cardiac arrest (OHCA) remains associated with a poor prognosis, with a survival rate of approximately 10% [1]. Only 40% of patients presenting with OHCA are successfully resuscitated, and only 25% of them survive to hospital discharge [1].
In many cases of OHCA associated with acute myocardial infarction, the cardiac arrest is caused by ventricular fibrillation, occurring during the first hours after the onset of symptoms, and before the patient being admitted to hospital [2]. In these critical cases, implementation of specific protocols and dedicated networks are crucial for providing effective advanced cardiac life support.
Several treatment modalities have been proposed to improve outcomes in the post-resuscitation period. One such measure is induced therapeutic hypothermia, consisting of administering cooling infusions to cool the patient down to 32-34⁰C, and maintaining this for 12-24 hours. Evidence shows that when initiated promptly, cooling improves neurological outcomes in survivors of OHCA [3,4]. However, there is no clear evidence that hypothermia would lead to a significant reduction in mortality in these patients. Current guidelines recommend early therapeutic hypothermia as a class Ib indication, in the post-resuscitation phase, after cardiac arrest in patients who are comatose or deeply sedated [2]. [More]

The review article published in this issue by Schwartz A et al [1] draws attention to the importance of cardiac arrhythmias and especially that of new-onset atrial fibrillation (AF) and the clinical outcome of septic patients. The incidence of this phenomenon varies in different reports, from 5.8% [2] to 31-40% [3-4].
Causes are numerous and different mechanisms have been described in the literature and by the authors of the review. Endotoxin induces tachycardia, increases the cardiac index, and reduces blood pressure and systemic vascular resistance without change in stroke volume [5]. Fluid administration results in a decrease in left ventricular ejection fraction and an increase in ventricular volumes even more than before the administration of fluid therapy [5].
An increased inflammatory response also plays an important role in pathogenesis of cardiac arrhythmias and dysfunction in septic patients. Increased plasma levels of C-reactive protein, IL-6 and TNF-α may contribute to the onset of AF in septic patients [1,6]. [More]

The critically ill patient with primary multiple traumas and having secondary complications, presents a complex challenge to the trauma team. The most commonly encountered primary injuries are traumatic brain, spinal cord, pulmonary and abdominal injuries or trauma to the pelvis and the extremities. Moreover, severe inflammations, infections, hyper-metabolism, as well as biochemical and physiological imbalances, lead to a significant increase in morbidity and mortality.
Most recently, the role of free radicals has been a largely debated and reported topic. Once produced in excess, free radicals are responsible for inducing oxidative stress. The redox species known to have a destructive effect on cells include the superoxide anion, the hydroxyl radical, hydrogen peroxide, nitric oxide, peroxynitrite, lipid peroxyl and alkoxy lipid. Under normal conditions, free radicals are produced in the human body in small amounts, their activity being minimized by the body’s physiologically anti-oxidant systems which include superoxide dismutase, catalase, glutathione, glutathione peroxidase, peroxiredoxins, and glutaredoxins.
In the critically ill patient, severe physiological and biochemical imbalances significantly reduce the body’s anti-oxidant capacity, disrupting the redox balance [1]. A series of biomarkers are in use, designed to quantify oxidative stress. These comprise interleukin 1 beta, interleukin 6, interleukin 10, tumor necrosis alpha, components of the complement, plasmatic levels of antioxidant enzymes and the microRNA species [2]. [More]

Sugammadex, a synthetic cyclodextrin sodium salt, was heralded and initially marketed as the first selective relaxant binding agent (SRBA) designed to reverse rocuronium [1]. This chemically modified cyclodextrin basically swallowed rocuronium removing it from the effector site, which was a “paradigm shift” from the then current methodology [2]. Following the launch of rocuronium and the rapidly spreading practice of intubation on rocuronium in rapid sequence instead of succinylcholine, a need to reverse muscle relaxation in case of intubation failure emerged. Moreover, the well-known undesirables side effects of cholinesterase inhibitors needing blunting by coadministration of muscarinic antagonists enlarged the odds of experiencing unwanted extra drug effects [3]. Further studies supported the use of sugammadex to reverse a life-threatening situation defined as “cannot intubate, cannot ventilate” [4]. It was a genuine revolutionary approach [5].Thus sugammadex appeared as a rescue drug. It was then used as the best, the most rapid and the safest if not the single solution to reverse curarization, although controversies as to the standard ofrapid sequence induction and intubation[6] are going on [7]. The odds were favorable and still are if it were not for certain voices to say “nay” to sugammadex as a routine drug based mainly on cost related issues. [More]