Neurointensive care medicine has experienced great advancements and developments of neuromonitoring techniques, allowing a better comprehension of acute brain injury early phase pathological mechanisms and an overall improvement of ICU management, currently based on the concept of individualized therapy, targeted to protect the brain against further secondary insults, by optimizing patient pathophysiology at the bedside . Individualized therapy in neurointensive care practice includes a number of pharmacological interventions, either general (or nonspecific, such as sedatives, hyperosmolar fluids, vasopressors, nutrition solutions, mineralocorticoids) or more specific (antiepileptic agents, desmopressin, vaptans). This neuroscience issue of Current Opinion in Critical Care is entirely dedicated to pharmacotherapy in neurointensive care. We invited several prominent experts to review recent advancements in the field and provide an update on current practices. The first article of the series focuses on sedatives and the classical paradigm of ‘pharmacologically induced coma’ aimed at reducing the cerebral metabolic rate of oxygen, and thereby protecting the brain against secondary insults (ischemia, hypoxia, seizures). Geert Meyfroidt and collaborators (pp. 97–104) discuss standard sedatives (mainly propofol) and the emerging role of alternative classical (ketamine, barbiturates) and novel (dexmedetomidine) agents. Their article very thoughtfully underlines the surprisingly low-level of clinical evidence for sedative practices in neurointensive care and the challenge of applying the current general ICU paradigm of minimizing sedation to acute brain injury patients. Management of intracranial pressure (ICP) with hyperosmolar fluids is a mainstay of therapy in neurointensive care. Suarez and collaborators (pp. 105–109) elegantly review current clinical evidence on the use of standard (crystalloids, balanced solutions, albumin) and hyperosmolar (mannitol, hypertonic saline) fluids in different patient populations (trauma, stroke, neoplasms). Steiner and Siegemund (pp. 110–116) tackle the difficult clinical question of the ‘optimal’ cerebral perfusion pressure (CPP) in neurointensive care, based on individual patient autoregulation curve. Although practically feasible, thanks to neuromonitoring improvements [e.g. using invasive ICP and mean arterial pressure (MAP) to calculate the pressure reactivity index (PRx)], clinical implementation and the level of clinical evidence are still limited. On the basis of low-evidence physiology studies, norepinephrine may be considered the agent of choice to improve MAP/CPP. Seizure management has greatly evolved in recent years, with the advent of various new antiepileptic pharmacological agents to manage ICU refractory status epilepticus. Allen and Vespa (pp. 117–125) critically revise the current guidelines and provide guidance to intensivists on available treatment options. ‘Food for thought: the brain needs fuel’: Quintard and Ichai (pp. 126–131) nicely review current best practices for metabolic and nutritional support in neurointensive care patients, a field of growing clinical research interest. Sodium disorders are frequent in neurointensive care patients and their management is challenging. Geeraerts and collaborators (pp. 132–137) provide an update of recent data and propose an algorithm on how to best approach pharmacotherapy of sodium and water imbalances in this setting.
Pharmacotherapy of acute cerebral diseases is complex and multifaceted, including many pharmacological agents targeting various secondary injury mechanisms. Current practices are derived from small sample size prospective physiological studies or nonrandomized large observational cohort analysis, and are currently based on an individualized care paradigm , targeted to restore or ameliorate cerebral hemodynamic, circulatory and metabolic functions.
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