Objectives: To review the neurocritical care aspects of patients supported by extracorporeal membrane oxygenation, including cerebral physiology, neurologic monitoring, use of sedatives and anti-seizure medications, and prevalence and management of extracorporeal membrane oxygenation associated brain injury. Data Sources: PubMed database search using relevant search terms related to neurologic complications, neurocritical care management, and brain injury management in patients with extracorporeal membrane oxygenation. Study Selection: Articles included original investigations, review articles, consensus statements and guidelines. Data Extraction: A detailed review of publications performed and relevant publications were summarized. Data Synthesis: We found no practice guidelines or management strategies for the neurocritical care of extracorporeal membrane oxygenation patients. Such patients are at high risk for hypoxic-ischemic brain injury, intracranial hemorrhage, cerebral edema, and brain death. Improving clinical outcomes will depend on better defining the neurologic complications and underlying pathophysiology that are specific to extracorporeal membrane oxygenation. Currently, insufficient understanding of the pathophysiology of neurologic complications prevents us from addressing their etiologies with specific, targeted monitoring techniques and interventions. Conclusions: A large knowledge gap exists in our understanding and treatment of extracorporeal membrane oxygenation-related neurologic complications. A systematic and multidisciplinary approach is needed to reduce the prevalence of these complications and to better manage the neurologic sequelae of extracorporeal membrane oxygenation in a way that will improve patient outcomes.

Purpose of review To discuss recent updates in fluid management and use of hyperosmolar therapy in neurocritical care. Recent findings Maintaining euvolemia with crystalloids seems to be the recommended fluid resuscitation for neurocritical care patients. Buffered crystalloids have been shown to reduce hyperchloremia in patients with subarachnoid hemorrhage without causing hyponatremia or hypo-osmolality. In addition, in patients with traumatic brain injury, buffered solutions reduce the incidence of hyperchloremic acidosis but are not associated with intracranial pressure (ICP) alteration. Both mannitol and hypertonic saline are established as effective hyperosmolar agents to control ICP. Both agents have been shown to control ICP, but their effects on neurologic outcomes are unclear. A recent surge in preference for using hypertonic saline as a hyperosmolar agent is based on few studies without strong evidence. Summary Fluid resuscitation with crystalloids seems to be reasonable in this setting although no recommendations can be made regarding type of crystalloids. Based on current evidence, elevated ICP can be effectively reduced by either hypertonic saline or mannitol.

OBJECTIVEBlood transfusions are given to approximately one-fifth of patients undergoing elective lumbar spine surgery, and previous studies have shown that transfusions are accompanied by increased complications and additional costs. One method for decreasing transfusions is administration of tranexamic acid (TXA). The authors sought to evaluate whether the cost of TXA is offset by the decrease in blood utilization in lumbar spine surgery patients.METHODSThe authors retrospectively reviewed patients who underwent elective lumbar or thoracolumbar surgery for degenerative conditions at a tertiary care center between 2016 and 2018. Patients who received intraoperative TXA (TXA patients) were matched with patients who did not receive TXA (non-TXA patients) by age, sex, BMI, ASA (American Society of Anesthesiologists) physical status class, and surgical invasiveness score. Primary endpoints were intraoperative blood loss, number of packed red blood cell (PRBC) units transfused, and total hemostasis costs, defined as the sum of TXA costs and blood transfusion costs throughout the hospital stay. A subanalysis was then performed by substratifying both cohorts into short-length (1–4 levels) and long-length (5–8 levels) spinal constructs.RESULTSOf the 1353 patients who met inclusion criteria, 68 TXA patients were matched to 68 non-TXA patients. Patients in the TXA group had significantly decreased mean intraoperative blood loss (1039 vs 1437 mL, p = 0.01). There were no differences between the patient groups in the total costs of blood transfusion and TXA (p = 0.5). When the 2 patient groups were substratified by length of construct, the long-length construct group showed a significant net cost savings of $328.69 per patient in the TXA group (p = 0.027). This result was attributable to the finding that patients undergoing long-length construct surgeries who were given TXA received a lower amount of PRBC units throughout their hospital stay (2.4 vs 4.0, p = 0.007).CONCLUSIONSTXA use was associated with decreased intraoperative blood loss and significant reductions in total hemostasis costs for patients undergoing surgery on more than 4 levels. Furthermore, the use of TXA in patients who received short constructs led to no additional net costs. With the increasing emphasis put on value-based care interventions, use of TXA may represent one mechanism for decreasing total care costs, particularly in the cases of larger spine constructs.

The cessation (ischemia) and restoration (reperfusion) of cerebral blood flow after cardiac arrest (CA) induce inflammatory processes that can result in additional brain injury. Therapeutic hypothermia (TH) has been proven as a brain protective strategy after CA. In this article, the underlying pathophysiology of ischemia-reperfusion brain injury with emphasis on the role of inflammatory mechanisms is reviewed. Potential targets for immunomodulatory treatments and relevant effects of TH are also discussed. Further studies are needed to delineate the complex pathophysiology and interactions among different components of immune response after CA and identify appropriate targets for clinical investigations.