Fulminant hepatic failure (FHF) is often accompanied by a myriad of neurologic complications, which are associated with high morbidity and mortality. Although appropriate neuromonitoring is recommended for early diagnosis and to minimize secondary brain injury, individuals with FHF usually have a high chance of coagulopathy, which limits the ability to use invasive neuromonitoring. Jugular bulb venous oxygen saturation (JvO₂) monitoring is well known as a surrogate direct measures of global brain oxygen use. We report the case of a patient with increased intracranial pressure due to FHF, in which JvO₂ was used for appropriate brain oxygen monitoring.
Brain Edema ; Brain Injuries ; Brain* ; Early Diagnosis ; Hepatic Encephalopathy ; Humans ; Intracranial Pressure ; Jugular Veins ; Liver Failure, Acute* ; Mortality ; Oxygen Consumption ; Oxygen*

Multimodality monitoring (MMM) is a recently developed method that aids in understanding real-time brain physiology. Early detection of physiological disturbances is possible with the help of MMM, which allows identification of underlying causes of deterioration and minimization of secondary brain injury (SBI). MMM is especially helpful in comatose patients with severe brain injury because neurological examinations are not sensitive enough to detect SBI. The variables frequently examined in MMM are hemodynamic parameters such as intracranial pressure, cerebral perfusion pressure, and mean arterial pressure; brainspecific oxygen tension; markers for brain metabolism including glucose, lactate, and pyruvate levels in brain tissue; and cerebral blood flow. Continuous electroencephalography can be performed, if needed. The majority of SBIs stem from brain tissue hypoxia, brain ischemia, and seizures, which lead to a disturbance in brain oxygen levels, cerebral blood flow, and electrical discharges, all of which are easily detected by MMM. In this review, we discuss the clinical importance of physiological variables as well as the practical applicability of MMM in patients with stroke.
Brain ; Brain Injuries ; Coma ; Critical Care ; Electroencephalography ; Glucose ; Hemodynamics ; Humans ; Hypoxia, Brain ; Intracranial Pressure ; Ischemia ; Lactic Acid ; Monitoring, Physiologic ; Neurologic Examination ; Oxygen ; Perfusion ; Pyruvic Acid ; Seizures ; Stroke

Prompt diagnosis and appropriate treatment is most important process in managing patients with acute stroke. The acute stroke treatment can be categorized as a specific treatment and general management. Specific treatment, including antithrombotic treatment or thrombolysis therapy, needs to be modified in individual patients. However, general management deals with common problems such as elevated blood pressure, high glucose level, respiratory difficulty, or fever, and those problems are commonly encountered in treating patients with acute stroke. This paper presents up-to-date recommendations for treating acute stroke with review of literatures.
Fever ; Glucose ; Humans ; Hypertension ; Stroke

No abstract available.
Echocardiography* ; Heart*

No abstract available.
Hip*

Although perioperative stroke is uncommon during low-risk non-vascular surgery, if it occurs, it can negatively impact recovery from the surgery and functional outcome. Based on the Society for Neuroscience in Anesthesiology and Critical Care Consensus Statement, perioperative stroke includes intraoperative stroke, as well as postoperative stroke developing within 30 days after surgery. Factors related to perioperative stroke include age, sex, a history of stroke or transient ischemic attack, cardiac surgery (aortic surgery, mitral valve surgery, or coronary artery bypass graft surgery), and neurosurgery (external carotid-internal carotid bypass surgery, carotid endarterectomy, or aneurysm clipping). Concomitant carotid and cardiac surgery may further increase the risk of perioperative stroke. Preventive strategies should be individualized based on patient factors, including cerebrovascular reserve capacity and the time interval since the previous stroke.
Anesthesiology ; Aneurysm ; Consensus ; Coronary Artery Bypass ; Critical Care ; Embolism ; Endarterectomy, Carotid ; Hemorrhage ; Humans ; Ischemia ; Ischemic Attack, Transient ; Mitral Valve ; Neurosciences ; Neurosurgery ; Stroke ; Thoracic Surgery ; Transplants

Targeted temperature management is a treatment strategy to lower core body temperature to achieve neuroprotection or reduce elevated intracranial pressure. Therefore, it has been increasingly used in the neurointensive care unit to manage various types of acute neurologic injuries.Current Concepts: Targeted temperature management can be divided into three distinct phases, including induction, maintenance, and rewarming, and each phase has risks and predictable complications. In patients with acute neurocritical illnesses, including traumatic brain injury, subarachnoid hemorrhage, intracranial hemorrhage, and ischemic stroke, brain edema is a potentially life-threatening complication as it raises the intracranial pressure, leading to brain herniation and permanent neurological damage. In this sense, targeted temperature management can be considered the final strategy for medical treatment for controlling an intracranial pressure crisis in patients with severe brain injury.Discussion and Conclusion: In the neurointensive care unit, applying targeted temperature management to patients with severe brain injuries may be challenging. Targeted temperature management in critically ill neurological patients is associated with an increased risk of systemic complications, as hypothermia is prolonged, requiring a comprehensive patient-by-patient assessment of the advantages and disadvantages of treatment. Except for cerebral pressure management, analyses of targeted temperature management in patients with traumatic brain injury and subarachnoid hemorrhage remain controversial regarding its effect on prognosis. Targeted temperature management should be reserved for selective patients, and further studies are needed to improve the efficacy of hypothermia for individual conditions, including intracerebral hemorrhage and ischemic stroke.

Mannitol and hypertonic saline are the most frequently used hyperosmolar agents to treat cerebral edema resulting from acute brain injury. However, there are several issues with using hyperosmolar therapies. Here, we focus on the potential adverse effects of hyperosmolar therapies and practical tips to overcome these issues in the neurointensive care unit.Current Concepts: Among the hyperosmolar agents used, mannitol may decrease intravascular volume and pose a potential risk of acute kidney injury for patients. Complications associated with using hypertonic saline include the risk of central pontine myelinolysis, coagulopathy, electrolyte imbalances, metabolic acidosis, and pulmonary edema. In addition, prolonged use of hypertonic saline increases the risk of hyperchloremic metabolic acidosis, which may be overcome with the concomitant use of sodium acetate.Discussion and Conclusion: Several laboratory variables were monitored in the neurointensive care unit to limit and possibly detect early complications related to hyperosmolar therapies. When using hyperosmolar agents, including mannitol and hypertonic saline, for therapeutic purposes in patients with cerebral edema, determining whether to use peripheral or central lines and determining the appropriate rate and infusion dose can minimize their adverse effects. Clinicians need to be aware of the potential adverse events of administering hyperosmolar agents.

Hyperosmolar therapy is an essential treatment method for increased intracranial pressure and cerebral edema. Mannitol and hypertonic saline are frequently used in clinical practice; however, more helpful recommendations are needed for the optimal management of cerebral edema in terms of the choice, dosage, and timing of these medications. This study aimed to introduce the characteristics and relative strengths of two agents, i.e., mannitol and hypertonic saline, and review clinical data supporting their use in various diseases.Current Concepts: Hyperosmolar therapy reduces intracranial pressure by removing water from the brain tissue and transferring it to the vascular space by creating an osmotic gradient. Mannitol improves cerebral blood flow by reducing the hematocrit, decreasing blood viscosity, and increasing deformability of red blood cells. Hypertonic saline increases intravascular volume, transiently increases cardiac output, and improves tissue oxygen partial pressure in the brain. Hypertonic saline has several advantages over mannitol, including quicker onset and longer-lasting reduction in intracranial pressure. However, no significant differences are noted in clinical, functional outcomes, or mortality between the two treatment agents.Discussion and Conclusion: Both mannitol and hypertonic saline are effective in reducing increased intracranial pressure. Clinicians should be able to select an appropriate agent in different clinical situations based on available evidence and patients’ individual medical conditions.

Increased intracranial pressure (ICP) is a pathological condition associated with severe neurological conditions in patients with acute brain injuries. Managing increased ICP based on optimal cerebral perfusion pressure (CPP) is crucial for improving outcomes.Current Concepts: Cerebral autoregulation, the intrinsic ability to maintain stable cerebral blood flow across a wide range of CPP, is impaired in several brain injuries. CPP, the difference between the mean arterial pressure and the ICP, is a critical factor in maintaining cerebral blood flow. Therefore, optimal CPP is important in managing patients with acute brain injuries. In addition, monitoring cerebral autoregulation and its response to pathological derangements can help diagnose, manage, and predict acute brain injury outcomes. Goal-directed therapy using cerebral autoregulation is beneficial in managing patients with ICP elevation. If blood pressure is excessively low in a patient with elevated intracranial pressure, a treatment to increase blood pressure should be considered as a first step, called optimizing cerebral perfusion pressure. However, if CPP is excessively high in a patient with elevated ICP, a treatment to lower CPP by controlling blood pressure to an appropriate level to prevent worsening of edema due to hyperperfusion should be considered.Discussion and Conclusion: Monitoring cerebral autoregulation to guide optimal management of increased ICP based on optimal CPP may be helpful in goal-directed therapy and improving prognosis among patients with acute brain injuries.