Intracranial pressure (ICP) monitoring and control is a cornerstone of neuroanesthesia and neurocritical care. However, because elevated ICP can be due to multiple pathophysiological processes, its interpretation is not straightforward. We propose a formal taxonomy of intracranial hypertension, which defines ICP elevations into 3 major pathophysiological subsets: increased cerebral blood volume, masses and edema, and hydrocephalus. (1) Increased cerebral blood volume increases ICP and arises secondary to arterial or venous hypervolemia. Arterial hypervolemia is produced by autoregulated or dysregulated vasodilation, both of which are importantly and disparately affected by systemic blood pressure. Dysregulated vasodilation tends to be worsened by arterial hypertension. In contrast, autoregulated vasodilation contributes to intracranial hypertension during decreases in cerebral perfusion pressure that occur within the normal range of cerebral autoregulation. Venous hypervolemia is produced by Starling resistor outflow obstruction, venous occlusion, and very high extracranial venous pressure. Starling resistor outflow obstruction tends to arise when cerebrospinal fluid pressure causes venous compression to thus increase tissue pressure and worsen tissue edema (and ICP elevation), producing a positive feedback ICP cycle. (2) Masses and edema are conditions that increase brain tissue volume and ICP, causing both vascular compression and decrease in cerebral perfusion pressure leading to oligemia. Brain edema is either vasogenic or cytotoxic, each with disparate causes and often linked to cerebral blood flow or blood volume abnormalities. Masses may arise from hematoma or neoplasia. (3) Hydrocephalus can also increase ICP, and is either communicating or noncommunicating. Further research is warranted to ascertain whether ICP therapy should be tailored to these physiological subsets of intracranial hypertension.

Inhaled anesthetics have been utilized mostly for general anesthesia in the operating room and oftentimes for sedation and for treatment of refractory status epilepticus and status asthmaticus in the intensive care unit. These contexts in the ICU setting are related to potential for prolonged administration wherein potential organ toxicity is a concern. Over the last decade, several clinical and animal studies of neurotoxicity attributable to inhaled anesthetics have been emerging, particularly in extremes of age. This review overviews potential for and potential mechanisms of neurotoxicity and systemic toxicity of prolonged inhaled anesthesia and clinical scenarios where inhaled anesthesia has been used in order to assess safety of possible prolonged use for sedation. High dose inhaled agents are associated with postoperative cognitive dysfunction (POCD) and other situations. However, thus far no strong indication of problematic neuro or organ toxicity has been demonstrated after prolonged use of low dose volatile anesthesia.

Awake intubation is frequently described in the literature as the preferred method for securing the airway in adult patients with epiglottitis, whereas children with epiglottitis are usually intubated following an inhalational induction. However, if topicalization is difficult due to the presence of an abscess or an uncooperative patient, an inhalational induction may still be a reasonable approach in the adult patient. In a review of the literature, only one recent case report had been found describing an inhalational induction with video laryngoscopy. However, this attempt was unsuccessful, mandating the need for a surgical airway. Our case report describes a successful inhalational induction and video laryngoscope intubation without the use of a paralytic agent in an adult patient with an epiglottic abscess and moderate airway stenosis.

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