الفهرس 
Consciousness and SleepOnly 14 pages are availabe for public view
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Abstract
General anesthesia can be defined as a reversible drug-induced state of unconsciousness, during which noxious stimuli can neither be perceived nor recalled (Brown et al., 2011). The concept of balanced anesthesia was developed by John Lundy to provide these elements of anesthesia by using multiple drugs at lower doses to minimize the adverse effects of each drug, while still providing appropriate anesthesia (Ellis et al., 2004). Ideally, on cessation of anaesthesia, the patient should be awake or easily arousable, protecting the airway, maintaining adequate ventilation and with their pain under control (Saranagi et al., 2009).
Although emergence from general anae¬sthesia has been characterized by large individual variability, there are defined problems that affect proper emergence from general anesthesia. These problems include delayed awakening, which has been defined as a state of unconsciousness that persists for more than 30 minutes after admission to the PACU. It poses as a serious anesthetic complication because impaired ventilatory efforts can lead to a greater incidence of hypoxia and hypercarbia that may culminate to cardiac arrest or permanent neurological sequels. (Faleiro and Sinclair, 2006) Post-operative delirium is defined as an acutely altered and fluctuating mental status with features of inattention and an altered level of consciousness (Robinson and Eiseman, 2008). Its incidence can be as high as 87% (Demeure and Fain, 2006), and is critically important because it is associated with poor outcomes including functional decline, longer hospitalization, greater medical costs, and higher mortality (Dasgupta and Dumbrell, 2006). Post-operative cognitive dysfunction is another disorder of emergence, which affects cognition in terms of memory, comprehension, and attention (Bryson and Wyand, 2006).
There are a plethora of risk factors that can impact a patient’s recovery of consciousness from general anesthesia. Postoperative delirium and postoperative cognitive dysfunction are quintessential geriatric complications (Inouye et al 2007; Newman et al. 2007). Patients suffering from kidney insufficiency and liver failure (Zafirova et al., 2010) are at a high risk of delayed emergence after surgery and anesthesia. Clinically hypothyroid patients can be especially slow to emerge from general anesthesia (Bostan et al., 2011), where-as patients with obstructive sleep apnea can be particularly sensitive to the depressant effects of opioids or inhalational anesthetics (Chung et al. 2008). Systemic sepsis significantly impairs mental status, both directly and secondarily through hypotension (Adam et al., 2013). Porphyrias may exhibit unconsciousness after exposure to barbiturates, propofol and other classes of medications (Pischik et al., 2009).
The type of surgical procedure is also a risk factor, depending upon the duration, the need of muscle relaxation, regional techniques and the degree of pain. Neurological procedures may be associated with intra-operative events that can affect emergence (Fabregas, 2007). Cardiac transplantation can be associated with neurological complications and coma (Vandebeeck et al., 2008). In liver transplantation, there are several reasons for neurological damage during and after the procedure including electrolyte disturbances, air embolism, cerebral hemorrhage, and bacterial encephalitis (Plachky et al., 2004). Endoscopic urological procedures can be associated with infusion injuries as dilutional hypo-natremia (Gupta et al., 2010) which can have neurological manifestations.
Residual pharmacological agents used in anesthesia are the foremost anesthetic factor for delayed emergence. Emergence from intravenous anesthetics depends on the drug’s dose, the rate of its absorption and distribution, the rate of its metabolism and excretion, and its pharmaco-kinetic and pharmaco-dynamic interactions (Bajaj et al., 2007). Emergence from volatile anesthetic agents depends on function of alveolar ventilation (V̇a), solubility of the anesthetic in plasma and tissues, tissue perfusion, and cardiac output (Katznelson et al., 2008). Profound neuromuscular blockade can also mimic delayed emergence at recovery (Faliero and Sinclair, 2006). The use of succinylcholine in genetic and acquired acetylcholinesterase deficiency can result in prolonged apnea that delays trials for patient arousal (Barker, 2003).
Respiratory disturbances leading to hypoxemia or hypercarbia can serve as both cause and complication of compromised emergence. Other factors like hypothermia can also hinder recovery (Feinstein, 2010).
The continuous research and development of ultra-short acting drugs in anesthesia has decreased the incidence of delayed emergence (Bajaj et al., 2007). In addition, monitoring tools have been introduced that assess the level of consciousness (as bi-spectral index monitoring and auditory evoked potential monitoring) (White et al., 2004) other tools that assess the success of respiratory efforts (as capnography and near-infrared spectroscopy) (Ghosh et al., 2012) and the neuromuscular state (such as TOF monitoring). All have allowed better management of emergence from anesthesia. When validated, DoA monitors can allow a total coverage of the dose–response relation. By measuring the patients’ individual response to a given drug dose, drug administration could be guided by a pharmacodynamic advisory system estimating the complete dose–response relationship. Additionally, closed-loop technology could be used. Such systems might help the anaesthetist in optimizing the titration of drug administration without overshoot, controlling physiological functions and guiding monitoring variables (Struys et al., 2004).
This work reviewed the factors that compromise emergence of consciousness from general anesthesia, outlined its assessment using current monitoring tools, and the mention of the optimal therapeutics that can prove effective in managing normal recovery of post-anesthetic consciousness.