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Intraoperative Awareness - Mechanisms and Management - Essay Example

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This paper "Intraoperative Awareness - Mechanisms and Management" focuses on the fact that intraoperative awareness is the uncomfortable sensation of awareness or partial consciousness that occurs in some individuals during surgical procedures in which the patient has been given general anaesthesia. …
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Intraoperative Awareness - Mechanisms and Management
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Intraoperative Awareness: Mechanisms and Management Introduction Intraoperative awareness is the uncomfortable sensation of awareness or partial consciousness that occurs in some individuals during surgical procedures in which the patient has been given general anesthesia. (Spitelle et al, 2002). Interoperative awareness (IOA) affects .1-.2% of patients receiving general anesthesia for surgical procedures, and has been estimated to affect up to 20,000 patients each year (Sebel et al, 2004). Furthermore, it is estimated that up to one-third of patients experiencing IOA suffer psychological trauma as a result of this experience (Osterman et al, 2001). IOA is more common in patients in whom anesthesia is administered intravenously as compared to patients anesthetized by inhalation. IOA occurs more frequently during cardiovascular surgery, Caesarian sections and. trauma surgery Research studies suggest that IOA is more likely to occur in individuals who have engaged in substance abuse, who have low hemodynamic reserve, smokers or who have a tendency to experience anxiety. Not surprisingly, the phenomenon is more commonly reported among patients whose anesthesia is carefully monitored to administer the minimum necessary dose due to potential complications (Sebel et al. 2004) General anesthetic drugs fall into two main categories: inhalational and intravenous. In general, both types of anesthetics are administered to surgical patients to induce general anesthesia. In general, anesthesia is administered intravenously for induction and maintenance is in the form of inhalational anesthetics (Rang et al, 2008). Inhalational drugs are in the form of gases or volatile liquids that are delivered as a mixture including oxygen, air and inhalational drug. Fluorinated hydrocarbons are the most useful inhalational anesthetics. The most commonly used inhalational anesthetics are desflurane, isoflurane and sevoflurane; these may be used in combination with nitrous oxide (Rang et al, 2008). Other inhalational agents that are sometimes used are halothane, enflurane and methoxyflurane. Research suggests that a primary site of action of general anesthetics is on the cell plasma membrane (Rang et al, 2008). Increased membrane fluidity resulting from the action of these hydrophobic agents appears to be an important component of the pharmacologic activity of these drugs. The primary site of action of general anesthetics is the CNS receptor. Inhibition of receptor mediated excitatory functions appears to be a major component of the pharmacologic action of this class of drugs. Among the affected receptors are n-acetylcholine receptors, glutamate receptors and 5-HT3 receptors. In addition, general anesthetics can excite inhibitory receptors such as GABA-subtype A receptors and TREK. The inhalational anesthetic isoflurane binds to several types of neurotransmitter receptors to produce muscle relaxation and decrease pain sensitivity. Among the target receptors are GABA receptors, glutamate and glycine receptlors. Isoflurane also blocks potassium channel conduction. The binding to glycine receptors effects muscular relaxation and blocks motor activities. Increased membrane fluidity increases the activity of calcium ATPase; the drug also binds to ATP synthase and NAD dehydrogenase. This class of drugs also appears to block gap junction intercellular interactions which may also contribute to depression of neural responses and its consequent anesthetic effects (Fee & Bovill, 2005). Intravenous anesthetics in most common use are propofol, etomidate, barbiturates, and benzodiazepines. Most intravenous agents and some inhalational agents increase the activity of the inhibitory GABAA subtype A and glycine channels and decrease the excitatory functions of neuronal nicotinic acetylcholine receptors (Fee& Bovill, 2005). Nitrous oxide (an inhalational agent)and ketamine both function by decreasing the activity of the N-methyl-D-aspartate receptors and by enhancing the activity of opioid mu receptors. Ketamine acts in the same way as inhalational agents; it is rapid acting, short term effects and functions as a non-competitive antagonist of the NMDA receptor. It binds at the phencyclidine site and blocks calcium influx The IV anesthetic etomidate activates GABA-subtype A receptors. Propofol is the most commonly used IV anesthetic. Its primary mechanism of action is to enhance GABA activity. Its effects are of short duration. (Fee & Bovill, 2005). The most common manifestations of IOA are the perception of sounds associated with conversations, the feeling of pain, the awareness of paralysis and a heightened state of anxiety and/or panic associated with this conscious awareness (Sneyd & Matthew, 2008). It is less common for the patient to experience visual sensation or to be aware of intubation. Other issues that relate to the incidence of IOA concern airway obstruction problems, difficulties in intubation and delayed extubation. Additional causes of IOA include the failure to monitor correctly the level of patient sedation during surgery either due to inadequate monitoring or difficulties in assessing consciousness levels (Osterman et al, 2001). In addition, variations in patient responses to pharmacologic agents used in anesthesia may make some individuals more likely to develop IOA (Sneyd & Matthew, 2008).Clearly, there are many important and probable contributory factors that may increase the risk of IOA> The types of general anesthetic drug protocols most commonly associated with IOA are those that include muscle relaxants, the use of total intravenous anesthesia, rapid sequence induction and the use of nitrous oxide –opioid anesthetics (Ranta et al, 1998). One of the greatest risk factors for IOA is the use of muscle relaxants such as succynylcholine that do not induce loss of consciousness and may prevent the patient from indicating that IOA is occurring. Another risk factor involves the use of light anesthesia for surgeries such as Caesarian sections or for patients with low cardiac reserve. Under these conditions, light anesthesia may be used as a precautionary measure, but may not be sufficient to prevent IOA (Thompson & Wafford, 2001). Each of these types of anesthetics has been implicated in increasing the risk for patient IOA, although there is some controversy among anesthesiologists as to the relative contributions of these general anesthetics and sedation approaches to the actual occurrence of OIA (Thompson & Wafford, 2001). There is some dispute as to whether the primary cause of IOA is more closely linked to patient profile and associated risk, the types of GA used and the role of dosing errors or equipment malfunction/poor monitoring as contributory factors. There are multifaceted effects of the pharmacologic agents used in general anesthesia on physiology, therefore, despite the conscious awareness level of the patient experiencing IOA, there may be little physical evidence associated with it (Ranta et al, 1998). For this reason, the surgical team may be unaware that the patient is exhibiting this distress unless it can be revealed by physiologic monitoring. The most common physiological manifestations associated with this type of stress, including muscular movement, hypertension, tacchycardia sweating and tears may be inhibited by the spectrum of pharmaceuticals used in general anesthesia (Ranta et al, 1998). In order to understand the biological mechanisms responsible for IOA, it is necessary to define the concept of consciousness and how drugs used in general anesthesia may affect this higher order brain function. The hypnotic aspect of anesthetics is the least well understood of the pharmacological properties of these agents, making the assessment of the physiological basis for IOA more difficult to explain.(Ghoneim, 2000) Consciousness is defined as the mental state in which an individual is able to process information about one’s surroundings. General anesthesia agents cause a loss of consciousness associated with the inability to experience serious pain. The main components of general anesthesia include hypnosis, analgesia, amnesia, muscle relaxation. Patients receiving general anesthesia require physiology support for respiration and cardiac function (Ghoneim, 2000). Recent research in this area includes the work of Allaire (2000) who has defined a “unified theory of narcosis” involving thalamic cortical networks who activity is directly affected by general anesthesia. In 2005, John and Prichep proposed an “anesthetic cascade” to account for the effects of general anesthesia. Important components involve depression of the brainstem, depression of the mesolimbic dorsolateral prefrontal cortex to inhibit memory, depression of the reticular activating system to affect thalamic cortical functions. Ultimately there is depression of parietal cortical associations that block cognition and awareness (Lenmarkin & Sandin, 2004). Some recommendations set forth by the ASA to reduce the likelihood of its occurrence include the rigorous monitoring of anesthesia during surgery, proper maintenance of equipment and the identification of patients who may be at risk for this occurrence in order to apply preventive protocols (Sandin et al, 2000). Difficulties in patient assessment for signs of IOA may result from the masking effect of pharmacologics used in anesthesia that may override increased blood pressure, heart rate, muscular contraction and other symptoms of stress that might otherwise be used to assess the presence of IOA. Some of these agents include beta blockers, calcium channel blocxkers and paralytic agents (Sandin et al, 2000). For these reasons, it is essential to utilize measure of brain activity as a tool for monitoring patient consciousness levels during surgery that may indicate the occurrence of IOA (Lenmarkin & Sandin, 2004). EEG devices that monitor consciousness levels are called level-of –consciousness, sedation level and and anesthesia-depth monitors can be used for this purpose (Sandin et al, 2000). monitoring of brain activity is an essential component of detection and prevention of IOA during surgery. However, the use of EEG is not a foolproof method of assessing patient brain consciousness levels during general anesthesia, as there are many factors that affect its accuracy and sensitivity (Ekman, 2004). These include sensitivity to beta-blockers and muscle relaxants, electrical equipment effects on readings, and other factors that may aff Conclusion Anesthesiologists are generally in agreement, however, that patientSome recommendations set forth by the ASA to reduce the likelihood of its occurrence include the rigorous monitoring of anesthesia during surgery, proper maintenance of equipment and the identification of patients who may be at risk for this occurrence in order to apply preventive protocols (Sandin et al, 2000). Difficulties in patient assessment for signs of IOA may result from the masking effect of pharmacologics used in anesthesia that may override increased blood pressure, heart rate, muscular contraction and other symptoms of stress that might otherwise be used to assess the presence of IOA. Some of these agents include beta blockers, calcium channel blocxkers and paralytic agents (Sandin et al, 2000).For these reasons, it is essential to utilize measure of brain activity as a tool for monitoring patient consciousness levels during surgery that may indicate the occurrence of IOA (Lenmarkin & Sandin, 2004). EEG devices that monitor consciousness levels are called level-of –consciousness, sedation level and and anesthesia-depth monitors can be used for this purpose (Sandin et al, 2000). monitoring of brain activity is an essential component of detection and prevention of IOA during surgery. However, the use of EEG is not a foolproof method of assessing patient brain consciousness levels during general anesthesia, as there are many factors that affect its accuracy and sensitivity (Ekman, 2004). These include sensitivity to beta-blockers and muscle relaxants, electrical equipment effects on readings, and other factors that may affect the sensitivity of EEG recordings. Recent research studies suggest that BIS which involves an algorhithm that converts single channel frontal EEG to a readable hypnotic level index may represent a very useful monitoring tool to prevent and/or detect the occurrence of IOA (Myles et al, 2004).A number of preventive measures has been recommended by anesthesiologists. These include patient premedication with drugs such as benzodiazepines or scopalomine that induce amnesia, avoiding muscle paralyzing agents or, if necessary, using these muscle relaxants stringently. It is also essential to monitor patients on beta blockers or calcium channel blockers for signs of conscious awareness by EEG scans. (Myles et al, 2004Conclusion Conclusion In conclusion, IOA represents an important clinical problem associated with general anesthesia. Although there exists some controversy within the medical profession as to the extent and significance of this problem, it is clear that when it does occur, IOA is an extremely stressful experience that can have a lasting impact on the patient, impede recovery and contribute to post traumatic stress disorder in some individuals. Research identifying important risk factors and the pharmacologic properties of drugs that may, under certain conditions, precipitate IOA represents an important step forward un developing new approaches to prevent this problem. Most importantly, better methods of detection of incipient IOA during general anesthesia, such as EEG-bispectral imaging, may help to alleviate this serious clinical issue. References Ekman A, Lindholm M L, et al 2004, ‘Reduction in the Incidence of Awareness Using BIS Monitoring,’ Acta Anaesthesiologica Scandinavica, vol. 48, pp.20-6. Fee Howard JP & Bovill GJ. 2005, Pharmacology for Anaesthesiologists. London: Taylor and Francis. Ghoneim M M., 2000,’Awareness during anesthesia,’ Anesthesiology, vol. 92, no.2, pp.:597-602. Lennmarken C.& Sandin R 2004, ‘Neuromonitoring for awareness during surgery’ Lancet, vol.363, pp.1747-8. Myles P S, Leslie K, et al, 2004,’Bispectral index monitoring to prevent awareness during anaesthesia: The B-aware randomised controlled trial," Lancet, vol.363, pp.1757-63. Osterman .E., Hopper,J., et al.,2001, ‘Awareness under anesthesia and the development of posttraumatic stress disorder,’ General Hospital Psychiatry, vol. 23, pp.198-204. Rang HP, Dale MM, Ritter JM, Flower RJ. 2008, Rang and Dale’s Pharamacology. 6th Edition. China: Churchill Livingstone Elseiver. Ranta SO-V, Laurila R, Saario J, Ali-Melkkila R, & Hynynen M. 1998, ‘Awareness with recall during general anesthesia: Incident and Risk Factors.’ Anesth Analg vol. 86, pp.1084-9. Sandin RH, Enlund G, Samuelsson P, & Lennmarken C.2000, ‘Awareness during anaesthesia: A prospective case study’. , vol. 355, pp.707-11. Sebel PS., Bowdle TA, et al, 2004, ‘The Incidence of Awareness During Anesthesia: A Multicenter United States Study’ Anesth Analg, vol. 99, pp.833-9. Sneyd JR & Mathews DM. 2008, ‘Memory and awareness during anaesthesia’. British Journal of Anaesthesia, vol.100, no. 6, pp. 742-4. Spitellie PH, Holmes MA, et al, 2002, ‘Awareness During Anesthesia,’ Anesthesiology Clinics of North America, vol. 20, pp.555-70. Thompson SA & Wafford K. 2001, ‘Mechanism of action of general anaesthetic- new information from molecular pharmacology. Currrent Opinion in Pharmacology, vol. 1, pp. 78 -83. Read More
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