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Intraoperative Awareness - Case Study Example

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The paper "Intraoperative Awareness" discusses that all general anaesthetic drugs, having different mechanisms of actions, provide unconsciousness only at the desired drug concentrations in the brain and consciousness will return as those concentrations decline from surgical anaesthesia stage…
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Intraoperative Awareness
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of Bradford Anaesthesia Awareness: Mechanism and Management Special Studies Abida Ansari UB: 07029228 /12 Essay submitted as part of the summative assessment for Special Studies 1. Word Count: 2039 Anaesthesia Awareness: Mechanisms and Management Introduction: Intraoperative awareness or anaesthesia awareness is the unintended awareness experienced by the patient while under general anaesthesia which manifests itself as the sensation of feeling or partial consciousness that occurs in some individuals during surgical procedures in which the patient has been given general anaesthetic.1, 2 In the UK extensive trials have demonstrated that anaesthesia awareness affects 1-2 cases per 1000 patients under going general anaesthesia for surgical procedures. It is estimated that up to one-third of patients experiencing anaesthesia awareness suffer psychological trauma as a result of this experience. 3-5 Anaesthesia awareness is more common in patients in whom anaesthesia is administered intravenously compared to patients anaesthetised by inhalation.5, 6, 7 It is not confined to any gender or age, but is reported to occur more frequently during cardiovascular surgery, 7, 8 caesarean sections and trauma surgery. Also, research suggests that anaesthesia awareness may be more prevalent in individuals with a history of substance misuse, which include chronic alcohol, anti-epileptic, opiate or other sedative drug use. Additional factors may also include limited cardiovascular reserve and a previous history of anaesthesia awareness; this may result in them developing anxiety disorders of varying severity and post-traumatic stress disorder (PTSD); which includes flashbacks, panic -attacks and the feeling of fear, anxiety and nightmares.8, 9, 10 Overview of General Anaesthetic Agents General anaesthetic agents fall into two categories: inhalation and intravenous. Inhalation drugs are in the form of gases or volatile liquids, and act either by amplifying inhibitory function or decreasing excitatory transmission at the nerve endings in the brain12, 22 Fluorinated hydrocarbons are the most useful inhalation anaesthetics.22-25 The most commonly used inhalation anaesthetics are desflurane, isoflurane and sevoflurane.25. Less commonly used inhalation agents include halothane, enflurane and methoxyflurane.27,28 On the other hand, intravenous anaesthetics are administered through the venous route instead of inhalation, wherein action of the drug is generally the same as inhalation general anaesthetics. The most commonly used intravenous general anaesthetic drugs are propofol, etomidate, ketamine and thiopentone.30, 31 Different general anaesthetic agents can be combined (e.g. isoflurane, then nitrous oxide)26. Common general anaesthetic agents are listed on Table 1. 19, 20, 21 Route Drugs Inhalation isoflurane desflurane nitrous oxide sevoflurane Intravenous propofol etomidate ketamine thiopentone Muscle relaxants* succinylcholine mivacurium atracurium vecuronium pancuronium Table 1. Drugs commonly used in anaesthesia, which are divided into those used intravenously, by inhalation and the muscle relaxants that are used in addition to that method. Mechanisms of Action of General Anaesthesia Agents It is now believed that the main site of action for general anaesthetics was in the CNS rather than the cellular plasma membrane. 12, 21, 22, 28 The more accepted mechanism of action for inhalation anaesthetic is the inhibition of receptor mediated excitatory functions which appears to be a major component of the pharmacologic action of this class of drugs.21, 24, 25 Among the affected receptors are nicotinic-acetylcholine receptors,30 glutamate receptors and 5-HT3 receptors,29 GABAA receptors and TREK channels.30,31,32 Recent research in the area of awareness includes the “unified theory of narcosis” involving thalamic cortical networks where activity is directly affected by general anaesthesia.37, 38 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.39, 40 Ultimately there is depression of parietal cortical associations that block cognition and awareness. For instance, the inhalation anaesthetic isoflurane binds to several types of neurotransmitter receptors to produce muscle relaxation and decrease pain sensitivity.27, 28, 29 Among the target receptors are GABA receptors, glutamate and glycine receptors.23-25 Isoflurane also blocks potassium channel conduction, the binding to glycine receptors effects muscular relaxation and blocks motor activities. The increase of the activity of calcium ATPase by binding to ATP synthase and NAD dehydrogenase results to increased membrane fluidity, which increases the membrane’s resistance to decrease the electrical potential (same principle in the Ohm’s law). This class of drugs also appears to block gap junction intercellular interactions by inhibiting electrical synapses that promote existing neuronal activities which may also contribute to depression of neural responses and its consequent anaesthetic effects.21, 29 NMDA receptor antagonists (e.g. Ketamine, Nitrous Oxide) bind to cellular glutamate, glycine and allosteric binding sites, thereby competing with NMDARs (glutamate, glycine), blocking the electrical signals between the neurons and the spinal column43. They also enhances the activity of opioid μ receptors.20,21,25,26 Ketamine also acts as a catecholamine re-uptake inhibitor, leading to sympathomimetic effects in vital signs and altered mental status.21,25 Benzodiazepines (e.g. midazolam) are used together with general anaesthesia to prolong the anaesthetic effect. Like the barbiturate thiopental sodium, these drugs also work with GABA receptors in enhancing its inhibitory action. By binding to the benzodiazepine site of the GABA receptor, opening frequency of the chloride ion channel is increased, allowing chloride ions flow inside the cell to produce an inhibitory effect to the activity on neurons, producing unconsciousness on adequate doses. Opioid anaesthetics (e.g. fentanyl), on the other hand, works with the opioid receptors to depress the CNS. General Anaesthesia and Anaesthesia Awareness Inadequate drug concentrations of these anaesthetics to the brain, beyond their anaesthetic dose, allows consciousness to return, thereby anaesthesia awareness is expected even if their analgesic effects retain. For example, without adequate amount of NMDA receptor antagonists, there is ineffective blocking of all available NMDA receptors, allowing glutamate and glycine to bind in some of these unblocked receptors, causing anaesthesia awareness. Another anaesthetic drug, isoflurane, when the amount of drug is not adequate enough to bind with all available GABA receptors, will result to failure of inhibiting all intracellular electrical synapses, which will result to anaesthesia awareness by the remaining unbounded GABA receptors. The role of general anaesthetic agents in anaesthesia awareness comes in when these drugs failed to reach the surgical anaesthesia stage. There is ongoing debate among anaesthesiologists as to the relative contributions of various general anaesthetics and sedation approaches to the prevalence of anaesthesia awareness.35,36,37 There is some dispute whether or not the primary cause of anaesthesia awareness is more closely linked to patient profile and its associated risks, the types of general anaesthetic used and the role of dosing errors or equipment malfunction/poor monitoring as contributory factors.7,9 The pharmacological agents used whilst inducing general anaesthesia have multifaceted physiological effects.12, 20 As a result the signs that a patient has regained awareness may be masked; for example the use of neuromuscular blockade prevents movement and thus signalling to the surgical team, cardiovascular signs may be blocked by beta blockers, which are used to control myocardial function, heart rate, blood pressure and vascular resistance.12, 16, 24 Muscle Relaxants and Anaesthesia Awareness This incidence of awareness is halved with the absence of a neuromuscular blockade, making the use of muscle relaxants (e.g. succinylcholine) as one of the greatest risk factor in developing anaesthesia awareness.12, 21, 24 These agents allow motor paralysis to facilitate the tracheal tube insertion (where inhalation anaesthetics are delivered) and to allow respirations to be controlled to adjust the dosage of inhaled anaesthetic agent.29,32 Consequentially, the patient will also lose the ability to communicate awareness through the use of motor muscles since we always check the patient’s motor responses to assess consciousness when we use the Glasgow Coma Scale (e.g. guarding behaviour as response from pain stimulus, decorticate and decerebrate positioning), and even the patient’s ability to blink or to cry.33-35 The use of muscle relaxants must be used only when necessary, avoiding its use when possible. Should the use of muscle relaxant is really necessary, other methods on assessing consciousness should be utilized (which will be discussed below). Management of Anaesthesia Awareness The phenomenon is more commonly reported where anaesthesia is exceptionally delicately balanced due to high levels of anaesthetic risk, ensuring that the minimum necessary dose is administered due to potential complications.9-11 The most commonly reported manifestations include perception of pain, awareness of paralysis, heightened anxiety and recall of intraoperative conversations. It is less common for the patient to experience visual sensation or to be aware of intubation.12 Additional possible causes of anaesthesia awareness may include individual variations at receptor level or in pharmacokinetics;11, 15 either innate or iatrogenic, difficulty assessing consciousness level5, 7 and inadequate intraoperative monitoring may make some individuals13, 14 more likely to develop anaesthesia awareness.16-18 Managing anaesthesia awareness begins with meticulous preoperative assessment, wherein the patient is asked about alcohol, nicotine and recreational drug use, and medications taken, including herbal and dietary supplement use.44 Some substances taken by the patient may have drug interactions with the anaesthetic to be used, for instance, zimelidine antagonizes thiopental sodium, so expect anaesthesia awareness to occur. Another solution is to ensure the proper administration of the anaesthetic drug, which lies mainly on the anaesthesiologist’s competence and experience in maintaining intraoperative surgical anaesthesia. Also discussed above is the role of muscle relaxants in suppressing the patient’s ability to express intraoperative consciousness to the anaesthesiologist. Consciousness is frequently assessed through the patient’s reaction to verbal command or to painful stimulus, but without the patient’s ability to express this response due to loss of motor functions, the patient is paralyzed but awake. Therefore, it is essential to utilise alternative measures to assess consciousness while the patient is paralyzed by muscle relaxants, through the monitoring of brain activity during surgery that may indicate the occurrence of anaesthesia awareness.41 Among those are the use of electroencephalogram (EEG), bispectral index monitor (BIS). Isolated forearm technique can be used when the general anaesthesia does not include the use of muscle relaxants or when it was still not yet administered. Electroencephalogram is the most common method of assessing intraoperative consciousness during general anaesthesia through monitoring the brain activity. The wave form of an awaken patient is different from the wave form of an unconscious patient. It also displays a number which indicates whether the patient is awake or not. However, there is an issue on its accuracy and sensibility. The anaesthesiologist must be experienced enough to detect EEG artefacts so that he will not be treating the monitor rather than the patient. 45 Bispectral Index Monitor, which also utilizes EEG, is a statistics-based index which can also predict intraoperative consciousness under general anaesthesia which displays a number to indicate the depth of patient’s unconsciousness.46 This can predict the probability of recovery from consciousness47 but a study shows that anaesthesia awareness still occur even within the value revealing unconsciousness48 making it an unproven way in protecting the patient from anaesthesia awareness.37 The isolated forearm technique can indicate wakefulness but not necessarily explicit awareness. A tourniquet is applied to the patient’s upper arm and inflating above the systolic blood pressure PRIOR to administration of muscle relaxant. Movement of arm indicates wakefulness but not necessarily explicit awareness, and no longer useful after the administration of the muscle relaxant. 39, 40, 42 A combination of consciousness-identification strategies is recommended to immediately signal the surgical team if the patient manifests anaesthesia awareness. It would also be advisable to have in place an emergency management plan if anaesthesia awareness is suspected.9, 10, 16, 23, 32, 37, 40 Conclusion Anaesthesia awareness represents an important clinical problem associated with general anaesthesia. Despite some controversy exists within the medical profession as to the extent and significance of this problem, it is clear that when it does occur, anaesthesia awareness 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 pharmacological properties of drugs that may precipitate anaesthesia awareness represent an important step forward in developing new approaches to prevent this problem. All general anaesthetic drugs, having differing mechanisms of actions, provide unconsciousness only at the desired drug concentrations in the brain and consciousness will return as those concentrations decline from surgical anaesthesia stage. Most importantly, better methods of detection of anaesthesia awareness during general anaesthesia such as EEG, bispectral imaging and isolated forearm technique (only prior to use or disuse of muscle relaxant) may help to alleviate this serious clinical issue though there is no current regimen to fully assure a patient not to experience an anaesthesia awareness experience intraoperatively. Further research is warranted on fully protecting patients from anaesthesia awareness even it rarely occurs. Word Count: 2039 References 1. Osterman E, Hopper J, Herran W, Keane T, van der Kolk B. Awareness under anesthesia and the development of posttraumatic stress disorder. Jr General Hospital Psychiatry 2003; 23: 198-204. 2. Sebel PS et al. The Incidence of awareness during anesthesia: a multicenter United States study. Anesthesia and Analgesia 2004; 99:833-9. 3. Osborne GA, Bacon AK, Runciman WB, Helps, SC. Crisis management during anaesthesia: awareness and anaesthesia. Quality and Safety in Health Care. 2005; 14:16. 4. Myles P. Prevention of awareness during anaesthesia. Best practice and research clinical anesthesiology 2007; 21: 345-55. 5. Ghoneim MM. Awareness during anesthesia. Anesthesiology 2000; 92: 597-602. 6. Davidson AJ et al. Detecting awareness in children by using an auditory intervention. Anesthesiology 2008; 109: 619-24. 7. Forman S. Awareness during general anaesthesia: concepts and controversies. Perioperative Medicine and Pain 2006; 25: 211-8. 8. Domino KB, Posner KL, Caplan AR, Cheney WF. Awareness during anesthesia. Anesthesiology 1999; 90: 1053-61. 9. Ranta SO-V, Laurila R, Saario J, Ali-Melkkila R, Hynynen M. Awareness with recall during general anesthesia: incident and risk factors. Anesthesia and Analgesia 1998; 86: 1084-9. 10. Sandin RH, Enlund G, Samuelsson P, Lennmarken C. Awareness during anaesthesia: a prospective case study. Lancet 2000; 355:707-11. 11. Ekman A, Lindholm M L, Lennmarken C, Sandin R. Reduction in the incidence of awareness using BIS monitoring, Acta Anaesthesiologica Scandinavica 2004; 48: 20-6. 12. Howard JP, Bovill GJ. Pharmacology for Anaesthesiologists. London: Taylor and Francis. 2005 13. Lennmarken C, Sandin R. Neuromonitoring for awareness during surgery. Lancet 2003; 363: 1747-8. 14. Myles PS, Leslie K, McNeil J, Forbes A, Chan MT. Bispectral index monitoring to prevent awareness during anaesthesia: the B-aware randomised controlled trial. Lancet 2004: 363: 1757-63. 15. Pollard JR, Coyle PJ, Gilbert LR, Beck EJ. Intraoperative awareness in a regional medical system. Anesthesiology 2007; 106: 269-74. 16. Rang HP, Dale MM, Ritter JM, Flower RJ. Rang and Dale’s Pharamacology 6th Edition. China: Churchill Livingstone Elseiver 2008. 17. Dowd PN, Cheng CHD, Karski MJ, Wong TD, Munro CJA, Sandler NA. Intraoperative awareness in fast track cardiac anaesthesia. Anesthesiology 1998; 5: 1068-73. 18. Sneyd JR, Mathews, DM. Memory and awareness during anaesthesia. British Journal of Anaesthesia 2008; 100:742-4. 19. Spitellie PH, Holmes MA, Domino, K. Awareness during anesthesia. Anesthesiology Clinics of North America 2002; 20: 555-70. 20. Kerssens C, Klein J, Bonke B. Awareness - monitoring versus remembering what happened. Anesthesiology. 2003;99:570-5 21. Thompson SA, Wafford K. Mechanism of action of general anaesthetic- new information from molecular pharmacology. Current Opinion in Pharmacology 2001; 1: 78-83. 22. Malamed FS, Quinn LC. Sedation - a guide to patient management. Missouri: Mosby 1995. 23. Dundee WJ, Clarke RSJ, McCaughey W. Clinical Anaesthetic Pharmacology. London: Longman Group 1991. 24. Vickers MD, Morgan M, Spencer PSJ, Read MS. Drugs in anaesthetic and intensive care practice 8th edition. Kent: Reed Educational and Professional Publishing Ltd. 1999. 25. McCaughey W, Clarke R, Howard Fee JP, Wallace FMW. Anaesthetic physiology and pharmacology. Hong Kong: Pearson Professional Ltd. 1997. 26. Peck TE, Williams MA. Pharmacology for Anaesthesia and Intensive Care. London: Greenwich Medical Media Ltd. 2000. 27. Naish J, Revest P, Court SD. Medical Sciences. Saunders Elsevier 2009. 28. Glass SAP. Anesthetic drug interactions, an insight into general anaesthesia – its mechanism and dosing strategies. Anaesthesiology. 1998; 88:5-6. 29. Mullins LI. Some physical mechanisms in narcosis. Chem Rev 1954; 54: 289–323 30. Miyazawa A, Fujiyoshi Y, Unwin N (2003). "Structure and gating mechanism of the acetylcholine receptor pore. Nature 2003; 423: 949–55. 31. Ishizawa Y. Mechanisms of anaesthetic actions and the brain. Anaesthesiology 2007; 21: 187-99. 32. Little HJ. How has molecular pharmacology contributed to our understanding of the mechanisms of general anaesthesia. Journal of Pharmacology Therapy. 1996. 69: 37 -58 33. Rosow CE. Anesthetic drug interaction: overview. Journal of Clinical Anaesthesia 1997; 9: 27S–32S. 34. Alkire MT, Haier RJ. Correlating in vivo anaesthetic effects with ex vivo receptor density data supports a GABAergic mechanism of action for propofol, but not for isoflurane. British Journal of Anaesthesia. 2001; 86: 618-26. 35. Mashour GA, Forman SA, Campagna. Mechanism of general anaesthesia: from molecules to mind. Best Practice and Research Anaesthesiology. 2005; 19: 349-364. 36. Mashour GA, Larock E. Inverse zombies, anesthesia awareness, and the hard problem of unconsciousness. Consciousness and Cognition. 2008; 17: 1163–1168 37. O’Connor MF, Daves MS, Tung A, Cook RI, Thisted R, Apelfaum J. BIS monitoring to prevent awareness during general anesthesia. Anesthesiology. 2001; 94: 520-2. 38. Samulesson P, Brudin L, Sandin HR. Late psychological symptoms after awareness among consecutively included surgical patients. Anesthesiology. 2007: 106: 26-32. 39. Apfelbaum, J et al. Practice Advisory for Intraoperative awareness and brain function monitoring. Anesthesiology. 2006; 104: 847-64. 40. Lennmarken C, Sydsjo. Psychological consequences of awareness and their treatment. Best Practice and Research Clinical Anaesthesiologist. 2007;21(3): 357-67. 41. Alkire MT, Haler RJ, Falon JH. Toward a Unified theory of narcosis: brain imaging evidence for a thalmocorticol switch as the neurophysiologic basis of anaesthetic induced unconsciousness. Consciousness and Cognition. 1999; 9 (3): 370–86. 42. Arnot Smith J, Smith FA. Patient safety incidents involving neuromuscular blockade: analysis of the UK National Reporting and Learning System. Data from 2006 to 2008. Journal of the association of anaesthetists of Great Britain and Ireland 2010; 65: 1106–1113. 43. Kim AH, Kerchner GA, Choi DW. Blocking excitotoxicity. CNS Neuroproteciton 2002: 3-36. 44. Black, J, Hawks JH. Medical-surgical nursing: clinical management for positive outcomes 7th edition. Singapore: Elsevier 2005. 45. Bennett C, Voss L, Barnard J, Sleigh J. Practical use of the raw electroencephalogram waveform during general anesthesia: the art and science. Anesthesia and Analgesia 2009; 109: 539-50. 46. Kaul HL, Bharti N. Monitoring depth of anaesthesia. Indian Journal of Anaesthesiology 2002; 46. 47. Flaishon R, Windsor A, Sigl J, Sebel, PS. Recovery of consciousness after thiopental or propofol: bispectral index and the isolated forearm technique. Anesthesiology 1997; 86: 613-619. 48. Avidan S et al. Anesthesia awareness and the bispectral index. The New England Journal of Medicine 2008; 358: 1097-1108. Read More
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