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Patients are usually kept at degrees during surgery to facilitate venous drainage. Paralyze adequately and achieve deep general anesthesia before DL, maintain PaCO2 of mm Hg during surgery, avoiding PEEP if possible, as it can impair venous return from the brain.

Avoid agitation on emergence. Additional means include administration of thiopental or lumbar catheter drainage if available.


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Following the craniotomy and dural incision, anesthetic requirements drop substantially, as the brain itself is insensate. Relaxants should be held until the head dressing is completely on, as movement in response to the endotracheal tube can be detrimental. Acta Neurochir Suppl 89, ].

Two recent studies have cast doubt on this common assumption — first, in a follow up study, Petersen et al. More recently, Gelb et al. Avoid ICP changes. Bed at degrees facilitates venous draininge from brain.

Hyperventilation only lasts hrs. Deeply paralyze for intubation, avoid agitated emergence. There is a known association between emergence hypertension and post-operative hemorrhage — Basali et. Mortality rate in patients who suffered POH increased from 1.

Note, however, that the overall POH rate was only 0. Anesthesiology 48, ] In order to prevent intraoperative hemorrhage on emergence, consider the following techniques: 1. From intracranial vascular procedures and major spine cases to functional neurosurgery and carotid endarterectomy, the learner in neuroanesthesia will find both a preview of what a prototypical case entails and a description of common critical events and concerns in the first half of this text. Special attention is given to preoperative assessment and postoperative complications for each class of procedure. Pediatric neuroanesthesia receives its own separate section, as does the discussion of an assortment of neurologic sequelae in other patient populations including pregnancy, liver failure, and nonneurosurgical procedures.

The second half of the text is given over to discussion of the intensive care of the neurosurgical patient. Topics covered include basics of the intensive care unit, such as management of hypotension, mechanical ventilation, and end-of-life issues, as well as common neurosurgical problems, such as vasospasm, hyponatremia, and status epilepticus. Good case selection and the close interrelationship of the neurosurgical intensive care unit and neurosurgical operating suite keep many of the vignettes directly translatable to intraoperative anesthesia care.

This section should also be considered essential reading for residents who are primarily concerned with the operating room environment. As with any overview or survey of a subspecialty, caveats regarding the level of detail and depth on any specific topic apply. With two to four pages of text allotted for each vignette, one cannot expect a thorough discourse on the subtleties of either surgical procedures or physiologic principles.

In this regard, the editors undertake a significant challenge by including such intricate problems as postarrest cooling and decooling and noncardiac surgery in a patient with a ventricular assist device. Although such topics might be soundly discussed over the course of several vignettes, as the editors do with aneurysm clipping and other major neurosurgical procedures, the brief treatment these topics receive in a single case description do well by mentioning the highlights and recommending other relevant resources.

Practitioners who encounter these entities in practice hopefully have a robust appreciation of the complexity involved with their management, and can draw upon the experiences of their colleagues for more guidance. The book provides ready reference for teaching in the operating room, and will be especially useful for correlation to the day's clinical experiences. It is suitable as a primary text for residents rotating in neuroanesthesia, and deserves a place on the bookshelf of fellows and other learners in neuroanesthesia as well.

This is a very successful first iteration of a sound and much-needed approach to teaching the subspecialty of neuroanesthesia. Get Permissions. Get Citation Citation. Landmark Papers in Anaesthesia. Handbook of Neuroanesthesia, Fifth Edition. Anaesthetists have historically not focused on delirium because it typically manifests when patients are no longer under their direct care. Delirium causes distress to patients and their families, and is a frustrating problem for clinicians as no treatments have been available to decrease its incidence or mitigate its duration.

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One of the reasons that delirium is difficult to prevent or treat is that several pathological pathways have been implicated, including neurotransmitter imbalance, neuroinflammation, endothelial dysfunction, impaired oxidative metabolism, and altered availability of large neutral amino acids. Nonetheless, there are important risk factors for delirium that should be prevented or alleviated. These include pain, acute medical conditions, sleep disturbance, sensory impairment, social isolation, daylight deprivation, infections, withdrawal syndromes, dehydration, blood loss, blood transfusion, electrolyte abnormalities, acid—base abnormalities, hypoxaemia, temperature derangements, seizures, and endocrine dysfunction.

Given that postoperative delirium is so common, any approach that prevented it or lessened its consequences would have major clinical impact. Evidence has recently emerged from randomized controlled trials that guiding both total i. However, if slightly deeper anaesthesia in vulnerable surgical patients were to increase the risk of postoperative delirium, we would expect regional anaesthesia to be associated with a considerably lower incidence of postoperative delirium than general anaesthesia. A meta-analysis of small trials that randomized surgical patients to regional albeit with light sedation or general anaesthesia surprisingly found no increased risk for delirium with general anaesthesia odds ratio, 0.

Various perioperative pharmacological agents have been investigated for the prevention of delirium and some success has been noted with low-dose haloperidol, subanaesthetic dose ketamine, and perioperative dexmedetomidine. After operation or in the critical care setting, the discomfort caused by limb restraints, bladder catheters, tracheal tubes, invasive lines, surgical drains, and enteral tubes increase agitation, and these should be discontinued when possible. However, when pain is severe, opioid medications have been reported both to alleviate pain and to decrease delirium.

The National Institute of Health and Care Excellence in the UK has highlighted clinical pathways covering risk, prevention, diagnosis, and management for patients at risk of delirium, although the focus on and evidence regarding surgical patients is limited pathways. POCD is a major concern for elderly surgical patients and their families. In , Bedford 43 warned in the Lancet that people older than 50 yr should avoid surgery if possible in view of the high risk of cognitive decline. Conceptually, POCD is a subtle and frequently transient cognitive decline that is often only detectable with appropriate neuropsychological tests and a comparison with preoperative cognition.


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  • The study found that at 7. As meaningful cognitive decline occurs with ageing, even from the age of 45 yr, 56 it is unsurprising that studies without appropriate age- and disease-matched controls have found cognitive decline in older patients with various morbidities during the intermediate- to long-term period after surgery. Many studies in this area have had major limitations including lack of appropriately matched non-surgical controls, absence of data on preoperative cognitive trajectories, suboptimal statistical approaches, and failure to contextualize cognitive outcomes considering the success of surgery and the general postoperative course.

    It would not be surprising if this hypothetical patient were to experience persistent POCD. Pain, inflammation, and acute illness carry a cognitive burden; 58—60 it is therefore to be expected that patients will experience cognitive impairment in the early postoperative period, analogous to sickness behaviour.

    However, when patients recover from the insult of surgery, they might revert to their predicted cognitive paths, based on their preoperative trajectories. Those who have improvement of their general health compared with the preoperative baseline might even experience relative cognitive improvement. This could occur when surgery results in decreased pain e. Although the notion that cognition could improve and decline after surgery is controversial, it is consistent with discoveries that the brain retains plasticity throughout life and preliminary research showing increased brain volumes or cognitive performance after successful surgeries, such as back surgery, joint surgery, carotid surgery, cardiac surgery, and ventricular assist device surgery.

    From the anaesthetist's perspective, whether or not general anaesthesia contributes to POCD remains uncertain and highly relevant. A recent meta-analysis aggregating 26 randomized trials that compared general and regional anaesthesia—albeit with light sedation—did not find that general anaesthesia was independently associated with POCD. It has become clear that postoperative cognition should not be assessed in a vacuum and cannot be dissociated from the general outcome of surgery. Given that even early POCD is associated with intermediate-term mortality and worse long-term quality of life, 49 , 50 efforts should be focused on general and cognitive perioperative rehabilitation in order to minimize persistent POCD, to return cognition to the preoperative trajectory, and where possible to promote relative cognitive improvement.

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    Perioperative stroke is defined as a cerebral infarction of ischaemic or haemorrhagic origin that occurs during or after surgery, with the postoperative time period sometimes defined as up to 30 days. Bucerius and colleagues 66 studied 16 consecutive patients presenting for cardiac surgery and identified a perioperative stroke incidence of 4. The multicentre GALA trial studied patients presenting for carotid surgery with general anaesthesia or local anaesthesia with sedation.

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    The incidence of stroke in the non-cardiac, non-vascular, and non-neurological surgical population is significantly lower. It is important to note that these data reflect the incidences of overt stroke, that is, stroke with a clinically obvious neurological deficit.

    Recent preliminary data derived from non-cardiac surgery in patients with cardiovascular risk factors NeuroVISION trial suggest that the incidence of covert stroke i. Perioperative strokes have varying aetiologies across different patient populations and surgical procedures, but are primarily ischaemic as opposed to haemorrhagic.

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    Strokes after cardiac surgery are most likely to be embolic, 71 whereas strokes occurring in the non-cardiac surgery population are of both embolic and thrombotic origin. One of the most consistent risk factors for perioperative stroke in cardiac and non-cardiac surgery is a history of cerebrovascular disease, as evidenced by past stroke or transient ischaemic attack. Intraoperative hypotension has been associated with perioperative stroke in the non-cardiac surgical population, but the effect size is minimal and the clinical significance is not yet clear.

    Risk factors for perioperative stroke. Modified with permission from Moore and colleagues, pp. Surgical patients with perioperative stroke have a higher mortality than propensity-matched surgical patients without stroke. Recent studies from Mashour and colleagues 76 and Ashes and colleagues 80 have found that the routine use of perioperative metoprolol is associated with stroke after non-cardiac surgery.

    If a stroke is identified in the postoperative setting, it is imperative to consult immediately with a stroke neurologist, arrange for neuroimaging non-contrast head computed tomography and possibly magnetic resonance imaging , and avoid physiological perturbations that can exacerbate neural injury e. It is important to remember that surgeries other than intracranial or spinal procedures are not an absolute contraindication to therapy with tissue plasminogen activator given i.

    Spinal cord ischaemia SCI is a potentially devastating complication associated with the surgical repair of thoracoabdominal aneurysms and dissections. The reported incidence of SCI is varied, likely because patient cohorts are heterogeneous with regard to aneurysm type, preventive modalities, and surgical technique. Immediate-onset SCI present on emergence from anaesthesia may be caused by interruption of the blood supply to the spinal cord at any point of the operation; a spinal cord infarction may be several hours old at the time of initial recognition.

    Description

    Native blood supply to the anterior spinal cord is from both the single anterior spinal artery and from multiple segmental radicular intercostal tributaries. Collateral artery ligation during surgical dissection, aortic cross-clamp application, and collateral artery coverage by an endovascular stent can all cause immediate SCI by interrupting blood flow through the intercostal arteries. Delayed-onset SCI may be because of postoperative collateral thrombosis or a decrease in spinal cord perfusion pressure [hypotension, increased cerebrospinal fluid CSF pressure of ischaemia—reperfusion, or both].

    The most widely accepted risk factor for SCI is the location and extent of the aortic aneurysm itself. Svensson and colleagues 84 and Conrad and colleagues 88 correlated the incidence of SCI and the location of the aneurysm, demonstrating a decreasing incidence from Crawford types I and II both high thoracic origin to type III mid-thoracic origin to type IV distal thoracic origin aneurysms. Other risk factors include cross-clamp time more important when distal reperfusion techniques are not utilized , emergency operations, aortic rupture or dissection, and possibly intraoperative hypotension.

    Identification and reimplantation of non-selected segmental intercostal arteries does not clearly reduce SCI risk but may be of benefit when extensive aortic replacement is necessary. Thoracic endovascular aneurysm repair may have a lower incidence of SCI, which is likely attributable to fewer risk factors associated with the procedure. This is despite the fact that multiple segmental arteries are covered in the course of the operation, again pointing to a varied set of SCI risk factors for any particular patient. A history of infrarenal abdominal aortic aneurysm repair or internal iliac artery obstructions decreased contributions to collateral flow may increase SCI risk in patients undergoing endovascular repair.

    Outcome after SCI is exceptionally poor. The protection provided to the spinal cord by CSF drainage has been demonstrated in case reports and case series for both open and endovascular repairs of thoracoabdominal aneurysms. In the largest prospective randomized controlled trial, it was demonstrated that CSF drainage was associated with a decreased incidence of SCI: 2.

    Risks of placement include infection, haematoma, spinal cord or nerve root injury, meningitis, retained drain fragments, and intracranial haemorrhage. Delayed SCI resulting in partial or complete paraplegia has been reported even several weeks after surgery, but it most commonly presents in the first several postoperative days. Hypotension is the most common cause and reflects the pressure-dependent nature of collateral flow. When delayed-onset paraplegia does present, immediate treatment e.

    Placement or replacement of a spinal drain has been successfully used to rescue patients with delayed-onset paraplegia in the postoperative period. POVL is a rare but devastating neurological complication of elective surgery and can be caused by central retinal artery occlusion, cortical blindness, and ischaemic optic neuropathy ION. Patil and colleagues 95 used the same database with different inclusion criteria and found a 0. Stevens and colleagues 96 reported an even higher incidence of POVL after spine surgery at three institutions, with 0.

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    Discrepancies in the incidence likely relate to the database used and also inclusion criteria. Collectively, the data suggest that cardiac surgery and posterior spine surgery are the highest risk categories for POVL and ION, although the complication is by no means limited to these surgeries. Risk factors associated with anterior ION in cardiac surgery include prolonged cardiopulmonary bypass, anaemia, excessive perioperative weight gain, and use of epinephrine and amrinone. Notably, neither anaemia nor haemodynamic variables were predictors; a single-centre case—control study was also unable to find haemodynamic differences associated with ION.

    Risk prediction for ION after posterior spine surgery. Given the rarity, the outcomes of POVL are difficult to assess.