- Email: [email protected]
Pressure support ventilation in tetraplegia
Correspondence
T. Asai K. Shingu Osaka, Japan
EditorÐThank you for the opportunity to respond to this correspondence. We described a temporal association between a devastating deterioration in neurological function and the insertion of a laryngeal mask airway. In our patient, there was probably pre-existing unrecognized damage to the posterior longitudinal ligament. This was worsened during the procedure to create a haematoma and result in critical cervical cord compression. The presence of a haematoma at the site of complete rupture on MRI scan and at surgical decompression was taken as a sign of recent injury. We acknowledged the potential reduction in spinal perfusion pressure that may accompany moderate arterial hypotension during anaesthesia.1 Cervical spinal cord injury produced by airway manoeuvres is extremely rare. We agree that if measures are taken to protect the neck in suspected cervical spine injury, then the airway can be secured safely. In our case, there was no suspicion of cervical spine abnormality and therefore no such protective measures were taken. Cadaveric and radiological studies may describe expected cervical spine movement in speci®c populations. However, there is still a place in the literature for a case report describing a catastrophic event as a result of a combination of unusual circumstances.
C. J. Edge V. Addy C. Kearns Oxford, UK 1 Edge CJ, Hyman N, Addy V, et al. Posterior spinal ligament rupture associated with laryngeal mask insertion in a patient with undisclosed unstable cervical spine. Br J Anaesth 2002; 89: 514±17 2 White AA, Johnson RM, Panjabi MM, Southwick WO. Biomechanical analysis of clinical stability in the cervical spine. Clin Orthop 1975; 109: 85±96 3 McLeod AM, Calder I. Spinal cord injury and direct laryngoscopyÐ the legend lives on. Br J Anaesth 2000; 84: 705±9 4 May DM, Jones SJ, Crockard HA. Somatosensory evoked potential monitoring in cervical surgery: identi®cation of pre- and intraoperative risk factors associated with neurological deterioration. J Neurosurg 1996; 85: 566±73 5 Weglinski MR, Berge KH, Davis DH. New-onset neurologic de®cits after general anesthesia for MRI. Mayo Clin Proc 2002; 77: 101±3 6 Coppleters MW, Van de Velde M, Stappaerts KH. Positioning in anesthesiology: toward a better understanding of stretch-induced peripheral neuropathies. Anesthesiology 2002; 97: 75±81
DOI: 10.1093/bja/aeg554
Pressure support ventilation in tetraplegia EditorÐI read with interest the case reports describing an apparent failure of ¯ow triggering when using pressure support ventilation (PSV) for two patients with high cervical cord lesions.1 Case 1 involved a 66-yr-old man with an odontoid fracture, managed with halo stabilization. Using the Puritan Bennett 7200 with inspiratory pressure support of 16 cm H2O and 7.6 cm H2O PEEP, the initial inspiratory pressure support trigger was pressure dependent, set at 0.5 cm H2O. It had been noted the patient was unable to trigger at a sensitivity of 1.0 cm H2O. A trial of ¯ow triggering (using `¯ow-by') at basal ¯ow 5 and trigger 3 litre min±1 resulted in a fall in respiratory rate from 25 bpm to 14 bpm. We are not told the corresponding tidal volume but that the vital signs were unchanged, the patient appeared comfortable and oxygenated, and no evidence of accessory muscle activity was apparent. `An error in the ¯ow-by settings was suspected', but it is not clear why? I would be surprised if this machine was not in working order when it was checked after this critical incident. This patient had advanced and profound weakness with complete tetraparesisÐthe requirement of a 0.5 cm H2O pressure trigger is evidence of this. Flow-by and ¯ow triggering generally were originally devised to meet the initial inspiratory `gas demand' of a dyspnoeic patient, and reduce the possible time delay to effective inspiratory pressure support delivery.2 Whether it achieves this or not remains controversial, with a number of con¯icting studies, as referenced in this report. However, having noted a failure to trigger at 1.0 cm H2O, the authors then tried a ¯ow trigger of 3 litre min±1: this is probably closer to an equivalent 1.0 cm H2O pressure trigger rather than the 0.5 cm H2O hoped for, especially as no triggering was observed.3 4 The patient was effectively moved to a higher trigger setting on ¯ow-by and so it should be no surprise if triggering `failed', but this is a direct consequence of patient weakness, not ventilator failure. The authors then increased the base ¯ows up to 20 litre min±1, with no change. This is not surprisingÐthe base ¯ow is largely irrelevant if the patient is too weak to even reach the trigger ¯ow. This is not a patient with a high initial inspiratory ¯ow requirement,
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authors stated in the discussion that `In our case, neck manipulation as a result of direct laryngoscopy or insertion of the LMA cannot be blamed'.1 It becomes obvious only when one reads the case presentation and discussion that the laryngeal mask was an unlikely cause of this damage. The patient had suffered from severe neck pain with weakness in the legs and some dif®culty in walking before the operation and, for whatever reason, the symptoms worsened after surgery. We believe that the title should re¯ect the contents of the article accurately, because busy clinicians would often only read the titles of the articles, particularly when an internet search is used. The abstract of the article does not rectify this misleading title. Second, their claim about the safety of laryngoscopy in patients with unstable necks is also misleading. In the introduction, the authors state that `[a]ccording to prevailing dogma, direct laryngoscopy is hazardous in the presence of cervical instability'.1 We should attempt to minimize movement of the head and neck during insertion of an airway device, as studies in cadavers and anaesthetized patients have shown some movement of the neck during insertion of an airway. Nevertheless, direct laryngoscopy and tracheal intubation have been performed routinely in numerous patients with unstable necks, and there have only been a few case reports of possible damage to the spinal cord from these procedures. It is reasonable to conclude therefore, that as long as we take careful measures to protect the neck (such as manual in-line head and neck stabilization), direct laryngoscopy and tracheal intubation can be performed safely without damaging the cervical spine in the majority of patients. The authors' claim is therefore unsubstantiated, and we fear that such a statement may mislead people, such as orthopaedic surgeons, patients, and lawyers. It would be sad if any case of tracheal intubation in a patient with an unstable neck was brought to the courts based on this unsound dogma. In this era of evidence-based medicine, we should summarize what we know, and improve our clinical practice further, based on reliable data and sound reasoning.
Correspondence
inspiratory trigger above 0.5 cm H2O. These levels of PEEP, for patients with no active expiration, will produce air trapping, closing the total thoracic pressure/volume ratio (compliance) to a less favourable level, requiring elevated inspiratory pressure support, and producing chronic lung hyperexpansion with associated baro/volutrauma, cardiovascular and neuroendocrine responses. The role of abdominal supports/splinting in aiding expiration for tetraplegia is often overlooked. The excellent accompanying editorial mentions the problems that may affect inspiratory/expiratory cycling with PSV and the consequences thereof.5 While high intrinsic PEEP is mentioned, extrinsic PEEP (which may produce the former) is not. When we set up ventilators we would do well to consider each setting and its consequences. The recent ARDS Network trial6 is a good example of the morbidity and mortality that an inappropriately set up ventilator will cause. Curiously, in neither article is mention made of volume support as an alternative to inspiratory pressure support for patients with inadequate inspiratory efforts. I think pressure and ¯ow triggering were probably both applicable for these two patients had they been set `equally'. I presume no faults were subsequently found on either ventilator. The odontoid fracture patient required evaluation of their diaphragm function. In both patients, inappropriately high levels of PEEP were used, for no clear reason. C. Morris Belfast, UK EditorÐThank you for the opportunity to reply to Dr Morris. The purpose of these case reports was to demonstrate that small changes in trigger sensitivity settings could be signi®cant in patients with severe muscle weakness. Studies assessing the various trigger modes and settings have shown that the time differences between them are in the range of milliseconds. In one study, the difference in the mean triggering time between a trigger sensitivity setting of 0.5 cm H2O and 3 litre min±1 was 17 ms (0.017 s).3 The difference between a trigger sensitivity of 1 cm H2O and 3 litre min±1 was 12 ms (0.012 s). We are not sure how many intensivists are aware of these tiny differences. In practice, for most patients, it does not matter whether the ¯ow sensitivity is 2 litre min±1 or 3 litre min±1. We wanted to emphasize the point that even the `default' trigger setting of 3 litre min±1 in ventilators such as the Puritan Bennett 7200 can prove to be `too much' for patients with severe muscle weakness. We suspect that the purpose of having such default setting in these ventilators was to avoid the possibility of `autotriggering'. We did not intend to blame the ventilator for the hypoventilation in these patients. If the patient fails to trigger the ventilator, there can be several other reasons apart from failure of the machine, which is unusual if it has undergone the preoperational checks. As to his query regarding the ®rst patient not being put on a ¯ow sensitivity of 1 litre min±1, it was not done so because, at that time, it was not suspected that the ¯ow sensitivity was the reason for failure to trigger. These two patients presented about two months apart. When the second patient also failed to trigger the ventilator at the default ¯ow sensitivity, a more sensitive trigger setting was tried. The decision to change over to ¯ow sensitivity was taken since a pressure sensitivity setting of 0.5 cm H2O carried the perceived risk of autotriggering,7 and the fact that the patient was unable to trigger the ventilator at a trigger sensitivity of 1 cm H2O. Dr Morris questions the suitability of using pressure support ventilation in the ®rst patient. This patient was quadriparetic when he was ®rst admitted to the hospital, but lost all motor power in his limbs subsequently. The patient was able to trigger the ventilator
704
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potentially left `gasping' by using a pressure trigger. The authors note that their second patient with an epidural abscess at C2±C4, could trigger at 1 litre min±1 and conclude `¼it is likely the ®rst patient could have responded in the same way'. Why was 1 litre min±1 not tried? A poorly set up ventilator is the fault of the clinician, and the title `Flow-By Induced Hypoventilation¼', implying ventilator failure, is misleading. I suspect that if like was compared with like, i.e. pressure trigger of 0.5 cm H2O vs ¯ow trigger 1±2 litre min±1, little difference would have been found. I am left wondering what the desired effect of ¯ow-by was in this patient and why the pressure trigger was ever changed; we are told this was an `assessment' of the patient's ability to trigger the ventilator. A patient with neuromuscular weakness is unlikely to require high initial ¯ows and the initial trigger, set at 0.5 cm H2O, appeared appropriate to the authors. I am also concerned about using the PSV mode for this patient. We are told that the patient suffered an odontoid fracture (C1/C2) with clinical involvement at least from below the C3 dermatome. The intercostal muscles will not therefore function and both phrenic nerves/hemidiaphragms are likely to be impaired. There is likely to be no respiratory innervation and therefore no facility for triggering inspiratory pressure support. This patient needs a more complete assessment. It is imperative to demonstrate diaphragmatic function/innervation with this C1±C3 lesion if PSV is to be used, otherwise triggering is impossible. In Case 2, we are told that ultrasonography revealed reduced diaphragmatic movements. The de®ciencies of this particular imaging technique for this purpose are alluded to in the accompanying editorial,5 but the patient was also observed making weak respiratory efforts on an (excessively) high set ¯ow trigger. This is at least compatible with the potential to trigger. In contrast, Case 1 may well have a `disconnected' diaphragm and chest wall. Electromyography, diaphragmatic ¯uoroscopy or even a Wright's respirometer should have been employed to determine the possibility of triggering, particularly when no respiratory efforts were noted. No diaphragm innervation makes pressure support ventilation meaninglessÐand one is left speculating as to what was triggering the ventilator on either trigger setting. Was false triggering (e.g. transmitted pulsations) on a low pressure trigger at 25 bpm erroneous, and the rate of 14 bpm on a higher ¯ow trigger nearer the endogenous neural rhythm, particularly if the patient appears comfortable and oxygenated on these settings? Finally, I am concerned by one small detail that makes a huge differenceÐthe PEEP setting. We have established that this patient's weakness prevented triggering above 0.5 cm H2O. Expiration at rest is a passive phenomenon, but during exercise (and possibly a trial of inappropriate trigger settings) this can become active, because of abdominal musculature contractionÐ not an option in tetraparesis. Patients cannot be expected to exhale against +7.6 cm H2O PEEP if they cannot generate ±0.5 cm H2O inspiratory trigger pressure. What was the indication for this excessive level of PEEP? Was it poor oxygenation; which is unlikely if the FIO2 was only 0.35. A more appropriate measure would be to increase the FIO2 slightly, accepting a mechanical bene®t for reduced oxygenation. Or was it recruitment of atelectatic lung? This is again inappropriate as tetraparesis reduces FRC to a signi®cant degree. Including occasional mandatory breaths (or speci®cally using the `automatic sigh' facility on the Puritan Bennett 7200) would achieve recruitment, as would physiotherapy. PEEP is a therapy titrated to end points of oxygenation and lung recruitment, and has the potential to cause harm. I would argue that PEEP much above physiological levels (>2.5 cm H2O) for patients with severe weakness is probably counterproductive and incompatible with PSV. Case 2 was also managed with 5 cm H2O PEEP while unable to tolerate an
Correspondence
S. Kannan N. Sherwood Birmingham, UK 1 Kannan S, Sherwood N, Arm®eld A. Flow-by induced hypoventilation in high spinal cord lesionsÐreport of two cases. Br J Anaesth 2002; 89: 512±14 2 Sykes K, Young JD. Modern ventilator technology. In: Hahn CEW, Adams AP, eds. Respiratory Support in Intensive Care. London: BMJ, 1999; 263±6 3 Goulet R, Hess D, Kacmarek RM. Pressure vs ¯ow triggering during pressure support ventilation. Chest 1997; 111: 1649±53 4 Hill LL, Pearl RG. Flow triggering, pressure triggering, and autotriggering during mechanical ventilation. Crit Care Med 2000; 28: 579±81 5 Watt JWH. Pressure support ventilation and the critically ill patient with muscle weakness. Br J Anaesth 2002; 89: 373±5 6 ARDS Network Investigators. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000; 342: 1301±8 7 Willatts SM, Drummond G. Brain stem death and ventilator trigger settings. Anaesthesia 2000; 55; 676±7 8 Shapiro BA, Cane RD, Harrison RA. Positive end expiratory pressure therapy on adults with special reference to acute lung injury: a review of the literature and suggested clinical correlations. Crit Care Med 1984; 12: 127±41
Tracheal intubation using a Macintosh laryngoscope or a GlideScopeâ in 15 patients with cervical spine immobilization EditorÐThe use of rigid ®brescopes that incorporate tracheal tubes does not allow for independent movement of the ®brescope to allow visualization of the glottis while inserting the tube.1±3 This produces particular problems in patients with cervical rigidity.4 In addition, these devices all suffer from fogging and obstruction of the lens.5 The GlideScopeâ (Saturn Biomedical Systems Inc, Burnaby, British Columbia, Canada; retail price US$6500±7000 including monitor) is a new video laryngoscope that may be a useful alternative in dif®cult airway management. The GlideScopeâ incorporates a high resolution digital camera located in the middle of the blade tip. The glottis is visualized through a video cable, using a high resolution LCD monitor. The blade design of the GlideScopeâ has several advantages; an embedded anti-fogging mechanism, a reduced overall thickness of 18 mm, and a 60° curvature to match the anatomical alignment (Fig. 1). The object of the study was to compare the Cormack grade6 obtained initially with a Macintosh laryngoscope and then with the GlideScopeâ, in 15 patients presenting for general anaesthesia who were wearing cervical collars. Informed written consent was required for inclusion in the study. The camera portion of the GlideScopeâ is inserted along the middle of the tongue and the tip is positioned in the vallecula. The epiglottis is elevated by lifting the blade into the vallecula. A view of the epiglottis and glottis is available on the monitor as soon as the camera section of the GlideScopeâ enters the mouth. The tube stylet is an important part of intubation with the GlideScopeâ. It is curved to follow the 60° angulation of the GlideScopeâ blade. The Cormack grade (I±IV) and ease of tracheal insertion were evaluated in each patient. The Cormack grading in 14 of the 15 patients (93%) was reduced by one when using the GlideScopeâ. One Grade IV patient and eight out of nine Grade III patients on direct laryngoscopy became Grades III and II respectively on using the GlideScopeâ. One patient classi®ed as Grade III using direct laryngoscopy remained a Grade III with the GlideScopeâ. This patient was intubated using a gum elastic bougie under continuous vision provided by the GlideScopeâ. In addition, ®ve Grade II patients became Grade I using the GlideScopeâ. The average time of intubation with the GlideScopeâ was 38 s. No complications,
DOI: 10.1093/bja/aeg558 Fig 1 The GlideScopeâ blade design: a reduced thickness of 18 mm and a 60° curvature. The tracheal tube stylet is curved to follow the 60° angulation.
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when pressure support ventilation was ®rst attempted with no evidence of autotriggering. The switch from pressure sensitivity to ¯ow sensitivity settings used at that time led to the `hypoventilation' because of failure to trigger. The time duration of ¯ow sensitivity settings was not continued beyond a couple of minutes for obvious reasons. This was possibly not long enough for the patient to exhibit discomfort or desaturation, especially when there was some ventilation of the lungs occurring. As regards the positive end expiratory pressure (PEEP) settings, the intention was to prevent atelectasis rather than alveolar recruitment. Alveolar recruitment generally needs a PEEP of 10 cm H2O or more.8 The ®rst patient had required a high inspired oxygen concentration during the preceding three weeks and the PEEP was being gradually brought down. Dr Morris has expressed concern about the possible complications of PEEP in these patients. If these patients did not have adequate expiration, auto-PEEP would have been inevitable. There was no evidence of this in either of these patients as seen on the ventilator graphic waveforms. Volume support was the back up mode for these patients in the event of pressure support failure. The inadequate inspiratory efforts were noted only during the trial of ¯ow sensitivity settings and not otherwise. Hence, pressure support ventilation was continued in both patients. We do not think that the ventilatory management in these two patients was inappropriate at any stage. Weaning quadriplegic patients from ventilatory support is a challenging task, probably best done in specialist centres, which may be more familiar with the triggering issues we have highlighted. However, because of service constraints, many patients similar to the two cases we have reported will continue to be cared for in non-specialist critical care units throughout the country.
T. Asai K. Shingu Osaka, Japan
EditorÐThank you for the opportunity to respond to this correspondence. We described a temporal association between a devastating deterioration in neurological function and the insertion of a laryngeal mask airway. In our patient, there was probably pre-existing unrecognized damage to the posterior longitudinal ligament. This was worsened during the procedure to create a haematoma and result in critical cervical cord compression. The presence of a haematoma at the site of complete rupture on MRI scan and at surgical decompression was taken as a sign of recent injury. We acknowledged the potential reduction in spinal perfusion pressure that may accompany moderate arterial hypotension during anaesthesia.1 Cervical spinal cord injury produced by airway manoeuvres is extremely rare. We agree that if measures are taken to protect the neck in suspected cervical spine injury, then the airway can be secured safely. In our case, there was no suspicion of cervical spine abnormality and therefore no such protective measures were taken. Cadaveric and radiological studies may describe expected cervical spine movement in speci®c populations. However, there is still a place in the literature for a case report describing a catastrophic event as a result of a combination of unusual circumstances.
C. J. Edge V. Addy C. Kearns Oxford, UK 1 Edge CJ, Hyman N, Addy V, et al. Posterior spinal ligament rupture associated with laryngeal mask insertion in a patient with undisclosed unstable cervical spine. Br J Anaesth 2002; 89: 514±17 2 White AA, Johnson RM, Panjabi MM, Southwick WO. Biomechanical analysis of clinical stability in the cervical spine. Clin Orthop 1975; 109: 85±96 3 McLeod AM, Calder I. Spinal cord injury and direct laryngoscopyÐ the legend lives on. Br J Anaesth 2000; 84: 705±9 4 May DM, Jones SJ, Crockard HA. Somatosensory evoked potential monitoring in cervical surgery: identi®cation of pre- and intraoperative risk factors associated with neurological deterioration. J Neurosurg 1996; 85: 566±73 5 Weglinski MR, Berge KH, Davis DH. New-onset neurologic de®cits after general anesthesia for MRI. Mayo Clin Proc 2002; 77: 101±3 6 Coppleters MW, Van de Velde M, Stappaerts KH. Positioning in anesthesiology: toward a better understanding of stretch-induced peripheral neuropathies. Anesthesiology 2002; 97: 75±81
DOI: 10.1093/bja/aeg554
Pressure support ventilation in tetraplegia EditorÐI read with interest the case reports describing an apparent failure of ¯ow triggering when using pressure support ventilation (PSV) for two patients with high cervical cord lesions.1 Case 1 involved a 66-yr-old man with an odontoid fracture, managed with halo stabilization. Using the Puritan Bennett 7200 with inspiratory pressure support of 16 cm H2O and 7.6 cm H2O PEEP, the initial inspiratory pressure support trigger was pressure dependent, set at 0.5 cm H2O. It had been noted the patient was unable to trigger at a sensitivity of 1.0 cm H2O. A trial of ¯ow triggering (using `¯ow-by') at basal ¯ow 5 and trigger 3 litre min±1 resulted in a fall in respiratory rate from 25 bpm to 14 bpm. We are not told the corresponding tidal volume but that the vital signs were unchanged, the patient appeared comfortable and oxygenated, and no evidence of accessory muscle activity was apparent. `An error in the ¯ow-by settings was suspected', but it is not clear why? I would be surprised if this machine was not in working order when it was checked after this critical incident. This patient had advanced and profound weakness with complete tetraparesisÐthe requirement of a 0.5 cm H2O pressure trigger is evidence of this. Flow-by and ¯ow triggering generally were originally devised to meet the initial inspiratory `gas demand' of a dyspnoeic patient, and reduce the possible time delay to effective inspiratory pressure support delivery.2 Whether it achieves this or not remains controversial, with a number of con¯icting studies, as referenced in this report. However, having noted a failure to trigger at 1.0 cm H2O, the authors then tried a ¯ow trigger of 3 litre min±1: this is probably closer to an equivalent 1.0 cm H2O pressure trigger rather than the 0.5 cm H2O hoped for, especially as no triggering was observed.3 4 The patient was effectively moved to a higher trigger setting on ¯ow-by and so it should be no surprise if triggering `failed', but this is a direct consequence of patient weakness, not ventilator failure. The authors then increased the base ¯ows up to 20 litre min±1, with no change. This is not surprisingÐthe base ¯ow is largely irrelevant if the patient is too weak to even reach the trigger ¯ow. This is not a patient with a high initial inspiratory ¯ow requirement,
703
Downloaded from http://bja.oxfordjournals.org/ by guest on March 24, 2015
authors stated in the discussion that `In our case, neck manipulation as a result of direct laryngoscopy or insertion of the LMA cannot be blamed'.1 It becomes obvious only when one reads the case presentation and discussion that the laryngeal mask was an unlikely cause of this damage. The patient had suffered from severe neck pain with weakness in the legs and some dif®culty in walking before the operation and, for whatever reason, the symptoms worsened after surgery. We believe that the title should re¯ect the contents of the article accurately, because busy clinicians would often only read the titles of the articles, particularly when an internet search is used. The abstract of the article does not rectify this misleading title. Second, their claim about the safety of laryngoscopy in patients with unstable necks is also misleading. In the introduction, the authors state that `[a]ccording to prevailing dogma, direct laryngoscopy is hazardous in the presence of cervical instability'.1 We should attempt to minimize movement of the head and neck during insertion of an airway device, as studies in cadavers and anaesthetized patients have shown some movement of the neck during insertion of an airway. Nevertheless, direct laryngoscopy and tracheal intubation have been performed routinely in numerous patients with unstable necks, and there have only been a few case reports of possible damage to the spinal cord from these procedures. It is reasonable to conclude therefore, that as long as we take careful measures to protect the neck (such as manual in-line head and neck stabilization), direct laryngoscopy and tracheal intubation can be performed safely without damaging the cervical spine in the majority of patients. The authors' claim is therefore unsubstantiated, and we fear that such a statement may mislead people, such as orthopaedic surgeons, patients, and lawyers. It would be sad if any case of tracheal intubation in a patient with an unstable neck was brought to the courts based on this unsound dogma. In this era of evidence-based medicine, we should summarize what we know, and improve our clinical practice further, based on reliable data and sound reasoning.
Correspondence
inspiratory trigger above 0.5 cm H2O. These levels of PEEP, for patients with no active expiration, will produce air trapping, closing the total thoracic pressure/volume ratio (compliance) to a less favourable level, requiring elevated inspiratory pressure support, and producing chronic lung hyperexpansion with associated baro/volutrauma, cardiovascular and neuroendocrine responses. The role of abdominal supports/splinting in aiding expiration for tetraplegia is often overlooked. The excellent accompanying editorial mentions the problems that may affect inspiratory/expiratory cycling with PSV and the consequences thereof.5 While high intrinsic PEEP is mentioned, extrinsic PEEP (which may produce the former) is not. When we set up ventilators we would do well to consider each setting and its consequences. The recent ARDS Network trial6 is a good example of the morbidity and mortality that an inappropriately set up ventilator will cause. Curiously, in neither article is mention made of volume support as an alternative to inspiratory pressure support for patients with inadequate inspiratory efforts. I think pressure and ¯ow triggering were probably both applicable for these two patients had they been set `equally'. I presume no faults were subsequently found on either ventilator. The odontoid fracture patient required evaluation of their diaphragm function. In both patients, inappropriately high levels of PEEP were used, for no clear reason. C. Morris Belfast, UK EditorÐThank you for the opportunity to reply to Dr Morris. The purpose of these case reports was to demonstrate that small changes in trigger sensitivity settings could be signi®cant in patients with severe muscle weakness. Studies assessing the various trigger modes and settings have shown that the time differences between them are in the range of milliseconds. In one study, the difference in the mean triggering time between a trigger sensitivity setting of 0.5 cm H2O and 3 litre min±1 was 17 ms (0.017 s).3 The difference between a trigger sensitivity of 1 cm H2O and 3 litre min±1 was 12 ms (0.012 s). We are not sure how many intensivists are aware of these tiny differences. In practice, for most patients, it does not matter whether the ¯ow sensitivity is 2 litre min±1 or 3 litre min±1. We wanted to emphasize the point that even the `default' trigger setting of 3 litre min±1 in ventilators such as the Puritan Bennett 7200 can prove to be `too much' for patients with severe muscle weakness. We suspect that the purpose of having such default setting in these ventilators was to avoid the possibility of `autotriggering'. We did not intend to blame the ventilator for the hypoventilation in these patients. If the patient fails to trigger the ventilator, there can be several other reasons apart from failure of the machine, which is unusual if it has undergone the preoperational checks. As to his query regarding the ®rst patient not being put on a ¯ow sensitivity of 1 litre min±1, it was not done so because, at that time, it was not suspected that the ¯ow sensitivity was the reason for failure to trigger. These two patients presented about two months apart. When the second patient also failed to trigger the ventilator at the default ¯ow sensitivity, a more sensitive trigger setting was tried. The decision to change over to ¯ow sensitivity was taken since a pressure sensitivity setting of 0.5 cm H2O carried the perceived risk of autotriggering,7 and the fact that the patient was unable to trigger the ventilator at a trigger sensitivity of 1 cm H2O. Dr Morris questions the suitability of using pressure support ventilation in the ®rst patient. This patient was quadriparetic when he was ®rst admitted to the hospital, but lost all motor power in his limbs subsequently. The patient was able to trigger the ventilator
704
Downloaded from http://bja.oxfordjournals.org/ by guest on March 24, 2015
potentially left `gasping' by using a pressure trigger. The authors note that their second patient with an epidural abscess at C2±C4, could trigger at 1 litre min±1 and conclude `¼it is likely the ®rst patient could have responded in the same way'. Why was 1 litre min±1 not tried? A poorly set up ventilator is the fault of the clinician, and the title `Flow-By Induced Hypoventilation¼', implying ventilator failure, is misleading. I suspect that if like was compared with like, i.e. pressure trigger of 0.5 cm H2O vs ¯ow trigger 1±2 litre min±1, little difference would have been found. I am left wondering what the desired effect of ¯ow-by was in this patient and why the pressure trigger was ever changed; we are told this was an `assessment' of the patient's ability to trigger the ventilator. A patient with neuromuscular weakness is unlikely to require high initial ¯ows and the initial trigger, set at 0.5 cm H2O, appeared appropriate to the authors. I am also concerned about using the PSV mode for this patient. We are told that the patient suffered an odontoid fracture (C1/C2) with clinical involvement at least from below the C3 dermatome. The intercostal muscles will not therefore function and both phrenic nerves/hemidiaphragms are likely to be impaired. There is likely to be no respiratory innervation and therefore no facility for triggering inspiratory pressure support. This patient needs a more complete assessment. It is imperative to demonstrate diaphragmatic function/innervation with this C1±C3 lesion if PSV is to be used, otherwise triggering is impossible. In Case 2, we are told that ultrasonography revealed reduced diaphragmatic movements. The de®ciencies of this particular imaging technique for this purpose are alluded to in the accompanying editorial,5 but the patient was also observed making weak respiratory efforts on an (excessively) high set ¯ow trigger. This is at least compatible with the potential to trigger. In contrast, Case 1 may well have a `disconnected' diaphragm and chest wall. Electromyography, diaphragmatic ¯uoroscopy or even a Wright's respirometer should have been employed to determine the possibility of triggering, particularly when no respiratory efforts were noted. No diaphragm innervation makes pressure support ventilation meaninglessÐand one is left speculating as to what was triggering the ventilator on either trigger setting. Was false triggering (e.g. transmitted pulsations) on a low pressure trigger at 25 bpm erroneous, and the rate of 14 bpm on a higher ¯ow trigger nearer the endogenous neural rhythm, particularly if the patient appears comfortable and oxygenated on these settings? Finally, I am concerned by one small detail that makes a huge differenceÐthe PEEP setting. We have established that this patient's weakness prevented triggering above 0.5 cm H2O. Expiration at rest is a passive phenomenon, but during exercise (and possibly a trial of inappropriate trigger settings) this can become active, because of abdominal musculature contractionÐ not an option in tetraparesis. Patients cannot be expected to exhale against +7.6 cm H2O PEEP if they cannot generate ±0.5 cm H2O inspiratory trigger pressure. What was the indication for this excessive level of PEEP? Was it poor oxygenation; which is unlikely if the FIO2 was only 0.35. A more appropriate measure would be to increase the FIO2 slightly, accepting a mechanical bene®t for reduced oxygenation. Or was it recruitment of atelectatic lung? This is again inappropriate as tetraparesis reduces FRC to a signi®cant degree. Including occasional mandatory breaths (or speci®cally using the `automatic sigh' facility on the Puritan Bennett 7200) would achieve recruitment, as would physiotherapy. PEEP is a therapy titrated to end points of oxygenation and lung recruitment, and has the potential to cause harm. I would argue that PEEP much above physiological levels (>2.5 cm H2O) for patients with severe weakness is probably counterproductive and incompatible with PSV. Case 2 was also managed with 5 cm H2O PEEP while unable to tolerate an
Correspondence
S. Kannan N. Sherwood Birmingham, UK 1 Kannan S, Sherwood N, Arm®eld A. Flow-by induced hypoventilation in high spinal cord lesionsÐreport of two cases. Br J Anaesth 2002; 89: 512±14 2 Sykes K, Young JD. Modern ventilator technology. In: Hahn CEW, Adams AP, eds. Respiratory Support in Intensive Care. London: BMJ, 1999; 263±6 3 Goulet R, Hess D, Kacmarek RM. Pressure vs ¯ow triggering during pressure support ventilation. Chest 1997; 111: 1649±53 4 Hill LL, Pearl RG. Flow triggering, pressure triggering, and autotriggering during mechanical ventilation. Crit Care Med 2000; 28: 579±81 5 Watt JWH. Pressure support ventilation and the critically ill patient with muscle weakness. Br J Anaesth 2002; 89: 373±5 6 ARDS Network Investigators. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000; 342: 1301±8 7 Willatts SM, Drummond G. Brain stem death and ventilator trigger settings. Anaesthesia 2000; 55; 676±7 8 Shapiro BA, Cane RD, Harrison RA. Positive end expiratory pressure therapy on adults with special reference to acute lung injury: a review of the literature and suggested clinical correlations. Crit Care Med 1984; 12: 127±41
Tracheal intubation using a Macintosh laryngoscope or a GlideScopeâ in 15 patients with cervical spine immobilization EditorÐThe use of rigid ®brescopes that incorporate tracheal tubes does not allow for independent movement of the ®brescope to allow visualization of the glottis while inserting the tube.1±3 This produces particular problems in patients with cervical rigidity.4 In addition, these devices all suffer from fogging and obstruction of the lens.5 The GlideScopeâ (Saturn Biomedical Systems Inc, Burnaby, British Columbia, Canada; retail price US$6500±7000 including monitor) is a new video laryngoscope that may be a useful alternative in dif®cult airway management. The GlideScopeâ incorporates a high resolution digital camera located in the middle of the blade tip. The glottis is visualized through a video cable, using a high resolution LCD monitor. The blade design of the GlideScopeâ has several advantages; an embedded anti-fogging mechanism, a reduced overall thickness of 18 mm, and a 60° curvature to match the anatomical alignment (Fig. 1). The object of the study was to compare the Cormack grade6 obtained initially with a Macintosh laryngoscope and then with the GlideScopeâ, in 15 patients presenting for general anaesthesia who were wearing cervical collars. Informed written consent was required for inclusion in the study. The camera portion of the GlideScopeâ is inserted along the middle of the tongue and the tip is positioned in the vallecula. The epiglottis is elevated by lifting the blade into the vallecula. A view of the epiglottis and glottis is available on the monitor as soon as the camera section of the GlideScopeâ enters the mouth. The tube stylet is an important part of intubation with the GlideScopeâ. It is curved to follow the 60° angulation of the GlideScopeâ blade. The Cormack grade (I±IV) and ease of tracheal insertion were evaluated in each patient. The Cormack grading in 14 of the 15 patients (93%) was reduced by one when using the GlideScopeâ. One Grade IV patient and eight out of nine Grade III patients on direct laryngoscopy became Grades III and II respectively on using the GlideScopeâ. One patient classi®ed as Grade III using direct laryngoscopy remained a Grade III with the GlideScopeâ. This patient was intubated using a gum elastic bougie under continuous vision provided by the GlideScopeâ. In addition, ®ve Grade II patients became Grade I using the GlideScopeâ. The average time of intubation with the GlideScopeâ was 38 s. No complications,
DOI: 10.1093/bja/aeg558 Fig 1 The GlideScopeâ blade design: a reduced thickness of 18 mm and a 60° curvature. The tracheal tube stylet is curved to follow the 60° angulation.
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when pressure support ventilation was ®rst attempted with no evidence of autotriggering. The switch from pressure sensitivity to ¯ow sensitivity settings used at that time led to the `hypoventilation' because of failure to trigger. The time duration of ¯ow sensitivity settings was not continued beyond a couple of minutes for obvious reasons. This was possibly not long enough for the patient to exhibit discomfort or desaturation, especially when there was some ventilation of the lungs occurring. As regards the positive end expiratory pressure (PEEP) settings, the intention was to prevent atelectasis rather than alveolar recruitment. Alveolar recruitment generally needs a PEEP of 10 cm H2O or more.8 The ®rst patient had required a high inspired oxygen concentration during the preceding three weeks and the PEEP was being gradually brought down. Dr Morris has expressed concern about the possible complications of PEEP in these patients. If these patients did not have adequate expiration, auto-PEEP would have been inevitable. There was no evidence of this in either of these patients as seen on the ventilator graphic waveforms. Volume support was the back up mode for these patients in the event of pressure support failure. The inadequate inspiratory efforts were noted only during the trial of ¯ow sensitivity settings and not otherwise. Hence, pressure support ventilation was continued in both patients. We do not think that the ventilatory management in these two patients was inappropriate at any stage. Weaning quadriplegic patients from ventilatory support is a challenging task, probably best done in specialist centres, which may be more familiar with the triggering issues we have highlighted. However, because of service constraints, many patients similar to the two cases we have reported will continue to be cared for in non-specialist critical care units throughout the country.