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Rapid Responses: Rapid Responses published:
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Classifying Types of Brain Injury
- Catriona C Morten, Michael Gilhooly, and Rakesh Khanna (31 May 2009)
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Rapid Sequence Induction
- Matthew J Jackson (10 June 2009)
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Early hyperpyrexia after severe traumatic brain injury – no clear evidence yet for role in secondary damage
- Charmaine Childs, Andrew T King. Fiona Lecky. (22 June 2009)
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Use of mannitol in the traumatic brain injury patient
- Debraj Mukherjee, M.D., M.P.H. Alfredo Quiñones-Hinojosa, M.D. (29 June 2009)
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Mannitol: does it accelerate depletion of intracerebral adenine nucleotide pools?
- Richard G Fiddian-Green (30 June 2009)
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Catriona C Morten, FY2 doctor Accident and Emergency Department, New Cross Hospital, Wednesfield Road, Wolverhampton, WV10 0QP, Michael Gilhooly, and Rakesh Khanna
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In the article Prehospital management of severe traumatic brain injury the authors stated that subdural and extradural haematomas are types of primary brain injury. However, traditionally subdural and extradural haematomas are categorised as types of secondary brain injury. This has clinical and prognostic implications. Primary brain injury occurs at the time of impact and results in axonal shearing and associated areas of haemorrhage(1). The primary injury may be diffuse (diffuse axonal injury) or localised(1). The relevance in the clinical context is that the brain injury is non reversible and there is likely to be little improvement. Secondary brain injury occurs from insults to the brain after the initial injury. This includes hypoxia, hypovolaemia and cerebral oedema(2). Subdural and extradural haematomas occur after the initial insult and exert their effects through raised intracranial pressure (ICP) and so should be classified as secondary brain injury(2). Although the vessel damage causing the bleeding will have occurred at the time of the injury and is therefore part of the primary brain injury the extradural or subdural haematoma develop some time after and are part of the secondary brain injury complex. Indeed, the term lucid interval has been used to describe the asymptomatic period between the initial injury and the development of symptoms as a result of an expanding intracranial haematoma(3). The resultant brain dysfunction is reversible and less likely to be permanent if surgical treatment is instituted quickly and ICP normalised. This traditional categorisation could be considered useful to differentiate between non-reversible and reversible causes of brain injury. However it is seldom used in modern guidelines for management of brain injury despite its practical use(4). 1. Wyatt J, Illingworth R, Graham C, Clancy M, Robertson C (eds.) Oxford handbook of Emergency Medicine. 3rd ed. Oxford: Oxford University Press; 2006 2. Kerr RCS, Maatvens NF. Craniocerebral Trauma. In Russell R, Williams N, Bulstrode C (eds.) Bailey and Love’s Short Practice of Surgery. 24th ed. London: Arnold Hodder Headline Group; 2004. p 594. 3. Kushner D. Mild Traumatic Brain Injury. Toward Understanding Manifestations and Treatment. Arch Intern Med [online] 1998;158: pp. 1617- 1624. Available from: http://archinte.highwire.org/cgi/content/full/158/15/1617#REF-IRA70860-23 [Accessed on 29th May 2009]. 4. NHS National Institute for Health and Clinical Excellence. Quick Reference Guide Head Injury. NICE clinical guideline 56, 2007. Available from: http://www.nice.org.uk/nicemedia/pdf/CG56QuickRedGuide.pdf[Accessed on 29th May 2009]. Competing interests: None declared |
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Matthew J Jackson, CT1 Anaesthesia Trafford General Hospital, M41 5SL
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I read with interest Hammell & Henning’s review of pre-hospital management of severe traumatic brain injury [1]. Their section on pharmacological adjuncts to intubation partially addresses the changing landscape of the rapid sequence intubation (RSI) as the traditional two-drug cocktail of suxamethonium and thiopentone gives way to alternative agents [2]. Of the four intravenous induction agents currently available in the UK, traditional teaching favours ketamine least for brain injury patients due to its adverse effects on intracranial pressure. In-line with recent review articles considering RSI in hypotensive patients, Hammell & Henning proposed ketamine as the intravenous anaesthetic agent of choice in traumatic brain injury – balancing the risk of secondary brain injury from raised intracranial pressure (ICP) with that from hypotension [3, 4]. The renewed interest in ketamine revolves around extrapolations from animal models, historical pharmacodynamic studies and case reports form the field. Whilst a true head-to-head comparison of ketamine with the other agents, in brain injury patients is lacking, such a study would be technically difficult. The discussion of anaesthetic agents did not extend to the neuromuscular blocking component of the rapid sequence induction. The traditional choice of suxamethonium is favoured due to its speed of onset and offset; however, speed is at the price of a transient raise of ICP [5, 6]. Following the advent of sugamadex, a specific reversal agent for rocuronium, an alternative rapidly acting, rapidly reversible option exists without some of the side effects of suxamethonium. A further missed opportunity was the lack of discussion of additional agents used to modify the sympathetic response to laryngoscopy such as rapidly acting opiates and beta-blockers. [6] [1] Hammell CL, Henning JD. Prehospital management of severe traumatic brain injury. BMJ 2009;338b1683 [2] Koerber JP, Roberts GEW, Whitaker R, Thorpe CM. Variation in rapid sequence induction techniques: current practice in Wales. Anaesthesia 2009;64:54-59 [3] Sehdev RS, Symmons DA, Kindl K. Ketamine for rapid sequence induction in patients with head injury in the emergency department. Emerg Med Australas. 2006;18:37-44. [4] Morris C, Perris A, Klein J, Mahoney P. Anaesthesia in haemodynamically compromised emergency patients: does ketamine represent the best choice of induction agent? Anaesthesia 2009;64:179-84 [5] Perry JJ, Lee JS, Sillberg VA, Wells GA. Rocuronium versus succinylcholine for rapid sequence induction intubation. Cochrane Database Syst Rev. 2003;(1):CD002788. [6] Reynolds SF, Heffner J. Airway Management of the Critically Ill Patient: Rapid-Sequence Intubation. Chest 2005;127:1397-1412 Competing interests: None declared |
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Charmaine Childs, Senior Research Fellow Brain Injury Research Group, Univesrity of Manchester, Andrew T King. Fiona Lecky.
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We note with interest the recent clinical review on pre-hospital management of severe traumatic brain injury by Hammel and Henning [1]. Starting with a short section on the definition and major causes of a severe head injury, the authors turn their attention to three potential secondary insults; hypoxaemia, hypotension and hyperpyrexia; the key contributing factors to the development of secondary (albeit avoidable) brain damage in man. Based on McHugh et al’s synthesis of results from randomised controlled trials (RCT’s) and observational studies from the IMPACT (International Mission on Prognosis and Clinical Trials [2]) database, Hammel and Henning’s review highlighting hypoxia and hypotension as risk factors warranting very early identification and treatment indeed has a basis in published evidence. Hyperpyrexia has no such basis. It is spontaneous hypothermia, not hyperpyrexia, which is the thermoregulatory event most strongly (OR 2.2, 95% CI 1.6-3.2) and convincingly associated with a poor outcome after human TBI and which, together with hypoxia and hypotension, is a powerful marker of adverse outcome [2]. So what of hyperpyrexia? What magnitude of temperature elevation do the authors suggest increases the risk of a secondary insult: a temperature within the febrile range commensurate with a mild to moderate fever or an ‘excessively high’ temperature commonly referred to as hyperpyrexia yet often without a specified range? Whilst raised temperature on admission to hospital after stroke has been shown to be an independent predictor of poor outcome [3] a recent study [4] failed to show the existence of such a relationship at three months. In our own research studies of patients receiving acute neurocritical care, we have repeatedly failed to show that mild to moderate fever-range temperature (brain temperature up to 39oC)is associated with a worse outcome after TBI [5,6.] On this evidence, we would wish to caution against the commonly held assumption proposed by Hammel and Henning…… “there is little doubt that hyperpyrexia is detrimental to outcome after severe traumatic brain injury”. Until studies are designed to test the hypothesis that raised temperature is harmful, we must retain some uncertainty that fever, with its long evolutionary history, is harmful, even in the case of the neurosurgical patient. References 1. Hammel CL, Henning JD. Prehospital management of severe traumatic brain injury. BMJ 2009; 338: 1262-1266 2. McHugh GS, Engel DC, Butcher I, Steyerberg EW, Lu, J, Mushkudiani N, Hernandez AV, Marmarou A, Maas AIR, Murray GD. Prognostic value of secondary insults in traumatic brain injury: Results from the IMPACT study. J. Neurotrauma 2007; 24: 287-293. 3. Reith J HS. Jorgensen HS, Pederson PM,Nakayama H, Raaschou HO, Jeppesen LL, Olsen TS. Body temperature in acute stroke: relation to stroke severity, infarct size, mortality and outcome. Lancet 1996; 347:422 -425. 4. den Hertog, HM, van der Worp, HB, van Genert, HMA, Koundstaal, PJ, Dippel, WWJ. Body temperature at 24 hours rather than initial body temperature is related to functional outcome in acute stroke. Cerebrovasc Dis. 2009; 27: (suppl 6) 14. 5. Childs, C., A. Vail, et al. (2006).Brain temperature and outcome after severe traumatic brain injury. Neurocritical Care; 5: 1-5. 6. Sacho, R.H. Brain temperature, inflammation and outcome after severe traumatic brain injury. University of Manchester, MD thesis 2009. Competing interests: None declared |
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Debraj Mukherjee, M.D., M.P.H. Alfredo Quiñones-Hinojosa, M.D., Co-Directors, Neuro-Oncology Surgical Outcomes Research Laboratory, Department of Neurosurgery Johns Hopkins University School of Medicine, Baltimore, Maryland, USA 21231
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To The Editors: We read with great interest the topical review article by Hammell and Henning [1]. The authors cogently summarized important guidelines on the prehospital management of patients with severe traumatic brain injury (TBI), including airway protection, maintenance of adequate cerebral perfusion, and mitigation of increased intracranial pressure (ICP), while transporting patients to neurosurgical centers expeditiously. The review also discussed arguments for and against the use of corticosteroids, cervical neck immobility, and hypothermia. We would like to add a few salient points to this important discussion, particularly with regard to reduction of ICP in patients with severe TBI. The authors cite a 2007 Cochrane review of prospective studies focusing on the use of mannitol for treatment of ICP in noting that “there was insufficient data to support prehospital administration of the drug” [2]. Given the body of literature supporting the use of mannitol, we seek to provide some clarification. While the single prospective study thus far conducted on prehospital use of mannitol for the treatment of increased ICP did not produce clinically improved outcomes, it should be noted that this study was significantly underpowered, with only 20 participants included in the mannitol group and 21 participants in the control group. Furthermore, no long term outcome data was reported, as patients were only followed for two hours after mannitol administration [3]. Had this prehospital study been more appropriately powered with patients followed for a longer period of time, such as the Smith et al. study of 80 patients with reported outcomes up to one year following treatment with mannitol, then results may have reflected other past literature demonstrating the efficacy of mannitol in significantly decreasing short-term ICP when given as a single dose to TBI patients [4-8]. Debraj Mukherjee, M.D., M.P.H. Alfredo Quiñones-Hinojosa, M.D. Co-Directors, Neuro-Oncology Surgical Outcomes Research Laboratory
References: 1. Hammell CL, Henning JD. Prehospital management of severe traumatic brain injury. BMJ 2009; 338: 1262-1266. 2. Wakai A, Roberts I, Schierhout G. Mannitol for acute traumatic brain injury. Cochrane Database Syst Rev 2007; 1: CD001049. 3. Sayre MR, Daily SW, Stern SA, Storer DL, van Loveren HR, Hurst JD. Out-of-hospital administration of mannitol does not change systolic blood pressure. Academic Emergency Medicine 1996; 3: 840–848. 4. Smith HP, Kelly DL Jr, McWhorter JM, Armstrong D, Johnson R, Transou C, et al. Comparison of mannitol regimens in patients with severe head injury undergoing intracranial monitoring. Journal of Neurosurgery 1986; 65: 820–824. 5. Cruz J, Minoja G, Okuchi K, Facco E. Successful use of the new high-dose mannitol treatment in patients with Glasgow Coma Scale scores of 3 and bilateral abnormal pupillary widening: A randomized trial. J Neurosurg 2004; 100: 376–383. 6. Sorani MD, Manley GT. Dose-response relationship of mannitol and intracranial pressure: A metaanalysis. J Neurosurg 2008; 108: 80–87. 7. James HE. Methodology for the control of intracranial pressure with hypertonic mannitol. Acta Neurochir 1980; 51: 161-172. 8. Marshall LF, Smith RW, Rauscher LA. Mannitol dose requirements in brain injured patients. J Neurosurg 1978; 48: 169-172. Competing interests: None declared |
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Richard G Fiddian-Green, FRCs, FACS None
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If the primary objective in managing head injuries is to limit secondary brain injury, by preventing an intracerebral energy deficit in regions adjacent injured brain and reperfusion injury not only in the injured region but also in the penumbra, then inducing a diuresis with mannitol might be subverting that objective by depleting intracerebral in addition to systemic adenine nucleotide pools(1,2). 1. Fluid volumes and the preservation of adenine nucleotide pools. Richard G Fiddian-Green (1 April 2009) eLetter re: D. R. McIlroy, D. V. Pilcher, and G. I. Snell Does anaesthetic management affect early outcomes after lung transplant? An exploratory analysis Br. J. Anaesth. 2009; 102: 506-514 2. Should permissive oliguria and anuria be added to permissive hypotension? Richard G Fiddian-Green (22 June 2009) eLetter re: E M Dempsey, F Al Hazzani, and K J Barrington. Permissive hypotension in the extremely low birthweight infant with signs of good perfusion Arch. Dis. Child. Fetal Neonatal Ed. 2009; 94: F241-F244 Competing interests: None declared |
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