Prehospital management of severe traumatic brain injury
BMJ 2009; 338 doi: https://doi.org/10.1136/bmj.b1683 (Published 19 May 2009) Cite this as: BMJ 2009;338:b1683
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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
Competing interests: No competing interests
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
Department of Neurosurgery,
Johns Hopkins University School of Medicine, 1550 Orleans Street, Cancer Research Building II Room 253, Baltimore, MD 21231
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
Competing interests: No competing interests
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
Competing interests: No competing interests
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
Competing interests: No competing interests
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
Competing interests: No competing interests
Re: Prehospital management of severe traumatic brain injury
Dear Editors,
Emergency air medical transport (EAMT) has become a major part of the modern trauma care system and is frequently used to transport patients from remote islands to a tertiary center. Data of all patients with traumatic brain injury and underwent EAMT were retrospectively retrieved from National Aeromedical Approval Center (NAAC). Patient data were analyzed by using the following parameters: age, gender, injury of severity score, and outcome within three days after air transport.
Between Oct 01, 2002 to Dec 31, 2012, there were 3195 EAMS requests from the four major remote islands to Taiwan Main Island. Among them, 2839 were approved (approval rate: 87.98%). Among the 2839 patients, 362 sustained head injury. Male predominates in the head injury patient populations(M:F=2.6:1). Patients between 21 and 30 years old comprised the majority (20%). There was higher percentage of moderate to severe head injury patients compared with ground transport. Moderately injured patients comprised 23%(82 patients) and severe head injury patients comprised 27%(99 patients). Of these 181 patients, 26% were intubated. Hypertonic saline and mannitol were routinely used. Twenty-seven patients expired within seven days after air medical transport. These findings demonstrated that airway maintenance is a key factor for traumatic brain injury patient transport both in air and ground.
Competing interests: No competing interests