Pragmatic Evidence-based Review Best-evidence Review of Acute Care for Moderate to Severe Traumatic Brain Injury Reviewer Mark Ayson MBChB DPH Date Report Completed August 2011 Important Note: It is not intended to replace clinical judgement, or be used as a clinical protocol. A reasonable attempt has been made to find and review papers relevant to the focus of this report; however it does not claim to be exhaustive. The document has been prepared by the staff of the Research Unit, ACC. The content does not necessarily represent the official view of ACC or represent ACC policy. This report is based upon information supplied up to 12 May 2011. Purpose The purpose of this brief report is to summarise the best evidence for acute care of people with moderate and severe traumatic brain injury. This report is focused on adults with moderate to severe TBI.
1 Key Messages 1.1 Pre-hospital setting The first priority is to treat the greatest threat to life and avoid further harm Assess and manage according to clear principles and standard practice such as the Advanced Trauma Life Support (ATLS) system Initiate prompt referral to an Emergency Department if there are risk factors for acute intracranial complications of TBI Rapid transfer to an Emergency Department using emergency services is appropriate if the signs of acute complications are more serious or there is deterioration of the person s condition, loss of consciousness, focal neurological deficit, skull fracture, or penetrating head injury, seizure or suspected neck injury The Glasgow Coma Scale (GCS) should be used for assessment and classification of people with a suspected TBI Full cervical spine immobilisation if GCS < 15, neck pain or tenderness, focal neurological deficit, paraesthesia in the extremities, or any other clinical suspicion of cervical spine injury Transport patient directly to a facility where TBI is managed in its entirety, if possible. Otherwise, transport the patient to a facility identified as having the appropriate resources to resuscitate, investigate and initially manage any patient with multiple injuries For people with a severe TBI (GCS 8), make a standby call to the destination to ensure appropriately experienced professionals are available to treat patient and to prepare for imaging Pain should be managed effectively because it can lead to a rise in intracranial pressure. Reassurance and splintage of limb fractures are helpful; catheterisation of a full bladder will reduce irritability 1.2 Emergency Department setting The priority is to stabilise airway, breathing and circulation before attending to other injuries All patients presenting to an emergency department with a head injury should be assessed by a trained member of staff within a maximum of 15 minutes of arrival at hospital Anyone presenting to an Emergency Department with a suspected traumatic brain injury should receive a triage assessment by a trained staff member on arrival. Part of this triage assessment should establish whether they are high or low risk for clinically significant brain injury and/or cervical spine injury, using validated CT rules Anyone presenting to an Emergency Department with impaired consciousness (GCS < 15) should be assessed immediately by a trained staff member (such as a triage nurse) In patients with a GCS 8 there should be early involvement of an anaesthetist or critical care physician early and an early referral to a neuroscience specialist should be made Depressed conscious level should be ascribed to intoxication only after a significant brain injury has been excluded 2
The primary investigation of choice for detection of clinically significant acute complication of TBI is CT imaging of the head Manage pain effectively because it can lead to a rise in intracranial pressure. Avoid the use of corticosteroids in the management of people with TBI of any kind 1.3 Hospital care Any person with a deteriorating GCS or GCS <15 after imaging, or any indication for CT scan should be admitted to hospital Minimum observations included GCS, pupil size and reactivity, limb movements, respiratory rate, BP, temperature, heart rate, blood oxygen saturation, and any unusual behaviour Consider immediate CT scan and reassessment of patient s condition if agitation or abnormal behaviour develops, decrease in GCS, severe or worsening headache, persistent vomiting or any new or evolving neurological symptoms or signs 1.4 Intensive care Optimum oxygenation, perfusion, nutrition, glycaemic control & temperature homeostasis are essential Benefits of prophylactic anti-seizure treatment must be balanced against the potential risks; recommended indications include penetrating brain injury & depressed skull fracture in patients with PTA >24 hours in whom a dural lesion is suspected Sedation & artificial ventilation are used to reduce brain swelling & raised intracranial pressure (ICP) in patients with severe TBI ICP should be monitored in all comatose patients with a TBI and an abnormal CT scan Osmotherapy is currently considered as second line treatment after sedation & artificial ventilation have failed to lower raised ICP. There is insufficient evidence to support the use of hypertonic saline over mannitol because of the risks of hypernatraemia with hypertonic saline. Osmotherapy is best reserved for patients in whom ICP is being monitored Hyperventilation has been used to reduce ICP effectively however there is a risk of worsening ischaemia. Arterial CO 2 < 30 mmhg should be avoided Decompressive craniectomy is controversial as it does not produce improved outcome in all people & has many side-effects, some severe. There is a consensus that the craniectomy should be large enough & done early & with duraplasty. 3
2 Findings 2.1 Pre-hospital setting 2.1.1 Pre-hospital assessment The goals of pre-hospital assessment are: To establish whether trauma to the head has occurred 1 To estimate the severity of any injury to the brain 1 To identify and prevent hypoxia and/or hypotension 1 2 Identify risk factors for acute complications of TBI which may require intervention *1 Identify other injuries that may require urgent treatment 1. 2.1.1.1 Hypoxia and hypotension Hypoxia (defined here as O 2 saturation < 90% or PaO 2 < 60 mmhg) and hypotension (systolic blood pressure < 90 mmhg) are very prevalent when assessed before hospital admission (44-55% of cases have a oxygen saturation below 90% and 20-30% are hypotensive 2 ). In addition, both hypoxia and/or hypotension increase morbidity and mortality from TBI 1-4 and are strongly associated with poor outcome (hypoxia odds ratio [OR] 2.1, 95% Confidence Interval [CI] 1.7-2.6; hypotension: OR 2.7, 95% CI 2.1-3.4). The importance of frequent or continuous monitoring of oxygen saturation has been shown in one study where any oxygen desaturation of <70% during intubation and any desaturation of <90% were associated with higher mortality (OR = 3.89, 95% CI 1.12-13.52 and OR = 3.86, 95% CI 1.18-12.61) 5. The only guidelines for pre-hospital management of severe TBI 5 make the following recommendations about the assessment of oxygenation and blood pressure: Patients with suspected severe traumatic brain injury (TBI) should be monitored in the prehospital setting for hypoxemia (<90% arterial hemoglobin oxygen saturation) or hypotension (<90 mmhg systolic blood pressure [SBP]) Percentage of blood oxygen saturation should be measured continuously in the field with a pulse oximeter Systolic (SBP) and diastolic blood pressure (DBP) should be measured using the most accurate method available under the circumstances Oxygenation and blood pressure should be measured as often as possible, and should be monitored continuously if possible 5. 2.1.1.2 Glasgow Coma Scale The Glasgow Coma Scale should be used for the assessment and classification of people who have had a head injury [C]. The risk of intracranial complications and consequent need for surgery increases as the GCS declines (RR = 5.58) 6. Urgent investigation and/or referral is indicated if there is a fall 2 or more points on the GCS, as this may represent the * especially intracranial bleeding 4
development of intracranial bleeding [GAP]. Hence GCS is included as a referral criterion as can be seen in Table 2. The GCS also allows the severity of the TBI to be assessed. An example of one classification system can be seen in Table 1. The severity of TBI will influence the consequent management including referral, the rapidity of transport, and medical intervention(s). For example, NICE (2007) 7 recommends that for all people with a GCS of 8 make a standby call to the destination to ensure appropriately experienced professionals are available to treat the patient and to prepare for imaging. Table 1: Criteria for classifying the severity of TBI Severity of Injury GCS Score Duration of PTA Mild 13-15 <24 hrs Moderate 9-12 1-6 days Severe 3-8 7 days Specific recommendations are made regarding the how and when to use the GCS, for example: Prehospital measurement of the Glasgow Coma Scale (GCS) should be used repeatedly to identify improvement or deterioration over time The GCS should be measured after airway, breathing, and circulation are assessed, after a clear airway is established, and after necessary ventilatory or circulatory resuscitation has been performed The GCS should be measured preferably prior to administering sedative or paralytic agents, or after these drugs have been metabolised 5. Other recommendations regarding the use of the GCS can be seen in the relevant evidence tables in the separate evidence table document. 2.1.1.3 Cerebral Herniation The clinical signs of cerebral herniation include dilated and unreactive pupils, asymmetric pupils, a motor examination that shows either extensor posturing or no response, or progressive neurological deterioration (a decrease in the GCS of >2 points from the prior best score in people with an initial GCS <9) 5. These signs are all part of the GCS assessment and the guideline for the pre-hospital management of severe TBI recommends that patients should be assessed frequently for clinical signs of cerebral herniation. 2.1.1.4 Risk factors for intracranial complications Many variables have been identified that elevate the risk of clinically important TBI and the acute intracranial complications of TBI (see Table 2). 2.1.1.4.1 Loss of consciousness: Altered consciousness after TBI is associated with an increased risk of developing an intracranial complication 1 6 7 although the absolute risk remains low 7. Loss of consciousness was found to have a relative risk (RR) of 2.23 of an intracranial lesion in one study 6. Loss of, or change in, consciousness may have other causes and the ACC (2006) 1 guideline recommends the routine check of blood glucose levels in all people with altered consciousness [GPP]. 5
2.1.1.4.2 Post-traumatic amnesia Amnesia of events before or after head injury increases the risk of intracranial complications 6 7, although the evidence on the type (before or after injury) and length of amnesia are less compelling than the evidence for other risk factors 1 7. 2.1.1.4.3 Neurological signs Focal neurological signs post-trauma are highly associated with the risk of an intracranial complication 1 6 7 (RR = 9.43) 6. 2.1.1.4.4 Bleeding disorders and use of anticoagulants People who have a bleeding or clotting disorder or who are taking anticoagulant medication, like warfarin, are at an increased risk of intracranial complications, however the strength of association has not been well established 1 6 7. People taking medications that have an antiplatelet effect, like aspirin and clopidogrel, should also be considered for referral to hospital 1 6 [GPP]. In addition, the ACC (2006) 1 guideline includes complementary and alternative medicines like Ginkgo biloba in this group. 2.1.1.4.5 Skull fracture People with a diagnosed skull fracture have a higher risk of intracranial complications. It is estimated that the risk of an intracranial haematoma to be 12 times higher in people with an x-ray detected skull fracture than in people without this diagnosis 1 7. Signs of a skull fracture are also a strong predictor of an intracranial lesion (RR = 6.13) 6. These signs include: clear fluid running from the ears or nose, black eye with no associated damage around the eyes, bleeding from one or both ears, new deafness in one or both ears, bruising behind one or both ears, penetrating injury signs, depressed or open skull injury, and visible trauma to the scalp or skull of concern to the professional 1 6 7. Of note, the routine use of skull x-rays is not recommended 1 7. 2.1.1.4.6 Seizure The rationale for the recommendations regarding post-traumatic seizure in the guidelines is inconsistent, even though seizure is included as a risk factor in all the guidelines. SIGN (2009) 6 reported an unadjusted RR of 3.37 (95% CI: 1.76-6.45) for seizure from a metaanalysis as predictive of intracranial injury whereas NICE (2007) 7 included seizure under the neurological signs criterion which was reported as being highly associated with the risk of intracranial complications. In contrast, ACC (2006) 1 reported that seizure alone, with no neurological signs and full recovery, is rarely a sign of an intracranial haematoma, however, alteration in consciousness (either as a result of the seizure itself or the drugs used to treat it) is indistinguishable from that caused by an intracranial bleeding complication of TBI. As a result, post-traumatic seizure is included as a criterion for referral to hospital. 2.1.1.4.7 Mechanism of injury High energy mechanism of injury is included in all three guidelines as a risk factor; however, what they are is difficult to define. However, one study has proposed that a pedestrian struck by a motor vehicle, an occupant ejected from a motor vehicle, and a fall of greater than 1 metre or more than five stairs, as high risk mechanisms for a clinically significant TBI 1 7. Mechanisms of injury that are risk factors for a significant cervical spine injury are also listed. They include: high-speed motor vehicle collision, rollover motor vehicle accident, ejection from a motor vehicle, and an accident involving a recreational vehicle or bicycle 1 7. 2.1.1.4.8 Age Increasing age is associated with an increased risk of intracranial complications 1 6 7 and a poorer prognosis following a TBI 1 7. An age threshold of over 65 yrs was chosen to be included in the referral criteria for two of the guidelines 1 7. 2.1.1.4.9 Alcohol or drug intoxication 6
Alcohol or drug intoxication can produce signs and symptoms that are risk factors for intracranial complications, including a reduction in the GCS. Drug and/or alcohol use has also been identified as independent risk factors for poorer outcomes following TBI, and may impact on rehabilitation from TBI 1. Although alcohol intoxication can reduce the Glasgow Coma Scale, it is always safer to assume that such signs are due to TBI or a complication of TBI rather than intoxication and proceed accordingly 1 6 7. 2.1.1.4.10 Headache Even though the evidence is conflicting 7, headache may be both a symptom associated with raised intracranial pressure and a risk factor for intracranial complications of a head injury 1 (RR = 1.02 for an intracranial lesion 6 ). Persistent headache is included in the referral criteria in two guidelines 1 7, and severe and persistent headache in the other 6. 2.1.1.4.11 Vomiting Vomiting is included in all guidelines as a risk factor for intracranial complications but there is some debate about the number of episodes required 1 6 7. 2.1.1.4.12 Irritability and altered behaviour Irritability and altered behaviour are included in two guidelines 1 7 as risk factors, even though it was reported that there was little evidence to support their use. However, they are an important sign in young children where other symptoms like headache and amnesia cannot be detected 1 7. 2.1.1.4.13 A history of cranial neurosurgical interventions A history of cranial neurosurgical interventions has been included in two guidelines as a referral criterion 1 7, based on expert opinion that such intervention is likely to increase the risk of developing a subdural haematoma 1. The ACC (2006) 1 guideline explicitly recommends that any cranial neurosurgery should be recorded, especially in the 6 weeks prior to injury, or if there is a shunt in place for hydrocephalus. 7
2.1.2 Referral to emergency department (ED) Consistent criteria was reported in the identified guidelines for referral to an ED for further assessment, based on the presence of risk factors for acute intracranial complications of TBI as discussed in a previous section. An example of these referral criteria can be seen in Table 2. Some of the details of the recommendations differ e.g. the NICE 7 guideline doesn t specify how many episodes of vomiting are required whereas the SIGN 6 guideline does, but for the purposes of brevity these differences will not be mentioned in this report. Table 2: Criteria for referral to ED (adapted from NICE 2007 7, ACC 2006 1 & SIGN 2009 6 ) Criteria for referral to a hospital emergency department, using the ambulance service if deemed necessary: Any of the following: Unconsciousness or lack of full consciousness Any loss of consciousness as a result of the injury GCS < 15 on initial assessment Any focal neurological deficit since the injury Any suspicion of a skull fracture or penetrating head injury since the injury Amnesia for events before or after the injury** Persistent headache since the injury Any vomiting episodes since the injury Any seizure since the injury Any previous cranial neurosurgical interventions(s) A high-energy head injury History of bleeding or clotting disorder Current anticoagulant therapy such as warfarin Current drug or alcohol intoxication e.g. problems keeping eyes open e.g. problems understanding, speaking, reading or writing; decreased sensation; loss of balance; general weakness; visual changes; abnormal reflexes; and problems walking. e.g. clear fluid running from the ears or nose, black eye with no associated damage around the eyes, bleeding from one or both ears, new deafness in one or both ears, bruising behind one or both ears, penetrating injury signs, visible trauma to the scalp or skull of concern to the professional. ** assessment of amnesia will not be possible in pre-verbal children and is unlikely to be possible in any child aged under 5 years. e.g. pedestrian struck by motor vehicle, occupant ejected from motor vehicle, fall from a height of greater than 1 m or more than five stairs, diving accident, high-speed motor vehicle collision, rollover motor accident, accident involving motorized recreational vehicles, bicycle collision, or any other potentially high-energy mechanism. 8
Age 65 years or older Suspicion of non-accidental injury Continuing concern by the professional about the diagnosis. In the absence of any the factors listed above, the professional should consider referral to an emergency department if any of the following factors are present depending on their own judgement of severity: Irritability or altered behaviour, particularly in infants and young children Visible trauma to the head not covered above but still of concern to the professional. Adverse social factors Continuing concern by the injured person or their carer about the diagnosis. [D] Other factors included in the guidelines include: Significant medical comorbidity6 People taking antiplatelet medication*** should be considered for referral to hospital6 [GPP] 2.1.3 Pre-hospital management Three guidelines referred to so far 1 6 7 do not give advice about specific pre-hospital management, but they do give these general recommendations: The first priority is to treat the greatest threat to life and avoid further harm 1 7 Assess and manage according to clear principles and standard practice such as the Advanced Trauma Life Support (ATLS) system 1 6 7 A person who has sustained a suspected traumatic brain injury should have full cervical spine immobilisation attempted 1 7 8 Transport patient directly to a facility where TBI is managed in its entirety, if possible 1. Otherwise, transport the patient to a facility identified as having the appropriate resources to resuscitate, investigate and initially manage any patient with multiple injuries 7. For people with a GCS 8, make a standby call to the destination to ensure appropriately experienced professionals are available to treat patient and to prepare for imaging 7. i.e. aged under 5 years. e.g, no one is able to supervise the injured person at home. *** e.g. aspirin, clopidogrel unless they have all of the following: no alteration of consciousness, no neck pain/tenderness, no focal neurological deficit, or no major distracting injury 9
Pain should be managed effectively because it can lead to a rise in intracranial pressure. Reassurance and splintage of limb fractures are helpful; catheterisation of a full bladder will reduce irritability 7. NB: ACC (2006) 1 makes no recommendations about pain relief in this setting and explicitly states to avoid strong systemic analgesia until a full assessment is done. Both NICE (2007) 7 and Reed (2007) 4 both recommend assessment and stabilisation of ABCDE s and the following management is then dependent on the severity of the TBI as assessed by the GCS score (using the same severity criteria as in Table 1). See section 2.2.2.1 and 2.2.2.2 for the initial management of severe and moderate TBI respectively for more details. One guideline 5 and one best evidence review 8 give specific guidance regarding the management of severe TBI. Rapid transfer to an appropriate secondary care facility is essential as time from injury to definitive neurosurgical care can affect outcomes for people with severe TBI; patients with mass lesions have a better outcome if they receive neurosurgical care within 4 hours of injury 8. Implementation of measures to expediate rapid transfer and prevent secondary brain injury from hypoxia and/or hypotension have been shown to improve outcomes when these parameters were specifically targeted in the prehospital setting 8. More specifically, the introduction of a system in the pre-hospital setting capable of normalising oxygenation and blood pressure has been associated with improved outcomes 2. The Brain Trauma Foundation 5 guideline for severe TBI makes the following recommendations: 2.1.3.1 Airway, Ventilation and Oxygen Hypoxemia should be avoided, and corrected immediately upon identification An airway should be established, by the most appropriate means available, in patients with severe TBI, who are unable to maintain an adequate airway, or who have hypoxemia not corrected by supplemental O 2 The routine use of paralytics to assist endotracheal (ET) intubation in patients who are spontaneously breathing, and maintaining an SpO 2 above 90% on supplemental oxygen, is not recommended Emergency services implementing ET intubation protocols should monitor blood pressure, oxygenation, and when feasible, end-tidal CO 2 (ETCO 2 ) Patients should be maintained with normal breathing rates (ETCO 2 35-40 mmhg), and hyperventilation (ETCO 2 < 35 mmhg) should be avoided unless the patient shows signs of cerebral herniation Airway compromise is common after severe TBI and has an important contribution to the development of secondary brain injury. The Hammell (2009) 8 review suggests that basic airway adjuncts should be used initially and high flow O 2 administered. Inevitably ET intubation is required in almost all patients with severe TBI, although the evidence for its benefit in the pre-hospital setting is controversial 8 ; several retrospective studies have shown that ET intubation by paramedics in this situation with minimal use of sedatives and muscle relaxants have a high risk of complications. A recent systematic review 9 of 17 studies (15, A = airway maintenance with cervical spine protection ; B = breathing; C = circulation; D = disability (neurological evaluation); E = exposure/environmental control 10
335 subjects) comparing pre-hospital intubation with other airway management concluded that the available evidence did not support any benefit from pre-hospital intubation and mechanical ventilation after TBI. Hammell (2009) 8 suggests that true rapid sequence induction of anaesthesia performed by physicians is more promising. Administering anaesthetic and neuromuscular blocking drugs to assist in intubation has been shown to lead to better outcomes in people with head injuries 8 and, after intubation, adequate sedation and neuromuscular blockade must be maintained to avoid rises in ICP due to coughing 8. According to Hammell (2009) 8, monitoring ETCO 2 is now considered a routine monitoring standard for all mechanically ventilated patients during transfer and has been shown to reduce the incidence of hyperventilation by 50%. Hyperventilation can lead to cerebral vasoconstriction and ischaemia and therefore should be avoided in patients with head injuries 8. 2.1.3.2 Hypotension and Fluid Resuscitation The ideal resuscitation fluid for patients with severe TBI is unknown, however, isotonic fluids are the commonest used fluid in the pre-hospital resuscitation of people with a TBI, however, little data has been published to support its use 5. Evidence for the efficacy of hypertonic fluids is inconsistent but suggestive of a survival benefit for hypertonic fluids in people with severe TBI 5. Hypotensive patients should be treated with boluses of no more than 250mls 10 of isotonic crystalloid fluids 8 Hypertonic resuscitation is a treatment option for TBI patients with a Glasgow Coma Scale Score (GCS) < 8 Patients with severe TBI who are hypotensive have a doubled risk of death compared to those who are normotensive and results in reduced cerebral perfusion and ischaemia. It is often multifactorial, however, Hammell (2009) 8 suggests that it is best to assume that the hypotension is due to hypovolaemia until proven otherwise 8 and that guidelines 10 have recommended the use of small boluses (250ml) of isotonic crystalloid fluids to correct hypotension in patients with severe TBI. 2.1.3.3 Raised ICP and cerebral herniation ICP is often raised in patients with severe TBI 8 and Hammell (2009) 8 recommends that specific treatment should be given to lower it if clinical signs are present **** and if transfer time allows and stresses that hypoxaemia, hypotension, hypercapnia and inadequate sedation (in an intubated patient) should all be addressed before specific treatment 8. Hammell (2009) then states that there is little evidence about strategies to reduce ICP in the pre-hospital environment. A recent Cochrane review concluded that there are insufficient data on the effectiveness of pre-hospital administration of mannitol 11. Hypertonic saline can be used as an alternative to mannitol, however the evidence is conflicting 8. Hyperventilation in the acute setting reduces ICP but has also been shown to decrease cerebral blood flow, a deleterious effect 5. People who are chronically hyperventilated in e.g. bag-valve-mask or O 2 administration **** includes: dilated and unreactive pupils, asymmetric pupils, a motor examination that shows either extensor posturing or no response, or progressive neurological deterioration (a decrease in the GCS of >2 points from the prior best score in people with an initial GCS <9) 11
hospital have been shown to have worse outcomes at 3 and 6 months but equivalent outcomes at one year but it appears that in some people with progressive cerebral oedema, hyperventilation can temporise impending herniation. In this situation the benefits of hyperventilation outweigh the potential detrimental effects 5. In the prehospital phase, clinical criteria must be used to identify people at risk of herniation (in contrast to the hospital setting where ICP is used), therefore hyperventilation is used as a temporising measure in people with severe TBI who shows signs of herniation 5. Mild or prophylactic hyperventilation (PaCO 2 < 35 mmhg) should be avoided, except as below In patients who are normoventilated, well oxygenated, and normotensive - and still have signs of cerebral herniation - hyperventilation should be used as a temporizing measure, and discontinued when clinical signs of herniation resolve. The goal of hyperventilation is ETCO 2 of 30-35 mmhg. 5. 12
2.2 Emergency Department setting The ED assessment and management of people with suspected TBI should focus on: Preventing and treating hypotension and hypoxia 1 Obtaining early imaging 1 Attending to co-existing injuries 1. 2.2.1 Assessment in ED The main focus of ED assessment in people who have sustained a head injury should be the identification of actual or potential hypotension and/or hypoxia 1, risk of clinically important brain injuries 1 7, appropriate referral for imaging 1 7 and injuries to the cervical spine 7. Due attention should also be paid to co-existing injuries and other concerns the clinician may have e.g. non-accidental injury, and early imaging, rather than admission and observation, will reduce the time to detecting life-threatening complications and is associated with better outcomes 7. 2.2.1.1 Hypoxia and/or hypotension Recommendations from the Brain Trauma Foundation severe TBI management guideline 3 : Blood pressure should be monitored and hypotension (systolic blood pressure < 90 mm Hg) avoided [II] Oxygenation should be monitored and hypoxia (PaO 2 < 60 mm Hg or O 2 saturation < 90%) avoided [III] 2.2.1.2 Investigation for clinically important brain injury The guidelines are unanimous that the primary investigation of choice for detection of clinically significant acute complication of TBI is CT imaging of the head 1 4 6 7. This guidance is based upon high level evidence, including a systematic review of the literature on diagnostic procedures and selection rules for imaging of people with head injury 1, however, for the purposes of this review, the details of this evidence will not be discussed. An example of selection rules for adults for CT imaging of the head can be seen in Table 3 below. There is some slight variation in the details of the guidance, particularly on the timing of the CT scan, but in general terms the criteria are consistent. The full criteria and criteria for the urgency in performing CT imaging of the head are included in the relevant evidence tables. 13
Table 3: Selection of Adults For Head CT(adapted from NICE 2007 7, ACC 2006 1 & SIGN 2009 6 ) CT scans should be immediately requested for adults who have sustained a head injury, if they have any one of the following risk factors: any deterioration in condition a GCS <13 when assessed, irrespective of the time elapsed since the injury a GCS <15 two hours after the injury a suspected open or depressed skull fracture any sign of basal skull fracture post-traumatic seizure focal neurological deficit one episode of vomiting amnesia for > 30 minutes for events before the injury. CT scanning should be immediately requested for adults with any of the following risk factors who have experienced an injury to the head with some loss of consciousness or amnesia since the injury: 65 years coagulopathy high-risk mechanism of injury. If patient presents out of hours and is: 65 years has amnesia for events > 30 minutes before impact or there was a dangerous mechanism of injury it is acceptable to admit for overnight observation, with CT imaging the next morning, unless CT result is required within 1 hour because of the presence of additional clinical findings listed above. 2.2.2 Management in ED: The following recommendations are taken from the Reed (2009) 4 guideline algorithm for the initial management of moderate and severe TBI which may occur in different settings but is included here for convenience. In addition, pain management, signs of neurological deterioration and indications for referral to neuroscience are included in this section. 14
2.2.2.1 Initial management of severe TBI (GCS 3-8) Standard care includes 4 : Early intubation Initial assessment & resuscitation of ABCDE s Supportive care of ABCDE s with appropriate attention, posturing (30 head up), basic nursing care and avoidance of hyperventilation Prevent secondary injury by avoiding hypoxia (O 2 saturation >90%) and hypotension (systolic BP <90) Early CT scan to identify neurosurgically correctable focal intracranial haematomas Early neurosurgical consult Consider ICP monitoring to guide management of cerebral perfusion pressure Optional use of anticonvulsants to prevent early post-traumatic seizures ICU admission Routine brain injury rehabilitation consult. 2.2.2.2 Initial management of moderate TBI (GCS 9-13) Standard care includes 4 Initial assessment & resuscitation of ABCDE s Early CT scan to identify neurosurgically correctable focal intracranial haematomas Period of ED observation Prevention of secondary brain injury by avoiding hypoxaemia (O 2 saturation <90%) & hypotension (systolic BP <90) Supportive care of ABCDE s Admit for prolonged hospital observation (24-48 hours) unless rapid clinical improvement, normal CT scan & absence of other risk factors Early neurosurgical consult if not clinically improving and/or abnormal CT scan Routine post-traumatic amnesia (PTA) testing and referral to brain injury rehabilitation service (or neurologist) due to high risk of cognitive behavioural social sequelae. 2.2.2.3 Pain Management: There is some apparent conflicting guidance regarding pain management. For example, NICE (2007) 7 recommends to manage pain effectively because it can lead to a rise in based on Brain Trauma Foundation 2000, Management & Prognosis of Severe TBI; American College of Surgeons Committee on Trauma 1997, Advanced Trauma Life Support for Doctors; and seven Cochrane reviews 2002-2003 see relevant evidence table for full details 15
intracranial pressure and to treat significant pain with low dose of intravenous opioids. They also recommend that reassurance and splintage of limb fractures are helpful; catheterisation of a full bladder will reduce irritability. In contrast, the ACC (2006) 1 guidance is that in general, people with a suspected TBI should not receive strong systemic analgesia until they have been fully assessed, so that an accurate measure can be made of consciousness and other neurological signs. No of the other guidelines make any recommendations concerning pain management. 2.2.2.4 Corticosteroids The ACC (2206) 1 and the ERABI 12 group recommend to avoid the use of corticosteroids in the management of people with TBI of any kind. This is an A grade recommendation based on a multicentre study of over 10000 participants with acute TBI which showed an increase of 18% in two-week all-cause mortality in the group receiving methylprednisolone. 2.2.2.5 Acute neurological deterioration 4 Indications of deterioration: GCS falls by 2 or more points Develops dilated pupil(s) Develops focal neurological deficit Delayed or focal seizure Cushing s response i.e. bradycardia & hypertension Clinical approach: Re-assess ABCDE s to exclude a non-head injury cause Supportive care of ABCDE s e.g. perfusion & oxygenation Consider early intubation & short term hyperventilation to PaCO 2 25-30 Immediate CT scan if available Consult neurosurgical service Consult retrieval service early Consider the use of mannitol boluses (1g/kg) in consultation with neurosurgical service, to reduce ICP for transfer Consider local burr holes under local anaesthesia in consultation with the neurosurgical service if transfer likely to take more than 2 hours & CT scanning is available and has demonstrated a large extra axial haematoma 2.2.2.6 Indications for referral to neuroscience Discuss the care of all patients with new, surgically significant ***** abnormalities on imaging with a neurosurgeon 1 4 6 7 statement revised after personal communication with Dr R Bullock 16
Regardless of imaging, other reasons for discussing a patient s care plan with a neurosurgeon include: persisting coma (GCS 8 ) after initial resuscitation 1 4 6 7 unexplained confusion for more than 4 hours 6 7 deterioration in GCS after admission (pay greater attention to motor response deterioration)7, especially a fall of 2, development of pupil dilation or other new neurological deficit 1 4 severe neurological deficit following TBI 1 progressive focal neurological signs 4 6 7 seizure without full recovery 6 7 definite or suspected penetrating injury 6 7 compound depressed skull fracture 4 6 cerebrospinal fluid leak 7 or other sign of a basal skull fracture 6 when a person fulfils the criteria for CT scanning but facilities are unavailable 6 normal CT but not improving 4. Reed (2007) 4 formats the recommendations with respect to severity but the guidance is very similar to above. Moreover, they recommend consultation with a neuroscience specialist when in doubt and that patients should be observed in facilities that can manage any complications that are likely to arise and that early neurosurgical consultation is advised. ***** definition of surgically significant to be developed by local neurosurgical unit and agreed with referring hospitals i.e. all people with severe TBI 17
2.3 Hospital care Included in this section are indications for admission, type and frequency of clinical observations, indications for review and management in intensive care. Again, as in the last section, the separation into the various clinical settings is artificial and are grouped here together for convenience. 2.3.3 Indications for admission These criteria are composed from the NICE (2007) 7, ACC (2006) 1 and SIGN (2009) 6 guidelines. Admit to hospital if there are ANY of the following: a deteriorating GCS 1 clinically significant abnormalities on imaging 1 7 GCS <15 after imaging 1 6 7 any indication for a CT scan 6 criteria for CT scanning are met but CT scanning is not possible 1 7 focal or abnormal neurological signs 1 early post-traumatic seizure 1 skull fracture high-risk mechanism of injury 1 continuing signs of concern to the clinician (e.g., vomiting, severe headaches, amnesia) 1 7 other reasons for clinician concern, including drug or alcohol intoxication, other injuries, shock, suspected non-accidental injury, signs of meningeal irritation, cerebrospinal fluid leak, where a scalp laceration overlies a fracture, or the person s age 1 7 when there is no responsible family/whanau member, caregiver or close friend under whose care the person could be discharged 1 6 where there are significant comorbidities 6 e.g. anticoagulant use mild head injuries with symptoms such as headache, photophobia, nausea and vomiting, or amnesia requiring management 1 Other relevant recommendations from the ACC (2006) guideline: People who require an extended period in a recovery setting due to the use of sedation or general anaesthetic during CT imaging should not normally require admission 1 Resuscitation and stabilisation of the injured person should be completed before transfer. A person persistently hypotensive despite resuscitation should not be transported until stabilised 1 People with multiple injuries should be admitted under the care of the team appropriate to their most severe and urgent problem 1. 18
2.3.3.1 In-hospital observation Minimum neurological observations should include ALL the following: GCS pupil size and reactivity limb movements respiratory rate heart rate blood pressure temperature 1 6 7 blood oxygen saturation 6 7 unusual behaviour or temperament or speech impairment 6. Perform and record observations at least every 15 minutes until GCS is 15 on two consecutive occasions 1 (NB: NICE (2007) 7 and SIGN (2009) 6 recommend half-hourly observations). The ACC (2006) 1 guideline also adds to assess for post-traumatic amnesia and focal neurological signs at regular intervals 1. For people with an initial GCS of 15, or who have returned to a GCS of 15 on two consecutive observations, the minimum frequency of observations following the initial assessment should be: half-hourly for the first two hours, then one-hourly for four hours, then two-hourly thereafter 1 7 If the person deteriorates to GCS <15 after initial 2-hour period, revert to 15 minute observations and follow original schedule 1 7 2.3.3.2 Indications for review Consider immediate CT scan, re-assess patient s clinical condition and manage appropriately, if Agitation or abnormal behaviour developed 6 7 GCS dropped by 1 point and lasted for at least 30 minutes (give greater weight to a drop of 1 point in the motor response score) 1 6 7 Any drop of 3 or more points in the eye-opening or verbal response scores, or 2 or more points 1 in the motor response score 6 7 Severe or increasing headache developed or persistent vomiting 1 6 7 New or evolving neurological symptoms or signs, such as pupil inequality or asymmetry of limb or facial movement 1 6 7. 19
In addition, if GCS 15 not achieved after 24 hours observation, but CT scan normal: consider further CT imaging or MRI scanning and discuss with radiology department 1 7. SIGN (2009) 6 has given the following additional guidance, mainly based on expert opinion: Clinical signs of shock in a patient with a head injury should be assumed, until proven otherwise, to be due to hypovolaemia caused by associated injuries Whilst an intoxicating agent may confuse the clinical picture, the assumption that deterioration or failure to improve is due to drugs or alcohol must be resisted If systemic causes of deterioration such as hypoxia, fluid and electrolyte imbalance, or hypoglycaemia can be excluded, then resuscitation should continue according to ATLS principles while anaesthetic help and neurosurgical advice are sought After traumatic brain injury remedial causes of agitation should be excluded before therapies are started. 2.3.4 Intensive care management The major focus for intensive care is: The prevention & limitation of ongoing brain damage 2 To provide the best conditions for natural brain recovery by reducing brain swelling & raised ICP 2 Due to the clinical complexity of patients who are admitted to intensive care for management of their TBI and the limited scope of this document, evidence will only be presented for the efficacy of interventions for post-traumatic seizures and treatment of raised ICP. As in general intensive care, optimum oxygenation, perfusion, nutrition, glycaemic control & temperature homeostasis are essential 2. 2.3.4.1 Post-traumatic seizure Benefits of prophylactic anti-seizure treatment must be balanced against the potential risks; recommended indications include penetrating brain injury & depressed skull fracture in patients with PTA >24 hours in whom a dural lesion is suspected 2 According to the ERABI 12 Research Group, seizure can occur with in hours of the initial head trauma (immediate seizures), within the first week of sustaining the injury (early seizures) or several months post injury (late seizures). These seizures can further complicate the injury has they can lead to increased damage. It has also been noted that the risk for developing or having late seizures post TBI is related to the severity of injury. The Brain Trauma Foundation 3 does not recommend the prophylactic use of phenytoin or valproate for preventing late post-traumatic seizures. Their prophylactic use results in similar incidences of early or late seizures and similar mortality rates 12. If late post-traumatic seizures occur, they recommend patients should be managed in accordance with standard approaches to patients with new onset seizures. The ERABI group 12 suggest, from one case study, that intramuscular midazolam may be effective for acute seizure cessation 12. It also appears to have less adverse effects than other commonly used intramuscular drugs such as diazepam and lorazepam 12. The Foundation also states that anticonvulsants are indicated to decrease the incidence of early post-traumatic seizures (within 7 days of injury). However, early post-traumatic seizures 20
are not associated with worse outcomes 3 and ERABI 12 conclude that anticonvulsants provided shortly post-tbi do not reduce long-term mortality, morbidity or late seizures and that anticonvulsants provided immediately post-tbi reduce the occurrence of seizures only within the first week. Phenytoin has been shown to reduce the incidence of early post-traumatic seizures 3 12 and may reduce the risk of late seizures 12. Valproate may have a comparable effect to phenytoin on reducing early post-traumatic seizures but may be associated with a higher mortality 3. On the other hand, levetiracetam is as effective as phenytoin in treating and preventing seizures in individuals in the intensive care unit post TBI 12. In addition, both phenytoin and carbemazepine have negative effects on cognitive performance, particularly those tasks with a motor and speed components 12. There is also some lower level evidence that carbemazepine improves seizure control and is less harmful to cognitive performance and behaviour than other anticonvulsants 12. 2.3.4.2 Raised Intracranial Pressure 2.3.4.2.1 Monitoring ICP should be monitored in all people with a severe TBI (in a coma) and an abnormal CT scan 3 There is evidence to support the use of ICP monitoring in people with a severe TBI who are at risk for intracranial haemorrhage 3. Not monitoring ICP while treating raised ICP can be deleterious and result in a poor outcome 3 2.3.4.2.2 Sedation and ventilation Sedation & artificial ventilation are used to reduce brain swelling & raised ICP in patients with severe TBI 2 13 The Brain Trauma Foundation 3 recommends propofol for the control of ICP, but not for improvement in mortality or 6 month outcome. In addition, high-dose propofol (>4mg/kg per hour 12 ) can produce significant morbidity 13. ERABI found that propofol may help to reduce ICP and the need for other ICP and sedative interventions when used in conjunction with morphine 12 13. High-dose barbiturate administration is also recommended to control elevated ICP that is refractory to maximum standard medical and surgical treatment. Of note, haemodynamic stability is essential before and during barbiturate therapy 3. ERABI 12 makes the further recommendations: there is conflicting evidence regarding the efficacy of pentobarbital over conventional ICP management measures 13 ; thiopental is more effective than pentobarbital for controlling unmanageable refractory ICP 13 ; pentobarbital is not better than mannitol for the control of elevated ICP 13 ; barbiturate therapy plus hypothermia may improve clinical outcomes ; patients undergoing barbiturate therapy should have their immunological response and systemic blood pressure monitored 13. 2.3.4.2.3 Hyperventilation Hyperventilation has been used to reduce ICP effectively however there is a risk of worsening ischaemia 2 Arterial CO2 < 30 mmhg should be avoided 2 Level 4 = case series, pre-post or post-study, or retrospective chart review based on one level 4 study 21
Prophylactic hyperventilation (pco 2 25 mmhg) is not recommended by the Brain Trauma Foundation but may be used as a temporising measure for the reduction of raised ICP 3. They also add that it should be avoided during the first 24 hours after injury when cerebral blood flow (CBF) is often critically reduced. If hyperventilation is used, they recommend that jugular venous oxygen saturation (SjO 2 ) or brain tissue oxygen tension (PbrO 2 ) measurements are used to monitor oxygen delivery 3. In addition ERABI make the following statements: hyperventilation below 34 mmhg PaCO 2 may cause an increase in hypoperfused brain tissue; tromethamine counteracts the detrimental effects of prolonged hyperventilation for the control of ICP leading to better outcomes post-tbi; hyperoxia may counteract the adverse effects of prolonged hyperventilation for the control of ICP post-tbi 12. 2.3.4.2.4 Osmotherapy Osmotherapy is usually considered as second line treatment after sedation and artificial ventilation have failed to control ICP ****** & interest in early & extensive craniotomies is increasing 2 There is insufficient evidence to support the use of hypertonic saline over mannitol because of the risks of hypernatraemia with hypertonic saline 2 Osmotherapy is best reserved for patients in whom ICP is being monitored Rapid administration of mannitol is among the first-line treatments recommended for the management of increased ICP. However, it is associated with significant diuresis and can cause acute renal failure, hyperkalemia, hypotension, and in some cases rebound increments in ICP 12. For these reasons, the Brain Trauma Foundation recommends that mannitol should only be used if a patient has signs of elevated ICP or deteriorating neurological status 12. The Brain Trauma Foundation 3 concludes that mannitol is effective in reducing ICP in the management of raised ICP post-tbi at doses of 0.25 gm/kg to 1 g/kg body weight. They add that arterial hypotension (SBP < 90 mm Hg) should be avoided and advise to restrict the use of mannitol (prior to ICP monitoring) only to patients with signs of transtentorial herniation or progressive deterioration not attributable to extracranial causes 3. ERABI 12 make the following statements regarding the use of mannitol for raised ICP: high dose mannitol results in lower mortality rates and better clinical outcomes compared with conventional mannitol 13 ; early out of hospital administration of mannitol does not negatively affect blood pressure 13 ; mannitol may only lower ICP when initial ICP values are abnormally elevated 13. With regard to hypertonic saline, the Brain Trauma Foundation 3 does not make any recommendations on its use because current evidence is not strong enough. The ERABI group, however, make the following statements: hypertonic saline reduces ICP more effectively than mannitol 13 ; hypertonic saline and Ringer s lactate solution are similar in lowering elevated ICP and result in similar clinical outcomes and survival up to 6 months post-injury 13 ; hypertonic saline may reduce elevated ICP uncontrolled by conventional ICP management measures; hypertonic saline may aid in resuscitation of brain injured patients by increasing cerebral oxygenation. 2.3.4.2.5 Decompressive craniectomy Decompressive craniectomy is controversial as it does not produce improved outcome in all people & has many side-effects, some severe 2. There is a consensus that the ****** recommendation revised after personal communication with Dr R Bullock personal communication with Dr R Bullock 22