Introduction References
Conclusion Annotated
Bibliography Questions
Severe
Traumatic Brain Injury
Case
Presentation
Coming back
from the weekly visit to his parents, FD, a 34 year old male while driving
on the highway, lost control of his car and crashed against the guard-rail.
The left side of the car was completely destroyed. In less than 14 minutes
he was rescued by an advanced life ambulance team with physician on
board. He was comatose, the airway was open, respiratory rate 32/m,
heart rate 135 bpm, systolic blood pressure 85 mmHg; the first Glasgow
Coma Score was 6 (V1; E1; M4). Unequal pupils (left > right pupil)
were detected; his abdomen appeared distended and an fracture of the
left leg was evident. He was suddenly intubated and ventilated after
administration of midazolam (0.1 mg/kg). A colloid infusion was started;
a cervical collar was placed on his neck and he was blocked on a pneumatic
matress and the left leg was splitted.
On arrival at
the ED, his neurologic condition was the same but he showed a downward
and external rotation of the left ocular bulb with a palpebral contusion.
Haemodynamic status deteriorated with a BP of 73/43, Hr 135 bpm; SpO2
was 100% and Hb on the coxymeter 4.5g/dl. A chest X ray was positive
for multiple chest rib fractures. Urgent abdominal US detected the presence
of a free blood collection. The patient was immediately transferred
to the OR where the fractured spleen was removed. At the end of the
operation, after multiple hemotransfusions and cristalloid infusion,
haemodynamics condition improved to a BP 125/76mmHg, Hr 95 bpm, SpO2
100% at a FiO2 .4 and Hb 9,.5 g/dl and remained stable. His neurological
condition did not improved after stabilization (GCS = 6; best mor response
a coordinate flexion to pain). His was then transferred to Radiology:
the first Ct scan showed only a modest brain swelling with no intracerebral
and/or extraassial blood collection.
He was then
transferred to ICU, sedated with remifentanyl (0.05 mcg/kg/m) and propofol
(2.5 mg/kg/h). An ICP monitoring through a intraparenchimal transducer
tipped catheter was placed and the first value detected was 15 mmHg.
Twelve hours later ICP increased to 25 mmHg refractory to a heavier
sedation and mannitol. A second CT showed a bilateral intraparenchymal,
subcortical blood collections that were considered as the expression
of a diffuse brain injury. There was no shift of the midline and no
indication for neurosurgical operation was given by the specialist.
Key Clinical questions
-
Brain ischemia
is the main cerebral blood flow pattern complicating head injury
-
Head injured
patients require aggressive approach in the acute phase for prevention
of secondary insults; hypoxia and hypotension are the most frequent,
important complications that should be prevented
-
Referral
to hospital with neurological facilities should be the gold standard
where surveillance, diagnosis and prompt surgical intervention could
be provided in case of detection of mass lesion.
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Severe
Traumatic Brain Injury
Introduction
Traumatic brain
injury (TBI) represents a relevant pathology in the ED and still remains
the leading cause of death among people younger than 25 years of age
(1) and the main single factor in determining prognosis in the polytraumatised
patient. Approximately 200 patients/100.000 inhabitants/year are admitted
in the ED for a TBI; among them 15-20 are severe TBI (STBI) patients
defined as patients scored with a GCS < 9.
What are the priorities in the treatment of severe head injuries?
-the role and prevention of cerebral ischemia
Prognosis in head injury has been strictly correlated with the degree
and duration of ischemia and more than 90% of autopsies on patients
dead after a head injury showed ischemic lesions of different severity
(2). Many causes have been advocated for posttraumatic cerebral ischemia
such as intracranial hypertension, arterial hypotension, brain edema
and swelling, focal tissue compression from intracranial hematomas and
involvement of microcirculation and vasospasm of large cerebral arteries.
Many in vivo studies have confirmed that ischemia is the predominant
cerebral blood flow pattern in the early postraumatic phase in head
trauma patients (3). In addition, early ischemia has been found to correlate
with poor outcome and early mortality. The correlation between CBF and
mortality is lost after this early period whereas it remains valid for
cerebral metabolic rate for oxygen (4). This pattern of early ischemia
cannot be attributed only to abnormally low cerebral perfusion pressure,
excessive hyperventilation or vasospasm, because it is still present
even after normalisation of the haemodynamic and respiratory parameters,
suggesting the presence of an increased distal vascular resistance due
to different factors (extrinsic microvascular compression by damaged
and edematous astrocytic processes, active muscular contraction of the
resistance arterioles caused by the trauma induced release of vasoactive
substances such as calcium, cathecolamines, prostaglandins, haemoglobin,
neuropeptides and intravascular thrombosis)(5).
This pattern
was demonstrated even with monitoring of brain parenchyma oxygen saturation
(6) and the measurement of glutamate and lactate concentration in interstitial
and CSF fluid (7,8).
-the ABCs
The cornerstones of emergency treatment of SHI must be aimed at the
assessment of the ABC's and the simultaneous resuscitation in the primary
survey to obtain a normal oxygenation (arterial haemoglobin oxygen saturation
> 95%), the maintenance of CO2 values at 30-35 mmHg (avoiding hyperventilation
with resulting hypocarbia and subsequent hypoperfusion), the rigorous
maintenance of normal systemic arterial pressure values (avoiding even
short episodes of arterial hypotension).
A=Airway patency
All comatose
patients (GCS < 9) should be intubated under sedation and analgesia
(9, 10). The indications for an early endotracheal intubation are the
following: any case of airway obstruction, the maintainance of an adequate
oxygenation and ventilation, the prevention of hyper and hypocapnia,
the protection from airways obstruction, the prevention of neurological
deterioration in hostile environments (transport, radiological procedures
etc). Oratracheal intubation is usually preferred. Blind nasotracheal
intubation should be avoided in any case of suspected basal or maxillary
fracture; moreover it needs the patient breathing spontaneously, there
is an high percentage of failures and it could give nasal bleeding.
A cervical spine lesion must ever be suspected in all comatose patient;
he/she should be treated as having a spine injury until demonstrated
otherwise.
But looking
at daily clinical behaviour, do we all act according to clinical guidelines?
A survey study performed in Italy on 1278 patients showed that about
12% in GCS 7 and 33% of GCS 8 were not intubated in the preH setting
(11).
Is prehospital endotracheal intubation a gold priority in the management
of the STBI?
Some papers
were recently published discussing the key role of prehospital intubation
of STBI. Murray (12) showed that prehospital intubation did not demonstrate
any improvement in survival, Bochicchio (13) demonstrated that prehospital
intubation in patients who survived more than 48 hours after the trauma
was associated with a significant increase in morbidity and mortality.
The conclusions of these studies must take into consideration the different
organisation of EMS and the technical skills of the first aid.
B = Breathing
All intubated
patients must be ventilated, to obtain:
a) adequate oxygenation (paO2 >90 mmHg, SaO2 >95%)
b) prevention of hyper- or hypocapnia, with PaCO2 of 35 mmHg.
Hypercapnia is avoidable as a factor aggravating brain injury and must
absolutely be corrected if not prevented. Cerebral acidosis or vasodilatation
can cause intracranial hypertension and secondary brain damage.
Why not to hyperventilate?
Hyperventilation,
which may lead to hypocapnia, is not advisable because cerebral vasoconstriction
induced by the drop in blood CO2 may cause cerebral hypoperfusion; this
worsens the already critical situation of diminished blood flow or inadequate
oxygen transport.
C = Circulation
Prehospital
hypotension, defined as a single observation of a systolic blood pressure
< 90 mmHg, has been found to be an independent predictor of outcome
(14). In the NeuroLink study (11) patients who did not show episodes
of hypoxia and hyptension had 52% of good outcomes with a mortality
rate of 19%; patients who simultaneously presented either hypoxia and
hypotension had 51% mortality and 18% good outcomes.
What is the optimal target for BP?
The value of
90 mmHg to delineate the threshold for hypotension has arisen arbitrarly
and is more statistical than a physiologic parameter (15). In facts
no studies have been performed to corroborate this. In the Italian Guidelines
for the treatment of the STBI a systolic pressure higher than 110 mmHg
was indicated as the target (10)
Is mean arterial blood pressure a better endpoint than systolic
blood pressure?
It may be valuable
to maintain mean arterial pressure above those represented by systolic
blood pressure (15)
What about sedation of the STBI?
Sedation and
analgesia is indicated for STBI. Hypnotics such as propofol and midazolam
are probably the most used drugs. Midazolam has a dose related effect
(16) and propofol can cause hypotension when administered in boluses
in the hypovolemic patient. To avoid these effects older drugs with
a lesser effect on hemodynamics are now coming back to a daily use such
as etomidate mostly in US and less in Europe (17) and Ketamine whose
effects on cerebral blood flow when used alone restricted his role in
TBI.
Intravenous
lidocaine (1.5 mg/kg) is useful in blunting the increase of ICP with
endotracheal intubation (18) but no study demonstrates that this was
helpful in making patients' outcome better.
Fentanyl or
morphine are the most used drugs for analgesia.
Muscle relaxation
could be used to facilitate endotracheal intubation; suxamethonium,
rocuronium or vecuronium are the most used drugs.
Sedation/analgesia
should be continued using short-acting drugs so that neurological assessments
can be made at regular intervals in the ED. Muscle relaxing drugs should
be avoided if possible.
How much to rely on the first CT for further evolution and prognosis?
Notwithstanding
all these assumptions, prompt diagnosis and early surgical treatment
of intracranial masses still remains the central point for the management
of TBI. For this reason cerebral CT scan should be performed following
protocols that could allow the detection of expanding masses. Servadei
(19) has demonstrated that even patients with normal CT scan have a
4% possibility to be complicated by a mass lesion; this percentage increases
to a 20% with a diffuse injury IV.
The Italian
guidelines for the care of the STBI advise to perform the first CT scan
as soon as possible and the second before 12 hours after the trauma
if the first CT was done within 3 hours or within 24 hours if done later
(10). In STBI an abnormal CT scan has arisk for raised ICP of 50-60%
(9).
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Severe
Traumatic Brain Injury
Reference
List
1. White R.J., Likavek
M.J. The diagnosis and initial management of head injury. N. Eng.
J. Med; 327:1507-1511,1992
2. Graham D.I., Adams
J.H. Ischemic brain damage in fatal head injuries. Lancet 1:265-266,
1971
3. Bouma G.J., Muizelaar
J.P., Choi S.C., Newlon P.G., Young H.F. Cerebral circulation and
metabolism after severe traumatic brain injury: the elusive role
of ischemia J. Neurosurg. 75:685-693, 1991
4. Della Corte F., Giordano
A., Pennisi M.A., Barelli A., Caricato A., Campione P., Galli G.
Cerebral blood flow determination with a new DSPET device: prognostic
implication in the first 48 hours after severe head injury. Acta
Neuchirurgica, Vol 139, n. 7, 636-642, 1997
5. Martin NA, Patwardhan
RV, Alexander MJ, Afrik CZ, Lee JH, Shalmon E, Hovda DA, Becker
DP Characterization of cerebral hemodynamic phases following severe
head trauma: hypoperfusion, hyperemia and vasospasm. J. Neurosurg.
87; 9-19, 1997
6. Van Den Brink (2000)
Brain oxygen tension in severe head injury. Neurosurgery 46(4):868-878
7. Yamamoto T, Rossi
S, Stiefel M, Doppenberg E, Zauner A, Bullock R, Marmarou A. CSF
and ECF glutamate concentrations in head injured patients. Acta
Neurochir Suppl (Wien). 1999;75:17-9.
8. Goodman JC, Valadka
AB, Gopinath SP, Uzura M, Robertson CS. Extracellular lactate and
glucose alterations in the brain after head injury measured by microdialysis.
Crit Care Med. 1999 Sep;27(9):1965-73.
9. Bullock R., Chesnut
RM, Clifton F, Ghajar J, Marion DW, Narayan RK, Newell DW, Pitts
LH, Rosner MJ, Wilberger JW Guidelines for the management of severe
head injury. New York: Brain Trauma Foundation, 1996
10. Recommendations for
the treatment of serious adult head injury. I. Initial evaluation,
prehospital observation and treatment, hospitalization criteria,
systemic and cerebral monitoring. Procaccio F, Stocchetti N, Citerio
G, Berardino M, Beretta L, Della Corte F, D'Avella D, Brambilla
GL, Delfini R, Servadei F, Tomei G. Minerva Anestesiol. 1999 Apr;
65(4):147-58.
11. G. Citerio, N. Stocchetti,
M. Cormio , L. Beretta : Neuro-Link, a computer-assisted database
for head injury in intensive care. Acta Neurochirurgica Vol. 142,
7, 769-776, 2000
12. Murray JA, Demetriades
D, Berne TV, Stratton SJ, Cryer HG, Bongard F, Fleming A, Gaspard
D. Prehospital intubation in patients with severe head injury. J
Trauma. 2000 Dec;49(6):1065-70.
13. Bochicchio GV, Ilahi O, Joshi M, Bochicchio K, Scalea TM. Endotracheal
intubation in the field does not improve outcome in trauma patients
who present without an acutely lethal traumatic brain injury. J
Trauma. 2003 Feb; 54(2):307-11.
14. Chesnut RM, Marshall
LF, Klauber MR et al. The role of secondary brain injury in determining
outcome from severe head injury. J Trauma; 34:216-222, 1993
15. The Brain Trauma
Foundation. The American Association of Neurological Surgeons. The
Joint Section on Neurotrauma and Critical Care. Prehospital management
of severe brain injury. http://www.braintrauma.org/index.nsf/Pages/Guidelines-main.
16. Davis DP, Kimbro
TA, Vilke GM. The use of midazolam for prehospital rapid-sequence
intubation may be associated with a dose-related increase in hypotension.
Prehosp Emerg Care. Apr-Jun;5(2):163-8,2001.
17. Tentillier E, Ammirati
Prehospital management of patients with severe head injuries C.Ann
Fr Anesth Reanim.19(4):275-812000.
18. Robinson N, Clancy
M. In patients with head injury undergoing rapid sequence intubation,
does pretreatment with intravenous lignocaine/lidocaine lead to
an improved neurological outcome? A review of the literature.Emerg
Med J. 2001 Nov;18(6):453-7. Comment in: Emerg Med J. 2001 Nov;18(6):419.
19. Servadei F, Murray
GD, Penny K, Teasdale GM, Dearden M, Iannotti F, Lapierre F, Maas
AJ, Karimi A, Ohman J, Persson L, Stocchetti N, Trojanowski T, Unterberg
A.The value of the "worst" computed tomographic scan in
clinical studies of moderate and severe head injury. European Brain
Injury Consortium. Neurosurgery. 2000 Jan;46(1):70-5; discussion
75-7.
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Severe
Traumatic Brain Injury
Conclusions
/ Recommendations
-
From the
pathophysiological point of view, in STBI brain ischemia is the most
relevant pattern. This is especially true in the first 24 following
trauma and is not necessarily correlated to cerebral perfusion pressure
even if lower systemic arterial blood pressure will worsen the damage.
-
STBI patients
require aggressive approach in the acute phase for the prevention
of secondary insults. Hypoxia and hypotension are the most frequent,
important (an preventable) complications.
-
Referral
to hospitals with neurosurgical facilities should be the gold standard
where surveillance, diagnosis and prompt surgical intervention could
be provided in case of detection of mass lesion.
TOP
Severe
Traumatic Brain Injury
Annotated
Bibliography
1. Bouma
G.J., Muizelaar J.P., Choi S.C., Newlon P.G., Young H.F. Cerebral circulation
and metabolism after severe traumatic brain injury: the elusive role
of ischemia J. Neurosurg. 75:685-693, 1991
The paper defined the role of ischemia in the first 24 hours after severe
TBI. The mean cerebral blood flow of 186 patients was 22.5ml/100gr/min
in the first 6 hours but increased significantly during the first 24
hours. One third of patients in the first 6 hours most of patients had
a cerebral blood flow lower than the ischemic threshold of 18 ml/100g/min.
The severity of ischemia was correlated with outcome but only in the
first 24 hours.
2. Bullock R., Chesnut
RM, Clifton F, Ghajar J, Marion DW, Narayan RK, Newell DW, Pitts LH,
Rosner MJ, Wilberger JW Guidelines for the management of severe head
injury. New York: Brain Trauma Foundation, 1996
These are the guidelines approved by the AANS. II edition in 2000
and an update on cerebral perfusion pressure in March 2003.
3. G. Citerio, N. Stocchetti,
M. Cormio , L. Beretta : Neuro-Link, a computer-assisted database
for head injury in intensive care. Acta Neurochirurgica Vol. 142,
7, 769-776, 2000
An italian prospective database collecting data from patients admitted
in four hospitals in the area of Milan. The number of patients is
relevant and higher than that published by the TCDB. The results are
of this study are of the greatest interest.
4. Chesnut RM, Marshall
LF, Klauber MR et al. The role of secondary brain injury in determining
outcome from severe head injury. J Trauma; 34:216-222, 1993
Even if published in 1993, this paper defines for the first time the
role of hypoxia and hypotension in the determination of prognosis
of the severe head injured patient. One of most frequently cited paper
in neurotraumatology.
5. The Brain Trauma
Foundation. The American Association of Neurological Surgeons. The
Joint Section on Neurotrauma and Critical Care. Prehospital management
of severe brain injury. http://www.braintrauma.org/index.nsf/Pages/Guidelines-main.
Even if published in 1999, they represent the most comprehensive document
on Guidelines for treatment of the severe head injured patient in
the prehospital phase. Free download from the Internet.
Severe
Traumatic Brain Injury
Questions
1. In the STBI endotracheal
intubation:
a. is considered
indicated in all patients with a GCS < 9
b. the nasotracheal approach is to be preferred because it does not
nedd neck extension
c. is indicated in all patients with GCS 13 even if they are able to
maintain a normal oxygenation
d. is not indicated until a cervical lesion is excluded in the comatose
patient
2. The appearance of unequal
pupils in an unconscious patient may allow:
a. to exclude
the presence of a subdural hematoma
b. to confirm a lesion of the 5th pair of cranial nerves
c. to indicate an immediate CT scan to detect an intracerebral hematoma
d. to diagnose an hypoxic cerebral lesion
3. If the first CT of
a STBI patient has been performed one hour after the trauma and it was
negative and patient anamnesis did not show any risk factor:
a. It is not
necessary to schedule a new CT scan until the next 24 hours
b. A CT scan should be done within the 12 hours after the trauma
c. There is no reason to continue sedation and analgesia and to schedule
another CT scan
d. The program should be based on ICP values trend
4. Brain ischemia after
a STBI is always related to:
a. Reduction
of cerebral perfusion pressure
b. To arterial blood hypoxia
c. To arterial blood hypercapnia
d. To a complex network of pathophysiological chain reaction triggered
by the impact
5. All STBI patients should
be intubated and ventilated. Which should be the target for paCO2?
a. PaCO2 less
than 30 mmHg
b. PaCO2 35 mmHg
c. PaCO2 > 40 mmHg
d. PaCO2 is not important in cerebral flow regulation, the only important
target should be PaO2 control
Answers
1. Answer a.
Endotracheal intubation,
if available, is the most effective procedure to maintain the airways
that should be secured in all patients with GCS < 9, when there is
the inability to maintain an adequate airway or when hypoxiemia is not
corrected by supplemental oxygen.
2. Answer b.
An unequal pupil is due to
the compression of the III cranial nerve. It appears more rapidly and
more frequently than signs of involvement of the motor nerves. It could
be due also to a peripheral paresis/palsy of the III cranial nerve or
to a direct contusion of the ocular bulb but in the comatose patient
it should indicate the suspect of an intracranial expanding mass until
proven otherwise.
3. Answer b.
It was demonstrated that even if the first CT in a STBI is normal, a
percentage of 4% of these patients could develop an intracranial surgical
mass that should be evacuated. This percentage increases with worsening
of the initial CT
4. Answer d.
Ischemia is the main pathophysiological multifactorial consequence of
a STBI especially in the first 24 hours after the trauma. Ischemic patterns
of flow are not strictly correlated to the cerebral perfusion and could
be present even if arterial pressure is maintained in normal value.
If arterial drops the cerebral ischemic damage will obviously deteriorate.
5. Answer b.
PaCO2 should be maintained around 35 mmHg. Hyperventilation will lower
paCO2 due to cerebral arteriolar vasoconstriction resulting in further
worsening of cerebral ischemia.
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