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26. Brooks SE, Peetz AB. Evidence-based care of geriatric trauma patients. Surg Clin N Am.
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27. Hruska K, Ruge T. The tragically hip: trauma in elderly patients. Emerg Med Clin N Am.
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28. Huls CK, Detlefs C.Trauma in pregnancy. Semin Perinatol. 2018;42(1):13–20.
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34. Jones AC, Woldemikael D, Fisher T, Hobbs GR, Prud’homme BJ, Bal GK.Repeated computed tomographic scans in transferred trauma patients: indications, costs, and radiation exposure. J Trauma Acute Care Surg. 2012;73(6):1564–9.
C. R. Parrino et al.
Chapter 12
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Severe Traumatic Brain Injury: AReview
fortheGeneral andTrauma Surgeon
CorradoP.Marini, JohnMcNelis, andPatrizioPetrone
Introduction
According to the Glasgow Coma Score (GCS), mild, moderate, and severe traumatic brain injury (TBI) correspond to decreasing GCS scores in the corresponding
ranges of 15–13, 12–9, and 8–3 [1, 2]. Another assessment method is shown in
Table 12.1. A more comprehensive denition of severe TBI (sTBI) includes a
depressed GCS (<8), loss of consciousness >24h, and/or amnesia >7days [3]. The
30-day mortality of patients with sTBI ranges from 35 to 45%. Those who survive
incur neurological sequelae for 6–12months or even longer, as revealed by Glasgow
Outcome Scale (GOS) or extended GOS (GOSE) [4]. Scores <4 are consistent with
poor functional results for both of them.
It is recommended that the initial GCS should be re-evaluated after completion
of the resuscitation and stabilization phases, in order to predict more accurately the
14-day and 6-months outcomes (CrasH or IMPACT [5, 6]).
C. P. Marini
New York Medical College, Jacobi Medical Center, Bronx, NY, USA
e-mail: corradom@nychhc.org
J. McNelis
Department of Surgery, Albert Einstein College of Medicine, Jacobi Medical Center,
Bronx, NY, USA
e-mail: John.McNelis@nychhc.org
P. Petrone (
Department of Surgery, NYU Grossman Long Island School of Medicine, NYU Langone
Hospital—Long Island, Mineola, NY, USA
e-mail: patrizio.petrone@nyulangone.org
Switzerland AG 2024
J. Faintuch, S. Faintuch (eds.), Recent Strategies in High Risk Surgery,
https://doi.org/10.1007/978-3-031-56270-9_12
*)
195© The Author(s), under exclusive license to Springer Nature
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Table 12.1
Severity GCS Loss of consciousness Structural imaging
Mild 13–15 <20min to 1h Normal
Moderate 9–12 1–24h Normal/abnormal
Severe 3–8 >24h Abnormal
GCS Glasgow Coma Scale
Alternate classication
Available andInnovative Variables
Intracranial pressure (ICP), bi-frontal near infrared spectroscopy regional oxygen
saturation (rSO2), brain tissue oxygen (PbtO2), external ventricular drainage (EVD),
cerebral blood ow (CBF), and cerebral microdialysis (CMD) are among the most
mentioned multimodality measures within this context. Other predictive tools such
as Marshall, Rotterdam, CrasH, and IMPACT, along with existing clinical and
patho-anatomic classications targeting injury subtypes, should not be overlooked
either [6–8].
Their utilization should obviously be examined in the light of invasiveness,
safety, convenience, and cost but also of potential advantages concerning both mortality and long-term recovery. In other words, the most favorable effectivity, risk/
benet, and cost/benet ratios should be sought.
Primary Lesions
Most centers classify sTBI in accordance with computerized tomography ndings
(CT scan) as follows: (1) epidural hematoma; (2) hemorrhagic contusion/hematoma; (3) diffuse axonal injury; (4) subdural hematoma; (5) subarachnoid/intraventricular hemorrhage; and (6) diffuse swelling, as a result of the trauma itself.
Secondary injury is frequent as a result of uncorrected hypoxemia, hypotension, and
intracranial uid dynamics. Instead of occurring in the initial seconds, it tends to
appear within hours or even many days, depending on restoration of brain perfusion
and physiology. Diffuse axonal injury or swelling, hemorrhagic contusions, and
intraventricular or parenchymal traumatic hemorrhage represent the most unpredictable lesions, as corrective interventions are often unavailable or ineffective,
allowing for ongoing neuronal damage.
Intracranial Pressure Dynamics
The Monro–Kellie hypothesis (1783) states that the sum of the three components
contained within the rigid skull, namely blood (arterial and venous blood, 10%),
cerebrospinal uid (CSF, 10%), and brain parenchyma (80%), is constant. An
Intracranial
marking closure of the aortic valve
e
P
P
P
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increase in one requires a reciprocal decrease in one or the other two. The intracranial pressure (ICP) represents the pressure within the brain parenchyma and
CSF.ICP increases with corresponding reductions in cerebral blood ow (CBF) can
be caused by elevated cerebral blood volume (arterial or venous), increased CSF
volume or enlarged brain parenchyma (edema), and also abnormal brain expansion
(mass lesion).
While most surgeons are familiar with the numeric value of ICP and of its implication on brain integrity, few can interpret the waveform of the ICP tracing and
understand the associated information that can be gathered from it. The three characteristic peaks, namely, P1, P2, and P3, have different physiologic meanings and
should be individually analyzed (Figs.12.1 and 12.2).
P1
P2
P3
ICP
Amplitude
Time
Fig. 12.1 ICP intracranial pressure, P1 P1 wave, P2 P2 wave, P3 P3 wave
3
2
1
Pressure Waveform
Arterial Pulse Waveform
Dicrotic notch
Fig. 12.2 P1 P1 wave, P2 P2 wave, P3 P3 wave
Intracranial
(mean) Pressur
Systolic
Blood Pressure
Diastolic
Blood Pressure
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P1/P2 Ratio
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C. P. Marini et al.
Intracranial Hypertension (IH)
IH affects the characteristics of the waveform. An increase in amplitude of the three
peaks indicates a mean increase in ICP.A reduced amplitude of P1 suggests decreased
cerebral perfusion pressure (CPP), and an increase in the P2 peak above P1 is indicative
of decreased cerebral compliance (CC). A P2/P1 ratio>1 correlates with increased ICP
and a loss of CC, with an r of 0.94 [9] (Fig.12.3). The mean P2/P1 ratio has a sensitivity
of 100%, specicity of 45.4%, a positive predictive value (PPV) of 36.8%, and negative
predictive value (NPV) of 100% to predict IH with a cutoff value of 1.06. Of note, P2/
P1>1 precedes the increase in the absolute mean value of the ICP.This supports the
hypothesis that morphological changes of the brain volume-pressure curve precede IH.
Cerebral Blood Flow (CBF)
Normal range of CBF is 50–65mL/100g/min, accompanied by low venous pressure
(2–5 mmHg) [10]. Brain vessels increase or reduce perfusion depending on oxygen
requirements, as a phenomenon of cerebral autoregulation (CA) [11].
CBF <10–15 mL/100 g/min (tissue oxygen tension/PbtO2 <15 mmHg) is usually
incompatible with neuronal survival. Reversible damages are triggered by CBF
15–20mL/100g/min and electroencephalographic aberrations around 25mL/100g/min.
Cerebral perfusion pressure (CPP)=mean arterial pressure (MAP) − ICP (Fig.12.4)
[12]. Constant CBF is linked to cerebral vessel resistance in the settings of increased or
decreased CPP, respectively. Above and below the lower and upper limits of 50 and
160mmHg, CA is lost and CBF becomes dependent on mean CPP in a linear fashion.
Impaired Cerebral Autoregulation
Some degree of loss is observed in 49–87% of affected cases soon after sTBI [13–
15], and it contributes markedly to secondary brain injury. Continuous transcranial
Doppler ultrasonography (TCD) of the middle cerebral artery ow and calculation
Fig. 12.3 P1/P2 ratio. P1 P1 wave, P2 P2 wave, P3 P3 wave
P1
P2
P3
Normal Compliance
P2
P1
P3
Decreased Compliance
CBF ml/100 g
CPP mm Hg
Cerebral autoregulation
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160
140
120
100
80
60
40
20
0
010203040506080 100 120 140 160 180 185
Fig. 12.4 Cerebral autoregulation. CBF cerebral blood ow, CPP cerebral perfusion pressure
199
of the pressure reactivity index (PRx), related to the slow waves in ICP and MAP,
are well known tools to follow CA.
MAP Norepinephrine Challenge
This is another option to test CA integrity, even though less reliable than PRx calculation. MAP is raised during 10–20min by norepinephrine infusion, and MAP, CPP,
ICP, and PbtO2 are repeatedly documented. ICP will diminish (2–5mmHg within
3–5min) if CA is present, whereas no change or elevation will be observed if CA
was lost [16].
Open Versus Closed TBI
In both circumstances, GCS is widely used, more recently complemented by the
Neurological Outcome Scale for Traumatic Brain Injury (NOS-TBI) [17]. Both
modalities of trauma are similarly followed by various degrees of vasospasm, which
may not alleviate before 5–7days, thus aggravating low tissue perfusion (Table12.2)
[18, 19].
Subsequent Brain Damage
After sTBI, several cellular and metabolic shifts can be detected, encompassing calcium inux into neuronal cells and increased tissue levels of glutamate, aspartate, and
free radicals. All of these contribute toward cerebral edema, intracranial hypertension,
impaired CA, and decreased CBF, further damaging the affected brain [20–22].
Systemic hypotension should be prevented, including after hospital admission, when
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Table 12.2
Behavior Response Score
Eye opening response Spontaneously 4
Best verbal response Oriented to time, space, and person 5
Best motor response Obeys commands 6
Total score Best response 15
Available at glasgowcomascale.org/
Glasgow Coma Scale
To speech 3
To pain 2
No response 1
Confused 4
Inappropriate words 3
Incomprehensible sounds 2
No response 1
Moves to localized pain 5
Flexion withdrawal from pain 4
Abnormal exion (decorticate) 3
Abnormal extension (decerebrate) 2
No response 1
Comatose ≤8
Unresponsive 3
the patient is transferred to the intensive care unit (ICU), as it is a strong driver of
mortality (55–150% elevation) [23, 24]. Marked brain edema is another well-described
ominous development, as brain herniation could precipitate abrupt demise.
CT Predictive Models
The Marshall model is more than 30years old; however, it is still useful, notably for
early outcome, in the rst 4 weeks. The Rotterdam guideline is deemed more trustworthy for long-term course, being recommended for 6-month prediction (Tables
12.3 and 12.4) [7, 25–27]. The International Mission for Prognosis and Analysis of
Clinical Trials (IMPACT) is also a recommended score and has the advantage of
online calculation (Table12.5) (tbi- impact.org/?p=impact/calc) [28].
Immediate Management
Upon arrival at the emergency unit, all patients with sTBI should be intubated and
ventilated to a PCO2 range of 35–45. In case of IH, the level is set at 32–35mmHg,
and an intermittent bolus of mannitol 0.25–1.0g/kg is prescribed. Normal saline
<2000 mL is preferred over Lactated Ringers based on the results of the
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Table 12.3
Category Denition
Diffuse injury I No intracranial pathology
Diffuse injury II Cisterns present with midline shift <5mm and/or lesion densities present.
Diffuse injury III Cisterns compressed or absent with midline shift 0–5mm
Diffuse injury IV Midline shift >5mm, no high or mixed density>25cm
Evacuated mass
lesion
Non-evacuated
mass lesion
Available at
Table 12.4 Rotterdam CT
classication
Marshall CT classication
No high or mixed density lesion >25cm
Any lesion evacuated surgically
High or mixed density lesion >25cm
radiopaedia.org/articles/marshall- classication- of- traumatic- brain- injury
CT nding Score
Basal cisterns 0
Normal 1
Compressed absent 2
Midline shift
≤5mm 0
>5mm 1
Epidural mass lesion
Present 0
Absent 1
Intraventricular or subarachnoid hemorrhage
Absent 0
Present 1
Sum score +1
Available at
score- of- traumatic- brain- injury
1 point is added as a sum score to make the grade
numerically total 6 points consistent with the motor
score of the GHCS and the Marshall Classication.
(Maas AI, etal. Neurosurgery 2005;57(6):1173–82)
3
3
3
, not evacuated surgically
radiopaedia.org/articles/rotterdam- ct-
PROMMTT study that showed the superiority of saline for prehospital uid
replenishment [29, 30]. Lactated Ringer’s solution seems superior when the
patient is hypothermic.
CT scan of the head is required in all patients suspected of having suffered for
sTBI. A group of patients with sTBI requires immediate craniotomy or primary
decompressive craniectomy. Those who do not require an immediate procedure
should undergo multimodality monitoring and goal-directed therapy, as soon as
they are resuscitated and transported to the ICU. The exceptions are those with
unsurvivable brain injuries, who could become organ donors depending on systemic
conditions and family ethical consent. These are basically cases with GCS 3 along
with xed or unreactive pupils, severe damage to the brain or brainstem, or absence
of cerebral blood ow with imaging methods.
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Table 12.5
(International Mission for
Prognosis and Analysis of
Clinical Trials in TBI)
IMPACT
Advanced Monitoring—ICP
Admission
characteristics Value
Core
Age (14–99)
Motor score 1–6
Pupils Both reactive, one, none
Core+CT
Hypoxia Yes or no
Hypotension Yes or no
CT classication Marshall I–IV, evacuated mass
tSAH on CT Yes or no
Epidural mass on CTYes or no
Core+CT+lab
Glucose (3–20mmol/L)
Hb (6–17g/dL)
Available at
Prediction models for 6-month outcome after TBI
ISAH intraventricular or subarachnoid hemorrhage, Hb
hemoglobin concentration
tbi- impact.org/?p=impact/calc
lesion, non-evacuated mass lesion
Parenchymal or intraventricular ICP monitoring is a widely recognized technique to prevent secondary brain injury from IH (ICP >20mmHg). In the USA,
90% of level I and II trauma centers adopt it; however, not more than 37% in
Europe [31]. Indeed, there is some controversy in the literature about its usefulness [32, 33]. Nevertheless most specialists admit that in conjunction with a
three-tier algorithm, it can improve clinical results [34, 35]. An external ventricular drain (EVD) encompassing a pressure transducer provides reliable ICP
monitoring and CSF drainage, in circumstances of marked pressure elevations.
ICP-guided therapy requires data on cerebral tissue oxygenation (PbtO
) for
2
optimal benets.
Near Infrared Spectroscopy (NIRS)–Regional Cerebral Oxygen
Saturation (rSO2)
Oxygen demand-supply aberrations in the territory of the anterior and middle cerebral arteries (rSO2<55%) can be followed with this technique. Usually, a low rSO2
is compatible with elevated oxygen extraction due to decreased CBF.
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Brain Tissue Oxygen Tension (PbtO2)
Current Guidelines for the Management of Severe Traumatic Brain Injury, fourth
ed., do not advise PbtO2 monitors for direct brain tissue oxygenation measurement;
however, a consensus of experts supports the use treatment protocols based on both
PbtO2 and ICP [36, 37]. The results of the BOOST II trial and of other studies provide further evidence of the usefulness of such an apporach [38, 39].
Raising Brain Tissue Oxygen Tension
When PbtO2 is <20mmHg, if ICP is >20mmHg, an oxygen challenge (5min 100%
FiO2) could be attempted. If positive, the percentage is reduced to <60% as persistent normobaric hyperoxia is dangerous. If ICP is <20mmHg, the norepinephrine
challenge (with intact CA) will benet CPP and PbtO2, however, not ICP.Brain
oxygen consumption can also be diminished, if CA is lost or does not respond to
elevation of CPP, with an infusion of fentanyl, midazolam, and propofol (burst suppression), as detected on continuous EEG.
Normothermia Versus Hypothermia
Fever above 38.3°C is frequent in the rst week after sTBI [40] and is deleterious
regarding brain edema [41–43]. Normothermic control seems safer, as therapeutic
hypothermia could increase mortality and long-term functional impairment [44].
Prophylactic hypothermia is not endowed with clear benets either [36, 45, 46].
Several temperature control devices are available in the market (Artic Sun,
Medivance, Inc.; Louisville, CO, USA, and others), and for patient comfort, antishivering therapy should be added [47–49].
Enteral Feeding
Basal calorie expenditure replenishment should be achieved in 5–7days [36]. Given
the impact of multiple prescribed drugs and possible associated injuries and complications, the calculation of calories requirements using conventional predictive equations such as the Harris-Benedict, Penn State University, or Mifin St Jeor or
ASPEN equations can lead to signicant variability; therefore, indirect calorimetry
is recommended [50, 51]. Selected patients may suffer from severe hypermetabolism (up to 160% elevation) and massive nitrogen loss (up to 16g/day) [52]. We
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