Head Injuries: Neurosurgical
and Orthopedic Strategies
Philip F. Stahel and Michael A. Flierl
Contents
6.1 Introduction
6.2 Pathophysiology of Head Injury
6.3 The “Deadly Duo”: Hypoxia and
Hypotension
6.4 Clinical Assessment and Management
6.5 Strategies of Fracture Fixation
in Head-Injured Patients
Conclusion
References
P.F. Stahel, MD, FACS (*)
Department of Orthopaedics, Denver Health Medical
Center, University of Colorado, School of Medicine,
777 Bannock Street, Denver, CO 80204, USA
Department of Neurosurgery, Denver Health Medical
Center, University of Colorado, School of Medicine,
Denver, CO, USA
e-mail: philip.stahel@dhha.org
M.A. Flierl
Department of Orthopaedic Surgery, Denver Health
Medical Center, University of Colorado, School of
Medicine, Denver, CO 80204, USA
e-mail: michael.a.flierl@gmail.com
© Springer-Verlag Berlin Heidelberg 2016
H.-C. Pape et al. (eds.), The Poly-Traumatized Patient with Fractures:
A Multi-Disciplinary Approach, DOI 10.1007/978-3-662-47212-5_6
6
6.1 Introduction
55
Traumatic brain injury (TBI) represents the lead-
56
ing cause of death in the trauma patient and is
associated with dramatic long-term neurological
56
sequelae among survivors [1–4]. One of the cen-
58 tral aspects of our current understanding of the
pathophysiology of TBI is that the extent of neu-
59 rological injury is not solely determined by the
60 traumatic impact itself, but rather evolves over
time [5]. The evolution of secondary brain injury
61
is characterized by a complex cascade of molecu-
lar and biochemical reactions to the initial trauma
which occur as a consequence of complicating
processes initiated by the primary traumatic
impact [6–8]. These events trigger an acute
inflammatory response within the injured brain,
leading to development of cerebral edema, break-
down of the blood-brain barrier (BBB), and leak-
age of neurotoxic molecules from the peripheral
blood stream into the subarachnoid space of the
injured brain [9–13]. Ultimately, the extent of
secondary brain injury, characterized by neuroin-
flammation, ischemia/reperfusion injuries, cere-
bral edema, intracranial hemorrhage, and
intracranial hypertension, represents the main
determinant for the poor outcome of head-injured
patients [14, 15]. In addition, iatrogenic factors,
such as permissive hypotension, prophylactic
hyperventilation, overzealous volume resuscita-
tion, and inappropriate timing and technique of
associated fracture fixation may contribute to a
55
56
deterioration of secondary brain injury [13, 16–19].
Despite recent advances in basic and clinical
research and improved neurointensive care, no
specific pharmacological therapy is currently
available which may attenuate or prevent the
development of secondary brain injuries [20].
Due to the complex underlying pathophysiology
and the high vulnerability of the injured brain to
“2nd hit” insults, it is imperative to closely coor-
dinate the timing and surgical priorities for the
management of associated injuries in head-
injured patients.
6.2 Pathophysiology of Head
Injury
The primary brain injury is a result of mechanical
forces applied to skull at the time of impact,
whereas secondary brain injury evolves over time
and cannot be detected on initial CT imaging
studies [21]. Evidence of secondary brain injury
has been found on autopsy in 70–90 % of all
fatally head-injured patients [22, 23]. Secondary
brain injury is initiated by a trauma-induced,
host-mediated inflammatory response within the
intracranial compartment, and is aggravated by
hypoxia, metabolic acidosis, cerebral fat emboli
from the fracture site, injury-triggered activation
of the coagulation system, and development of
cerebral edema [6, 14, 17]. The immunological
and pathophysiological sequelae of TBI are
highly complex, and involve numerous brain-
derived proinflammatory mediators, such as
cytokines, chemokines, complement anaphyla-
toxins, excitatory molecules, electrolyte distur-
bances, and blood-derived leukocytes which are
migrating across the BBB [11, 24, 25].
The resulting complex neuroinflammatory
network leads to a proinflammatory environment
with brain edema and brain tissue destruction by
leukocyte-released proteases, lipases, and reac-
tive oxygen species [26, 27]. In addition, these
events culminate in the break-down of the BBB
and allow neurotoxic circulating molecules
to enter the brain. As a result, the traumatized
brain is highly susceptible to secondary injuries
caused by intracerebral inflammation, as well as
P.F. Stahel and M.A. Flierl
systemic neurotoxic molecules, which are nor-
mally blocked under physiological conditions
(Fig. 6.1).
In TBI patients who have sustained con-
comitant extracerebral trauma to the mus-
culoskeletal system, a profound systemic
inflammatory response is triggered in parallel,
involving cytokines/chemokines, complement
activation products, the coagulation system,
stress hormones, neuronal signaling, and numer-
ous inflammatory cells [28].
The treating surgeon has to be aware of the neu-
ropathology of TBI as well as the systemic inflam-
matory invents when deciding on the optimal
management approach in this challenging patient
population, as inappropriate treatment may result
in an iatrogenic secondary insult to the brain.
6.3 The “Deadly Duo”: Hypoxia
and Hypotension
Episodes of hypoxia and hypotension represent
the main independent predictive factors for poor
outcome after severe brain injury [8, 29]. In a
landmark article published in 1993, Chesnut et al.
analyzed the impact of hypotension, as defined as
a systolic blood pressure (SBP) <90 mmHg, either
during the resuscitation phase (“early”) or in the
ICU (“late”), on the outcome of head-injured
patients prospectively entered into the Traumatic
Coma Data Bank (TCDB) [15]. Early hypotension
occurred in 248 of 717 patients (34.6 %) and was
associated with a doubling of postinjury mortality
from 27 to 55 % [15]. Late hypotension occurred in
156 of 493 patients (31.6 %), of which 39 patients
(7.9 %) had combined early and late hypotensive
episodes. For 117 patients with an exclusive hypo-
tensive episode occurred in the ICU, 66 % either
died or survived in a vegetative state, as defined
by a Glasgow Outcome Scale (GOS) score of 1
or 2 points [15]. The authors furthermore deter-
mined that mortality is drastically increased in
combination with hypotension (SBP <90 mmHg)
and hypoxia (PaO2 ≤60 mmHg) [7]. A different
study by Elf et al. confirmed the notion, that severe
secondary insults occur during the neurointensive
care period in more than 35 % of all head-injured
6 Head Injuries: Neurosurgical and Orthopedic Strategies
Fig. 6.1 Schematic of priorities in the management of associated orthopedic injuries in patients with severe head inju-
ries, based on the understanding of the underlying immunological pathophysiology
patients, including episodes of hypoxia, hypo-
tension, elevated intracranial pressure (ICP) and
decreased cerebral perfusion pressure (CPP) [14].
The prevention of hypoxemia and hypotension
represents the “key” parameter for avoiding sec-
ondary insults to the injured brain and improving
outcomes of TBI patients [29, 30]. National
guidelines by the Brain Trauma Foundation man-
date that blood pressure and oxygenation be mon-
itored in all head-injured patients, and advocate to
maintain a systolic blood pressure >90 mmHg
and a PaO2 >60 mmHg, respectively [31]. This
notion is of particular importance in view of the
ongoing debate on the controversial concept of
“permissive hypotension” in patients with trau-
matic hemorrhage from penetrating or blunt torso
injuries [32, 33]. The strategy of “permissive
57
hypotension” is mainly based on a landmark arti-
cle from the 1990s advocating a modified prehos-
pital resuscitation concept for hypotensive patients
with penetrating torso injuries, by delaying fluid
resuscitation until arrival in the operating room
[34]. This proactive concept is certainly intuitive
from the perspective that traditional resuscitation
with aggressive fluid administration may lead to
increased hydrostatic pressure and displacement
of blood clots, a dilution of coagulation factors,
and an undesirable hypothermia in critically
injured patients [35]. However, in light of the vul-
nerability of the injured brain to secondary insults
mediated by hypoxia and hypotension during the
early postinjury period, the concept of hypoten-
sive resuscitation, which has seen an unjustified
expansion from penetrating to blunt trauma, in
58
absence of high level evidence [32, 36], appears
contraindicated for patients with traumatic brain
injuries [33, 37].
6.4 Clinical Assessment
and Management
Head-injured patients are initially assessed and
resuscitated according to the American College
of Surgeons’ Advanced Trauma Life Support
(ATLS®) protocol [35]. The severity of head
injury is diagnosed by the combination of (1)
mechanism of trauma, the (2) clinical/neurologi-
cal status, and (3) imaging by computed tomog-
raphy (CT) scan. The neurologic status is assessed
after stabilization of vital functions [38]. The
level of consciousness is rapidly evaluated by the
Glasgow Coma Scale (GCS), which grades the
severity of TBI as mild (GCS 14/15), moderate
(GCS 9–13), and severe (GCS 3–8) [21]. The
postresuscitation GCS score is of clinical impor-
tance due to the significant correlation with
patient outcome [21]. A head CT should be
obtained under the following circumstances: (1)
altered level of consciousness with GCS <14
(moderate or severe brain injury); (2) abnormal
neurological status; (3) differences in pupil size
or reactivity; (4) suspected skull fracture; (5)
intoxicated patients; and should be repeated
whenever the patient’s neurologic status deterio-
rates [21].
Elevated intracranial pressure (ICP) above
15-20 mmHg has been associated with poor out-
comes after severe TBI [39]. Monitoring of ICP
by indwelling catheters is recommended under
the following conditions [40–43]:
1. Severe TBI (GCS ≤8) and abnormal admis-
sion CT scan
2. Severe TBI (GCS ≤8) with normal CT scan,
but prolonged coma >6 h
3. Surgical evacuation of intracranial hematomas
4. Neurological deterioration (GCS ≤8) in
patients with initially mild or moderate extent
of TBI
5. Head-injured patients requiring prolonged
mechanical ventilation, for example, for man-
agement of associated extracranial injuries,
unless the initial CT scan is normal
P.F. Stahel and M.A. Flierl
The indications and benefits of emergency
craniotomy or decompressive craniectomy are
beyond the scope of this chapter, and the reader is
deferred to the pertinent peer-reviewed literature
[44–46].
Maintenance of an adequate cerebral per-
fusion pressure (CPP) is recommended above
70–80 mmHg, which is calculated as the mean
arterial pressure (MAP) minus ICP [39, 41, 47].
This notion reflects on the imperative not to
allow any period of hypotension in head-injured
patients, as discussed above [29, 37]. In addition
to the outlined dangers of hypoxemia and hypo-
tension, hypercarbia, and hypoglycemia should
be strictly avoided or rapidly corrected to mini-
mize the risk of developing secondary brain inju-
ries [14]. Hyperosmolar therapy with mannitol
or hypertonic saline is recommended for reduc-
tion of cerebral edema and increased ICP, and in
patients displaying clinical signs of trans-tentorial
herniation, progressive neurological deteriora-
tion, or bilaterally dilated and nonreactive pupils
[48]. However, the routine use of osmotherapy for
management of brain edema represents a topic of
heavy debate [49–51]. Similarly, the concept of
therapeutic hypothermia for patients with severe
head injuries remains controversial [46, 51, 52].
This noninvasive modality of neuroprotection
has been investigated for decades in patients with
head injuries, cerebrovascular stroke, cardiac
arrest, and spinal cord injury [53]. The underly-
ing rationale of moderately lowering the patient’s
body temperature is aimed at slowing down the
acute inflammatory processes in the injured CNS,
and to reduce the extent of traumatic and isch-
emic tissue injury [54]. Interestingly, the historic
euphoria in the 1990s for applying therapeutic
hypothermia to patients with severe head injuries
[55] was revoked later on in additional validation
studies, and the debate on the appropriateness
of cooling down the injured brain remains unre-
solved until present [52, 56]. Despite increased
understanding of the pathophysiology of second-
ary brain injury, the pharmacological “golden
bullet” for treating TBI patients and prevent-
ing or reducing incidence of secondary cerebral
insults has not yet been identified [20]. However,
there is unequivocal consensus that the use of ste-
roids is considered obsolete and contraindicated
6 Head Injuries: Neurosurgical and Orthopedic Strategies
for patients with traumatic brain injuries, since
the failure of the large-scale “CRASH” trial was
published in 2004 [57, 58].
6.5 Strategies of Fracture
Fixation in Head-Injured
Patients
Head-injured patients with associated orthope-
dic injuries represent a vulnerable population
due to the high risk of “2nd hit” insults, particu-
larly in presence of femur shaft fractures [17].
The benefits of early definitive fracture stabili-
zation in multiply injured patients are well
described and include early unrestricted mobil-
ity in conjunction with a decreased “antigenic
load” related to stress, pain, and systemic
inflammation [13, 59, 60]. Clearly, the question
regarding the “optimal” timing and modality of
long bone fracture fixation in patients with
associated head injuries remains a topic of
ongoing discussion and debate [18, 61–64].
Even though the benefits of early femur frac-
ture stabilization have been unequivocally dem-
onstrated in Dr. Bone’s landmark study more
than 20 years ago [65], not all multiply injured
patients are able to tolerate early definitive frac-
ture fixation due to hemodynamic instability,
refractory hypoxemia, or intracranial hyperten-
sion [62]. Impressively, experimental studies in
sheep showed that femoral reaming and nailing
leads to increased ICP levels above 15 mmHg
in models of hemorrhagic shock/resuscitation
with or without associated traumatic brain
injury [19, 66]. A clinical study in 33 blunt
trauma patients with TBI revealed that early
definitive fracture fixation within 24 h was
associated with adverse neurological outcomes
and increased mortality, associated with early
episodes of hypoxia and hypotension, com-
pared to TBI patients whose orthopedic injuries
were stabilized definitively at a later time-
points (>24 h) [67]. A larger 10-year study on
61 patients with severe TBI revealed that early
femur fracture fixation within <24 h is associ-
ated with an increased incidence of secondary
brain injury, related to significantly increased
rates of hypotension and decreased CPP
59
<70 mmHg [68]. These data were corroborated
by a different study analyzing changes in ICP
and CPP in 17 patients with severe head inju-
ries undergoing reamed intramedullary nailing
of associated femur fractures [69]. The authors
showed that the CPP dropped below a minimal
threshold of 75 mmHg intraoperatively during
the fracture fixation in all patients, with an
average decrease in CPP of Δ18 mmHg [69].
The decrease in CPP was attributed to intraop-
erative episodes of systemic hypotension, and
patients with early femoral nailing within 24 h
had statistically significant lower CPP values
than the rest of the cohort [69].
Overall, there is unequivocal evidence – both
from experimental animal studies and from clini-
cal trials in patients with severe TBI – that the
early (<24 h) definitive fixation of associated
femur shaft fractures in head-injured patients
leads to significant adverse effects, including
intraoperative episodes of hypotension, increases
in ICP and critical decreases in CPP, all of which
ultimately constitute preventable “2nd hits” and
contribute to secondary brain injury and poor
long-term outcomes (Fig. 6.1).
Consequently, alternative strategies to provide
early fracture stabilization of long bones, while
avoiding the risk of “early total care”, have been
proposed, including skeletal traction and “dam-
age control” external fixation [70]. The con-
cept of “damage control” surgery was extended
beyond its initial applications in abdominal and
thoracic trauma, to the initial management of
major fractures in the severely injured, particu-
larly in presence of associated head injuries [62,
71]. The principal is to provide early fracture
stabilization by external fixation as a bridge to
definitive fracture care once the patient is physi-
ologically stable, and the injured brain less vul-
nerable to iatrogenic “2nd hit” insults [17]. The
delayed conversion from external fixation to
intramedullary nailing of femur shaft fractures
is considered safe once the ICP has normalized
and/or patients are awake, oriented, and fully
resuscitated [35]. In other words, the second pro-
cedure related intramedullary reaming and nail-
ing of long bone fractures should be performed
outside of “priming” window, once the postin-
jury hyperinflammatory response has subsided
60
Fig. 6.2 Risks and benefits of distinct management strategies for acute immobilization of femoral shaft fractures in
head-injured patients
(Fig. 6.1). When compared to early total care, the
“damage control” approach with delayed conver-
sion to definitive care has been shown to decrease
the initial operative time and intraoperative blood
loss without increasing the risk of procedure
related complications such as infection and non-
union [72, 73].
The risks and benefits of distinct modalities
for acute management of femur shaft fractures in
head-injured patients, namely (1) skeletal trac-
tion [70], (2) “damage control” external fixation
[71, 72], and (3) “early total care” by reamed
intramedullary nail fixation [69] are depicted in
Fig. 6.2.
Conclusion
Head-injured patients with associated long
bone fractures represent a very vulnerable
patient population [17]. These patients have a
high risk of sustaining secondary cerebral
insults related to hypotension, increased ICP,
and decreased CPP, all of which contribute to
increased mortality and adverse neurological
outcomes [19, 66–69]. The subspecialties
P.F. Stahel and M.A. Flierl
involved in the early management of multiply
injured patients with head injuries and associ-
ated long bone fractures include ED physi-
cians, trauma surgeons, neurosurgeons, and
orthopedic surgeons. They all should be on the
same page in terms of understanding the
underlying pathophysiology of TBI and the
time-dependent vulnerability of the injured
brain to iatrogenic “2nd hit” insults [17, 21].
When the patient with combined orthopedic
and neurosurgical injuries is evaluated in the
emergency department, several questions need to
be answered. A rapid neurologic exam must be
performed to assess the severity of brain injury.
A noncontrast craniocerebral CT scan is obtained
as the first-line adjunctive diagnostic work-up in
stable patients. An ICP monitor (either fiberoptic
or ventricular) may be placed in the ED if the
patient is too hemodynamically unstable to jus-
tify a trip to the CT scanner.
Any patient with a suspected brain injury who
needs to be taken to the operating room and will
be unable to undergo follow up neurologic exam-
ination needs to have ICP monitoring. The exact
6 Head Injuries: Neurosurgical and Orthopedic Strategies
ICP threshold of when not to proceed to the
operating room is unknown, though sustained
pressures beyond 15–20 mmHg should be an
indication to proceed to the ICU for resuscitation.
Any patient with a progressively worsening neu-
rological exam is also at high risk as is the patient
with unexplained changes in ICP. Hypoxia and
hypotension significantly increase mortality in
the patient with brain injury.
Despite recent advances from basic research
and clinical studies [74], the current literature
remains conflicting in terms of identifying a clear-
cut management strategy for timing and modality
of fracture fixation in severely head-injured
patients [17, 18, 61, 64, 67, 68]. This notion
emphasizes the pressing need for well-designed
prospective controlled multicenter trails aimed at
comparing the standard treatment strategies for
initial management of long bone fractures in
patients with severe head injuries (Fig. 6.2).
Until higher level evidence-based recommen-
dations are available, the clinical approach for the
management of this vulnerable cohort of patients
must be based on the basic principle of “do not
further harm” by applying simple measures of
“damage control” – when in doubt – which
respect the underlying pathophysiology of trau-
matic brain injury and the hyperinflammatory
response of the combination of multiple critical
injuries [13]. We recommend the following spe-
cific management strategy for associated ortho-
pedic injuries in head-injured patients, based on a
combination of empiric experience and review of
the available pertinent literature in the field:
1. “Damage control orthopedics” by spanning
external fixation in all patients with severe TBI
(GCS ≤8, intracranial pathology on CT scan,
including cerebral edema, midline shift, sub-/
epidural bleeding, or open head injuries).
2. Optional “damage control orthopedics” in all
patients with moderate TBI (GCS 9–13), or
patients with GCS of 14/15 with “minor”
intracranial pathology on CT scan (e.g., trau-
matic subarachnoid hemorrhage that warrants
observation only). Concomitant neurosurgical
procedures may be performed at the same
time as DCO, for example, an emergency
craniotomy.
61
3. No additional operations (2nd hit) in patients
with refractory intracranial hypertension or
unexplained deterioration in neurologic exam.
4. Conversion from external to internal fixation
in TBI patients who recovered from a coma-
tose state and are awake and alert (GCS
13–15), or comatose patients with a stable
ICP (<20 mmHg) and CPP in a normal range
(>80 mmHg) for more than 48 h.
5. “Early total care” for long bone fractures all
patients with mild TBI (GCS 14/15) and nor-
mal initial craniocerebral CT scan.
6. Temporary skeletal traction as a valid adjunct
for patients “in extremis”, that is, in severe
protracted traumatic-hemorrhagic shock and
coagulopathy, who are unsafe to be taken to
the operating room until adequately
resuscitated.
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