This presentation addresses the treatment of moderate and severe head trauma patients
Neurotrauma, the so-called “silent epidemic”,
is the main cause of mortality and disability in the population under
40 years old. It is also
the leading cause of years of productive life loss.
Neurotrauma has predilection for young working males between
15 and 30 years old and a notorious inverse relationship with family
In 1998, in Buenos Aires, Argentina, Previgliano and Ferrari studied the incidence of Head Injury in the Emergency Department of the Fernandez county Hospital. Out of 15300 patients, two percent of the visits (310) were due to Head Injury and out of that, 92% were minor, 4% were mild, and 3.5% were severe, according to Rimel’s classification. Sixty-four percent were male and the average age was 35 ±16yo. This rate of males to females was constant in all different publications.
Even though some studies showed a higher rate of head
injury in blacks, we suppose that this finding is related to the poor
economic conditions. According to Cooper, the rate of injury was inversely
correlated to family income. Rates were highest in the lowest income
strata and were more often caused by motor vehicles and assaults.
Regarding mortality, Torner, in 1996, stated that it
was near 1% for minor injury, 18% for mild, and 48% for severe head
injury. As regards severe
head injury, mortality has been changing since that report.
Which are the factors that lead to that change?
1- Prehospitalary care
The widespread knowledge of the American College of Surgeons
ATLS® Courses improved the initial management of trauma
victims. This approach
is based on the identification of the sequential variables that could
cause the victim’s death:
A: airway with cervical spine control
B: breathing (hemo or pneumothorax)
C: circulation (maintenance of blood pressure, control
D: disability (Glasgow Coma Scale)
E: exposure (examination from head to toe)
S: secondary evaluation
The GCS will allow to classified head injury victims:
13 – 15: Minor
9 – 12: Moderate
3 – 8: Severe
Moderate head injury is an object of controversies.
The Italian Society of Neurosurgery excluded GCS 13 patients
from minor head injury. A
prospective research of our group reveal that there are significant
differences in the CT findings between GCS 13 and 14-15 patients,
so we included these patients in the moderate group.
Our approach to moderate head injury is based on the
clinical status and the CT findings (figure 1). According to the severity
patients are hospitalized in the general ward, in an Intermediate
Care Unit or in the Intensive Care Unit. This also implied a therapeutic
option: the less severe the lesion the less complexity in treatment,
so in this manner patients with moderate head injury could be treated
as minor o severe head injury, following the different guidelines.
We will focus on Severe Head Injury Management Guidelines
Severe head injury management has been outlined in different
Guidelines (Brain Trauma Foundation and European Brain Injury Consortium).
I will summarize the first ones.
Even though the presentation of the Guidelines in an
abbreviated format is not recommended mainly due to the process by
they were developed, I think that this way of presentation would motivate
the auditorium to read the complete text.
Guidelines were developed according to the standards
of the evidence-based medicine with three levels of evidence:
Class I evidence (Standards):
controlled trials, the gold standard of clinical trials.
However some may be poorly designed, lack sufficient patient
numbers or suffer from other methodological inadequacies.
Class II evidence (Guidelines):
Clinical studies in
which the data was collected prospectively, and retrospective analyses
that were based on clearly reliable data (observational, cohort, prevalence
and case control studies).
Class III evidence
Most studies based
on retrospectively collected data (clinical series, databases or registries,
case reviews, case report) Expert opinion.
With this methodology
they analyzed the following topics:
Resuscitation of blood pressure and oxygenation
Indications for intracranial pressure monitoring
Intracranial pressure treatment threshold
Recommendations for intracranial pressure monitoring technology
for cerebral perfusion pressure
Use of Mannitol
10. Use of barbiturates in the control of intracranial
11. Role of steroids
12. Critical pathway for the treatment of established
14. Role of antiseizure prophylaxis following head injury
1- Trauma system
All regions should
have an organized trauma care system
have an organized and responsive system of care for patients with
neurotrauma. They should
initiate neurotrauma care planning, including pre-hospital management
and triage, direct trauma center transport, maintain appropriate call
schedules, review trauma care records for quality improvement and
participate in trauma education programs
Trauma facilities treating
neurotrauma must have a neurosurgery service, an in-house trauma surgeon,
a continuously staffed and available operating room, intensive care
unit and laboratory. A CT scanner must be immediately available.
In rural or weather-bound
communities without a neurosurgeon, a surgeon should be trained to
perform accurate neurological assessment, including training to perform
life-saving surgical treatment of an extracerebral hematoma in a deteriorating
2- Initial management
The fundamental goals of resuscitation of the head-injured patient are the restoration of circulating volume, blood pressure, oxygenation, and ventilation. The physician should initiate maneuvers that serve to lower ICP and do not interfere with these aims as early as possible during resuscitation of any patient with a head injury. Treatment modalities such as hyperventilation and mannitol administration that have the potential of exacerbating intracranial ischemia or interfering with resuscitation should be reserved for patients who show signs of intracranial hypertension such as evidence of herniation or neurological deterioration.
A brain-oriented resuscitation has been developed in
an option level. In figure 2 you will find it. The numbers correspond
to the experience in the Fernandez General Hospital of Buenos Aires
City, with 52 consecutive patients treated according the guidelines.
Some groups, especially the Cochran one, have criticized
both the Guidelines and the ATLS® based in the weak evidence
in which they are based. Whatever you agree or not with them the result
of applying a systematized plan is encouraging.
of blood pressure and oxygenation
Hypotension (SBP < 90 mmHg)
or hypoxia (apnea, cyanosis or SaO2 < 90%) must be avoided
and scrupulously avoided, if possible, or corrected immediately in
severe TBI patients.
The MAP should be maintained above
90 mmHg through the infusion of fluids throughout the patient’s course
to attempt to maintain CPP > 70 mmHg.
Patients with GCS < 9 who are unable to maintain their airway
or who remain hypoxemic despite supplemental O2 required that their
AW be secured, preferably by endotraqueal intubation.
Early post-injury episodes of hypotension or hypoxia
greatly increase morbidity and mortality from severe head injury.
At present, defining level of hypotension and hypoxia is unclear
in these patients. However, ample class II evidence exists regarding
hypotension, defined as a single observation of a systolic blood pressure
of <90/mm Hg, or hypoxia, defined as apnea/cyanosis in the field
or a PaO2 < 60 mm Hg by arterial blood gas analysis, to warrant
the formation of guidelines stating that these values must be avoided,
if possible, or rapidly corrected in severe head injury patients.
A significant proportion of adult and pediatric TBI patients are discovered
to be hypoxemic or hypotensive in the pre-hospital setting. Patients
with severe head injury that are intubated in the pre-hospital setting
appear to have better outcomes. Strong class II evidence suggests
that raising the blood pressure in hypotensive, severe head injury
patients improves outcome in proportion to the efficacy of the resuscitation.
As is shown in figure 3, in our experience the incidence
of hypoxia and hypotension was reduced from 1987 to 1997. This changes
reach statistical significance (Chi square test p 0.01) and also reflected
mortality diminish and augmentation of survival as will be shown below.
4- Indications for
intracranial pressure monitoring
Comatose head injury
patients (GCS 3-8) with abnormal CT scans should undergo ICP monitoring.
Comatose patients with normal CT scans have a much lower incidence
of intracranial hypertension unless they have two or more of the following
features at admission: age over 40, unilateral or bilateral motor
posturing, or a systolic blood pressure of less than 90 mm Hg. ICP
monitoring in patients with a normal
CT scan with two or
more of these risk factors is suggested as a guideline.
Routine ICP monitoring
is not indicated in patients with mild or moderate head injury. However,
it may be undertaken in certain conscious patients with traumatic
mass lesions at the discretion of the treating physician.
In many papers is highlighted that
there is no evidence that ICP monitoring is really useful in diminish
mortality or morbidity in severe head injury and that ethics will
forbid the realization of a randomized controlled trial. By chance,
we had the experience of test the improvement in those results as
it is shown in figure 4 (p > 0.0001).
5- Intracranial pressure
An absolute ICP threshold
that is uniformly applicable is unlikely to exist.
Current data, however, support 20-25 mm Hg as an upper threshold
above which treatment to lower ICP should generally be initiated.
treatment of ICP based on any threshold should be corroborated by
frequent clinical examination and CPP data.
6- Recommendations for intracranial
pressure monitoring technology
In patients who require
ICP monitoring, a ventricular catheter connected to an external strain
gauge transducer or catheter tip pressure transducer device is the
most accurate reliable method of monitoring ICP and enables therapeutic
CSF drainage. Clinically
significant infections or hemorrhage associated with ICP devices causing
patient morbidity are rare and should not deter the decision to monitor
ICP. Parenchymal catheter
tip pressure transducer devices measure ICP similar to ventricular
ICP pressure but have the potential for significant measurement differences
and drift due to the inability to recalibrate. These devices are advantageous
when ventricular ICP is not obtained or if there is obstruction in
the fluid couple. Subarachnoid or subdural fluid coupled devices and
epidural ICP devices are currently less accurate
A prospective randomized trial comparing complications
of subdural pediatric feeding tubes (SPFT) and intraparenchimal fiberoptic
(IF) devices was performed at our ICU. We didn’t found statistical
differences in the infection rate (2% vs 0%) neither in the hemorrhage
incidence (0% vs 4%). As SPFT are cheaper than IF (U$45 vs U$ 1200)
we decided to use the first ones as first choice and the second only
when the patient needed monitoring beyond day 3.
7- Guidelines for
cerebral perfusion pressure
Maintenance of a CPP
above 70 mm Hg is a therapeutic option that may be associated with
a substantial reduction in mortality and improvement in quality of
survival and is likely to enhance perfusion to ischemic regions of
the brain following severe TBI.
No study has demonstrated that the incidence of intracranial
hypertension, morbidity, or mortality is increased by the active maintenance
of CPP above 70 mm Hg, even if this means normalizing the intravascular
volume or inducing systemic hypertension.
In a poster presented
at the ICP 2000 in Cambridge we shown a statistical correlation between
CPP and outcome (figure 5), the higher the CPP the better the outcome.
General critical care physicians following the guidelines, with the
CPP management as second their therapy, managed all these patients.
In the absence of increased
ICP chronic prolonged HV therapy (PaCO2 < 25
mmHg) should be avoided after TBI.
The use of prophylactic
HV (PaCO2 < 30 mmHg) during the first 24 hrs
after severe TBI should be avoided because it can compromise cerebral
perfusion during a time when CBF is reduced.
HV may be necessary for brief periods when there is acute neurological deterioration or for longer periods if there is refractory intracranial hypertension. SjO2, AJDO2, PtiO2 and CBF monitoring may help to identify cerebral ischemia if HV is necessary
Chronic prophylactic hyperventilation therapy should
be avoided during the first 5 days after severe TBI and particularly
during the first 24 h. CBF measurements in patients with severe TBI
demonstrate that blood flow early after injury is low and strongly
suggest that in the first few hours after injury the absolute values
approach those consistent with ischemia.
AVdO2 and SjO2 and brain tissue O2 measurements corroborate
these findings. Hyperventilation
will reduce CBF values even further, but will not consistently cause
a reduction of ICP and may cause loss of autoregulation.
The cerebral vascular response to hypocapnia is reduced in
those with the most severe injuries (subdural hematomas and diffuse
contusions), and there is substantial local variability in perfusion.
While the CBF level at which irreversible ischemia occurs has not
been clearly established, ischemic cell change has been demonstrated
in 90% of those who die following TBI, and there is PET evidence that
such damage is likely to occur when CBF drops below 15-20 cc/100 g/min.
A prospective randomized clinical trial has determined that
outcomes are worse when TBI patients are treated with chronic prophylactic
hyperventilation therapy. Within the standard, guideline, and options,
specific paCO2 thresholds have been described that are
different for each of the three parameters. These individual thresholds
were selected based on the preponderance of literature supporting
those thresholds in the contexts of the statements, which included
them. With the exception of the threshold included for the standard
in this guideline, it is emphasized that the paCO2 threshold
is not as important as the general concept of hyperventilation. The
preponderance of the physiologic literature concludes that hyperventilation
during the first few days following severe traumatic brain injury,
whatever the threshold, is potentially deleterious in that it can
promote cerebral ischemia.
Again the Cochran group sustained that the evidence for
this standard is very weak and they possibly have reason in this specific
matter because Bouma’s paper could have some alpha errors due to the
small number of patients. Nevertheless it confirmed many of the physiology
theories concerning hyperventilation and hypoxia.
Mannitol is effective for control of raised ICP after severe TBI. Effective doses range from 0.25 to 1 g/kg/body weight.
Indications to it use prior to ICP monitoring
are signs of transtentorial herniation or neurological worsening not
attributable to extracranial explanations. Hypovolemia should be avoided
by fluid replacement.
Serum osmolarity should be kept below 300
mOsm because of concern for renal failure.
Euvolemia should be maintained by adequate
fluid replacement. A Foley catheter is essential in these patients.
Intermittent boluses may be more effective
than continuous infusion.
In presence of hypovolemia mannitol administration could be deleterious (“paradox effect”) due to a further increase in renal salt and water excretion that could lead to a drop in MAP with a consequent drop in CPP that could start the so-called vasodilatadory cascade and increase ICP.
10) Use of barbiturates in the control of intracranial hypertension.
High-dose barbiturate therapy is efficacious
in lowering ICP and decreasing mortality in the setting of uncontrollable
ICP refractory to all other conventional medical and surgical ICP-lowering
treatments, in salvageable TBI patients. Utilization of barbiturates for the prophylactic treatment
of ICP is not indicated.
The potential complications attendant on this form of therapy mandate that its use be limited to critical care providers and that appropriate systemic monitoring be undertaken to avoid or treat any hemodynamic instability. When barbiturate coma is utilized, consideration should also be given to monitoring arteriovenous oxygen saturation as some patients treated in this fashion may develop oligemic cerebral hypoxia.
As a standard practice we use Swan Ganz catheters and
arterial lines in these patients.
11- Role of steroids
The majority of available evidence indicates that steroids
do not improve outcome or lower ICP in severely head-injured patients.
The routine use of steroids is not recommended for these purposes.
to the Cochran Data Base Collaborative Group the evidence that support
this standard is weak and furthermore a meta-analysis of the group
revealed a useful effect of steroids in mortality. This findings lead
to the CRASH trial, which could be the highest head injury trial ever
performed, randomizing 20000 patients all over the world. Some aspects
of this trial could be discussed during the questions.
our experience, the lack in using steroids improved the outcome of
HI patients, as is shown in figure 6.
12- Critical pathway for the treatment of established intracranial hypertension
This critical pathway is summarized in figure 7. In it
you will see a comprehensive management that is very useful for the
general ICU practitioners. Some experts criticized this pathway considering
it “too simple”.
Second their therapies could be chosen according to the
physician’s knowledge. In our Hospital we choose CPP management as
the first line second their therapy, controlled hyperventilation as
the second and high dose barbiturates as the third (figure 7).
A promising second their therapy is the so-called “Lund
therapy” that is based in a complete different pathophysiological
Replace 140% of resting metabolism expenditure in nonparalyzed
patients and 100% in paralyzed patients using enteral or parenteral
formulas containing at least 15% of calories as protein by day 7 after
The preferable option is use of jejunal feeding by gastrojejunostomy due to ease of use and avoidance of gastric intolerance.
Data show that starved head-injured patients lose sufficient nitrogen to reduce weight by 15% per week. Class II data show that 100-140% replacement of resting metabolism expenditure with 15-20% nitrogen calories reduces nitrogen loss. Data in non-head injured patients show that a 30% weight loss increased mortality rate. Class I data suggests that non-feeding of head-injured patients by the first week increases mortality rate. The data strongly support feeding at least by the end of the first week. It has not been established that any method of feeding is better than another or that early feeding prior to 7 days improves outcome. Based on the level of nitrogen wasting documented in head-injured patients and the nitrogen sparing effect of feeding, it is a guideline that full nutritional replacement be instituted by day 7.
Our practice is to start nutritional support as soon as the patient recovers the GI transit if ICP and CPP are in the desired range without the use of vasoactive drugs.
of antiseizure prophylaxis following head injury
Prophylactic use of phenytoin, carbamazepine,
phenobarbital or valproate, is not recommended for preventing late
Anticonvulsivants may be used to prevent early PTS in patients at risk. This prevention does not indicate an improvement in outcome.The majority of studies do not support the use of the prophylactic anticonvulsants studied thus far for the prevention of late PTS. Routine seizure prophylaxis later than 1 week following head injury is, therefore, not recommended. If late PTS occur, patients should be managed in accordance with standard approaches to patients with new onset seizures. Phenytoin and carbamazepine have been shown to reduce the incidence of early PTS. Valproate may also have a comparable effect to phenytoin on reducing early PTS but may also be associated with a higher mortality. It is, therefore, an option to use phenytoin or carbamazepine to prevent the occurrence of seizures in high-risk patients during the first week following head injury.
The EBIC Guidelines for management of Severe Head Injury in adults.
The EBIC guidelines don´t differ too much from the American
ones. Differences lie in the format and in the order in which therapeutic
options are proposal. They
enrich them with the surgical treatment timing and indications that
could be summarized as follows:
Acute epidural or subdural hematomas
Significant hematomas should
be evacuated immediately upon detection.
For small hemorrhagic contusions
or other small intracerebral lesion a conservative approach is generally
adopted. But operation should be considered urgent for large intracerebral
lesions with high or mixed density on CT scan.
Specific indications for operations include:
Size > 1cm thick extracerebral clot. Volume > 25
– 30 ml in intracerebral hematomas.
Midline shift > 5 mm.
Enlargement of contralateral ventricle (temporal horn).
Obliteration of basal cisterns or third ventricle.
Raised or increasing ICP
3- Skull Fractures
Operations definitely indicated only if it
is a compound (open) fracture (not over sagittal sinus) or if the
fracture is so extensive that it causes mass effect.
Closed depressed skull fractures are usually
treated conservatively, but operation may be appropriate in selected
cases to reduce mass effect or correct defigurement.
4- Descompresive craniotomy
be considered in exceptional situations.
In spite of all these consideration the best way to treat
moderate and severe head injury lays on a simple but complex alternative:
Tables and Figures
Figure 2- Brain oriented resuscitation.
Figure 5- Statistical differences (two tails) for CPP were found for: GOS 2 - 5 against GOS 1 (p < 0.01), GOS 4 - 5 against GOS 1 - 3 (p < 0.01), GOS 5 against GOS 3 (p 0.02), GOS 5 against GOS 2 (p 0.01) and GOS 5 against GOS 1 (p < 0.01).
Differences in the use of steroids between 1987 and 1997. This difference
was statistically significant (p > 0.0001) for morbimortality.