Management of Moderate and Severe Head Injury

Case Presentation

This presentation addresses the treatment of moderate and severe head trauma patients


Management of Moderate and Severe Head Injury



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 incomes.


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 of hemorrhage)

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


2- 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):

Prospective randomized 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 (Options):

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:

1.     Trauma Systems

2.      Initial management

3.      Resuscitation of blood pressure and oxygenation

4.      Indications for intracranial pressure monitoring

5.      Intracranial pressure treatment threshold                      

6.      Recommendations for intracranial pressure monitoring technology

7.       Guidelines for cerebral perfusion pressure

8.      Hyperventilation

9.      Use of Mannitol                                                   

10.  Use of barbiturates in the control of intracranial hypertension                                      

11.  Role of steroids                                                            

12.  Critical pathway for the treatment of established intracranial hypertension

13.  Nutrition                                                         

14.  Role of antiseizure prophylaxis following head injury


1- Trauma system



All regions should have an organized trauma care system



Neurosurgeons should 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 patient.


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.



3- Resuscitation 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 treatment threshold



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.



Interpretation and 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.



8- Hyperventilation



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.



9- Use of Mannitol                                                   



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.


There are two "class 1" studies, and one "class 2" study, and a large body of "Class 3" data, which can be used to support mannitol. The evidence supporting use of mannitol for ICP control is sufficiently strong to warrant guideline status.  Mannitol is effective in reducing ICP, and its use is recommended as a guideline in the management of traumatic intracranial hypertension. Serum osmolalities >320 mOsm and hypovolemia should be avoided. There is some data to suggest that bolus administration is preferable to 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.


According 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.


In 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 approach.



13- Nutrition



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 injury.



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.


14- Role of antiseizure prophylaxis following head injury



Prophylactic use of phenytoin, carbamazepine, phenobarbital or valproate, is not recommended for preventing late posttraumatic seizures.


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:


1- Acute epidural or subdural hematomas

     Significant hematomas should be evacuated immediately upon detection.


2-  Contusions

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:

a)      Clinical deterioration

b)      Size > 1cm thick extracerebral clot. Volume > 25 – 30 ml in intracerebral hematomas.

c)      Midline shift > 5 mm.

d)      Enlargement of contralateral ventricle (temporal horn).

e)      Obliteration of basal cisterns or third ventricle.

f)        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

May 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: PREVENTION.



Management of Moderate and Severe Head Injury

Reference List

  • Guidelines for Severe Head Injury Mangement - J Neurotrauma 2000;17(6-7):471-8

  • EBIC Guidelines for Management of Severe Head Injury in Adults. Acta Neurochir (Wien) 1997;139:286-294


Management of Moderate and Severe Head Injury

Tables and Figures



 Figure 1- Algorithm for moderate head injury management


Figure 2- Brain oriented resuscitation.


Figure 3- Differences in the incidence of hypoxia and hypotension in the Emergency Room, between 1987 and 1997 (p 0.01).


Figure 4- Differences in the use of intracranial pressure monitoring devices between 1987 and 1997.


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).




Figure 6- Differences in the use of steroids between 1987 and 1997. This difference was statistically significant (p > 0.0001) for morbimortality.




Figure 7- Algorithm for established intracranial hypertension