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Exploring the Guidelines for the Management of Severe Head Injury.

Abstract: A significant improvement in patient outcomes can be achieved by in-hospital interventions aimed at the prevention of secondary brain injury. The Guidelines for the Management of Severe Head Injury is a scientific, evidence-based document that evaluates the current evidence for practice and interventions to reduce secondary brain injury and improve outcome for traumatic brain injury (TBI) patients. The Guidelines covers a wide range of topics including trauma systems, oxygenation and blood pressure resuscitation, intracranial pressure monitoring, intracranial hypertension, nutrition, and pharmacological interventions for the severe TBI patient in the intensive care environment. Head injury care requires an interdisciplinary approach involving emergency room personnel trauma nurses, and critical care nurses. Critical care nurses will find this document especially applicable because secondary brain injuries are often the result of events that occur in the ICU setting: hypoxemia, hypotension, and intracranial hypertension.


Critical care neuroscience nurses are confronted every day with making treatment choices for patients with severe traumatic brain injury (TBI). Treatment often varies depending on the region of the country, hospital facilities, and physician and nurse experience. These variations in treatment were documented in a survey published in 1995 by Ghajar et al.[10] Level I, II, and III trauma centers were questioned about their treatment protocols for managing patients with TBI. Of all trauma centers surveyed, only 28% routinely performed intracranial pressure (ICP) monitoring. Corticosteroids were administered more than half of the time in 64% of the centers, and one-third of the centers reported utilizing hyperventilation with a goal of maintaining the partial pressure of arterial carbon dioxide [Pa[CO.sub.2]] less than 25 mm Hg. This report sparked the neurosurgical community to re-examine its role in providing quality care to neurotrauma patients.

The Brain Trauma Foundation, in a joint initiative with the American Association of Neurological Surgeons (AANS) and the Joint Section on Neurotrauma and Critical Care, developed a task force that researched the scientific basis for past and present treatments for TBI patients. The end result was the Guidelines for the Management of Severe Head Injury.[11] The Guidelines, endorsed by the AANS and the World Health Organization's Neurotrauma Committee, is the first scientific evidence-based document that evaluates the current evidence for practice and intervention: to reduce secondary brain injury and improve outcome for TBI patients. The Guidelines covers a variety of topics ranging from trauma systems, prehospital resuscitation, ICP monitoring, treatment of intracranial hypertension, and critical care management of TBI patients. This article reviews the interventions aimed at preventing secondary brain injury and the role of the neuroscience critical care nurse in implementing treatments to prevent or correct the events leading to secondary brain injury in TBI patients.


The practice parameters discussed in the Guidelines are defined as standards, guidelines, or options.[11] Standards are considered the accepted principles of patient care management. They represent the highest degree of clinical certainty and are based on Class I evidence. Prospective randomized controlled trials are considered Class I evidence. Guidelines represent a range of treatment strategies with a moderate degree of clinical certainty as documented with Class II evidence. Studies with less strength, nonrandomized cohort studies and case control studies are designated as Class II evidence. Options address the remaining treatment strategies for which there is unclear clinical certainty. Options are based on Class III evidence. Studies based on retrospective data collection, clinical series, databases, case reports, or registries are classified as Class III evidence. The relationship between treatment strategies and evidence classification is illustrated in Table 1. Very few Class I studies exist; therefore most practice parameters are listed as guidelines or options.

Table 1

Comparison of Standards, Guidelines, and Options
 Degree of Clinical Classification of
Recommendations Certainty Evidence

Standards High Class I

Guidelines Moderate Class II

Options Unclear Class III

Recommendations Examples

Standards Prospective randomized
 controlled data

Guidelines Prospective and retrospective
 clinical studies; observational
 studies, cohort studies,
 prevalence studies, case
 control studies

Options Retrospective data collection;
 clinical series databases or
 registries, case reports, case
 reviews and expert opinion

Secondary Brain Injury

The Guidelines describes the management for severe head injury patients and focuses on prevention of secondary brain injury associated with hypotension, hypoxemia, cerebral edema, and intracranial hypertension. Interventions aimed at preventing secondary brain injury begin at the accident scene with adequate resuscitation and continue to management in the hospital setting. Appropriate critical care treatment of these patients can significantly reduce TBI-associated deaths. The areas of critical care management of greatest concern include oxygenation and blood pressure (BP) support, ICP monitoring and cerebral perfusion pressure (CPP) management, and hyperventilation techniques.

Blood Pressure and Oxygen Resuscitation


Episodes of hypotension (systolic blood pressure less than 90 mm Hg) and hypoxia (partial pressure of arterial oxygen [Pa[O.sub.2]] less than 60 mm Hg) should be avoided whenever possible in severe head injury patients or, at the very least, corrected immediately.[11] Along with age, admission motor score, pupillary response, and the presence of mass lesions, hypotension and hypoxia have been associated with a poor prognosis.


The mean arterial pressure (MAP) should be maintained above 90 mm Hg throughout the patient's course in an attempt to maintain CPP greater than 70 mm Hg.[11]

Hypotension (systolic blood pressure less than 90 mm Hg) has a significant detrimental effect on patient outcome. As early as 1981, Miller et al. described a doubling of mortality from severe head injury when hypotension and hypoxia were present.[18] Marmarou et al. examined the effects of ICP instability and hypotension on outcome with severe head injury patients.[16] The study examined ICP and BP of TBI patients in intensive care units. For this group, hypotension was defined as systolic BP less than 80 mm Hg and ICP instability as ICP greater than 20 mm Hg as recorded at the end of each hour by the critical care nurse. A total of 428 patient records were reviewed. Approximately 50% of the patients were monitored for 5 days or more. Outcome was measured at 6 months using the Glasgow Outcome Scale.[13] Twenty percent of the patients were not available for outcome evaluation due to institutionalization, missed appointments, or unknown whereabouts. However, 32% had favorable outcomes (good or moderate disability), while 49% had poor outcomes (severe disability, vegetative, or dead). An ICP greater than 20 mm Hg emerged as a highly significant factor in explaining poor outcome, and systolic BP less than 80 mm Hg also demonstrated a significant detrimental effect on outcome.[16]

With the development of the Traumatic Coma Data Bank (TCDB) came an opportunity to reinvestigate the role of hypotension and hypoxia on the outcome of patients with severe head injury. Chesnut et al.[8] went on to further clarify the role of hypotension and hypoxia on the outcome of patients with severe head injury.[8] They discovered that hypotension was a major determinant in overall increased morbidity and mortality of patients with severe brain injury.[8] Mutually exclusive categories for hypotension and hypoxia were analyzed.

In the TCDB series, 699 patient records were reviewed from the time of arrival at the TCDB hospital emergency room. Of these patients, 113 (16.2%) suffered one or more episodes of hypotension, which resulted in a 60.2% mortality rate. In the subgroup of patients who experienced hypotension and hypoxia, 52 patients (7.4%) had a mortality rate of 75%. For the 456 patients (65.2%) with no known episodes of hypotension or hypoxia, the mortality rate was only 27%. Clearly, hypotension with or without hypoxia doubles the mortality rate for patients with severe head injury (Table 2).[8]

Table 2

Outcome of TBI Patients with Associated Secondary Insults
Secondary No. of Percentage of
Insults Patients Total Patients

Total cases 699 100.0
Neither 456 65.2
Hypoxia(*) 78 11.2
Hypotension(**) 113 16.2
Both 52 7.4

 Glasgow Outcome Score (%)
Secondary Good Severe
Insults Moderate Vegetation Dead

Total cases 42.9 20.5 36.6
Neither 51.2 21.9 27
Hypoxia(*) 44.9 21.8 33.3
Hypotension(**) 25.7 14.1 60.2
Both 5.8 19.2 75

(*) Hypoxia = Pa[O.sub.2] < 60 mm Hg

(**) Hypotension = SBP < 90 mm Hg

The avoidance of hypoxemia and hypotension is the goal for all critical care patients. The neuroscience critical care nurse plays an important role through close monitoring of the hypotensive effects of diuretics, sedatives, barbiturates, and narcotics. All these drugs have the potential to result in hypotensive events. Diligent pulmonary toilet, repositioning, endotracheal suctioning, and keen assessment of breath sounds and oxygen saturation monitoring all are effective methods of reducing the risk of atelectasis and pneumonia and thereby reducing the incidence of hypoxemia.

ICP Monitoring


ICP monitoring is appropriate in patients with severe head injury (Glasgow Coma Scale [GCS] score of 8 or less and an abnormal computed tomography [CT] scan).[11]

If the CT scan is normal but the patient meets two of three criteria--over 40 years of age, unilateral or bilateral motor posturing, and a systolic BP less than 90 mm Hg--then ICP monitoring should also be initiated. In patients with mild or moderate head injury, ICP monitoring is not routinely indicated.[11]

The largest single group of patients in whom we routinely monitor ICP are those patients with severe head injury, defined as a GCS score of 8 or less. Within this group exists a subgroup of patients with a higher incidence of intracranial hypertension (ICH). In patients with severe head injury, ICH is responsible for brain ischemia, severe neurologic dysfunction, and even death. Three noteworthy studies clearly outline the association of intracranial hypertension with higher mortality rates. Miller et al. examined 106 severe head injury patients who underwent ICP monitoring. Of the 71 patients (44%) who exhibited ICP readings greater than 20 mm Hg; 40% died.[17] Narayan's study showed similar results with 207 severe head injury patients: of the 96 patients (46%) who had ICP readings beyond 20 mm Hg, 50% died.[20] Saul and Ducker ran two series of data examining early versus late treatment of increased ICP. They reported that early aggressive treatment based on ICP monitoring significantly lessened the incidence of ICH and reduced the overall mortality rate of severe head injury patients from 84% to 69% without causing a disproportionate number of severely disabled or vegetative patients.[22] It has been well established that early CT scanning for the presence of mass lesions, surgical removal of mass expanding lesions, and early aggressive management of elevated ICP produced a 10%-20% increase in survival rates from severe head injury.[18]

The correlation between elevated ICP and mortality illustrates the importance of ICP monitoring in severe head injury patients. ICP monitoring alone does not improve morbidity or mortality of severe head injury patients, but it does provide the only means of confirming or excluding the presence of ICH. If ICH is indeed present, ICP monitoring provides the only way of adequately assessing the effectiveness of medical therapy. In the setting of ICH, ICP monitoring allows the practitioner an early opportunity to switch to alternative therapies if the present treatment is unsuccessful. However, if increased ICP is not present, the patient is spared therapy that carries some degree of risk.

Sound judgment and clinical experience are necessary in caring for a TBI patient with an ICP monitor. The critical care nurse must be able to troubleshoot problems associated with the ICP device, interpret false high or low readings due to malposition of the transducer and diagnose faulty equipment. In addition, continuous patient assessment by the neuroscience critical care nurse allows rapid implementation of therapies to reduce ICH and timely evaluation of their effectiveness.


The ventricular catheter connected to an external strain gauge transducer is still considered the "Gold Standard" for ICP monitoring.[11] The reasons are twofold. First, the ventricular catheter is the only monitoring device that not only allows monitoring of ICP but also provides the additional benefit of cerebrospinal fluid drainage as a mechanism for treating elevated ICP. Second, the external strain gauge transducer is accurate, inexpensive, reliable, and easy to calibrate.

Parenchymal ICP monitoring with fiberoptic or stain gauge catheter tip transduction is similar to ventricular ICP monitoring but has the potential for measurement drift. Subarachnoid, subdural, and epidural monitors are currently less accurate.[11]

In large randomized prospective studies, there are no reports associating ICP monitoring with a significant risk of intracranial infection. Infection rates using ventricular catheters range from 0% to 9.5%.[1,9,20,23] All the cited studies demonstrated minimal risk of infection for those patients who were monitored for less than 3 days. Similarly, the data reflect an increased incidence of infection when the ventricular monitoring devices were left in place longer than 5 days. Infections were classified as positive cerebrospinal fluid (CSF) cultures (ventriculitis with or without meningitis) or positive wound cultures.

Recent advances in technology have been made to replace the fluid coupled catheter and the strain gauge transducer with a more sophisticated monitoring system. A new ventricular catheter with a fiberoptic-tipped transducer showed accuracy over a wide range, with readings, on average, 1.15 mm Hg higher per day than those obtained by the traditional external strain gauge transducer. Of the readings made with the fiberoptic device, 97% were within 5 mm Hg of those of the strain gauge transducer.[5]

The incidence of malfunction that occurred in the fiberoptic catheter tip transducers ranged from 9% to 40%, often requiring reinsertion of a new fiberoptic device.[5,6,24] Ventricular catheters with miniature strain gauge (microsensor) transducers within the ventricular catheter demonstrated a 0.5 [+ or -] 2.6 mm Hg difference per day compared to the fluid coupled catheters with external strain gauge transducers. Of the readings made with the ventricular catheter, 98% were within 4 mm Hg of those made with the external strain gauge transducer.[12] Both the microsensor and fiberoptic ventricular catheter devices provide an alternative to the traditional external strain gauge transducer used with the fluid coupled ventricular catheters, however, catheter malfunction and the degree of drift must be considered when extended ICP monitoring is anticipated.

As technology in the field of ICP monitoring advances, so must the level of expertise of the critical care nurse caring for the TBI patient. The nurse must become intimately familiar with the type of ICP device utilized in the critical care unit.

In addition, the critical care nurse must monitor the ventriculostomy site for signs of infection and maintain aseptic technique while performing dressing changes and obtaining CSF samples.

Cerebral Perfusion Pressure


The minimum threshold for cerebral perfusion pressure is 70 mm Hg.[11]

In the past, systemic hypertension was viewed as potentially harmful to neurotrauma patients. Research during the last decade shows that ICP changes very little and often decreases when BP rises in head injury patients, despite the status of autoregulation.[2,3,4] In addition, there is mounting evidence that autoregulation remains intact in many cases of TBI.[7] With intact autoregulation, reduced blood pressure sharply increases ICP due to vasodilatation and the concurrent increase in cerebral blood flow. Bouma and colleagues explain this phenomenon by the fact that autoregulatory vasoconstriction is much smaller (maximum approximately 8%-10% of baseline diameter) than autoregulatory vasodilatation (up to 65% of baseline diameter).[3,14]

Cerebral perfusion pressure plays an important role in this analysis. When ICP is elevated, there is a vasodilatation of cerebral vessels, which causes an increase in cerebral blood volume and cerebral blood flow. In addition, if the MAP remains unchanged, then a concurrent decrease in CPP is likely to occur. If the process is interrupted and CPP is increased through vasoconstriction, there is a reduction in cerebral blood volume and a subsequent reduction in ICP.[7,21] Systemic blood pressure can be artificially raised via vascular expansion through the administration of red cell transfusions, concentrated albumin other synthetic colloids or by pharmacological therapy aimed at vasoconstriction. Elevation of the MAP can indirectly result in an increased CPP. Since cerebral blood vessels have few adrenergic receptors, administration of vasopressors will not lead to pharmacological cerebral vasoconstriction. However, with intact autoregulation, cerebral vasoconstriction will occur due to increased blood pressure (Fig 1). Recent mortality rates range from 18% to 21% when CPP remains greater than 70 mm Hg.[15,21]


The neuroscience critical care nurse plays an important role in the monitoring and tracking of physiologic parameters such as ICP, MAP, and CPP. Activities that lower MAP or raise ICP may in effect alter CPP. The nurse's role is to monitor the patient's physiologic responses to sedation, diuretics, and medical and nursing procedures. Prior to initiating CPP therapy, the neuroscience critical care nurse must have firsthand accurate knowledge of the patient's baseline hemodynamic status. Once therapy has begun, the nurse must carefully titrate vasoactive infusions to obtain the optimum physiologic response while monitoring for the adverse effects that often accompany vasopressor use.



In the absence of increased intracranial pressure, chronic prophylactic hyperventilation therapy (Pa[CO.sub.2] less than 25 mm Hg) should be avoided after severe head injury.[11]


The use of prophylactic hyperventilation therapy (Pa[CO.sub.2] less than 35 mm Hg) during the first 24 hours after severe TBI should be avoided because it can compromise cerebral perfusion during a time when cerebral blood flow is reduced.[11]


Hyperventilation therapy may be necessary for brief periods of time when acute neurologic deterioration is observed or for longer periods of time when there is ICH refractory to sedation, paralysis, CSF drainage, and osmotic diuretics.[11]

Carbon dioxide and hydrogen ion concentrations have a profound effect on cerebral vasculature. Low pH and hypercarbia (Pa[CO.sub.2] greater than 45 mm

Hg) result in cerebral vasodilatation while vasoconstriction occurs in the presence of a high pH and hypocarbia (Pa[CO.sub.2] less than 35 mm Hg). In the clinical setting hyperventilation was thought to be an effective and rapid way to reduce increased intracranial pressure. For years, hyperventilation was the mainstay of treatment for elevated ICP in severe head injury patients. Prophylactic hyperventilation (Pa[CO.sub.2] between 25 and 35 mm Hg) was used to theoretically reduce the associated cerebral edema that occurred following severe traumatic brain injury.

Muizelaar studied the issue of hyperventilation in TBI patients; 113 patients were randomized into one of three groups: control group, hyperventilation group, or hyperventilation plus buffer substance.[19] In groups with GCS motor scores of 4 or 5, at the 3-month outcome evaluation, the hyperventilation group demonstrated a lower mortality than the other two groups. However, the hyperventilation group presented with the largest number of patients in the severely disabled or vegetative category. These results were similar when GCS scores at 6 months were analyzed. Again at the 12-month follow-up, there remained a higher percentage of severely disabled or vegetative patients in the hyperventilation group compared to the control or hyperventilation plus buffer substance group. However, the results lost their statistical significance in this time period.

Research conducted by Bouma et al. demonstrated a reduction in cerebral blood flow during the early period after severe head injury (15-16 ml/100gm/min).[4] Cerebral blood flow below the threshold for infarction (less than 18 ml/100 gm/min) was associated with a significantly higher mortality and worse outcome for survivors. Hyperventilation may turn borderline ischemia into frank ischemia, resulting in neuronal cell death. In some cases, reducing hyperventilation and inducing arterial hypertension were found to reverse the effects of ischemia. The combination of early cerebral ischemia, coupled with hyperventilation, can seriously increase mortality and morbidity.

Careful monitoring of Pa[CO.sub.2] is crucial to avoiding unnecessary ischemic events in the TBI patient. The critical care nurse must carefully monitor the patient's arterial blood gasses and report variations in Pa[CO.sub.2] from normal limits to the physician. It is the critical care nurse's clinical observations of the patient's neurologic exam along with ICP that should guide treatment decisions related to hyperventilation.


During the past two decades, understanding of the pathophysiology of traumatic brain injury has increased remarkably. One central concept is now known: all neurologic damage does not occur at the moment of impact (primary injury), but rather evolves over the ensuing minutes, hours, and days after a severe traumatic brain injury. This secondary injury can result in increased mortality and more disabling injuries. While the Guidelines for the Management of Severe Head Injury was developed to guide physicians in their care of the severe traumatic brain-injured patient, the concepts are applicable to neuroscience critical care nurses as well. The same practice parameters that guide physician decisions should be incorporated by critical care nurses to guide their care of the TBI patient.


[1.] Aucoin PJ, Kotilainen HR, Gantz NM et al: Intracranial pressure monitoring: Epidemiologic study of risk factors and infections. Am J Med 1986; (80): 369-376.

[2.] Bouma GJ, Muizelaar JP: Relationship between cardiac output and cerebral blood flow in patients with intact and with impaired autoregulation. J Neurosurg 1990; 73: 368-374.

[3.] Bouma GJ, Muizelaar JP, Bandoh K, Marmarou A: Blood pressure and intracranial pressure volume dynamics in severe head injury: Relationship with cerebral blood flow. J Neurosurg 1992; 77: 15-19.

[4.] Bouma GJ, Muizelaar JP, Choi SC et al: Cerebral circulation and metabolism after severe traumatic brain injury: The elusive role of ischemia. J Neurosurg 1991; 75: 685-693.

[5.] Chambers IR, Kane PJ, Choksey MS, Mendelow AD: An evaluation of the Camino ventricular bolt system in clinical practice. Neurosurgery 1993; 33(5): 866-868.

[6.] Chambers IR, Mendelow AD, Sinar EJ, Modha P: A clinical evaluation of the Camino subdural screw and ventricular monitoring kits. Neurosurgery 1990; 26: 421-423.

[7.] Chesnut RM: Treating raised intracranial pressure in head injury. Pages 455-469 in: Neurotrauma, Narayan RK, Wilberger JE, Povlishock JT (editors). McGraw-Hill, 1996

[8.] Chesnut RM, Marshall LF, Klauber MR et al: The role of secondary brain outcome from severe head injury. J Trauma 1993; 34 (2): 216-222.

[9.] Clark WC, Muhlbauer MS, Lowrey R et al: Complications of intracranial pressure monitoring in trauma patients. Neurosurgery 1989; 25(1): 20-24.

[10.] Ghajar J, Hariri RJ, Narayan RK et al: Survey of critical care management of comatose, head-injured patients in the United States. Crit Care Med 1995; 23(3): 560-567.

[11.] Guidelines for the Management of Severe Head Injury. The Brain Trauma Foundation and The American Association of Neurological Surgeons, 1995.

[12.] Gopinath SP, Robertson CS, Contant CF et al: Clinical evaluation of a minature strain gauge transducer for monitoring intracranial pressure. Neurosurgery 1995; 36(6): 1137-1140.

[13.] Jennett B, Bond M: Assessment of outcome after severe brain damage. A practical scale. Lancet 1975; 1: 480-484.

[14.] Kontos HA, Wei EP, Navari RM et al: Responses of cerebral arteries and arterioles to acute hypertension and hypotension. Am J Physiol 1978; 234: H371-H383.

[15.] Marion DW, Obrist WD, Carlier PM et al: The use of moderate therapeutic hypothermia for patients with severe head injuries: A preliminary report. J Neurosurg 1993; 79: 354-362.

[16.] Marmarou A, Anderson RL, Ward JD et al: Impact of ICP instability and hypotension on outcome in patients with severe head trauma. J Neurosurg 1991; 75 [suppl]: 59-66.

[17.] Miller JD, Becker DP, Ward JD et al: Significance of intracranial hypertension in severe head injury. J Neurosurg 1977; 47: 503-516.

[18.] Miller JD, Butterworth JF, Gudeman SK et al: Further experience in the management of severe head injury. J Neurosurg 1981; 54: 289-299.

[19.] Muizelaar JP, Marmarou A, Ward JD et al: Adverse effects of prolonged hyperventilation in patients with severe head injury: A randomized clinical trial. J Neurosurg 1991; 75:731-739.

[20.] Narayan RK, Kishore PR, Becker DP et al: Intracranial pressure: To monitor or not to monitor? J Neurosurg 1982; 56: 650-659.

[21.] Rosner MJ, Daughton S: Cerebral perfusion pressure management in head injury. J Trauma 1990; 30: 933-941.

[22.] Saul TG, Ducker TB: Effect of intracranial pressure monitoring and aggressive treatment on mortality in severe head injury. J Neurosurg 1982; 56: 498-503.

[23.] Winfield JA, Rosenthal P, Kanter RK, Casella G: Duration of intracranial pressure monitoring does not predict daily risk of infectious complications. Neurosurgery 1993; 33(3): 424-430.

[24.] Yablon JS, Lantner HJ, McCormack TM et al: Clinical experience with a fiberoptic intracranial pressure monitor. J Clin Monitor 1993; 9(3); 171-175.

Questions or comments about this article may be directed to: Laura A. Iacono, MSN RN CNRN CCRN, at the Brain Trauma Foundation, 523 East 72nd Street, 8th Floor, New York, NY 10021. She is the education coordinator at the center.
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Author:Iacono, Laura A.
Publication:Journal of Neuroscience Nursing
Geographic Code:1USA
Date:Feb 1, 2000
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