Glasgow Coma Scale

The prehospital assessment of a patient’s neurologic condition serves as a guide to the appropriate triage of an individual following a TBI. When transported directly from the scene of injury to a trauma center, patients with severe TBI have lower mortality rates than those who are first taken to nontrauma centers.⁵ Furthermore, severely brain-injured patients who are admitted and treated at level I trauma centers have improved survival rates and experience better outcomes compared to matched counterparts treated at level II facilities.⁶

Over the years, many assessment schemes have been created to determine the neurologic status of head-injured patients, with the Glasgow Coma Scale (GCS) being the most commonly used tool to determine the severity of TBI (Table 132-1). Developed in 1974 by Teasdale and Jennett, the GCS gauges a patient’s level of consciousness through an assessment of eye opening, verbal response, and motor response.⁷ For patients who are mechanically ventilated by an endotracheal tube or via a tracheostomy, thus precluding the patient’s ability to communicate verbally, a GCS score of 1 point is given for the verbal response score with a “T” following to indicate the intubated status of the patient. There are instances in which accurately determining a GCS score is difficult or when the applicability of a score is of limited utility, as with the presence of concomitant facial trauma, ingestion of sedative drugs such as alcohol or barbiturates, or iatrogenic paralysis of patients for intubation. Moreover, physiologic derangements such as hypotension and hypoxia at the time of assessment hinder a patient’s neural response to stimuli; therefore, they represent important factors that may also lead to inaccurate GCS scores, as well as contributing to secondary brain injury.

Table 132-1 Glasgow Coma Scale

From Teasdale G, Jennett B. Assessment of coma and impaired consciousness: A practical scale. Lancet 2:81-84, 1974.

Severe TBI is classified by total GCS scores of 3 to 8 points, while scores of 9 to 12 points indicate moderate TBI and those between 13 to 15 points denote mild TBI. GCS scores correlate significantly with outcome, with the motor component of the score being most reproducible and yielding the most prognostic information.⁸ Patients whose GCS scores decrease by 2 points or more between the field and the emergency department are more likely to require surgical intervention.⁹ Nearly 80% of patients with an initial hospital GCS score of 3 to 5 points have an eventual outcome of death, severe disability, or vegetative state, with a mortality rate of 65% seen in patients with an initial GCS score of 3 points.^8,10,11 Among individuals with a GCS score of 3 points on presentation, only 13% have good functional outcomes at the 6-month mark.¹² Age, pupil reactivity, radiologic findings on head computed tomography (CT) scan, and extent of extracranial injuries suffered during the trauma serve as additional independent predictors of patient outcome following severe TBI.^13–15

Pupillary Examination

The pupillary examination is a critical component of a patient’s initial neurologic assessment following TBI. A dilated pupil that does not constrict in response to light indicates ipsilateral uncal herniation, until proved otherwise. Bilaterally dilated pupils can be seen with hypoxia, hypotension, bilateral oculomotor nerve dysfunction, or severe irreversible brain stem injury. A change in the pupillary examination is the most reliable indicator in determining the side with a mass lesion and carries an 80% positive predictive value. Moreover, pupillary size and reactivity are especially important in the assessment of trauma patients with an admission GCS score of 3 points, because those with bilaterally fixed and dilated pupils have a universally dismal prognosis, with mortality rates of upward of 100%.^16–18

Motor Examination

Mass lesions or intracranial hypertension sometimes precipitates a medial displacement of the temporal lobe on the same side. The compression of the midbrain against the tentorium cerebelli and the resultant interruption of corticospinal input from fibers within the ipsilateral cerebral peduncle cause a patient to present with hemiparesis contralateral to the side with the mass lesion. The manifestation of hemiparesis is a key focal neurologic deficit that is useful in establishing the laterality of a mass lesion following TBI. However, the surgeon must be aware that a false localizing sign occurs in cases of the Kernohan notch phenomenon, in which a mass lesion may manifest with ipsilateral hemiparesis due to compromise of the contralateral cerebral peduncle that is pushed against the contralateral tentorial edge.

Primary Brain Injury

Primary brain injury refers to damage suffered as a direct result of the initial traumatic event and may be caused by penetrating, blunt, or blast trauma. Bullets and other projectiles often create a significant amount of destruction to brain tissue along their track and can result in injury to brain parenchyma due to fragments of depressed skull. In addition, laceration of cerebral blood vessels can lead to subarachnoid hemorrhage and/or formation of intracerebral hematomas.¹⁹ Blunt trauma can result in brain injury because of transmission of force directly at the point of impact or at a point distant from impact due to the displaced brain rebounding against the inner surface of the skull, an event referred to as contrecoup injury.²⁰ The primary injuries of blast TBI are only now becoming understood and represent a regrettable reality of modern warfare and civilian terrorism.

Primary brain injury can be broadly divided into focal and diffuse injuries (Table 132-2). The specific type of injury suffered depends on the nature of the impact during injury (contact or inertial loading), the resultant forces delivered during the impact (rotational, translational, or angular acceleration), and the magnitude and duration of the impact itself.

Table 132-2 Types of Structural Primary Brain Injury

Focal injuries include traumatic intracranial hematomas and contusions. Based on data from the Traumatic Coma Data Bank (TCDB), diffuse injuries are more common and constitute upward of 60% of severe TBI, as they span a wide clinical spectrum ranging from concussion to diffuse axonal injury. Higher mortality rates have been seen with focal injuries,²¹ highlighting the necessity of expedient cranial imaging in evaluating TBI patients via CT scan, which can confirm the presence of a mass lesion and, in turn, prompt emergent surgical intervention if warranted.

Secondary Brain Injury

Secondary brain injury occurs when local phenomena within the skull or systemic factors cause further damage that manifests at the cellular level over the ensuing hours to days following the original insult. The reduction of mortality from severe TBI, even when adjusted for injury severity, age, and other admission prognostic parameters, from 50% to less than 25% over the past 30 years reflects the impact of preventing secondary brain injury specifically through avoiding and treating aggravating factors, such as hypotension, hypoxia, inadequate cerebral perfusion pressure (CPP), and intracranial hypertension.²² These unwanted physiologic perturbations result in cerebral ischemia, which can significantly compound the effects of the initial injury. The decrement in mortality and improvement in outcomes from TBI that has been achieved is largely attributable to the use of evidence-based protocols, which hold avoidance of cerebral ischemia—through intensive monitoring of neurophysiologic parameters and maintenance of adequate cerebral perfusion—as paramount.^23,24 Knowing and understanding the pathophysiologic basis underlying cerebral ischemia and intracranial hypertension, the indications for monitoring, and the available treatments directed toward preventing or mitigating their effects are crucial to any neurosurgeon involved in the care of patients with severe TBI.

Pathophysiology

At autopsy, 80% of patients who die after TBI have evidence of cerebral ischemia.²⁵ Cerebral ischemia is defined as cerebral blood flow (CBF) that is inadequate to meet the metabolic demands of the brain. While the brain constitutes only 2% to 3% of the body’s weight, it consumes 25% of its oxygen and receives about 20% of its cardiac output. The brain is almost completely reliant on adequate blood flow: nearly 95% of the brain’s metabolism is oxidative without a significant oxygen storage capacity and limited glucose and glycogen reserves. Delivery of oxygen to the brain is contingent on the oxygen content of the blood and CBF; likewise, delivery of glucose and other substrates of metabolism are based on CBF. In turn, a discrete metabolic autoregulatory mechanism exists to couple CBF with the cerebral metabolic rate of oxygen (CMRO₂) so that adequate perfusion exists to support local metabolic needs. This principle is illustrated by the Fick equation CMRO₂ = CBF × AVDO₂, where AVDO₂ is the arteriovenous difference in oxygen (in milliliters per deciliter) and is measured by subtracting the jugular venous oxygen content from the systemic arterial oxygen content. Under physiologic conditions, changes in CMRO₂ are paralleled by changes in CBF, with AVDO₂ remaining constant. In states in which decreased CBF occurs, as in systemic hypotension or when aberrant cerebral pressure autoregulation exists, the brain increases its extraction of oxygen to avoid ischemia. Current evidence suggests that episodes of inadequate CBF, evidenced by low jugular venous oxygen saturation (S_jvO₂) values of less than 50%, portend bad outcomes, because they are associated with increased morbidity and mortality in patients with severe TBI.²⁶

Two other important homeostatic mechanisms are involved in prevention of cerebral ischemia. The first mechanism indirectly links CBF to CPP via the partial pressure of carbon dioxide (P_aCO₂) within the arterial system.²⁷ In this process, arteriolar dilation and constriction occurs secondary to changes in P_aCO₂ and concomitant changes in the pH within the perivascular space, with hypercapnia causing vasodilatation and hypocapnia resulting in vasoconstriction. The second mechanism, referred to as pressure autoregulation, similarly links CBF to CPP.

CBF and CPP

Pressure autoregulation is a fundamental concept in cerebrovascular physiology and is distinct from metabolic autoregulation. Pressure autoregulation allows a constant supply of oxygen and metabolic substrates to be delivered to the brain by maintaining a constant CBF over a range of CPPs. CPP is defined as the mean arterial pressure (MAP) minus the intracranial pressure (ICP). Under normal circumstances, CBF remains relatively constant over a range of CPPs between 50 and 150 mm Hg, ensuring adequate oxygen delivery through a dynamic system of arteriolar vasoconstriction and dilation. Hence, in situations of low perfusion pressures, arteriolar vasodilation occurs, resulting in decreased cerebral vascular resistance and, in turn, increased CBF to normal. On the contrary, when a state of high perfusion pressure exists, arteriolar constriction leads to a decrease in CBF toward normal levels. At CPPs outside the autoregulatory threshold, however, CBF is unable to be maintained within its normal parameters—an exceedingly low perfusion pressure results in arteriolar collapse and a consequent decrement in CBF; hyperemia occurs at high CPPs outside of the limit of autoregulation due to vessels reaching their capacity for vasoconstriction (Fig. 132-1).

FIGURE 132-1 Cerebral pressure autoregulation.

(From White H, Venkatesh B. Cerebral perfusion pressure in neurotrauma: a review. Anesth Analg 107:979-988, 2008.)

The surgeon must also be able to distinguish CBF from cerebral blood volume (CBV). As already mentioned, CBF is the physiologic parameter that governs cerebral perfusion and oxygen delivery. CBV represents the total volume of blood within the intracranial compartment and is a key component of ICP per the Monro-Kellie doctrine. In efforts to control ICP, CBV may be manipulated while maintaining an adequate degree of CBF.

Low CPP has been shown to be associated with higher mortality rates and increased morbidity among survivors following TBI,^28–30 especially when systemic hypotension occurs concomitantly.³¹ Moreover, the normal response of cerebral arterioles to changes in CPP is frequently absent or impaired in 49% to 87% of patients after severe TBI.^32–34 Aberrant pressure autoregulation at a range outside normal physiologic parameters may occur after TBI (Fig. 132-2),^35,36 with significant consequences. Shifting the lower limit of autoregulation from 50 mm Hg to a supranormal range of 70 to 90 mm Hg could precipitate cerebral ischemia,^29,37,38 which is especially noteworthy when considering that up to 60% of patients with severe brain injury experience a reduction in CBF during the first few hours following their trauma.³⁹ Prolonged systemic hypotension or aggressive hyperventilation therapy would further exacerbate ischemia in vulnerable areas and could lead to subsequent cerebral edema. Conversely, autoregulation occurring at a lower-than-typical range of CPPs could result in malignant hyperemia or significant damage to the microcirculation, leading to secondary hemorrhages.⁴⁰ Thus, absent or impaired cerebral pressure autoregulation represents a particularly significant risk factor for development of secondary brain injury, especially early in the postinjury period.⁴¹

FIGURE 132-2 Aberrant cerebral pressure autoregulation after severe TBI.

(From Rangel-Castilla L, Gasco J, Nauta HJ, et al. Cerebral pressure autoregulation in traumatic brain injury. Neurosurg Focus 25:1-8, 2008.)

Based on the preceding information, CBF is assumed to have a linear relationship with CPP in managing patients with severe TBI. Other key factors that affect CBF include local factors such as physical compression of vessels by mass lesions or edematous brain, reduced cerebral metabolism of oxygen, and post-traumatic vasospasm.^42,43 Nearly 33% of severely head-injured patients have CBF values near the ischemic threshold (less than 18 ml/dl) within the first 24 hours after primary injury,^44,45 which is seen most often in individuals with diffuse cerebral edema or acute subdural hematomas.^46–48 Low CBF values during the first 7 days after injury are associated with significantly higher mortality rates and increased morbidity.^{32,39,49–51}

CPP thus serves as an important gauge of the adequacy of CBF and, in turn, must be monitored and maintained in patients with severe TBI. Through studies of brain tissue oxygen tension (P_btO₂) and S_jvO₂ that correlate with unfavorable outcomes, some investigators have suggested a treatment and maintenance threshold CPP of 60 mm Hg,^52,53 while other groups recommend a higher value of 70 mm Hg^54,55 to avoid cerebral oxygen desaturation. Based on the results of cerebral microdialysis monitoring, others have discussed a lower CPP threshold of 50 mm Hg.⁵⁶ In a prospective study in which a CPP-focused management strategy was used, Rosner et al.⁵⁷ demonstrated a mean mortality rate of 21% in patients with severe TBI when CPP is maintained above 70 mm Hg, as compared to the 40% mortality rate in the TCDB series. Current practice guidelines dictate a threshold around 60 mm Hg due to concern over causing secondary brain injury in patients with aberrant pressure autoregulation, with further adjustments based on ancillary neurophysiologic monitoring of CBF, oxygenation, metabolism and the individual patient’s pressure autoregulatory status.⁵⁸

Monitoring

Therapies directed toward avoidance of cerebral ischemia are founded on CPP calculation. Thus, systemic blood pressure and ICP monitoring via direct transduction of blood pressure by an indwelling arterial catheter and an ICP monitor, respectively, is warranted. Systemic arterial oxygen saturation and blood hematocrit are also monitored as standard practice among all trauma patients.

Management Principles

Avoidance of secondary brain injury due to cerebral ischemia is a fundamental principle guiding care following severe head injury. The surgical team must ensure adequate CBF by keeping CPPs around 60 mm Hg, as well as avoiding systemic hypotension, hypoxia, and anemia. Maintenance of CPPs above 70 mm Hg via use of vasopressors and volume expansion has been shown to carry a significantly increased risk of developing acute respiratory distress syndrome, thus obviating the need to aggressively treat patients in such a manner.^53,71

In patients with inadequate CPP, systemic causes of hypotension such as cardiac or spinal cord injury, tension pneumothorax, and bleeding must be ruled out. Intravascular volume must also be assessed via central venous pressure monitoring. Administration of intravenous isotonic fluids is a mainstay of management, but vasopressors are often necessary to maintain adequate CPP. The profiles of commonly used vasopressors are listed in Table 132-3. All listed agents are sympathomimetics, with phenylephrine being the most commonly used.^72–75 Though these agents are of significant importance in the management of patients following severe head injury, their use may be associated with complications such as pulmonary edema and/or expansion of preexisting hematomas or contusions⁷⁶ and therefore must be used with caution.

Delivery of oxygen to brain tissue is predicated on not only sufficient CBF but also oxygen content of the blood. As such, anemia can lead to cerebral ischemia. Despite evidence indicating that low hematocrit is associated with increased mortality⁷⁷ and morbidity^77a in patients with severe TBI, no consensus exists as to a particular threshold for transfusion of blood. While anemia is associated with worse outcomes, there is little support for the aggressive use of packed red blood cells to correct for anemia based on extant data: some studies have noted increasingly negative neurologic outcomes in patients with severe TBI who underwent transfusion,⁷⁸ while other authors have shown no difference in mortality rates among patients treated under an aggressive transfusion protocol as opposed to those treated along a more restrictive one.⁷⁹ Interestingly, studies have demonstrated that between 26% and 43% of patients with severe head injuries experience a paradoxical decrement in P_btO₂ values in the setting of blood transfusion,^80,81 with no effect seen on cerebral metabolism.⁸¹

Animal experiments, however, have shown that a hematocrit in the range of 30% to 33% provides an optimal balance between blood viscosity and oxygen-carrying capacity.⁸² Kee and Wood⁸³ noted that brain tissue oxygen delivery begins to decrease at a hematocrit less than 33%, lending credence to the belief that maintenance of a hematocrit of approximately 30% to 33% is optimal.⁸⁴ Most centers initiate transfusion of packed red blood cells at a hematocrit of less than 30%. As with all trauma patients, a hematocrit refractory to blood transfusion should prompt a search for extracranial bleeding sources.

Pathophysiology

Intracranial contents include blood, brain, and cerebrospinal fluid (CSF). Under physiologic conditions, the intracranial vasculature contains 75 ml of blood, most of which is located within the venous system; CSF occupies a volume of approximately 75 ml and is primarily contained in the ventricles. The intracranial contents are enclosed within the rigid, nonexpansile skull. Based on the principle that the total volume available to intracranial contents is fixed, ICP is determined by the dynamic interplay among the individual components, as delineated by the Monro-Kellie doctrine. Therefore, an increase in an existing component—as seen with hydrocephalus or with post-traumatic cerebral edema—occurs with a concomitant decrease in another. The same concept holds true when a mass lesion occurs, because an additional component has been added to the intracranial space. In this way, in cases of hydrocephalus, post-traumatic cerebral edema, and even new mass lesion development, ICP may remain within normal limits through compensations of the intracranial vascular volume, CSF volume, and brain parenchyma (Fig. 132-3). Physiologic volume-buffering mechanisms exist through which intracranial vascular volume may reduce via increased arteriolar constriction and increased venous outflow, and CSF volume may decrease by being displaced into the thecal sac surrounding the spinal cord. It is estimated that in some instances upward of 100 to 150 ml of new intracranial volume can manifest without any significant increases in ICP, provided that the new mass does not present acutely.⁸⁵ However, an uncompensated increase in one or more existing compartments or the presence of a new component results in an ICP higher than the normal range of 5 to 15 mm Hg.^86,87

FIGURE 132-3 Monro-Kellie doctrine.

CSF normally circulates through the lateral ventricles, the interventricular foramen of Monro, the third ventricle, the cerebral sylvian aqueduct, and the fourth ventricle and out the foramina of Luschka and Magendie. It courses over the spinal cord and the brain and is eventually absorbed into the arachnoid granulations and superior sagittal sinus by means of passive transport. In situations in which there is no intracranial mass lesion, increased ICP following TBI occurs due to perturbations in CSF flow or CBV, as well as because of the development of vasogenic or cytotoxic edema.⁸⁸ Breakdown products of blood secondary to traumatic subarachnoid hemorrhage preclude the passive absorption of CSF at the arachnoid granulations, which leads to an overall increase in CSF. Increase in CBV occurs when normal pressure and chemical autoregulatory mechanisms are compromised in severe TBI. Vasogenic and cytotoxic edema are the result of a disrupted blood–brain barrier and osmotic dysregulation in ischemic cells.

ICP rises exponentially when an uncompensated state exists. The shape of the pressure–volume curve reflects that as the ICP increases, the brain compliance decreases. The slope of the curve represents the intrinsic compliance of the brain without the influence of ICP. Marmarou et al.⁸⁹ illustrated this by plotting ICP and volume on a semilogarithmic axis (thus removing the influence of ICP) and obtaining a linear relationship. The slope of the straight line is the pressure–volume index and is the amount of volume necessary to raise pressure 10-fold (Fig. 132-4).

FIGURE 132-4 ICP–volume relationships. A, A classic pressure–volume curve depicts the exponential increase in ICP once compensatory mechanisms of handling additional intracranial volume are exhausted. In the patient with severe head injury, additional volume may take the form of increased CSF from poor absorption, increased CBV, vasogenic edema from a compromised blood–brain barrier, and cytotoxic edema. B, In a pressure–volume index, change in volume is plotted against ICP before (ICPo) and after (ICPi) logarithmic volume change.

(From Marmarou A, Shulman K, Rosende RM. A nonlinear analysis of the cerebrospinal fluid system and intracranial pressure dynamics. J Neurosurg 48:332-344, 1978.)

Elevated ICP, known as intracranial hypertension, leads to brain herniation and a decrement in the CPP (since CPP is defined as MAP-ICP). Herniation refers to an event in which brain parenchyma is displaced from its normal location through holes in the dura and skull. This may manifest as subfalcine herniation, uncal herniation, central downward herniation, external herniation of the brain through an open skull fracture, or tonsillar herniation (Fig. 132-5).

FIGURE 132-5 Herniation types. a, Subfalcine herniation. b, Uncal herniation. c, Central downward herniation. d, External herniation of the brain through an open skull fracture. e, Tonsillar herniation.

Monitoring

Intracranial hypertension is known to have a significant deleterious impact on patient outcome after severe TBI.^10,59,90,91 The institution of modern neurocritical care protocols, predicated on monitoring of ICP and other important neurophysiologic parameters, has been credited with improved patient outcomes following severe TBI when compared to historic cohorts.^92–94 The question of which patients benefit from ICP monitoring is based on risk stratification for developing intracranial hypertension. The presence of an abnormal head CT is one key factor in predicting which patients with severe brain injuries develop elevated ICPs. Narayan et al.⁹⁵ found that the incidence of intracranial hypertension in this population is between 53% and 63%. Per findings of the same study and other investigations, individuals with a negative head CT scan on admission following severe TBI have a much lower risk of this occurring, with upper estimates in the range of 10% to 15%.^14,96 Interestingly, among this particular subset of patients, the risk of developing intracranial hypertension was comparable to those with abnormal imaging findings if at least two of three risk factors (age over 40 years, unilateral or bilateral motor posturing, or systolic blood pressure less than 90 mm Hg) was present.⁹⁵

Apart from their basic utility in guiding therapy involving the management of ICP and CPP, ICP monitors may also serve an important diagnostic purpose by indicating the development of worsening intracranial lesions, as a trend of progressively rising ICP values often correlates with the evolution of intracranial pathology.⁹⁷

ICP Monitoring Devices, Indications, and Techniques of Usage

The Association for the Advancement of Medical Instrumentation has developed the American National Standard for Intracranial Pressure Monitoring Devices, which dictates performance requirements of currently available ICP monitoring devices. These parameters include the ability to (1) measure ICP readings from 0 to 100 mm Hg, (2) be accurate within 2 mm Hg in pressure ranges of 0 to 20 mm Hg, and (3) have a maximum error of 10% in pressure ranges of 20 to 100 mm Hg. Current technology allows for ICP measurement by external strain gauge transducers, microtip catheter strain gauge transducers, fiberoptic transducers, and coupling to a pneumatic transducer. There are many possible intracranial locations in which a particular ICP monitoring device may be placed, including within the ventricle, the brain parenchyma, the subdural space, the subarachnoid space, and epidurally. When considering which device to use, attention must be paid to accuracy, reliability, cost, and potential for patient morbidity. A ventricular catheter coupled to an external strain gauge transducer by fluid coupling is the gold standard.⁹⁸

In the setting of severe TBI, placement of an external ventricular drain (EVD), or ventriculostomy, for ICP monitoring also allows for CSF diversion and is useful for patients believed to be at risk for development of intracranial hypertension or hydrocephalus. As such, it has a crucial role in guiding therapy, as well as serving as a therapeutic modality by reducing ICP on a sustained basis.⁹⁹ The most common complications associated with the procedure are hemorrhage, infection, and malfunction. A recent meta-analysis estimated the risk of hemorrhage due to EVD placement as 5.7%, with only 0.61% of hemorrhages being clinically significant¹⁰⁰; however, the significantly higher overall hemorrhage rates reported by other investigators highlight that obtaining postprocedural head CT scans may be a confounding factor.¹⁰¹ Lozier et al.’s¹⁰² review of ventriculostomy-associated infections (VAIs) cited a rate between 6% and 9%. Other important considerations involving VAIs include the significant association of CSF infections with increasing duration of EVD catheterization, the utility of administering prophylactic antibiotics prior to EVD placement, and the use of antimicrobial-impregnated catheters, which have been shown to reduce the risk of EVD-related infections.¹⁰³ Based on the previously cited review of VAIs, prophylactic catheter exchange to reduce VAI rates is not efficacious. EVD malfunctions are usually attributable to obstruction in the fluid coupling mechanism by which the external strain gauge catheter transduces ICP, a complication estimated to occur in 2.5% of patients.¹⁰⁴

At our institution, right-sided EVDs are preferred to avoid the dominant hemisphere. The patient is maintained in a supine position with the head brought to the edge of the bed; the head of the bed is elevated to roughly 45 degrees. Hair clippers are used to widely shave the head on the same side of the EVD cannulation, and the head is prepared in the standard sterile fashion. Two lines are drawn on the scalp to establish Kocher’s point: one line in the midline from the nasion to a point 10 cm back and another from the previous point to a spot 3 cm lateral to it. This location is where the bur hole placement will occur and should be in the ipsilateral midpupillary line. Finally, two lines are drawn that guide the trajectory of ventricular cannulation: one line from Kocher’s point to the ipsilateral medial canthus of the eye and a second line from Kocher’s point to a point roughly 1.5 cm anterior to the ipsilateral tragus (Fig. 132-6). After administration of a local anesthetic containing epinephrine, a small linear skin incision is made down to bone and the periosteum is scraped off. A twist drill is used to open the cranium, bone fragments and dust are removed, and the dura and pia mater are pierced with a scalpel or sharp object. Using the demarcated lines as a guide, the trajectory at which the drill is used to create the bur hole is the same trajectory used for passing the ventricular catheter: aiming in the coronal plane toward the medial canthus of the ipsilateral eye and in the anteroposterior plane toward a point 1.5 cm anterior to the ipsilateral tragus. This trajectory is exceedingly important because it delineates the trajectory of the ventricular cannulation; if the bur hole is not created in an appropriate trajectory, the EVD cannot be optimally positioned due to its being limited by its bony opening, especially if the cranium is thick (Fig. 132-7). The ventricular catheter is passed to a depth of 6.25 cm using the previously described trajectory. The surgeon may alternatively pass the ventriculostomy using Dandy’s principle, which states that employing a trajectory directly perpendicular to the skull allows ventricular cannulation. Regardless, the ventricular catheter is never passed to a depth greater than 7 cm due to the risk of damaging the brain stem. Once the EVD is in place, it is tunneled through the skin away from the incision through a separate stab incision and is secured in place. A postprocedural head CT is then obtained.

FIGURE 132-6 Ventriculostomy anatomy.

FIGURE 132-7 Suboptimal EVD trajectory and placement.

There are cases in which ventricular cannulation can challenge even the most experienced of neurosurgeons. Our experience is to always use the landmarks and trajectory as outlined earlier, regardless of whether a mass lesion or significant shift is present. Most often, errant EVD passes are due to a lateral trajectory (Fig. 132-8), and the neurosurgeon must pay particular attention to avoiding an injury to the ipsilateral internal capsule. In cases in which the ventricle is believed to be cannulated with no egress of CSF, the neurosurgeon may consider attaching a small, plungerless syringe filled with sterile saline to the ventriculostomy catheter. If the ventricle is indeed cannulated, saline should flow from the syringe, through the catheter, and into the ventricle. If the neurosurgeon does not obtain CSF flow through the ventriculostomy after 3 passes, the EVD is left in place and a head CT scan is obtained to determine its position.

FIGURE 132-8 Errant EVD passes.

Other ICP monitoring devices are frequently used in centers, sometimes as an adjunctive means of monitoring ICP when they are placed in tandem with an EVD and at other times when slit-like ventricles preclude EVD placement. The scalp incision is made in the exact location as for a ventriculostomy, with a smaller drill bit and small stylet used to puncture the dura. When using microtip strain gauge or fiberoptic parenchymal monitors, the probe is advanced between 1 and 2 cm into the brain parenchyma. The microtip strain gauge probe must be tunneled through the skin via a separate stab incision and then be secured in place. However, the fiberoptic monitor can be held in place by a fixation bolt screwed into the skull. The reduced accuracy and reliability, increased propensity for malfunction, and high cost in comparison to EVD placement are factors that must be considered prior to using these alternative ICP monitors.

Management Principles

Current practice guidelines recommend that an ICP treatment threshold of 20 mm Hg be used,¹⁰⁵ based on investigations showing that the incidence of morbidity and mortality among severely brain-injured patients is significantly associated with ICPs exceeding 20 mm Hg.^59,95,106 The rationale behind treatment of intracranial hypertension is to prevent cerebral ischemia by ensuring adequate CPP and preventing brain herniation. ICP values, however, must be considered as part of the larger clinical picture, together with exam findings and imaging findings, such that established treatment thresholds are considered guidelines that do not preclude treatment at lower values, especially in light of herniation potentially occurring at ICP values less than 20 mm Hg.¹⁰⁷

Several methods may be employed to decrease ICP. A stepwise, protocol-based approach to treatment of intracranial hypertension is best suited to prevent the utilization of an excessive number of modalities concomitantly. Maneuvers to optimize venous outflow from the intracranial vascular volume are first used, followed by pharmacotherapy and CSF diversion (Fig. 132-9).

FIGURE 132-9 Stepwise protocol for ICP management.