Special Feature
Critical Care Management of the Patient with Elevated Intracranial Pressure
By Andrew M. Luks, MD, Pulmonary and Critical Care Medicine, University of Washington, Seattle, is Associate Editor for Critical Care Alert.
Dr. Luks reports no financial relationship to this field of study.
Elevated intracranial pressure (ICP) occurs as a complication of neurosurgical emergencies including traumatic brain injury (TBI) and intracranial hemorrhage or due to medical illnesses, such as meningitis or fulminant hepatic failure. While management of this problem usually falls within the purview of neurosurgeons and neurointensivists, recent efforts to assure intensivist involvement in the management of all ICU patients increases the likelihood that general intensivists will manage patients with this complication. In addition, intensivists at smaller institutions may manage these patients prior to transfer to centers with more specialized neurosurgical resources. As a result, general intensivists must be facile with the treatment of ICP problems. The purpose of this special feature is to review this issue in greater detail; it begins by discussing important background concepts regarding intracranial hypertension and then considers the different management approaches to this important problem.
Basics of ICP: Definitions, Physiology, and Monitoring
In supine adults, normal ICP resides between 5-15 mm Hg, whereas intracranial hypertension is present when ICP rises above 20 mm Hg. Transient spikes above this level occur in response to coughing or other stimuli, but the primary concern is sustained elevations above this threshold, as it is these situations that cause adverse consequences, including cerebral ischemia or herniation, and are associated with poor outcome. Although increased ICP typically happens within the first few days of injury, ICP problems can arise 5 or more days following TBI.1
A key principle underlying ICP problems is the Monroe-Kellie doctrine, which emphasizes that the intracranial compartment is comprised of three components — blood, cerebrospinal fluid (CSF), and brain tissue — residing within a fixed space defined by the cranium. Increases in the size of one component must be matched by decreases in the size of other components or ICP will rise. In the early phases of injury, compensatory mechanisms are invoked and prevent pressure elevation according to this principle. For example, with increasing brain edema, CSF is squeezed out of the ventricles provided the basal cisterns are patent. Eventually, however, compensatory mechanisms are exhausted and pressure rises in response to further changes in the size of the core components, with the magnitude and timing of ICP changes varying among individuals based on compliance of their intracranial compartment.
Current guidelines recommend monitoring ICP in TBI patients with Glasgow coma score (GCS) < 8 and an abnormal CT or with GCS < 8 and a normal CT if the patient has two or more of the following: age > 40, SBP < 90 mm Hg, or motor posturing.2 ICP monitors are occasionally used in non-traumatic situations, such as severe meningitis, but guidelines dictating when to place them are lacking and practices vary among institutions.
The gold standard for monitoring ICP remains the ventriculostomy drain,3 which can be placed at the bedside through a craniostomy. The advantage of this system is that it allows drainage of CSF and can be recalibrated in situ, while disadvantages include an increased risk of infection and hemorrhage relative to other modalities. Alternative monitoring systems include the subarachnoid bolt and fiberoptic catheters. Also placed at the bedside, these systems are used when tight ventricles prevent placement of a ventriculostomy drain and carry lower rates of infection and bleeding. Disadvantages include the fact that they measure pressure in one hemisphere and may not reflect pressure in all compartments and the fact that the fiberoptic systems cannot be recalibrated when measurement drift occurs. Less invasive modalities, such as optic nerve sheath diameter monitoring,4 have not become part of standard clinical practice.
While focusing on ICP is important, clinicians should also consider another important variable, cerebral perfusion pressure (CPP), which is defined as the difference between mean arterial pressure (MAP) and ICP. Patients may have elevated ICP, but with adequate MAP, cerebral perfusion can be maintained in an appropriate range, thereby preventing ischemic injury. Similarly, modestly elevated ICP may be poorly tolerated in the setting of marginal blood pressure. Although the data do not clearly support a mortality benefit from CPP-focused management and debate exists about the proper CPP threshold, current TBI guidelines recommend maintaining CPP between 50 and 70 mm Hg through the use of fluids and vasopressors and avoiding strategies focused on maintaining CPP > 70 mm Hg due to concerns about provoking acute lung injury or acute respiratory distress syndrome (ARDS).5
Management of Elevated ICP
General Principles
Treatment should be initiated with sustained increases in ICP above 20 mm Hg6 and should be guided by several general principles. First, although many treatment modalities are available, management is usually conducted using a tiered approach whereby less aggressive measures are used first and more aggressive steps are reserved for refractory pressure elevation. The specific approach varies among institutions but the concept of a staged approach is relatively consistent across centers. Second, while implementing these measures, it is important to identify and treat other factors contributing to the ICP beyond the head injury itself, such as hypercarbia, an overly tight cervical collar decreasing internal jugular outflow, or intra-abdominal hypertension. Finally, although surgical decompression is considered a final option in patients with refractory hypertension, certain patients have indications for acute surgical management (e.g., epidural hematoma with > 30 cm3 blood volume)7 regardless of other clinical features. The clinician must recognize these indications and arrange for urgent neurosurgery input if it has not already been obtained.
Lower-tier Interventions
When patients are first noticed to have elevated ICP, a series of less aggressive steps can be implemented.
Fever Control
Fever, which is associated with worse outcomes in many forms of acute neurologic injury,8 increases the cerebral metabolic rate and causes cerebrovascular dilation, two factors that increase cerebral blood flow and contribute to elevated ICP. For these reasons, aggressive fever control with acetaminophen and cooling blankets is employed in intracranial hypertension. While fever is often due to the head injury itself, effort should be made to identify and eradicate sources of infection.
Head of Bed Elevation
In what is likely the simplest and cheapest intervention in the ICU, the head of the bed should be elevated to 15-30° and the head maintained in a neutral position. This maneuver improves ICP by improving cerebral venous outflow and movement of CSF to the spinal canal and without impairing cerebral perfusion or oxygen delivery.9,10
Seizure Prevention
Seizures increase cerebral metabolic rate and ICP and should be treated aggressively. Data support use of phenytoin for prophylaxis in the first 7 days following TBI,11 but prophylactic use of anticonvulsants in other causes of elevated ICP has not been established. A significant proportion of post-TBI seizures are subclinical and consideration could be given to electroencephalographic monitoring to detect this problem.
Airway Management and Mechanical Ventilation
Intensivists should use a low threshold for intubating patients with elevated ICP, as altered mental status, impaired airway patency, and inadequate ventilation can cause hypoxemia and hypercarbia, which in turn lead to increased cerebral blood flow (CBF) and worsening ICP. Traditional teaching emphasized intentional hyperventilation in mechanically ventilated patients to decrease CBF and improve ICP, but this practice has lost favor due to concern that excessive hypocarbia induces cerebral vasoconstriction, impairing perfusion through swollen brain tissue and worsening oxygen delivery. Current practice is to target PaCO2 to 35-40 mm Hg and reserve the short-lived benefits of intentional hyperventilation for episodes of acute decompensation to buy time to get the patient to the CT scanner or the operating room. Increasing PEEP can be used to support oxygenation but clinicians should avoid raising PEEP to levels approaching ICP, as, depending on lung compliance, this may raise cerebral venous pressure sufficiently to impair cerebral venous return.12
Sedation and Analgesia
Because agitation raises ICP, care should be taken to ensure adequate sedation and analgesia. Aside from a small study comparing a propofol-morphine combination with a morphine-only combination,13 there is no good evidence supporting the use of one particular regimen over another. Propofol and bolus administration of fentanyl, however, do offer the advantage of rapid offset and thereby facilitate frequent neurologic assessment as compared to longer acting agents like lorazepam. In cases of poorly controlled ICP, more aggressive sedative measures may be necessary (discussed below).
Higher-tier Interventions
When the ICP remains elevated despite the above interventions, more aggressive measures are necessary.
Hyperosmolar Therapy
Bolus administration of intravenous mannitol (0.25-1 mg/kg) has long been the mainstay of severe ICP management, but hypertonic saline, given as a bolus or a continuous drip at concentrations between 3% and 23% NaCl, is being used with greater frequency. Both agents increase serum osmolarity and, as a result, draw fluid from the extravascular to the intravascular space. Hypertonic saline is the better agent for patients with marginal or low blood pressure, as the diuretic effect of mannitol can cause hypovolemia and lower blood pressure even further. Frequent monitoring of serum sodium and osmolarity is necessary with goal serum osmolarity of 300-320 mOsm/L and serum sodium of 140-150 mEq/L. When using hypertonic saline, care must be taken to avoid hypernatremia as well as sudden decreases in sodium concentration upon cessation of therapy, as such drops may cause intracerebral fluid shifts and worsen ICP. Concerns persist that either agent may cross the altered blood-brain barrier in injured brain and, paradoxically cause fluid movement into the injured and swollen tissue.14
Increased Sedation
With severely elevated ICP, aggressive sedation is necessary to decrease cerebral metabolic activity and oxygen demand. Possible regimens include adding a benzodiazepine to propofol or using propofol at very high doses. The latter regimen carries important risks, however, including hypotension, hypertriglyceridemia, and the propofol infusion syndrome, a severe complication marked by the onset of lactic acidosis and multiorgan failure that can occur after several days of high-dose therapy (> 50 mg/kg/min). When ICP remains elevated despite these measures, barbiturate coma can be induced using pentobarbital. This therapy has been shown to decrease ICP15 with no clear effect on mortality, but carries a risk of hypotension and prevents neurologic examination for significant periods of time. Failure to respond to this therapeutic intervention is associated with mortality rates approaching 85%.16
Vasopressors
Agents such as norepinephrine or phenylephrine can be used to raise MAP to supranormal levels in an effort to maintain CPP between 50 and 70 mm Hg. The choice of vasopressor does not matter significantly because cerebral vascular autoregulation is impaired in neurologic injury and any increase in MAP leads to improvements in cerebral blood flow.
CSF Drainage
In patients with ventriculostomy drains, CSF can be removed to decrease the total volume of the intracranial compartment. Ventriculostomy placement may be difficult, however, if brain swelling causes decreased ventricle size. CSF should not be drained through lumbar drains or periodic lumbar puncture, however, as excessive CSF flow through the spinal compartment could provoke a herniation syndrome.
Other Modalities
Paralysis may be considered with severe intracranial hypertension. Data demonstrating benefit are lacking and this intervention is generally avoided in less severe situations due to the risks of provoking ICU polyneuropathy and myopathy. Induced hypothermia has been considered for refractory ICP elevation, but the available evidence does not support a clear outcome benefit. Corticosteroids do not have a benefit in traumatic brain injury patients,17 but may have benefit in cases of pneumococcal meningitis and cerebral tumors. Limited experimental data suggest that albumin may reduce edema in the regions around contused brain,18 but randomized, controlled data demonstrating benefit are lacking and it is reserved for very severe cases.
When All Else Fails
When patients fail to respond to aggressive medical interventions, consideration is given to decompressive craniectomy. Removal of the part of the cranium eliminates the central problem in the Monroe-Kellie doctrine — fixed intracranial space — and allows swollen brain tissue to expand, thereby relieving pressure. More recent data from case series19 suggest outcomes may be better than those shown in earlier studies,20 but randomized controlled data supporting a benefit and clear guidelines for when to proceed with this option in refractory intracranial hypertension are still lacking.
References
- Stocchetti N, et al. Time course of intracranial hypertension after traumatic brain injury. J Neurotrauma 2007:24:1339-1346.
- Bratton SL, et al. Guidelines for the management of severe traumatic brain injury. VI. Indications for intracranial pressure monitoring. J Neurotrauma 2007:24(Suppl 1):S37-S44.
- Bratton SL, et al. Guidelines for the management of severe traumatic brain injury. VII. Intracranial pressure monitoring technology. J Neurotrauma 2007:24(Suppl 1):S45-S54.
- Soldatos T, et al. Optic nerve sonography in the diagnostic evaluation of adult brain injury. Crit Care 2008:12:R67.
- Bratton SL, et al. Guidelines for the management of severe traumatic brain injury. IX. Cerebral perfusion thresholds. J Neurotrauma 2007:24(Suppl 1):S59-S64.
- Bratton SL, et al. Guidelines for the management of severe traumatic brain injury. VIII. Intracranial pressure thresholds. J Neurotrauma 2007:24(Suppl 1):S55-S58.
- Bullock MR, et al. Surgical management of acute epidural hematomas. Neurosurgery 2006:58(3 Suppl):S7-S15.
- Jones PA, et al. Measuring the burden of secondary insults in head-injured patients during intensive care. J Neurosurg Anesthesiol 1994:6:4-14.
- Feldman Z, et al. Effect of head elevation on intracranial pressure, cerebral perfusion pressure, and cerebral blood flow in head-injured patients. J Neurosurg 1992:76:207-211.
- Ng I, et al. Effects of head posture on cerebral hemodynamics: Its influences on intracranial pressure, cerebral perfusion pressure, and cerebral oxygenation. Neurosurgery 2004:54:593-597.
- Temkin NR, et al. A randomized, double-blind study of phenytoin for the prevention of post-traumatic seizures. N Engl J Med 1990:323:497-502.
- Caricato A, et al. Effects of PEEP on the intracranial system of patients with head injury and subarachnoid hemorrhage: The role of respiratory system compliance. J Trauma 2005:58:571-576.
- Kelly DF, et al. Propofol in the treatment of moderate and severe head injury: A randomized, prospective double-blinded pilot trial. J Neurosurg 1999:90:1042-1052.
- Rangel-Castilla L, et al. Management of intracranial hypertension. Neurol Clin 2008:26:521-541.
- Eisenberg HM, et al. High-dose barbiturate control of elevated intracranial pressure in patients with severe head injury. J Neurosurg 1988:69:15-23.
- Marshall LF, et al. The outcome with aggressive treatment in severe head injuries. Part I: The significance of intracranial pressure monitoring. J Neurosurg 1979:50:20-25.
- Gudeman SK, et al. Failure of high-dose steroid therapy to influence intracranial pressure in patients with severe head injury. J Neurosurg 1979:51:301-306.
- Elliott MB, et al. Effects of crystalloid-colloid solutions on traumatic brain injury. J Neurotrauma 2007:24:195-202.
- Aarabi B, et al. Outcome following decompressive craniectomy for malignant swelling due to severe head injury. J Neurosurg 2006:104:469-479.
- Kjellberg RN, et al. Bifrontal decompressive craniotomy for massive cerebral edema. J Neurosurg 1971:34:488-493.
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