45: Increased Intracranial Pressure and Traumatic Brain Injury

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CHAPTER 45 Increased Intracranial Pressure and Traumatic Brain Injury

Matthew Hall, MD

1 Define elevated intracranial pressure

Elevated intracranial pressure (ICP) is usually defined as a sustained pressure of greater than 20 mm Hg within the subarachnoid space. The normal ICP is approximately 10 to 18 mm Hg.

2 What are the determinants of intracranial pressure?

The space-occupying contents of the skull, the brain (85%), the cerebrospinal fluid (CSF) (10%), and cerebral blood volume (15%), are all contained in the virtually fixed volume of the cranium. Once compensatory mechanisms are exhausted (mostly translocation of CSF), any increase in volume will cause a rise in ICP.

3 How is intracranial pressure measured?

Various techniques are available, including ventricular catheters, subdural-subarachnoid bolts, epidural transducers, and intraparenchymal fiber-optic devices. The standard method is a ventriculostomy, in which a plastic catheter is introduced into the anterior aspect of the lateral ventricle via a burr hole in the cranium. The catheter is attached to saline-filled tubing, and the pressure is transduced. In addition, this catheter can be used to drain CSF via a pop-off valve set at 20 cm H₂O. Another common method is the subarachnoid bolt, which is also placed through a burr hole but does not require insertion through brain tissue or identification of the position of the ventricle. A third technique involves the insertion of a fiber-optic bundle through a small burr hole. The fiber-optic bundle senses changes in the amount of light reflected off a pressure-sensitive diaphragm at its tip. However, the fiber-optic bundle is subject to drift in the measurements over time and cannot be recalibrated in situ. In addition, the intraparenchymal and subdural methods are limited by the inability to withdraw CSF and manage ICP. Newer generations of fiber-optic ICP monitors allow simultaneous measurement of ICP, local cerebral blood flow (CBF) with Doppler, pH, PO₂, and PCO₂ and avoid the potential infectious problems of a fluid-filled transducing system.

4 Summarize the conditions that commonly cause elevated intracranial pressure

See Table 45-1.

TABLE 45-1 Common Causes of Elevated Intracranial Pressure

Increased CSF Volume	Increased Blood Volume	Increased Brain Tissue Volume
Communicating hydrocephalus	Intracerebral hemorrhage (aneurysm or AVM)	Neoplasm
Obstructing hydrocephalus	Epidural or subdural hematoma	Cerebral edema (CVA, encephalopathic, metabolic, traumatic)
	Malignant hypertension	Cysts

AVM, Arteriovenous malformation; CSF, cerebrospinal fluid; CVA, cerebrovascular accident; ICP, intracranial pressure.

5 Describe the symptoms of increased intracranial pressure

Symptoms associated with increased ICP alone include headache, vomiting, papilledema, drowsiness, loss of consciousness, and behavioral changes. Several other symptoms such as pathologic (decerebrate) posturing, oculomotor nerve palsy, abnormalities of brainstem reflexes, and abnormal respiratory patterns (including apnea), are probably caused by brainstem distortion or ischemia secondary to impending herniation. The Cushing reflex, consisting of hypertension and reflex bradycardia, is likely caused by medullary ischemia and occurs when ICP approaches systemic arterial pressure.

6 Discuss the possible consequences of increased intracranial pressure

In addition to producing the previously mentioned symptoms, increased ICP can lead to a decrease in cerebral perfusion pressure, which may result in regional or global cerebral ischemia. Further elevations in ICP may result in herniation of brain contents (across the falx cerebri, tentorium, or foramen magnum).

7 What are the determinants of cerebral perfusion pressure?

Cerebral perfusion pressure (CPP) is usually defined as the difference between mean arterial pressure (MAP) and ICP or central venous pressure, whichever is higher.

8 What is intracranial elastance? Why is it clinically significant?

Intracranial elastance, commonly misnamed intracranial compliance, refers to the variation in ICP in accordance with intracranial volume. Because intracranial components can shift their volumes to an extent (e.g., CSF movement from the intracranial compartment to the spinal compartment), ICP remains somewhat constant over a certain range of volume. However, when compensatory mechanisms are exhausted, ICP rises rapidly with further increases in volume (Figure 45-1).

Figure 45-1 Intracranial elastance. ICP, Intracranial pressure.

9 How is cerebral blood flow regulated?

CBF is coupled to cerebral metabolic rate by an uncharacterized mechanism but may involve potassium, hydrogen, calcium ions, adenosine, nitric oxide, and prostaglandins. In general, increases in the cerebral metabolic rate for oxygen (CMRO₂) lead to increases in CBF, although the increase in flow is delayed by 1 to 2 minutes. Several other parameters influence flow. Specifically an increase in the partial pressure of carbon dioxide in arterial blood (PaCO₂) is a powerful cerebral vasodilator, with CBF increasing/decreasing 1 to 2 ml/100g/min with a 1-mm Hg change in PaCO₂. Similarly, a decrease in the partial pressure of oxygen (PaO₂) in arterial blood below 50 mm Hg greatly increases flow. Variations in MAP also may result in large increases or decreases in flow, but over a broad range (50 to 150 mm Hg) flow is nearly constant. This constancy of flow over a range of pressures is known as autoregulation. Chronic hypertension shifts the autoregulation curve to the right. Following a brain injury such as stroke, tumor accompanied by edema, or trauma, autoregulation may be disrupted, and flow becomes pressure dependent (Figure 45-2).

Figure 45-2 Regulation of cerebral blood flow (CBF). BP, Blood pressure; MAP, mean arterial pressure.

10 What is the goal of anesthetic care for patients with elevated intracranial pressure?

Because patients with elevated ICP may be approaching the upslope of the elastance curve, in which a small change in volume leads to a large increase in ICP, the goal of anesthetic care is to use all possible measures to reduce intracranial volume while maintaining cerebral perfusion.

11 Can this goal be aided by preoperative interventions?

Traditionally several techniques have been used to decrease intracranial volume before surgery. Mild fluid restriction (intake of one third to one half of daily maintenance requirements) may decrease ICP over a period of several days. Corticosteroids are particularly effective in decreasing edema associated with tumors.

12 How is the goal of reduced intracranial volume achieved at induction of anesthesia?

The measures used at induction of anesthesia are chosen to reduce cerebral blood volume. Thiopental and propofol are the preferred intravenous induction agents because they reduce both CBF and CMRO₂. Ketamine and etomidate should be avoided because ketamine increases CBF and ICP and the propylene glycol formulation of etomidate may induce neurologic deficits in at-risk tissue. Opioids have a variable effect on CBF but are commonly used to blunt the sympathetic response to laryngoscopy and tracheal intubation. However, administer opioids cautiously in the spontaneously breathing patient since hypoventilation can lead to an increase in PaCO₂ and thus CBF. Common adjuncts used at induction include intravenous lidocaine, a cerebral vasoconstrictor that blunts the response to intubation, and short-acting β-blockers such as esmolol that blunt systemic hypertension caused by laryngoscopy.

13 How is intracranial pressure moderated during maintenance of anesthesia?

Most intraoperative maneuvers for controlling ICP rely on reduction of cerebral blood volume or total brain water content. Blood volume is minimized by hyperventilation to lower PaCO₂ (25 to 30 mm Hg), which results in transient cerebral vasoconstriction, and by using anesthetic agents that decrease CBF. Halogenated volatile agents should be limited to less than 1 minimum alveolar concentration. Nitrous oxide should be avoided because it increases both CBF and CMRO₂ and may be neurotoxic. Maintaining the patient in a slightly head-up position promotes venous drainage. Brain water can be decreased acutely with diuretics such as mannitol (0.25 to 1g/kg bolus) and/or furosemide. In addition, intravenous fluids are limited to the minimal amount necessary to maintain cardiac performance. The surgeon may drain CSF directly from the surgical field or use an intraventricular catheter to decrease total intracranial volume. If oxygenation is not problematic, positive end-expiratory pressure (PEEP) should be avoided because it can be transmitted to the intracranial compartment. If PEEP is necessary for ventilation, the head of the bed should be elevated to avoid the increase in ICP caused by decreased venous return.

14 Is hyperventilation a reasonable strategy for long-term intracranial pressure management?

Hyperventilation (achieving a PaCO₂ of 0 to 25 mm Hg) decreases ICP as a result of cerebral vasoconstriction, decreasing cerebral blood volume. This effect is mediated by an elevation in cerebral pH. This response occurs and is effective over the course of several hours. However, cerebral pH decreases by a gradual decrease in the bicarbonate concentration in newly formed CSF. Thus hyperventilation becomes ineffective for lowering ICP after 24 to 48 hours. Hyperventilation below a PaCO₂ of 25 mm Hg should be avoided out of concern for focal cerebral ischemia caused by profound decreases in CBF.

15 Which intravenous fluids are used during surgery to minimize intracranial pressure?

In general hypotonic crystalloid infusions should be avoided because they may increase brain water content. Normal saline may be superior to lactated Ringer’s because of the higher sodium and lower free water content. Some centers resuscitate with small volumes (4 ml/kg) of hypertonic saline to minimize free water in the setting of elevated ICP. Glucose-containing solutions are avoided because of evidence of worsened neurologic outcome if ischemia occurs in the setting of hyperglycemia. Hyperglycemia (serum glucose >180 mg/dl) should be treated with insulin. Colloidal solutions are not superior to crystalloid solutions.

16 What are the effects of volatile anesthetics on cerebral blood flow?

All of the commonly used inhaled anesthetics have been noted to increase CBF and decrease CMRO₂. The response of CBF to changes in PaCO₂ is preserved.

17 How do neuromuscular blocking agents affect intracranial pressure?

Succinylcholine has been reported to increase ICP, but the clinical significance of this transient increase is probably not of concern. Therefore, in cases of emergent surgery in patients with a full stomach, rapid-sequence induction with succinylcholine is acceptable. Commonly used nondepolarizing agents have no effect on ICP and can be used safely.

18 Discuss strategies for controlling intracranial pressure at emergence from anesthesia

β-Blockers such as esmolol and labetalol can be titrated to attenuate the increased sympathetic tone present at emergence. They are particularly useful in their ability to cause peripheral dilation without cerebral vasodilation, which can increase CBF. Nitroprusside, a direct-acting vasodilator, is also useful in controlling blood pressure when administered by infusion but can worsen ICP through cerebral vasodilation. The head of the bed should be elevated, and hypercarbia should be avoided.

KEY POINTS: Factors Affecting CBF

4. Metabolism (CMRO₂)

19 If the previously mentioned measures fail to control intracranial pressure, what other measures are available?

Barbiturate coma has been used in patients who are refractory to other methods of ICP control. Typical doses of pentobarbital are 10 mg/kg given over 30 minutes to load, followed by three hourly doses of 5 mg/kg. This regimen usually provides a therapeutic serum level of 30 to 50 mcg/ml. Maintenance is usually achieved by dosing of 1 to 2 mg/kg/h.

KEY POINTS: Agents to Avoid in the Setting of Elevated ICP

2. Nitrous oxide

3. Hypotonic or glucose-containing intravascular fluid

4. High concentrations of inhalation agents

20 What are the mechanisms behind traumatic brain injury?

The damage to the brain after traumatic injury can be divided into two categories:

1. Damage from the primary mechanism of injury

2. Damage from secondary insults (hypotension, hypoxia)

The primary mechanism (e.g., motor vehicle crash, gunshot) can result in focal or global damage to the brain tissue. Focal injuries are primarily caused by penetrating trauma, contusions, or intracranial hemorrhage. On the other hand, global injuries are often the result of diffuse axonal injury in which rapid deceleration and rotation result in shearing between neocortical grey and white matter. The primary insult may not be responsive to therapeutic interventions. In contrast, secondary injuries from hypoperfusion or hypoxia that often occur in the intensive care unit or operating room should be prevented lest there be further deterioration in the patient’s status.

21 What are the anesthetic goals in a patient with traumatic brain injury?

As previously mentioned, the anesthetic goals for managing a patient with traumatic brain injury (TBI) should be geared to prevent secondary injury. The already damaged brain tissue is extremely susceptible to hypoperfusion and hypoxia. Intubation should be achieved rapidly, with hemodynamic stability ensured and adequate oxygenation maintained. Adequate cerebral perfusion should be closely monitored, and a CPP between 60 to 80 mm Hg maintained. A MAP of >90 is generally accepted and should be achieved with fluid resuscitation and vasopressors. Increases in ICP should also be addressed by measures previously discussed. Of note, cerebral autoregulation is commonly disrupted in TBI; and hypertension can similarly be deleterious by worsening vasogenic edema, resulting in an increased ICP and a subsequent decrease in CPP. In TBI oxygen demand may be increased as a result of a disproportional release of excitatory neurotransmitters, and hypoxia can worsen the ischemic injury.

22 In a patient with traumatic head injury, how should fluid resuscitation be prioritized and what fluids are beneficial?

As a general rule, hemodynamic stability takes precedence because cerebral hypoperfusion is clearly detrimental. The choice of resuscitative fluids in TBI is an ongoing debate. Traditionally Ringer’s lactate and normal saline (0.9%) have been used. Ringer’s lactate has an osmolarity (273 mOsm/L) less than serum osmolarity, which in large volumes can decrease serum osmolarity and increase cerebral blood volume. In some institutions Ringer’s lactate is limited to 2 L to minimize this effect. Normal saline has an osmolarity closer to serum osmolarity and does not result in a decrease in serum osmolarity. Some institutions use hypertonic saline (3% or 7.5%) for fluid resuscitation. Small quantities of hypertonic saline can be used to maintain intravascular volume because they result in movement of water from the intracellular space to the extracellular space. This may improve hemodynamics and decrease ICP. However, hypertonic saline does not reliably improve cerebral oxygen delivery and can result in electrolyte abnormalities. Colloid solutions (Hextend, albumin) can provide acute intravascular volume expansion. However, albumin has been implicated in increases in morbidity and mortality in TBI, and hetastarch has been associated with an elevation of prothrombin and partial thromboplastin times when given in volumes >20 ml/kg. In the event of acute or continued blood loss, packed red blood cells provide excellent volume expansion.

SUGGESTED READINGS

1. Bedell E., DS Prough D.S. Anesthetic management of traumatic injury. Anesthesiol Clin North Am. 2002;20:417-439.

2. Bendo A., et al. Anesthesia for neurosurgery. In: Barash P.G., Cullen B.F., Stoelting R.K., editors. Clinical anesthesia. ed 5. Philadelphia: Lippincott Williams & Wilkins; 2005:746-789.

3. Moppett I.K. Traumatic brain injury: assessment, resuscitation and early management. Br J Anaesth. 2007;99:18-37.

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