Increased intracranial pressure s and traumatic brain injury

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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.

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.

TABLE 45-1. COMMON CAUSES OF ELEVATED INTRACRANIAL PRESSURE

Increased CSF

Increased Blood

Increased Brain Tissue

Volume

Volume

Volume

Communicating

Intracerebral

Neoplasm

hydrocephalus

hemorrhage

(aneurysm or AVM)

Obstructing

Epidural or subdural

Cerebral edema (CVA,

hydrocephalus

hematoma

encephalopathic, metabolic,

traumatic)

Malignant hypertension

Cysts

AVM, Arteriovenous malformation; CSF, cerebrospinal fluid; CVA, cerebrovascular accident;

ICP, intracranial 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).

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).

50 MAP (mmHg) 150 20 PaC02 ioo 10 Pa02 200

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 ol 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 p-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.

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