61
Acute Intracranial Problems
Kristen J. Costello
http://evolve.elsevier.com/Lewis/medsurg/
CONCEPTUAL FOCUS
Cognition Mobility
Functional Ability Safety
Intracranial Regulation Sensory Perception
LEARNING OUTCOMES
1. Explain the mechanisms that maintain normal intracranial 6. Compare the types, clinical manifestations, and
pressure. interprofessional care of patients with brain tumors.
2. Describe the common etiologies, clinical manifestations, 7. Discuss the nursing management of the patient with a brain
and interprofessional care of the patient with increased tumor.
intracranial pressure. 8. Describe the nursing management of the patient
3. Describe the nursing management of the patient with undergoing cranial surgery.
increased intracranial pressure. 9. Distinguish among the primary causes and interprofessional
4. Compare types of head injury by mechanism of injury and and nursing management of brain abscess, meningitis, and
clinical manifestations. encephalitis.
5. Describe the interprofessional and nursing management of
the patient with a head injury.
KEY TERMS
cerebral edema head injury
coma intracerebral hematoma
concussion intracranial pressure (ICP)
contusion meningitis
diffuse axonal injury (DAI) nuchal rigidity
encephalitis subdural hematoma
epidural hematoma unconsciousness
Glasgow Coma Scale (GCS)
The body has various mechanisms by which it regulates the and cerebrospinal fluid (CSF) (Fig. 61.1). Brain tissue makes up
intracranial space to promote optimal brain function. Acute about 78% of this volume. Blood in the arterial, venous, and
intracranial problems can disrupt these processes, leading to capillary network makes up 12% of the volume. The remaining
increased intracranial pressure (ICP), reduced blood flow to 10% is the volume of CSF.
the brain, and brain tissue damage. This chapter discusses the We categorize brain injury in 2 phases, primary and second-
mechanisms that maintain normal ICP and problems that lead ary injury. Primary injury occurs at the initial time of an injury
to increased ICP. (e.g., impact of car accident, blunt-force trauma). It results in
displacement, bruising, or damage to any cranial component
(brain tissue, blood, CSF).
INTRACRANIAL REGULATION Secondary injury is the resulting hypoxia, ischemia, hypoten-
Understanding the dynamics of ICP is important in caring for sion, edema, or increased ICP that follows the primary injury.
patients with neurologic problems. The skull is an enclosed Secondary injury can occur several hours to days after the ini-
space with 3 essential volume components: brain tissue, blood, tial injury. It is the modifiable concern when managing brain
1483
,1484 SECTION 12 Problems Related to Movement and Coordination
Initially an increase in volume does not increase ICP because
Cerebrospinal fluid: 10%
of these compensatory mechanisms. However, there is a lim-
ited ability to compensate for changes in volume. As the volume
Intravascular blood: 12% increase continues, ICP rises. Decompensation occurs. This
results in compression and ischemia.
Brain tissue: 78% Cerebral Blood Flow
Cerebral blood flow (CBF) is the amount of blood in milliliters
passing through 100 g of brain tissue in 1 minute. The global
CBF is about 50 mL/min/100 g of brain tissue. Maintaining
blood flow to the brain is critical because the brain requires a
constant supply of O2 and glucose. The brain uses 20% of the
body’s O2 and 25% of its glucose.3
Fig. 61.1 Components of the brain. Autoregulation of Cerebral Blood Flow
The brain regulates its own blood flow in response to its meta-
bolic needs despite wide fluctuations in systemic arterial pres-
injury. Management of the patient with an acute intracranial sure. Cerebral autoregulation is the automatic adjustment in the
problem must include managing secondary injury and prevent- diameter of the cerebral blood vessels by the brain to maintain a
ing increased ICP. constant blood flow with changes in arterial BP. The purpose of
autoregulation is to ensure a consistent CBF to provide for the
Normal Intracranial Pressure metabolic needs of brain tissue and maintain cerebral perfusion
Intracranial pressure (ICP) is the hydrostatic force measured pressure (CPP) within normal limits.
in the brain CSF compartment. Under normal conditions in The lower limit of systemic arterial pressure at which auto-
which intracranial volume stays relatively constant, the balance regulation is effective is a mean arterial pressure (MAP) of 70
among the 3 components (brain tissue, blood, CSF) maintains mm Hg. Below this, CBF decreases, and symptoms of cere-
ICP. Factors that influence ICP under normal conditions are bral ischemia, such as syncope and blurred vision, occur. The
changes in (1) arterial pressure, (2) venous pressure, (3) intraab- upper limit of systemic arterial pressure at which autoregula-
dominal and intrathoracic pressure, (4) posture, (5) tempera- tion is effective is a MAP of 150 mm Hg. When this pressure
ture, and (6) blood gases, especially CO2 levels. The degree to is exceeded, the vessels are maximally constricted and further
which these factors increase or decrease the ICP depends on the vasoconstrictor response is lost.
brain’s ability to adapt to changes. The cerebral perfusion pressure is the pressure needed to
The Monro-Kellie doctrine states that the 3 components ensure blood flow to the brain. CPP is equal to the MAP minus
must stay at a relatively constant volume within the closed skull. the ICP (CPP = MAP − ICP). See the example in Table 61.1.
If the volume of any 1 of the 3 components increases within Normal CPP is 60 to 100 mm Hg. As CPP decreases, autoregu-
the skull and the volume from another component is displaced, lation fails and CBF decreases. A CPP of less than 50 mm Hg is
the total intracranial volume will not change.1 This hypothesis associated with ischemia and neuron death. A CPP of less than
is applicable only in situations in which the skull is closed. The 30 mm Hg results in ischemia. It is incompatible with life. This
hypothesis does not apply in persons with displaced skull frac- is why it is important to maintain MAP when ICP is increased.
tures or craniectomy (removal of part of the skull). Although CPP is clinically useful, it does not consider the
We can measure ICP in the ventricles, subarachnoid space, effect of cerebrovascular resistance. Cerebrovascular resistance
subdural space, epidural space, or brain tissue with a pressure is generated by the arterioles within the cranium. It links CPP
transducer.2 Normal ICP ranges from 5 to 15 mm Hg. A sus- and blood flow as follows:
tained pressure greater than 20 mm Hg is abnormal.
CPP = Flow × Resistance
Normal Compensatory Adaptations
In applying the Monro-Kellie doctrine, the body can adapt to When cerebrovascular resistance is high, blood flow to brain
volume changes within the skull in 3 different ways to maintain tissue is impaired. Normally, autoregulation maintains an ade-
a normal ICP. The first compensatory mechanisms can include quate CBF and CPP by adjusting the diameter of cerebral blood
changes in CSF volume. CSF volume can be changed by alter- vessels and metabolic factors that affect ICP.
ing CSF absorption or production, and by displacing CSF into CPP may not reflect perfusion pressure in all parts of the
the spinal subarachnoid space. Second, changes in intracranial brain. There may be local areas of swelling and compression
blood volume can occur through the collapse of cerebral veins that limit perfusion pressure. Thus these patients may need a
and dural sinuses, regional cerebral vasoconstriction or dila- higher CPP to prevent localized tissue damage. For example, a
tion, and changes in venous outflow. Third, brain tissue volume patient with an acute stroke may need a higher BP, increasing
compensates through distention of the dura or compression of MAP and CPP, to increase perfusion to the brain and prevent
brain tissue. further tissue damage.
, CHAPTER 61 Acute Intracranial Problems 1485
TABLE 61.1 Calculating Cerebral Perfusion PATHOPHYSIOLOGY MAP
Pressure (CPP)
CPP = MAP − ICP Insult to brain
MAP = DBP + (SBP − DBP)
OR
SBP + 2 (DBP) Tissue edema
MAP =
3
Example: Systemic BP = 122/84 mm Hg ↑ ICP
MAP = 97 mm Hg
ICP = 12 mm Hg
CPP = 85 mm Hg Compression of ventricles
Factors Affecting Cerebral Blood Flow Compression of blood vessels
CO2, O2, and hydrogen ion concentration affect cerebral blood
vessel tone. An increase in the partial pressure of CO2 in arte-
↓ Cerebral blood flow
rial blood (PaCO2) relaxes smooth muscle, dilates cerebral ves-
sels, decreases cerebrovascular resistance, and increases CBF. A
decrease in PaCO2 constricts cerebral vessels, increases cerebro- ↓ O2 with death of brain cells
vascular resistance, and decreases CBF.
Cerebral O2 tension of less than 50 mm Hg results in cerebro-
vascular dilation. Dilation decreases cerebrovascular resistance, Edema around necrotic tissue
increases CBF, and increases O2 tension. However, if O2 tension is
not increased, anaerobic metabolism begins, resulting in a buildup
of lactic acid. As lactic acid increases and hydrogen ions accumu- ↑ ICP with compression of brainstem
and respiratory center
late, the environment becomes more acidic. Within this acidic
environment, further vasodilation occurs in a continued attempt
to increase blood flow. The combination of a severely low partial Accumulation of CO2
pressure of O2 in arterial blood (PaO2) and increased hydrogen ion
concentration (acidosis), which are both potent cerebral vasodila-
tors, may produce a state in which autoregulation is lost and com- Vasodilation
pensatory mechanisms do not meet tissue metabolic demands.
CBF can be affected by cardiac or respiratory arrest, systemic
bleeding, and other pathophysiologic states (e.g., diabetic coma, ↑ ICP resulting from ↑ blood volume
infections, toxicities). Regional CBF can be affected by trauma,
tumors, cerebral bleeding, or stroke. When regional or global
autoregulation is lost, CBF is no longer maintained at a con- Death
stant level but is directly influenced by changes in systemic BP,
Fig. 61.2 Progression of increased ICP.
hypoxia, or catecholamines.
INCREASED INTRACRANIAL PRESSURE It is critical to maintain CBF to preserve tissue and
thus minimize secondary injury. Sustained increases in
Mechanisms of Increased Intracranial Pressure ICP result in brainstem compression and brain herniation.
Increased ICP is a potentially life-threatening situation that Herniation occurs as the brain tissue is forcibly shifted from
results from an increase in any or all the 3 components (brain a compartment of greater pressure to a compartment of less
tissue, blood, CSF) within the skull. Increased ICP is clinically pressure.
significant because it decreases CPP and increases risks for brain Displacement and herniation of brain tissue can cause a
ischemia and infarction. It has a poor prognosis.4 Common potentially reversible process to become irreversible. Ischemia
causes of increased ICP include a mass (e.g., hematoma, contu- and edema are further increased, compounding the preex-
sion, abscess, tumor) and cerebral edema (from brain tumors, isting problem. Compression of the brainstem and cranial
hydrocephalus, head injury, brain inflammation). nerves (CNs) may be fatal. Fig. 61.3 shows types of herniation.
These cerebral insults increase the formation and spread of Herniation forces the cerebellum and brainstem downward
cerebral edema. This may result in hypercapnia, cerebral acido- through the foramen magnum. If compression of the brainstem
sis, impaired autoregulation, and systemic hypertension. Edema is unrelieved, respiratory arrest will occur due to compression
distorts brain tissue, further increasing the ICP, and leads to of the respiratory control center in the medulla. In this situa-
even more tissue hypoxia and acidosis. Fig. 61.2 shows the pro- tion, intense pressure is placed on the brainstem. If herniation
gression of increased ICP. continues, brainstem death is imminent.
, 1486 SECTION 12 Problems Related to Movement and Coordination
Normal brain
Intact skull
Falx cerebri
Lateral
ventricles
Intracranial
hematoma
A Uncus
B
Uncal herniation
Calvarial herniation
Intracranial through craniectomy
hematoma site
C D
Central herniation Subfalcine
herniation
Fig. 61.3 Herniation. (A) Normal relationship of intracranial structures. (B, C, and D) Shifts of intracranial
structures.
TABLE 61.2 Causes of Cerebral Edema There are 3 types of cerebral edema: vasogenic, cytotoxic,
and interstitial. A patient may have more than 1 type.
Cerebral Infections Toxic or Metabolic
• Encephalitis Encephalopathies Vasogenic Cerebral Edema
• Meningitis • Hepatic encephalopathy
Vasogenic cerebral edema is the most common type of cerebral
• Lead or arsenic intoxication
Head Injuries and Brain • Uremia edema. It occurs mainly in the white matter. It results from disrup-
Surgery tion of the blood-brain barrier. This allows large molecules (pro-
• Contusion Vascular Insult tein, blood products) to enter brain tissue. This exposes brain cells
• Hemorrhage • Anoxic and ischemic episodes to toxic products from the blood and results in an osmotic gradi-
• Posttraumatic brain swelling • Cerebral infarction (thrombotic or ent that causes fluid to flow from the intravascular to extravascular
embolic) space. The result is an increase in the extracellular fluid volume.
Mass Lesions • Venous sinus thrombosis Systemic BP, site of the brain injury, and extent of the blood-brain
• Brain abscess
• Brain tumor (primary, metastatic) barrier defect influence the extent of the spread of edema.
• Hematoma (intracerebral, Edema may produce a continuum of symptoms. These range
subdural, epidural) from headache to a decrease in consciousness, including coma
• Hemorrhage (intracerebral, (profound state of unconsciousness) and focal (specific to a cer-
cerebellar, brainstem) tain area of the brain) neurologic deficits. In cases of cerebral
edema, a headache can quickly progress to coma and death. So,
you must be vigilant in your assessment.
Cerebral Edema
There are a variety of causes of cerebral edema (increased Cytotoxic Cerebral Edema
accumulation of fluid in the extravascular spaces of brain tis- Cytotoxic cerebral edema results from disruption of the integrity
sue) (Table 61.2). Cerebral edema results in an increase in tis- of the cell membranes. It develops from destructive lesions or
sue volume that can increase ICP. The extent and severity of the trauma to brain tissue, resulting in cerebral hypoxia or anoxia
original insult are factors that determine the degree of cerebral and syndrome of inappropriate antidiuretic hormone (SIADH)
edema. secretion. In this type of edema, the blood-brain barrier stays
Acute Intracranial Problems
Kristen J. Costello
http://evolve.elsevier.com/Lewis/medsurg/
CONCEPTUAL FOCUS
Cognition Mobility
Functional Ability Safety
Intracranial Regulation Sensory Perception
LEARNING OUTCOMES
1. Explain the mechanisms that maintain normal intracranial 6. Compare the types, clinical manifestations, and
pressure. interprofessional care of patients with brain tumors.
2. Describe the common etiologies, clinical manifestations, 7. Discuss the nursing management of the patient with a brain
and interprofessional care of the patient with increased tumor.
intracranial pressure. 8. Describe the nursing management of the patient
3. Describe the nursing management of the patient with undergoing cranial surgery.
increased intracranial pressure. 9. Distinguish among the primary causes and interprofessional
4. Compare types of head injury by mechanism of injury and and nursing management of brain abscess, meningitis, and
clinical manifestations. encephalitis.
5. Describe the interprofessional and nursing management of
the patient with a head injury.
KEY TERMS
cerebral edema head injury
coma intracerebral hematoma
concussion intracranial pressure (ICP)
contusion meningitis
diffuse axonal injury (DAI) nuchal rigidity
encephalitis subdural hematoma
epidural hematoma unconsciousness
Glasgow Coma Scale (GCS)
The body has various mechanisms by which it regulates the and cerebrospinal fluid (CSF) (Fig. 61.1). Brain tissue makes up
intracranial space to promote optimal brain function. Acute about 78% of this volume. Blood in the arterial, venous, and
intracranial problems can disrupt these processes, leading to capillary network makes up 12% of the volume. The remaining
increased intracranial pressure (ICP), reduced blood flow to 10% is the volume of CSF.
the brain, and brain tissue damage. This chapter discusses the We categorize brain injury in 2 phases, primary and second-
mechanisms that maintain normal ICP and problems that lead ary injury. Primary injury occurs at the initial time of an injury
to increased ICP. (e.g., impact of car accident, blunt-force trauma). It results in
displacement, bruising, or damage to any cranial component
(brain tissue, blood, CSF).
INTRACRANIAL REGULATION Secondary injury is the resulting hypoxia, ischemia, hypoten-
Understanding the dynamics of ICP is important in caring for sion, edema, or increased ICP that follows the primary injury.
patients with neurologic problems. The skull is an enclosed Secondary injury can occur several hours to days after the ini-
space with 3 essential volume components: brain tissue, blood, tial injury. It is the modifiable concern when managing brain
1483
,1484 SECTION 12 Problems Related to Movement and Coordination
Initially an increase in volume does not increase ICP because
Cerebrospinal fluid: 10%
of these compensatory mechanisms. However, there is a lim-
ited ability to compensate for changes in volume. As the volume
Intravascular blood: 12% increase continues, ICP rises. Decompensation occurs. This
results in compression and ischemia.
Brain tissue: 78% Cerebral Blood Flow
Cerebral blood flow (CBF) is the amount of blood in milliliters
passing through 100 g of brain tissue in 1 minute. The global
CBF is about 50 mL/min/100 g of brain tissue. Maintaining
blood flow to the brain is critical because the brain requires a
constant supply of O2 and glucose. The brain uses 20% of the
body’s O2 and 25% of its glucose.3
Fig. 61.1 Components of the brain. Autoregulation of Cerebral Blood Flow
The brain regulates its own blood flow in response to its meta-
bolic needs despite wide fluctuations in systemic arterial pres-
injury. Management of the patient with an acute intracranial sure. Cerebral autoregulation is the automatic adjustment in the
problem must include managing secondary injury and prevent- diameter of the cerebral blood vessels by the brain to maintain a
ing increased ICP. constant blood flow with changes in arterial BP. The purpose of
autoregulation is to ensure a consistent CBF to provide for the
Normal Intracranial Pressure metabolic needs of brain tissue and maintain cerebral perfusion
Intracranial pressure (ICP) is the hydrostatic force measured pressure (CPP) within normal limits.
in the brain CSF compartment. Under normal conditions in The lower limit of systemic arterial pressure at which auto-
which intracranial volume stays relatively constant, the balance regulation is effective is a mean arterial pressure (MAP) of 70
among the 3 components (brain tissue, blood, CSF) maintains mm Hg. Below this, CBF decreases, and symptoms of cere-
ICP. Factors that influence ICP under normal conditions are bral ischemia, such as syncope and blurred vision, occur. The
changes in (1) arterial pressure, (2) venous pressure, (3) intraab- upper limit of systemic arterial pressure at which autoregula-
dominal and intrathoracic pressure, (4) posture, (5) tempera- tion is effective is a MAP of 150 mm Hg. When this pressure
ture, and (6) blood gases, especially CO2 levels. The degree to is exceeded, the vessels are maximally constricted and further
which these factors increase or decrease the ICP depends on the vasoconstrictor response is lost.
brain’s ability to adapt to changes. The cerebral perfusion pressure is the pressure needed to
The Monro-Kellie doctrine states that the 3 components ensure blood flow to the brain. CPP is equal to the MAP minus
must stay at a relatively constant volume within the closed skull. the ICP (CPP = MAP − ICP). See the example in Table 61.1.
If the volume of any 1 of the 3 components increases within Normal CPP is 60 to 100 mm Hg. As CPP decreases, autoregu-
the skull and the volume from another component is displaced, lation fails and CBF decreases. A CPP of less than 50 mm Hg is
the total intracranial volume will not change.1 This hypothesis associated with ischemia and neuron death. A CPP of less than
is applicable only in situations in which the skull is closed. The 30 mm Hg results in ischemia. It is incompatible with life. This
hypothesis does not apply in persons with displaced skull frac- is why it is important to maintain MAP when ICP is increased.
tures or craniectomy (removal of part of the skull). Although CPP is clinically useful, it does not consider the
We can measure ICP in the ventricles, subarachnoid space, effect of cerebrovascular resistance. Cerebrovascular resistance
subdural space, epidural space, or brain tissue with a pressure is generated by the arterioles within the cranium. It links CPP
transducer.2 Normal ICP ranges from 5 to 15 mm Hg. A sus- and blood flow as follows:
tained pressure greater than 20 mm Hg is abnormal.
CPP = Flow × Resistance
Normal Compensatory Adaptations
In applying the Monro-Kellie doctrine, the body can adapt to When cerebrovascular resistance is high, blood flow to brain
volume changes within the skull in 3 different ways to maintain tissue is impaired. Normally, autoregulation maintains an ade-
a normal ICP. The first compensatory mechanisms can include quate CBF and CPP by adjusting the diameter of cerebral blood
changes in CSF volume. CSF volume can be changed by alter- vessels and metabolic factors that affect ICP.
ing CSF absorption or production, and by displacing CSF into CPP may not reflect perfusion pressure in all parts of the
the spinal subarachnoid space. Second, changes in intracranial brain. There may be local areas of swelling and compression
blood volume can occur through the collapse of cerebral veins that limit perfusion pressure. Thus these patients may need a
and dural sinuses, regional cerebral vasoconstriction or dila- higher CPP to prevent localized tissue damage. For example, a
tion, and changes in venous outflow. Third, brain tissue volume patient with an acute stroke may need a higher BP, increasing
compensates through distention of the dura or compression of MAP and CPP, to increase perfusion to the brain and prevent
brain tissue. further tissue damage.
, CHAPTER 61 Acute Intracranial Problems 1485
TABLE 61.1 Calculating Cerebral Perfusion PATHOPHYSIOLOGY MAP
Pressure (CPP)
CPP = MAP − ICP Insult to brain
MAP = DBP + (SBP − DBP)
OR
SBP + 2 (DBP) Tissue edema
MAP =
3
Example: Systemic BP = 122/84 mm Hg ↑ ICP
MAP = 97 mm Hg
ICP = 12 mm Hg
CPP = 85 mm Hg Compression of ventricles
Factors Affecting Cerebral Blood Flow Compression of blood vessels
CO2, O2, and hydrogen ion concentration affect cerebral blood
vessel tone. An increase in the partial pressure of CO2 in arte-
↓ Cerebral blood flow
rial blood (PaCO2) relaxes smooth muscle, dilates cerebral ves-
sels, decreases cerebrovascular resistance, and increases CBF. A
decrease in PaCO2 constricts cerebral vessels, increases cerebro- ↓ O2 with death of brain cells
vascular resistance, and decreases CBF.
Cerebral O2 tension of less than 50 mm Hg results in cerebro-
vascular dilation. Dilation decreases cerebrovascular resistance, Edema around necrotic tissue
increases CBF, and increases O2 tension. However, if O2 tension is
not increased, anaerobic metabolism begins, resulting in a buildup
of lactic acid. As lactic acid increases and hydrogen ions accumu- ↑ ICP with compression of brainstem
and respiratory center
late, the environment becomes more acidic. Within this acidic
environment, further vasodilation occurs in a continued attempt
to increase blood flow. The combination of a severely low partial Accumulation of CO2
pressure of O2 in arterial blood (PaO2) and increased hydrogen ion
concentration (acidosis), which are both potent cerebral vasodila-
tors, may produce a state in which autoregulation is lost and com- Vasodilation
pensatory mechanisms do not meet tissue metabolic demands.
CBF can be affected by cardiac or respiratory arrest, systemic
bleeding, and other pathophysiologic states (e.g., diabetic coma, ↑ ICP resulting from ↑ blood volume
infections, toxicities). Regional CBF can be affected by trauma,
tumors, cerebral bleeding, or stroke. When regional or global
autoregulation is lost, CBF is no longer maintained at a con- Death
stant level but is directly influenced by changes in systemic BP,
Fig. 61.2 Progression of increased ICP.
hypoxia, or catecholamines.
INCREASED INTRACRANIAL PRESSURE It is critical to maintain CBF to preserve tissue and
thus minimize secondary injury. Sustained increases in
Mechanisms of Increased Intracranial Pressure ICP result in brainstem compression and brain herniation.
Increased ICP is a potentially life-threatening situation that Herniation occurs as the brain tissue is forcibly shifted from
results from an increase in any or all the 3 components (brain a compartment of greater pressure to a compartment of less
tissue, blood, CSF) within the skull. Increased ICP is clinically pressure.
significant because it decreases CPP and increases risks for brain Displacement and herniation of brain tissue can cause a
ischemia and infarction. It has a poor prognosis.4 Common potentially reversible process to become irreversible. Ischemia
causes of increased ICP include a mass (e.g., hematoma, contu- and edema are further increased, compounding the preex-
sion, abscess, tumor) and cerebral edema (from brain tumors, isting problem. Compression of the brainstem and cranial
hydrocephalus, head injury, brain inflammation). nerves (CNs) may be fatal. Fig. 61.3 shows types of herniation.
These cerebral insults increase the formation and spread of Herniation forces the cerebellum and brainstem downward
cerebral edema. This may result in hypercapnia, cerebral acido- through the foramen magnum. If compression of the brainstem
sis, impaired autoregulation, and systemic hypertension. Edema is unrelieved, respiratory arrest will occur due to compression
distorts brain tissue, further increasing the ICP, and leads to of the respiratory control center in the medulla. In this situa-
even more tissue hypoxia and acidosis. Fig. 61.2 shows the pro- tion, intense pressure is placed on the brainstem. If herniation
gression of increased ICP. continues, brainstem death is imminent.
, 1486 SECTION 12 Problems Related to Movement and Coordination
Normal brain
Intact skull
Falx cerebri
Lateral
ventricles
Intracranial
hematoma
A Uncus
B
Uncal herniation
Calvarial herniation
Intracranial through craniectomy
hematoma site
C D
Central herniation Subfalcine
herniation
Fig. 61.3 Herniation. (A) Normal relationship of intracranial structures. (B, C, and D) Shifts of intracranial
structures.
TABLE 61.2 Causes of Cerebral Edema There are 3 types of cerebral edema: vasogenic, cytotoxic,
and interstitial. A patient may have more than 1 type.
Cerebral Infections Toxic or Metabolic
• Encephalitis Encephalopathies Vasogenic Cerebral Edema
• Meningitis • Hepatic encephalopathy
Vasogenic cerebral edema is the most common type of cerebral
• Lead or arsenic intoxication
Head Injuries and Brain • Uremia edema. It occurs mainly in the white matter. It results from disrup-
Surgery tion of the blood-brain barrier. This allows large molecules (pro-
• Contusion Vascular Insult tein, blood products) to enter brain tissue. This exposes brain cells
• Hemorrhage • Anoxic and ischemic episodes to toxic products from the blood and results in an osmotic gradi-
• Posttraumatic brain swelling • Cerebral infarction (thrombotic or ent that causes fluid to flow from the intravascular to extravascular
embolic) space. The result is an increase in the extracellular fluid volume.
Mass Lesions • Venous sinus thrombosis Systemic BP, site of the brain injury, and extent of the blood-brain
• Brain abscess
• Brain tumor (primary, metastatic) barrier defect influence the extent of the spread of edema.
• Hematoma (intracerebral, Edema may produce a continuum of symptoms. These range
subdural, epidural) from headache to a decrease in consciousness, including coma
• Hemorrhage (intracerebral, (profound state of unconsciousness) and focal (specific to a cer-
cerebellar, brainstem) tain area of the brain) neurologic deficits. In cases of cerebral
edema, a headache can quickly progress to coma and death. So,
you must be vigilant in your assessment.
Cerebral Edema
There are a variety of causes of cerebral edema (increased Cytotoxic Cerebral Edema
accumulation of fluid in the extravascular spaces of brain tis- Cytotoxic cerebral edema results from disruption of the integrity
sue) (Table 61.2). Cerebral edema results in an increase in tis- of the cell membranes. It develops from destructive lesions or
sue volume that can increase ICP. The extent and severity of the trauma to brain tissue, resulting in cerebral hypoxia or anoxia
original insult are factors that determine the degree of cerebral and syndrome of inappropriate antidiuretic hormone (SIADH)
edema. secretion. In this type of edema, the blood-brain barrier stays
