Course
Objectives Upon
completion of this course, the student will be able to:
Discuss the major components
of the brain
Describe how the different
compartments of the brain are separated
Explain the theory behind
the Monroe-Kellie Doctrine
List the three types of
Supratentorial Herniation
Describe 3 early symptoms of
Uncal herniation and 3 late stage symptoms of Uncal herniation
Discuss nursing care and
management of the patient with increased intracranial pressure
List the 3 goals of therapy
for increased intracranial pressure
Definition
of Herniation The
definition of brain herniation is the protrusion of the brain tissue
from one compartment (of higher pressure) to a compartment of lower
pressure. With this shift of brain tissue, blood and oxygen supplies
are diminished causing herniating tissue to suffer from ischemia,
hypoxia and finally cell death. To better understand the different
herniation syndromes, lets take a look at what the brain is comprised
of and how it is divided. The components of the brain include:
Parenchyma - The
essential tissue (Brain in this case) of an organ distinct from its
surrounding connective tissue. This is the largest intracranial volume
(80%).
Blood vessel - The
volume of blood in the cerebral arteries is an important determinant of
intracranial pressure (10%).
Cerebral Spinal Fluid -
CSF is comprised of fluid in the ventricles and subarachnoid spaces and
is produced by the choroid plexus. Approximately 500 cc is
produced daily (10%).
The
Monroe-Kellie
Doctrine simply states that
in a non-expandable, non-contractable, freely communicating space, the
pressure of the fluid contents and the brain itself, must be directly
porportional to eachother in order to maintain a constant pressure. If
one of these pressures increases, another must decrease in order to
compensate. In
addition to the parenchyma, blood vessels and CSF, the brain is also
comprised of several individual compartments that are separated by
folds of fibrous and relatively rigid dura mater. Two of the major dura
folds include: Falx
Cerebri – which is a double fold of dura mater that drops
into the longitudinal fissure and partially, divides the supratentorial
space into the left and right side. Tentoruim
Cerebelli – this is also a double fold of the dura mater that
forms a tent like partition (higher in the middle), between the
cerebrum and cerebellum. (The area above the tentorium is the
supratentorium space and the area below is known as the infratentorial
space).
Note: Because it is
surrounded by strong bone and it is comprised of several small
compartments divided by dura mater, the brain is at greater risk then
other body organs for herniation. Types
and Location of Herniation Syndromes Supratentorial
Herniation (descending) – There are three major types of
herniation that are caused by expanding supratentorial lesions, these
include: Cingulate
Herniation – This occurs when the cingulated gyrus is forced
under the falx cerebri, displacing it to the opposite side. Cingulate
herniation alone is not considered to be life threatening, but because
it displaces the falx cerebri and can cause compression and/or loss to
local blood supply and surrounding cerebral tissue, it can lead to
increases in ICP, which can contribute other and more devastating forms
of herniation. Signs
and symptoms from Cingulate Herniation are not well defined, but
thought to include:
Increased ICP
Cerebral Edema
Altered LOC
Change in Neuro Exam
Note:
Though Cingulate Herniation is without defined symptomatology; it is
often thought to be a precursor to other more serious herniation
syndromes. Central
Transtentorial Herniation (Central Syndrome) – This occurs
when a downward shift or displacement, pushes the cerebral hemispheres,
basal ganglia, diencephalons, mid-brain and finally the medulla through
the tentorial incisura (notch). Progression of signs and symptoms vary
depending on whether herniation is in the early (reversible) or late
(irreversible) stage. These include: Early
herniation to the diencephalons region (reversible):
Change in LOC
(decreased alertness, agitation, drowsiness)
Pupils are small
(1-3mm) but reactive
Conjugate or slightly
disconjugate pupils at rest
Early hemiparesis or
hemiplegia develop bilateral signs
Purposeful to painful
stimuli
Babinski’s
sign absent
Respiratory will show
deep sigh, yawns and occasional pauses
Herniation
to the Midbrain/Upper Pons (Middle phase of Central Herniation):
Deep Coma
Pupils midpoint (3-5mm)
and non-reactive
Disconjugate pupils
with limited horizontal movement
Decorticate posturing
changes to decerebrate posturing
Babinski’s
sign present
Gradual respiratory
change to sustained hyperventilation
Diabetes Insipidus (not
seen early)
Hyperthermia (not seen
early)
Herniation
to the Medulla (Late phase of Central Herniation and irreversible):
Deep Coma
Pupils dilated and
non-reactive
Absent pupil movement
Flaccid extremities at
rest, occasional flexor response to deep pain
Slow irregular
respiratory rate, ataxia and periods of apnea
Note:
The underlying pathophysiology is that in the early phase of Central
Transtentorial Herniation, ischemia and compression, which are, both
thought to be reversible conditions, are the basis for signs and
symptoms of diencephalic involvement. In the later phase after the
midbrain becomes involved, it is thought that infarction of brain
tissue has begun and it is at this point that the damage is
irreversible. Uncal
Transtentorial Herniation (Uncal Syndrome) – This occurs when
the uncus or hippocampal gyrus (or both), shift from the middle fossa
through the tentorial notch and into the posterior fossa. When this
occurs, there is compression of the ipsilateral third cranial nerve,
then contralateral third cranial nerve and finally the mesencephalon.
When Uncal Herniation occurs, the diencephalons and mid-brain are
shifted to the opposite side of the brain. As with Central
Transtentorial Herniation, signs and symptoms of Uncal herniation are
considered to be reversible in the early stages and irreversible in the
late stages. These signs and symptoms include: Early
herniation to the diencephalons region (potentially reversible):
LOC may not be impaired
initially
Unilateral sluggish,
dilating pupil (Ipsilateral to primary lesion)
Full extraocular
movement
Pupils react to
“Cold Carolics”
No motor function
abnormality
Babinski’s
sign absent
Normal respiratory
pattern and rate
Herniation
to the Midbrain/Upper Pons (Middle phase of Uncal Herniation):
Deep Coma
Pupils contralaterally
fixed and either completed dilated or enlarged to 5-6mm
No extraocular movement
Bilateral decerebration
Bilateral positive
Babinski’s sign
Hyperventilation
(usually with rate 20-4- per minute)
Herniation
to the Medulla (Late phase of Uncal Herniation and irreversible):
Deep Coma
Bilateral and fully
dilated and fixed pupils
No extraocular movement
Flaccid extremities
with occasional flexor response to deep painful stimuli
Slow and irregular
respirations with occasional gasps and periods of apnea
Note:
The result of continued and unresolved downward displacement from any
of the supratentorial herniation syndromes is ultimate brainstem
herniation. When the medulla, which controls such vital functions as
respiration and cardiac function, herniates into the foramen magnum,
death is immediate. Infratentorial
Herniation (ascending) – Lesions of the infratentorial
compartment that contribute to herniation are much less frequent then
supratentorial herniation syndromes. Included in the infratentorial
compartment are the brainstem and the cerebellum. There are three
possible effects of an expanding lesion in the infratentorial
compartment and they include:
Direct compression of
the brainstem, cerebellum or the vascular supply to each area
Upward transtentorial
herniation of the brainstem and cerebellum
Downward herniation of
one or both cerebellum tonsils through the foramen magnum, to the
cervical spine. When this occurs, the medulla is compressed and death
is immediate.
The signs and symptoms
of an Infratentorial Herniation vary widely depending on the brainstem
involvement. In addition to medullary compression, an infratentorial
lesion can also encroach on a portion of the ventricular system (3rd
and 4th ventricle), which causes acute hydrocephalus. Nursing
Care and Management of Increased Intracranial Pressure:
Monitor LOC using
Glasgow Coma Scale (or other objective scale)
Assess motor response
(bilaterally)
Check for positive
Babinski’s sign
Assess sensory
responses (place emphasis on side opposite of injury)
Include the following
in assessment of pupils:
Comparing pupil size,
shape and equality bilaterally
Check pupils with the
direct light reflex (check each eye individually)
Check that pupils are
equal, round reactive to light accommodation (PERRLA)
Assess 6 cardinal
fields of gaze (Cranial Nerves 3, 4 and 6)
Assess for
Doll’s eye phenomenon in unconscious patients (indicates
brain stem damage)
Monitor vital signs
(Notify MD for deviation from set parameters)
Provide nursing
measures r/t respiratory care including:
Suctioning
ABG’s
Providing O2
Monitoring O2 saturation
Monitoring ventilator
settings
Position pt to maintain
venous outflow from brain
Elevate HOB to 30
degrees (except for dural tear)
No pillow under head
(can interfere with venous flow)
Turn by logrolling q 2
hrs
Administer prescribed
medications
Control noise and
stimuli
Provide rest/activity
balance (stagger tasks)
Maintain desired
temperature range (use antipyretics or hypothermia blanket)
Provide nursing care to
prevent damage to eyes, skin, oral mucous
Marini,
J., J. & Wheeler, A., P. (2006). Critical care medicine: the
essentials.(3rd ed.). Lippencott, Williams and Wilkes. Philadelphia Arbour,
R., (2004). Intracranial hypertension: Monitoring and nursing
assessment. Critical Care Nurse. Oct. 2004. Hickey,
J., V., (2002). The Clinical Practice of Neurological and Neurosurgical
Nursing. (5th ed.) Lippencott. Philadelphia S Peterman,
G., M.D., & Smirniotopoulos, J., G., M.D. (2005). Brain
herniation. Retrieved on December 5, 2006 at: http://rad.usuhs.mil/rad/herniation/herniation.html Neurological
Nursing NU 454. (2000). Retrieved on December 20, 2004 at: http://www.muw.edu/nursing/acuteneuro.html
Nursing CE Course
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